Graph about cancer

Cancer: Discussion & Support

2008.06.17 23:23 Cancer: Discussion & Support

This is a place for people with cancer and caregivers who are asking specific questions to come together and provide support for each other.
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2015.07.02 19:04 SulfurousAsh GraphQL

A place for interesting and informative GraphQL content and discussions.
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2012.09.22 10:13 bc87 All about Graph Theory

Nodes and edges.
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2024.05.07 04:42 JustthatoneDoomguy Transmogrified Imperator: Metamorphosis

A little idea that I had, Evolved Godzilla in GxK was just way too fucking cool, and I feel he was kind of underutilized. Especially for the extra little additions he had in his design, and in this story I want to put him up against the main threats that Goji himself had previously fought in the Monsterverse, just with his evolved state instead.
Will this be fair? Absolutely not lol, but will it be fun to write? Hell yeah.
Ao3 link if you want to read it there: https://archiveofourown.org/works/54956917/chapters/139311436
No one could have foreseen such a catastrophic event.

Ishiro Serizawa's heart pounded in his chest, threatening to burst entirely as sweat poured from his weary head. He couldn't sit straight upon the metal seat he had confined himself to, no one at Monarch could say otherwise too. The subtle rocking of the aircraft carrier certainly didn't help the pounding sensation in his head either, further adding to the stress placed upon the old doctor's mind. The sleepless nights ever since... it broke out had taken their toll upon the man, his brows furrowing as he clasped his hands together.

He had seen it for himself after all, to say Janjira was an absolute disaster would be the greatest understatement in the past century of human history. They thought they had everything under control, how could they not at this point? They had studied it for a decade without an end in sight, making sure that they could pull the plug on it. The kill field around the spore was capable of outputting enough electricity to power half a damn city...
And it shrugged it off like it was a jolt of carpet static.
In hindsight,he could do nothing but mentally curse himself over their own hubris. Monarch had become another example of mankind prancing its supposed control over the world, and the world was quick to put their arrogance into the ground. Nature came knocking, and its message was one that was echoed through the annals of human history.
Nature was a beast, a beast like no other. No amount of technology, science, religion or whatever else Mankind could conjure would ever be truly able to conquer and tame it. The creature that sprouted from the ancient spore exemplified such a thought like no other. Those deep crimson slits it had for eyes spoke of total and utter malevolence, like the world itself bored back into their souls... seeing red at them playing god.
"Sensei..."
He was broken out of his crushing thoughts upon the soft voice of one Doctor Graham, who was quick to sit beside the Japanese man when she had seen her mentor so deep and stuck in thought. The brit was always a comforting presence to him and to many other people at Monarch. Even if it did little to alleviate the old doctor's stress at the moment, it was something at the very least.
"Ah, Forgive me for my current state... there has been much on my mind."
A dry scoff emanated from the woman upon hearing his words, looking to the side of the doctor's head.
"There's been a lot on everyone's minds as of late."
Her shoulders sagged as she sighed, a finger of hers going up and rubbing one of her temples. The old doctor leaned back a little, looking up at his apprentice who looked no better than him in this state. The bags under her eyes said it all, she too was at the containment site when the creature emerged. They were lucky to have escaped relatively unscathed, the same could not be said for the Brody's.
"Has it been located?"
The old doctor's thick accented voice asked, rearing his head from his palm to look towards his apprentice. The expression on her face said it all, the shake of her head only cemented such a fact. The thought of that creature, being completely left unattended to and free to wreak havoc upon... anywhere for all god knew in the world was beyond horrifying to Serizawa.
"No... but I saw something in the audio readings..."
She paused, standing up and going towards one of the computer screens of the control room they were in. Tapping on the keyboard and bringing up something on the green tinted screen. The old doctor sat down in front of the computer, seeing that it was the audio patterns recorded through the minutes of hell when the creature broke free. He was unsure on what Graham wanted him to see, but she looked over from behind the screen and briefly gazed at him.
"Keep scrolling, before the EMP." She urged, as he complied to her request. Skimming through the readings, just seeing the spikes in audio through the graph made those chilling noises ring out in his ears again, but he kept going.
"This." She pointed and tapped on the screen, an all too familiar pattern to the both of them at this point. The call of the thing. But what really caught his attention was what sat right next to it.

A second call... a response.
Serizawa looked back to his apprentice at the realization of such a thing. It couldn't have been... could it? That second spore...
"A response." He muttered, his eyes wide as he considered the possibility of another MUTO having been awakened. But how? That second spore from the Philippine dig site that decade ago was wheeled off to storage probably far, far away from any source of radiation, unlike the spore in Janjira...At least to his knowledge. Writing this fact down onto his notes, he pondered such a scenario. As if things couldn't have possible gotten even more grim for not only Monarch but the world.
Vivienne went off to talk about with the other personnel present in the room, but quickly the attention of all those present was drawn to something else.
"We've received reports of a nuclear Akula 50, disappeared about 50 nautical miles from Hawaii." The voice of the officer was both heard by Admiral Stenz and the two Monarch scientists in earshot. Instantly that caught their attention, making Serizawa spring up from his seat and Vivienne to look over to face the Admiral. Stenz's gaze upon the two scientists still exhumed an underlying hint of contempt, one that the both scientists picked up on but disregarded for the time being. There were far better things to worry about at the moment anyways.

"A Russian sub's up and disappeared off the coast of Hawaii... could be the Muto." The admiral reiterated their own assumption that they thought of, and the screens behind the Admiral showed that they were about to get their answers soon enough...

---


The depths of the world were a place that human hands had not touched in many millennia. In times immemorial, when man walked alongside their gods... their titans, both lived in coexistence with each other. It was not one without conflict of course, but it was an existence of stability thanks to the efforts of beings were larger than life, to the eyes of men who were but ants to their splendor.
But as time flowed and the great wars began, when the aureate storm came and ravaged the lands, and when the crimson tyrant obsessed over total dominion upon nature...

One stood.

A king amongst the old gods of the world, the one that cheated death. The last one of a once great race, a guardian to all those who sided with his cause, that being the continued stability of nature. But to those that basked in anarchy, spreading it forth like a malignant cancer...
He was a monster.

And as the great wars raged on across the lands, the monster set forth upon innumerable battlefields. The auric wings of destruction found their match against the wrathful king, forging a rivalry etched into the very fabric of the world. The crimson tyrant learned to feel fear in his blackened soul, weeping in the shadow of the God-King.
In the end of it all, the king emerged victorious. But it was not a victory without bloodshed, not only of his enemies and himself but also of those he held dearest to him. The unwavering martyred in his name, The little ones caught in-between the battles of titans, his beloved queen...
Never again, he promised to himself. For all his might he couldn't save them. The queen would return, he knew that she wouldn't just fade away into nothingness like that. But that never erased the sorrow, the pain, the grief on his soul. He may have won the wars in placing the golden death in an icy prison and locking away the crimson tyrant deep below, but he was nearly destroyed in the process.
Defeat was never an option, and the wars had been the absolute closest the lord of the titans was to being gobbled up by the jaws of defeat. As of late the king of the monsters had decided that his form was not sufficient enough to cement his dominance over his enemies. Evolution was in order, to be a proverbial step ahead over what threats lied in wait, threats that he knew would come one day to jumpstart the cycle once more.
Evolve he did, the primordial minerals of the Hollow was something his kind always had been able to utilize, blessed with the ability to draw power from the crystalline materials. That was how they were blessed with their fire after all, but some sources yielded more interesting results. Said sources however were considered taboo to him and his lot, as there was really no telling what could possibly come out of consuming such things, the ones that did try usually succumbed to madness or explosive demises at the hands of volatile energies.
It was a gamble really, but one that ended up paying off. That fucshia-tinted nest of the serpent was quite the deposit of the volatile energy, one that she would never have let go without a fight. She was to be removed and besides, he already had a distaste for Tiamat anyway. Robbing him of the satisfaction of bringing down the rival that had cast him out from his territory long ago, and having the gall to side with the Golden One in the great war, and her being in the way of power that would make his job easier in the future was another thing to add onto the pile.

It was either her life or the world potentially being in jeopardy in the future.
A very easy decision that was to the leviathan.

Now transmogrified in the depths he remained, the crushing pressure of the entire ocean at this level made sure that very little life persevered here, let alone life that was intelligent enough to do anything to pose a threat to him. He rather enjoyed the relative silence, the only things being audible to him was the low churning of the rock all around him and the water rushing against his gargantuan form as he effortlessly glided through the water. Some peace and quiet was exactly what he sought, taking in those magenta crystals was quite the process he had to endure, but one that was worth the time to evolve.
The new form that he wore now was taking some getting used to, it felt like he had put on a completely new layer of skin to replace what once was. The lack of bulk in some areas was something he would have to rectify at a later occasion, but even then he hadn't felt so spry and filled with energy in a very, very long time. The more armored scales all over himself was something that he very much appreciated, the extra plates on his elbows and tail-tip were welcome additions of weaponry to use. Sustenance was in order if he wanted to regain his bulk and his home deep below would be able to quell the hunger he felt at the moment.

The peace ever since the last freeze proved to be a long one, but peace never was a permanent thing especially to him despite how much he would yearn and plead silently that it was. Despite the little ones unearthing him relatively recently, nothing seemed to come of it except for the strange incident at the remote atolls. Whether the little ones wanted to feed him or kill him was something that still eluded the leviathan but he definitely was displeased at seeing the damages that were incurred by the strange cylinder's detonation.
Continuing to trudge through the abyss and back to his home, the thought of him being overtly paranoid about all this crossed his mind. The innumerable sun cycles ever since the deep freeze started by the mother of ice marked a strange and silent point in his existence. At first it seemed too good to be true, but that first millennia going by without incident after the freeze started lulled him into a sense of security. Perhaps he was being overtly cynical about all this, evolving for threats that may never rear their ugly heads ever again. Had the Moth been around, perhaps the two of them could have finally gotten to "living a little." as the queen said to him.
A low grumble escaped the leviathan's throat, unheard to anyone in the depths as those bitter memories reemerged. How much he had wanted to have the "happy ending" that the goddess wanted not only for her, but for the both of them. A true sense of happiness was something that became a rarity to him long ago, when the wars first broke out at the auric death's arrival, it might as well have died alongside the queen in the last stretch of the conflict. He knew she would return, she would never be content to just fade way like that, even if it took millions upon millions of sun cycles for her to return, he would count down each and every day. In the meantime, he would ensure he did her and his own kind proud, continuing to tend to the lands as they always had done. But for now, home was calling.
When she did return, he would make sure that she would never fall to death's clutches ever again.

Come heaven or hell, he would make sure of it.


---

The air was tense upon the carrier, the two doctors watching the screens displaying the body cams of personnel on the ground. If a Nuclear submarine had gone up and missing near a relatively high-populated area like Hawaii would definitely be a cause for concern.

Especially considering there was a two hundred foot tall winged monster on the loose.

The nuclear submersible disappearing alongside the fact that the titan's main source of nourishment being radiation certainly painted a grim picture in their heads... that thing possibly being around, completely free to trample over the isles was a mortifying thought. The possibility of Monarch's secrecy to the public had now completely gone up in flames, but that was secondary to the potential millions that the existence of but one active titan could do. It was a nightmare born straight out of the darkest conceivable timeline to both Dr Graham and Serizawa, the top priority now in this dire situation would be to get a visual on the MUTO, and assess how to deal with it from there.
The men continued to march through the brush, being watched over by the two doctors from the screens, the night vision of the body cameras still doing little to give the clear picture to both of them. The disturbance that was picked up by the military at the very least was being taken completely seriously, both men on the ground and the air force had been called in for this, for a disturbance near Honolulu, combined with that sudden disappearance of that sub on top of the MUTO's escape probably had everyone on edge at the moment.

"We played god..." The old doctor thought to himself. How much he wished he could turn back time, destroy the damn spore the moment it had come to Janjira and nestled itself atop the irradiated wasteland. Nature was certainly giving him and everyone else at Monarch a hell of a lesson in not playing with flames they should never have even stoked in the first place.
"The consequences were bound to rear their heads at us eventually." Another thought ran through his mind, as he wiped the sweat from his weary head. Were they even able to do anything to the creature had they found it? He hated to be pessimistic, but considering the kill field around it's spore didn't even earn so much as a twitch from the thing as it was electrocuted... he had his doubts.

Though now... the prospect of him emerging again became very, very real.

"Gojira..." The old man whispered under his breath, to which his apprentice picked up on.
"Do you think he will come, sensei?" Graham replied back.

Had the tales been true, the old legends of a wrathful king emerging to weed out anything and everything that threatened the natural balance, Serizawa could only pray that forgiveness was something in Gojira's forte. They certainly did not give the King of the Monsters a welcoming taste of the modern world considering the in retrospect, utterly futile attempt on the King's life back in 1954 with Castle Bravo.
The aged man reared his bespectacled head to Graham, a look of uncertainty shining through his eyes.
"If the tales are to be believed... he will come. Nature's power will rise to alleviate the blight we have wrought upon it."
"We can only pray, that he does not consider us among the blighted."
Such words made chills run down Vivienne's spine, when Serizawa spoke in that way, she knew he was being more than serious. Others may have called his reverence of Godzilla as ludicrous, foolish even for placing his faith to tales of ancient 'uncivilized' humans, venerating what was 'just' a big animal. Serizawa saw it differently though, and while she couldn't exactly know why, she too believed in the old man's faith.
"I suppose we'll see." The English woman replied back, uncertain yet cautiously optimistic about it. Had Godzilla emerged due to the MUTOs, he would likely be at very least, focusing on them first and foremost. Whether he somehow knew that humanity was responsible for their reawakening was a scenario that she silently pleaded not to happen.

The eyes of all in the control room returned to the array of screens showing the men finally laying their vision upon something... it was hard to make out from the fuzzy vision of the cameras projecting the image and the nighttime darkness, but there was some sort of vague shape stuck up in the tree line. Was it the creature again? They got their answers quickly, when the group reared their lights upon the shape...
"Looks like we found your Russian sub." The stunned voice of one of the soldiers came over the comms, his camera completely frozen and transfixed upon the vehicle in very much not the appropriate terrain for it.
To everyone's total horror it was indeed the very submarine that was reported missing, stuck dozens of feet up in the tree line and from the looks of things, covered in some sort of viscous substance. Both the people watching from the carrier as well as the boots on the ground were all in utter shock, there could only be one thing responsible for the submersible's current predicament. The searchlights from the choppers above quickly got to scanning the immediate vicinity and from behind the suspended submarine... there was movement.
The choppers reared their way towards the flanks of the submarine, and everyone both watching and on the ground at that moment gasped from the sheer horror. It was not immediately spotted, but now with the illumination upon the side, the abyssal tinted hides of the MUTO once again showed itself... those crimson slits it had for eyes shining at the cameras like the uncaring gaze of a malevolent demon, the almost insectoid creature's dagger toothed jaws had been clamping down and munching upon the nuclear payload of the submarine. Just like they had suspected, these titans fed upon radiation. The question of if this MUTO was feeding just out of hunger or for something else crossed Serizawa and Graham's minds, but their current shock pushed it into the back of their minds.

"Cat's out of the bag now doctor..." The admiral's glare at Serizawa now returned, still maintaining a sense of calm but subtly the Doctor could tell that the current situation had definitely struck a chord within the man.
"No more keeping things under wraps, the public's safety is our utmost priority now." The admiral added, before going off elsewhere in the room as nearly everyone was sent into a complete panic as all hands on deck were sprung into action quickly, for the situation has now reached levels of potential danger that bode a grim outlook upon the local population on Hawaii.
Amidst all the panic now though, the doctors overheard another announcement from an officer manning the Radar...
"Second signature's coming in from the Pacific!"
Immediately, both doctors present knew immediately just who was coming... and just how utterly out of proportion this horrid situation that they already found themselves in had just gotten.

The king was coming.

For decades the great leviathan had remained docile and under the radar despite the uncalled provocation that was the welcoming he had received from Humanity in 1954, but now that Humanity had truly tipped the scales of the natural balance in a way that had never been shifted for countless millennia. Nature's power was to be called upon once more and Serizawa definitely wanted to be one of the first to witness such an event.
He sprung into action, quickly making his way out of the control room and into the busy halls of the manic carrier.
"Where are you going?!" Graham shouted as she followed the old man, nearly falling over due to the sudden rush.
"I have to see this!" Serizawa yelled back, his stride not breaking in the slightest as he practically sprinted for the main deck of the aircraft carrier.

As if History hadn't already been changed enough with the return of a Titan, now the very King of all the Titans was now coming. From the tales he knew of Gojira, while benevolent to the continued safety of the Planet he was also as capable of destruction like no other. As wrathful as he was merciful, for he himself was a true paragon of the two sides of Mother Nature itself, like the oceans as beautiful as they were yet capable of raging like no other...

He could only pray the his mercy graces humanity.

---

He had heard it.

Those familiar calls... reverberating through the murk, immediately being picked up by his senses.
A parasite.

The time of peace and introspection had now passed... and a king's work had to be done. Disorder had dawned upon the lands once more, and his services had been called upon once again.
Effortlessly, the leviathan shifted his course from headed back towards his undersea home and in the direction of the calls. The water around him raged and surged, heralding the king's incoming movements as he began to rise quickly towards the ocean surface from the crushing depths. This new body of his already proved its usefulness, the increased levels of energy that surged all around every ounce of his being giving him far greater speed than ever before. All that much better to address this tumor upon the balance he had tended and watched over from the shadows for all this time.
Rising and rising ever closer towards the water's surface, the moonlight gleaming through the waves that now swelled to be as large as trees to the beast's gigantic body waded past the waves. The adrenaline running through Gojira's veins were much like the very waves that he had kicked up now, driving him further and further as he felt his dorsal plates protruding above the ocean and knifing through the frigid air.
Focusing his eyes forwards and now seeing the deep abyss of the ocean give way to outline of land beneath the waves, he was close to making landfall now. Rearing the still massive bulk of his evolved form further and further towards the surface as he continued to trudge along... the subtle swishing of the air was audible to him, followed by the beating of what seemed to be... wings?
His momentary confusion was only furthered, as beams of light from all around traced over him and the beating and swishing grew louder and more intense as he travelled closer and closer inland. Averting his eyes up above and even through the rough waves he was kicking up, the lights seemed to have been coming from strange creatures that were tracking and following him as he swam.
They were nothing like he had ever seen before, those 'wings' that he had heard earlier spun around in a circular motion atop their strange looking frames, the lights attached to them were more like lamps that the little ones would use though even these ones were nothing like what he knew. What was stranger still, was that he could sense the little ones riding these metallic looking 'birds'. Truly strange creatures they had tamed, or maybe had even created but that was of little concern to him now.

If they still knew who he was, then they would stay out of his way.

Looking forwards once again now, the king was forced to slow down his current pace as what seemed to be an island came into his trajectory. Only upon another momentary inspection... this was no island at all. It was floating atop the water, the metallic material that made up it's land was a hallmark of being made by the little ones, much like the 'birds' that were illuminating him at the moment. It was less of an island and more like a manmade whale, and here too he could sense countless amounts of the little ones within and atop the 'whale'.
Rearing his body down below the waves once more, his dorsal plates narrowly missed ripping straight through the 'whale'. They were not his concern at the moment, and it would do him nothing to cause needless casualties towards the little ones when a potential disaster was running amok on the lands ahead.

Leaving the metal 'whale' behind but still having the 'birds' follow him from above, he picked up speed once more.

Land was ahead now... and a legend would voice his will once again.



















submitted by JustthatoneDoomguy to Monsterverse [link] [comments]


2024.05.02 07:03 UstroyDestroy AI Advancements: Hugging Faces Computer Vision Course, Coheres Partnership with MongoDB, and NVIDIAs AI Research with MIT

startups #tool #event #release #leaders #science #vc #bigtech #hardware #api #feature #update #paper #major_players #scheduled

The Hugging Face community has launched a computer vision course as part of its educational resources aimed at democratizing artificial intelligence through open source and open science [1]. Cohere has announced a partnership with MongoDB to assist enterprises in developing advanced AI applications using their scalable Command and Embed models [2][3].
Demis Hassabis, in his first TED Talks appearance, discussed the potential of AI in accelerating scientific discovery and solving major issues like cancer and climate change [4]. Goldman Sachs' secret weapon during the 2008 financial crisis was the SecDB, a real-time risk data tool. In a podcast episode of "In The Vault," RMartinChavez discusses how this technology edge influenced the crisis and how AI is set to revolutionize finance [5][6].
Google has introduced five AI-powered tools aimed at enhancing outdoor experiences and providing useful information for outdoor activities [7]. NVIDIA AI Developer has announced a new ChatRTX update with more LLM models, image search, and voice support, aiming to enhance AI capabilities on RTX-powered devices [8][17]. NVIDIA has also achieved significant advancements in AI research with MIT, including 48X SAM acceleration with no quality degradation and the development of usable apps and UI code using TensorRT [9].
NVIDIA AI Developer announced the release of DBRX, a large language model developed by Databricks, optimized with NVIDIA NIM for improved performance [10]. A webinar titled "Empowering Future Engineers and Scientists With AI and NVIDIA Modulus" will discuss the integration of physics-informed machine learning (physics-ML) with NVIDIA Modulus [11]. NVIDIA and Red Hat are partnering to reshape the landscape of AI in the enterprise, with a keynote featuring NVIDIA's Justin Boitano and Red Hat's Stefanie Chiras at the Red Hat Summit [18].
Satya Nadella has shared a commitment to building and deploying AI responsibly, releasing an inaugural report detailing their approach to AI [12]. The user's messages cover a wide range of topics related to high-performance computing, AI/ML, and hardware architecture, including various talks and seminars, discussions on the Fugaku supercomputer, high-performance sparse tensor operations, and the use of FPGAs for cloud-scale inference at Microsoft Bing [13].
Groq Inc has made API keys available to anyone and is co-sponsoring the first-ever Llama 3 hackathon at SHACK15 in San Francisco [14][15]. Groq Inc has been recognized as a leading provider in the LLM market and is poised to play a significant role in AI model development in the future [16].
AI is transforming retail by enabling personalized promotions to enhance customer engagement and increase profits [19]. Daniel Rohrer, VP of Product Security at NVIDIA, will be participating in a keynote panel at #RSAC, discussing the rise of AI safety and its implications for the future of AI and cybersecurity [20].
Google AI is excited about an upcoming event and encourages followers to register for I/O [21]. The Google Research Scholar program for 2024 has selected 78 professors from 55 universities and 14 countries to work on various projects related to a wide range of research areas [22]. The Google AI team has developed the TeraHAC algorithm for hierarchical agglomerative clustering of trillion-edge graphs [23].
Anthropic has introduced a new Team plan and iOS app for Claude, offering increased usage for team members, easy user and billing management, and the ability to tackle complex tasks with a large 200K context window [24][25]. Anthropic AI will be releasing collaboration features in the upcoming weeks, which will include citations from reliable sources to verify AI-generated claims and integrations with data repositories like codebases and CRMs [26]. The Claude iOS app by Anthropic is now available for download on the App Store, offering users an AI assistant for tasks ranging from writing to analysis to math [27].
Anthropic offers an AI assistant named Claude that aims to boost team productivity through knowledge sharing, research support, and cross-functional collaboration [30][31][32][35]. Claude from Anthropic AI assists in saving time for teams by streamlining tasks from brainstorming to execution, allowing them to focus on important tasks [33][34].
1. Hugging Face @huggingface https://twitter.com/huggingface/status/1785624867473097157
2. cohere @cohere https://twitter.com/cohere/status/1785645731367297487
3. cohere @cohere https://twitter.com/cohere/status/1785645733091172629
4. Demis Hassabis @demishassabis https://twitter.com/demishassabis/status/1785646721252336084
5. a16z @a16z https://twitter.com/a16z/status/1785640581726654674
6. a16z @a16z https://twitter.com/a16z/status/1785675159216476245
7. Google @google https://twitter.com/google/status/1785669675319169025
8. NVIDIA AI Developer @NVIDIAAIDev https://twitter.com/NVIDIAAIDev/status/1785691749785997813
9. NVIDIA AI Developer @NVIDIAAIDev https://twitter.com/NVIDIAAIDev/status/1785704487815934263
10. NVIDIA AI Developer @NVIDIAAIDev https://twitter.com/NVIDIAAIDev/status/1785716121087152248
11. NVIDIA AI Developer @NVIDIAAIDev https://twitter.com/NVIDIAAIDev/status/1785761115214930241
12. Satya Nadella @satyanadella https://twitter.com/satyanadella/status/1785714562601529831
13. Groq Inc @GroqInc https://twitter.com/GroqInc/status/1785660443958100367
14. Groq Inc @GroqInc https://twitter.com/GroqInc/status/1785714196904358280
15. Groq Inc @GroqInc https://twitter.com/GroqInc/status/1785732226052767900
16. Groq Inc @GroqInc https://twitter.com/GroqInc/status/1785777460480495861
17. NVIDIA AI @NVIDIAAI https://twitter.com/NVIDIAAI/status/1785685931845956050
18. NVIDIA AI @NVIDIAAI https://twitter.com/NVIDIAAI/status/1785702673590706252
19. NVIDIA AI @NVIDIAAI https://twitter.com/NVIDIAAI/status/1785746033160470765
20. NVIDIA AI @NVIDIAAI https://twitter.com/NVIDIAAI/status/1785808359397941322
21. Google AI @googleai https://twitter.com/googleai/status/1785713270659400055
22. Google AI @googleai https://twitter.com/googleai/status/1785758220558242202
23. Google AI @googleai https://twitter.com/googleai/status/1785763979748601888
24. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785685692988940509
25. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785685699183972828
26. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785685697275552210
27. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785701418546180326
28. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785785917967634545
29. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785785997374169128
30. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786122972623320
31. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786210243461220
32. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786262072578419
33. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786296075682138
34. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786333002416357
35. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786358587666592
36. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786385309569149
37. Anthropic @anthropicai https://twitter.com/anthropicai/status/1785786418004205676
submitted by UstroyDestroy to ai_news_by_ai [link] [comments]


2024.05.01 18:32 Note4forever YSK Academic Search engines that leverage Large Language models for capabilities - a view of the landscape and some advice.

Introduction
Hi all, since I wrote the wildly popular - YSK There are free literature review mapping tools that can automatically generate relevant related papers based on relevant seed papers + visualize them in a map/graph in 2020 (See my list of citation based literature mapping tools), the effectiveness of Large Language Models (so called "AI) meant new capabilities could be added to search (I focus obviously on academic search).

As an aside, I see many people lumping ConnectedPapers, ResearchRabbit etc into AI tools. While I think "AI" is a loose term, we probably want to distinguish tools that use LLMs and those that do not to better understand their strengths and weaknesses. ConnectedPapers for example tell me that they do not class their tool as a AI tool. Typically these tools use network or bibliometric techniques to recommend papers not LLMs. Some tools like Litmaps may be starting to use semantic search (contextual embeddings) to recommend papers on similarity of titles and abstracts but this isn't common yet. Another possible use I have seen is tools like CiteSpace use LLMs to label clusters
One of the first user facing commerical academic tools was Elicit (now Elicit.com), that was an early partner of OpenAI using GPT3/3,5 (Perplexity.ai was the general web counterpart) since 2021. Since then the number of academic search tools that leverage on LLMS have exploded.
Some of the earliest offerings are naturally from startups including Elicit, Consensus.ai, Scite.ai assistant, Scispace, OpenRead , Wonders AI , Epsilon.ai .
But traditional players in the academic search space and publishers have also responded e.g Scopus AI, Dimensions Research GPT, and Clarivate which owns a huge chunk of the academic workflow via Proquest databases and Web of Science and Exlibris Summon, and Primo have also responded with their own AI offerings that will be out by end of 2024. These include Web of Science™ Research Assistant, Proquest Research Assistant, Alethea Academic Coach.
Academic librarians reading this should be aware that in particular, Primo and Summon (which are the default search engine on most academic libraries) will launch the CDI Research Assistant by 2Q 2024, I do not believe this is a optional module, so by end of 2024, all your users will see direct generated answers!
See my list of academic search systems that use Large Language Models to generate answers (I exclude academic search that only use contexual embeddings for search ranking). I also exclude "ask PDF" type tools where you upload papers where such tools do not include an index of their own.

Three ways - Large Language models are used to improve search
I see three main ways in which LLMs are used to improve academic search engines
  1. LLMs are used to improve relevancy of search (semantic search)
  2. LLMs are used to extract answers to directly answer questions by extraction of text from papers
  3. LLMs are used to create "research matrix" of papers by extraction of text from papers (this is special case of #2)
See Possible impact of AI on academic search video

  1. LLMs are used to improve relevancy of search (semantic search)
This is probably the least appreciated of the changes since everything changed is under the hood. In the field of information retrievial , researchers talk about a 2019 "post BERT" (this is a "cousin" of the more famous auto-generative GPT, but both based on the transformer architecture) revolution , where the ability of search engines to understand queries and docs has drastically improved due to the incorporate of transformer based architeures like BERT, leading to huge improvements in info retrieval benchmarks results.
From the user point of view, this means that a typical "AI powered search" using contextual embeddings can "understand" natural language queries.
There are multiple terminology used to talk about this new type of search including embedding based search, neural search, semantic search etc.
Not only can you use natural language when searching, there is evidence both from formal studies and my own ancedotal testing that you actually often get better results searching in natural language than trying to search "keyword" style where you drop stop words (this can be very counter intutive after two decades of web searching).
Without going into detail, the latest information retrievial algos go beyond old bag of words techniques (BM25, TF-IDF) and can actually take into consideration not just the context of words but also the order of words. In other words the long promised Semantic Search!
If you are interested in a high level overview see this blog post
If you consider how ChatGPT can understand you well even with typos, this shouldn't surprise you!
That is why the results are actually better if you search in natural language! Google and Bing for example has already implemented BERT into interpreting search as far back as 2019! In Google's example, they show how Google is able to interprete correctly
2019 Brazil traveller to US need via
as a brazil traveller going to US as opposed to the other way around.
Let me give you an academic example. I was reading this news story from The Mirror that reported a research study on the risks of cancer by occupation,annoyingly like many news story it did not directly link to the research paper, nor give the title and author of the paper. It just stated a team from... and the journal.
By taking the full-text of the story and tossing it into either Elicit or Scispace, you would find the very first result in the search is the paper! This is amazing when you realize a lot of the text from the research paper has been paraphrased in the news and yet the semantic search was able to figure out the right paper that was closest in meaning!
Note this is not to say that keyword or lexical search is outdated, there are situations where it shines over "semantic search" for example when searching for very specific entities like proper names or protein names where you do not want "similar" entities. See for example this study.
A good way to combine two techniques is to use keyword or even boolean first, then use semantic search tools to see if you missed out anything (because a different keyword was used).
Alternatively if you have very little sense of what are the right keywords, use a semantic search based search engine like Elicit, or Scispace and look at what relevant papers appear. Then use those for structured keyword searching.
In practice many modern academic search tools like Elicit.com, or Scispace combine results from both keyword/lexical search and semantic search before reranking so you will be looking at combined results from both sets.
In pratice it can be hard to tell if the academic search you are using is using semantic search (there are lexical keyword search methods that are non-boolean) but in general if you can throw in a large chunk of text and there are still a lot of results, it is highly suggestive of some sort of closest neighbour embedding match of query and document,,,,

Adapt your search style depending on tool
In fact there are now three possible ways of searching which can be confusing
  1. Traditional Keyword search - - fasting regularly longer life spans
  2. Natural language search - Does fasting regularly lead to longer life spans
  3. Prompt engineering style - You are a top researcher in the area of longivitiy. Do a deep literature review on the topic does fasting regularly lead to longer life spans. Do include emperical studies and meta analysis but exclude opinion pieces...
The third style is still somewhat rarely supported by AI academic search, but some like Scite.ai assistant , Undermind.ai do so.
When using these new tools, pay attention to the hints they give on how to search, either in support documents, or the examples used in their marketing material or demos. Or if all else fails ask their engineers.

2. LLMs are used to extract answers to directly answer questions by extraction of text from papers
This is probably the most eye catching feature for most people. These new Ai powered search, will in fact cite text from papers to generate a direct answer instead of just providing a list of documents that might answer the question!
How does this work? Almost all such systems use variants of the popular RAG (Retrieval augmented generation) technique. In a typical example, a retriever (search engine) is used to find documents (or more commonly sections of documents) that might answer the question.
How it finds relevant documents or chunked text is typically using a semantic style search from #1, though in theory it could do traditional keyword search or even ask a LLM to come up with a boolean search strategy (see CoreGPT.
The chunked text of retrieved text is then passed over to the LLM with a prompt to ask it to try to answer the question if possible with the retrieved chunks of text (typically it is also instructed to say it does not have a answer if it is appropiate).
I've seen systems use RAG to answer questions in two ways.
Firstly and more commonly, the system will generate a paragraph or two of text trying to answer your query from the top N papers in the search (e.g. Elicit, Scispace, Scopus AI). More customizable ones like Scite.ai assistant allow you to customize things like number of references, length of generated text, search strategy used to find papers, where every generated statement needs a citation (or let the model decide) or even specify they must cite from a pool of papers etc.
These new AI search indexes tend to have mostly title and abstract from sources like Semantic Scholar, OpenAlex, Crossref and while this is almost always comprehensive for titles and abstracts (200 Million etc, though this inclusive set means you won't get only high impact journal papers), they tend to draw only on limited full text that is open access, this is why many tools are starting to allow you to upload full-text to supplement it. (e.g. Elicit, Scispace, Scite.ai assistant)
Secondly, there are some systems that only try to generate one answer per paper with no attempt to merge everything together into one coherent answer . e.g. Wonders AI , Studyflow , Consensus.ai used to only do this, but it now as a synethize model that creates a paragraph of answer with cites from multiple papers.
Caution : Many vendors of such tools will claim their tool is 99.9% free of hallucinations.
Often what they mean is a very limited way of defining "hallucinations". Often this is just saying that the papers cited using RAG techniques will always be real papers (as they were retrieved from search) unlike the free ChatGPT that might hallucinate or makeup papers. This is like the difference between asking you to try to remember which papers might answer a question (ChatGPT free) and asking you to use Google Scholar to find papers that are relevant first and cite them.
GPT4 (either via ChatGPT+ or GPT4 API) hallucinates less than earlier models but if it is not triggered to search it can hallucinate papers too.
The main issue is while RAG based search will not make up papers they can still "mis-interprete" papers. In other words, the generated statement might cite a paper but when you look at the cited papers, it does not support the generated statement or answer at all.
One of the earliest papers on the subject using Bing Chat, Perplexity and two other general web search using RAG, found that on average mere 51.5% of generated sentences are fully supported by citations and only 74.5% of citations support their associated sentence. It also provides a scary result where they found people who rated the generated answers as "helpful" or "fluent" these answers were negative correlated to citation precision and recall. In other words, fluent and useful answers tend to have invalid citations! If you think a while, you can understand why this is so....
There is now hundreds of papers studying when and how RAG fails.
It's a difficult problem, and there are many ways RAG can go wrong, and hundreds of proposed techniques to address this as this is an area of active research.
Unfortunately currently there isn't a lot of rigorous research out on the accuracy of RAG generated answers for specific tools, there's for example a mini study of Elicit, Consensus, Scopus AI and Scite assistant which amount other issues noted
Sometimes these tools may inaccurately conclude based on the the introductory or general statements from the abstracts instead of specific findings or conclusions, potentially leading to biased summaries. There are also instances where these tools quote secondary sources, e.g. Consensus – Ref. 4, or where Elicit and Consensus both quote a “Note” Benson (2018) – which is only a brief summary of another research article. These could also introduce inaccuracies or bias into the summary.
I can confirm from my own use this is quite common. For example, a paper may have a abstract that says "it is believed ...X" but the paper goes on to show X isn't true and this may trip up many such systems to thinking the paper says X.
Papers in areas like psychology with multi- part studies etc can confuse such systems too.
Often these systems also just generate an answer from the top N papers retrieved and because many of these systems do no weight citations and focus on pure semantic relevancy (see above), the generated answers may sometimes cite odd or very poor quality papers. Again some of the more customizable systems allow you to work around this by picking papers you want to try to use to answer or control search strategies used etc

3. LLMs are used to create "research matrix" of papers by extraction of text from papers
Many of these AI search engines also allow you to go to individual papers and "Chat with papePDF". A more interesting approach which I first saw in Elicit.com and now Scispace is that it generates a "research matrix" of papers, where each row is a paper, and there are columns that describe the charestistics of the papers.
For example, in Elicit,com you can add columns for abstract summary, main findings, methodology, population charateristics, data set used intervention, outcome measured, limitations etc. You are not limited to those default columns and you can create your own e.g. Sample Size, use of placebo etc, discipline covered etc, the sky's the limit.
Elicit.com even allows you give specific instructions beyond just naming the columns, for example for "participants age" you can instruct it to classify into 1-12, 12-20, 20-45, 45+
As you might appreciate it, the LLM is going through each paper and try to answer the "question" such as "what is the paricipants age" and extract the answer into the table. Sometimes the LLM might not give an answer , this is particularly so if it can't find the answer because all it has access is to the title, abstract and not full-text. That is why such tools also tend to allow you to upload full-text to work on.
How accurate are such extracts, in an infograph, Elicit not only claims 98% accuracy and claims to be 13-26% in absolute % points more accurate than "trained staff" doing manual extraction! This seems to me to be a very bold claim, but as of now, I do not see any details of the study showing this
If this is true, this will be a great boon to not just usual narrative reviews but also to evidence synthesis!
Some other thoughts on use of these tools
We are in the very early stage of these tools, so many of these tools are "free". But many of them will disappear as they are outcompeted (the "moat" is very low, as many are using the same source of data from Semantic Scholar, OpenAlex, OA papers, with LLM techniques that are not exactly hard to duplicate) , or just acquired so be careful about building your criticial whole workflow around them.
The source of the data underlying these tools should be considered. A lot of them use say Semantic Scholar, OpenAlex is >200M papers which is huge (Scopus is around 80M) and is typically good enough for most disciplines but it is still worth a check. For example, such sources pretty much have no clinicial trials reports so if you need those, these AI tools alone is not helpful (even if you upload them, they might not be properly parsed).
It might be that the final winners will be the established content owners because they have access to paywalled data that the startups do not. They may for example acquire the more popular ones.
While tools like Connectedpapers, LitMaps, remained free for a fairly long time and some like ResearchRabbit, Inciteful, Pure Suggest are still effectively free, these AI search tools using LLMs will be likely to be less generous because the cost of running each search is much higher due to LLM costs.
It is also unclear if the hallunication problem can be solved, but i hear many creators of these tools are taking for granted that as the base LLM model improves in reasoning etc (GPT5->GPT6 etc) their tools will also automatically improve , it is unclear though if improvements in LLM have levelled off. The more promising tool makes have their coders experimenting with various RAG techniques to improve the results.
Odds an ends
Knowledge graphs and LLMs seem to be the next thing people are trying as they are complementary technologies, where one is top down and structured while the other is bottom up and unstructured. Many ideas include using Knowledge graphs to act as a retriever to provide information of RAG systems or use LLMs to extract data for knowledge graphs. System Pro is one example.
Another interesting idea is agent based LLM type systems that
AKA It tries to mimic a real researcher. First of such tools I know about is Undermind.ai, see my blog post about this.

What do I recommend?
There are way too many such tools for me to try everything but these are the ones I have the most experience with (because they are relatively older).
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2024.04.26 08:47 healthmedicinet Health Daily News April 25 2024

DAY: APRIL 25 2024

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2024.04.24 19:00 windrequiem I am stuck.

Unsure if this is going to make any sense, but over a year ago I had “top surgery.” Really what they did was just a mastectomy with nipple graphs, but they removed all breast tissue so my chest looks concave and there’s residual fat/tissue above and below so it looks extra emphasized. Long story short, I should have chosen a better doctor and felt pressured to just get a mastectomy because breast cancer flags + allegedly it would have been cheaper by insurance, so my own stupidity for believing when they said it’d have the same results as top surgery. When I talked to them about fixing some of the issues aesthetically, they said it wouldn’t be covered by insurance since they can “fix the issue with liposuction” and it’s “not medically necessary since it’s aesthetics based.” I don’t know how legit of a fix it is, but when I called other surgeons in the area they told me they’d also just liposuction around the area. I can’t help but feel like that won’t fix the issue, but I don’t know if I’m just having trust issues about it…
TLDR i look like i got a botched mastectomy and i don’t know if lipo would do anything for me?? 🥲
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2024.04.19 21:49 Important-Monk-7145 Response CASS report

I will try to go through the post point for point. Firstly, I would like to just give some context about me so you know where I am coming from with this post since I have never posted here.
I have worked with LGBTQ+ organisations since 2012-2013. I have both studied gender studies and lgbtq+ psychology, and in 2021 I wrote about the trans healthcare system where I live. As I wanted to write my thesis on this, I continued doing research on the subject, but as I got a comprehensive overview of the research on the subject, I realized that the research foundation was homogenous, scarce and of low quality. I tried warning people that this would be used by conservatives to scale back or eliminate access to healthcare for trans people. Unfortunately, most people saw my concerns as paranoid, and they were brushed off. I decided to change paths and now I teach method subjects at university/college level.
The important takeaways from this is:
  1. I am going into this with the opinion that quite a lot of the studies are of poor quality.
  2. My goal is that trans people get the best possible healthcare, that means it has to be accessible, safe and scientifically robust.
I am currently in the process of reading the full report, I will not have time to fine read it until the weekend. I have read the interim report and parts of the full report. (it just takes a while to read everything with the citations etc).
1-3: I would not start with these points. If you want to repost this elsewhere, I would move them to the bottom with your last point and I would frame it as a failure to disclose and a reflexive error. Having contact with Hunter is not a bad thing per se. If you are evaluating healthcare, you should survey all sides or as many as possible. It is the committee’s failure to disclose this that is the problem.
4: They had panels and studies consisting specifically of people who were experts and clinicians: Research
The researchers who published the reviews are experts in their field, their fields are broad and relevant to the subject.
It is a valid criticism to levy that they did not do enough to get more people who are experienced in GH. However, since they had a substantial amount of them as participants in one of their studies, this would exclude them. Subsequently it is also not entirely ethical to have people working for the NHS GH to evaluate the NHS GH, that would ofc be biased – they would be evaluating themselves. I do applaud them for including the practitioners’ opinions in a panel. But I also think they should have included GH experts and practitioners from other countries on their board.
5: Nothing wrong with that, it is wrong if they did not disclose it properly and did might not have reflexively engaged with the information provided by the groups. If I wanted to evaluate the American military – it would be fine for me to interview or let anti-military organisations to give their input, but I would have to disclose it properly and keep that in mind when engaging with the material. (See point 1-3)
6-7: Trillby Langton did work at the Travistock centre for 10 years and later became a whitsleblower. Anastassis Spiliadis was one of the original whistleblowers for the travisstock centre. The fact that they are whistleblowers for the institution that is currently being evaluated is IMO. a far stronger argument that them publishing in . Both should have been included in a pane of whitcleblowers, but they should not be presented as neutral actors because of their whistleblower status.
It is kind of like asking Chelsea manning to evaluate the American military, she would undoubtedly have enough experience and competency to do so. But she would not be neutral and unbiased, because she was a whistleblower. The same thing applies here.
I would also caution against using "anti-trans methodology" - I would rather say that the report comittee fails to disclose their theoretical lens and assumptions. (The report is methodically bad, regardless of it being anti- or pro-trans). If they used the same method and arrived at a less problematic conclusion, their bad method should have still been called out.
8: Her references to zucker is to provide the historical context. That is how you do a review, you give context and outline the development. She even presents criticisms levied at the study: "Papers from this period were criticised because the children were not formally diagnosed using ICD or DSM. At that time, it was rare for children to have socially transitioned before being seen in clinic." (page 163)
She did not use the studies to say that trans kids grow out of being trans. she used it to see if socially transitioning before getting treatment would solidify GI or if the kids who socially transitioned before treatment where the ones with the most intense GI. She concludes that there could not be established any causality
9: It is surprising that so much focus have been put on the "double blind" aspect of the report (when it is barely mentioned) this might be because that it is the methodical standard most laypeople are familiar with? I'm not sure why people focus on this. (see point 34)
It would not be impossible to do blinded studies. There are multiple different therapeutic modularities that could be single- double or- triple blinded (different types of hormones, different types of therapies, social interventions, different types of healthcare structures. etc. etc.)
The main problem with cohort studies is that the number of participants dropping out is very high compared to other conditions. Over 20% would be a red flag. Some of the studies often cited to claim the 1% detransition, had a dropout rate of 45%.
"And to do robust tests you'd likely have to refuse treatment to actual trans kids while giving non-trans kids cross-gender hormones" - You would absolutely not need to give ciskids cross sex hormones. What would lead you to think that? That would not be a robust test at all because it would not answer the research question: is HRT effective and safe for trans people?
10: Different types of claims/fields/methodologies have different types of evidentiary/quality standards. The report does not cite the 2018 debunked study, it cited a study from 2021 by Littman. If you are going through the history of research on detransitioning, it would be natural to cite the Littman study as it most certainly is well-known. (And they actually chose not to cite it, they cited a later study by littman.)
A study on how detransitioners “feel” is different from a study on whether a medical treatment is effective/safe/treats the right patient group. Different quality standards because they have different ontological and epistemological underpinnings.
11: She is saying that the studies does not produce evidence of high quality. That does not mean the research is on par with other fields in medicine. Studies that have a very poor, poor, average and above average quality of evidence, all fall within this category. In the field of psychology/healthcare we tend to be a little more polite and cautious with our words compared to other fields. The research is of poor quality. Trans people deserve better. A substantial part of the research on trans healthcare make some of the same mistakes Littman was criticised for in her 2018 study.
12: Yeah the proposals are terrible.
13: (Personal opinion) I tend to think that both people are right/wrong here. For some they are given treatment too fast, while others are unfairly made to wait long or denied treatment. There is very little oversight and control of what happens inside the clinics and the teams that work on it are small and insular. The procedure and process vary greatly depending on where and to who you go.
Slowing down and limiting trans healthcare is not going to solve anything – because it does not address the main problem. The main problem is not quantitative (i.e. too little or too much trans healthcare) it is qualitative (the type of healthcare trans people receive are of low quality).
14: They are not American they do not use the DSM 5. They use the ICD. The diagnosis F64. 2024 ICD-10-CM Codes F64*: Gender identity disorders (icd10data.com) was operational until February 2022 when the new ICD-11 offically came into effect. The new version uses Gender incongruence, it can be indexed as "disorder of gender-identity or role in childhood" under the new version. We don't use the same diagnosis and language here as you do in America. The ICD considers the term "gender dysphoria" to be deprecated as a diagnostic term.
(Another example of this is that "homophile" if sometimes used in other non-english languages and calling someone "homosexual" would be considered rude. While in America it would be the other way around. This is because the homophile movement had a much stronger foothold here.)
15: I could not find this claim in the review. Are you referring to this: “Early research cited in Chapter 2 found low rates of persistence of childhood gender incongruence into adulthood, around 15% (for example, Zucker, 1985). Papers from this period were criticised because the children were not formally diagnosed using ICD or DSM” (page 67 and 163).
The review is going through the history. They also cite studies from 2008 and 2015. That is how you do a review.
If the claim is elsewhere the please direct me to it.
16: The quoted sentences were not in the report. I could not locate these claims.
17:
Figure 15: Number of referrals over time by country – from 2000 to 2015/17/18/19 (page 88)
Figure 16: Referrals to the National Gender Clinic for children and young people in Norway – this figure is from early 2000 to 2022. (Page 89)
I am assuming you are referring to Figure 17 – this one is in the USA and Europe from 2013-2015/16 (Page 89)
I would appreciate it if you could provide some info on where you think the plate is? It is difficult for me to fact check that aspect of your claim since your provide no sources for it. But the graph from Norway has numbers from 2022 and show an even bigger increase. The Norwegian healthcare system have to report the amount of people each centre treats every year, that is likely why there is recent information from there:Nasjonal behandlingstjeneste for kjønnsinkongruens - 2022 - (If you have any questions I can answer or translate for you)
18: Yeah the suggestion in the report is kind of dumb.
19: Most of them are bad and should be dismissed. Most studies have their follow up within 1 year. Very few follow up after 5 years. This is bad. (a few studies do long term follow ups Sci-Hub
Most also only interview the people currently getting treatment and not the people who no longer receive treatment/dropped out. (i.e the studies exclude the group most likely to have regrets). The vast majority also only have self-reports and no biological data. The questionaries used are also seldomly properly vetted. The lost goes on in regards to the studies lack of quality.
(Personal opinion) Instead of defending indefensible studies we should acknowledge that most studies are inadequate. What we should focus on dismantling is the notion that this has been done to fit the “trans agenda”. That is not the reason. Trans people have historically and are still to this day subjected to unethical research. The current situation we are in is just another iteration of scientific and medical malpractice against trans people.
20: Yeah this is a fair point.
21: Most of the research I have seen used by LGBT organisations are not sufficient to answer this question. I do not know which studies you are referring to. It would be great with some citations.
22: A report about a healthcare service, discloses the approximate number of referrals to the healthcare service. It would be unethical not do disclose it. We have fought a long time to dicourage people from using the size of a patient group as an argument in regards to evaluating the healthcare intervention. Let us not introduce it again. You are offering conservatives a reason to perform budget cuts that will gut trans healthcare services on a silver plate. (I don't think you are doing this intentionally but it is one of the effects of this kind of dicourse.)
23: You cannot reasonably say that the report frames transness as something that is a social contagion and will pass, and also think it is odd of them to recommend managing symptoms. The recommendation is completely logical and in line with their view. It is the premises the logic builds on that is incorrect. i.e transness is not a social contagion. Not the logic.
24: I think you might have worded this point oddly. Because now it seems that you are suggesting that the report should have included criticisms of the report, in the report. (How can you expect them to include something that came after the report was published).
The organizations you mentioned are also American and use a completely different diagnostic system, I am not sure why they should focus on American organizations for a British review.
25: We do not have sufficient information to conclude that...at all. It could be worse; it could not be worse; it could be equivalent. We do not know. This is speculation.
26: There should most certainly be a lot more investigations into hormonal treatments for cis people as well you are correctly pointing out a big hypocrisy here.
The paper they cited in the report recommending this is from 2023, so I am not sure where you get the claim that “that modern vaginoplasty has long not required this.”
27: The quotes don’t exist in the report so it made it a little harder to find.
Saying there is no established definition (technically not what they said, the quote comes further down) does not mean you cannot introduce a concept including the term there is not an established definition for. Pointing out that there is not one single definition of the term is good scientific praxis. It allows the reader to understand that the researcher chose one definition but that there are others out there.
“There is no single definition of social transition, but it is broadly understood to refer to social changes to live as a different gender such as altering hair or clothing, name change, and/or use of different pronouns” (page 31)
The second perceived inconsistency, is also hardly an inconsistency.
Formal diagnosis does not predict gender incongruency.
Diagnosis can be developed to be predictive of positive outcomes.
That is not an inconsistency at all (and this is using the posters framing). They are saying that we should not use diagnostic tests to determine who are trans or not, we should use it to determine who will benefit from treatment.
For the third part, there is offer no evidence offered that the graphs are manipulated. See my points on the graphs above.
28: I was not able to find this. The report suggest that kids who socially transition should get into the healthcare system as soon as possible and should not wait like it is done now: “Recommendation 4: When families/carers are making decisions about social transition of pre-pubertal children, services should ensure that they can be seen as early as possible by a clinical professional with relevant experience” (page 32)
But that is not equivalent to what your are suggesting so I might have missed where this is. Can you direct me to which page?
29: Yes this is in line with most recent European reviews and changes (see the recent changes in Norway, Sweden etc.)
30: Yes
31: I am not sure what you mean here. Gender incongruence being a mental health disorder is an etiological claim not a claim on the efficacy of intervention. There seems to be a huge leap in your logic here so I would look over your argument. You need to better establish what the current etiological claim is and how that differs from the understanding in the cass report, then you would need to establish how the etiological claim effects the choice of treatment, then provide the evidence for the effectiveness and possible harms of the treatment.
32: This is the situation today as well; it is just not standardized and varies greatly depending on what treating team you get. Having set criteria to qualify for a diagnosis is the foundation of our medical care system if we do not have a condition to treat it would be an elective treatment (like plastic surgery for example). I think your argument here is that you disagree with the criteria cass proposes? Or are you suggesting Europe should adopt the American model – if so, why? It would be a lot easier for conservatives to hinder access to trans healthcare if we have the American model.
Your point on hormones acquired externally is in line with some Scandinavian treatment models. It is a dumb addition, and will be particularly bad if the guidelines are used in countries with less functioning public healthcare systems.
33: I think you need to change this argument. Having safeguarding protocols for children who have obtained hormones or other drugs illegally is not inherently bad and is a good measure. The problem is when it is combined with restricting the public and legal access to those hormones/drugs.
Some hormone drug iterations have been linked to liver cancers and other types of cancers (and as a result is not commonly used). If the parents give those to the child - there should be an investigation into the parents. The best deterrent for this is to make hormones accessible tho.
34: No it is not a throwback to the medicalization of homosexuality. Medicalization is: the process by which human conditions and problems come to be defined and treated as medical conditions, and thus become the subject of medical study, diagnosis, prevention, or treatment.
If we de-medicalize gender incongruency we deny trans people ALL access to healthcare. We would be defining them out of the healthcare system. This was okay to do with gay people because there was no need for treatment. But most trans people need treatment – that is what they are fighting to get.
submitted by Important-Monk-7145 to u/Important-Monk-7145 [link] [comments]


2024.04.15 05:15 samuel_1000 Seaweed is a Conspiracy

Seaweed is a Conspiracy
This might sound fake, but I assure you that this is 100% real. The seaweed industry is a lie. You see, good deposits of seaweed are found way too deep to be attainable in a cheap way. Because of this, Big Seaweed is taking small amounts of seaweed found in shallow waters and adding a lot of filler chemicals to make it seem like there is more seaweed then there actually is in their product. The seaweed you buy is only like 30% real seaweed. This isn't even the worst part though. 75% of the additives that they use are known carcinogens. They use these chemicals just because they're cheap and allow them to make a huge profit, despite the known risks. No one has bothered to look into this because no one cares enough about seaweed, but as an avid seaweed lover, I felt it was my duty to bring this horrible truth to light. Seaweed is causing cancer, and we need to take action NOW. I have attached a graph detailing the similarities between seaweed consumption rates and cancer cases from 1970 to 2020. Please stay safe out there and always keep your eyes and mind open.
https://preview.redd.it/4ft6lqjl9kuc1.png?width=681&format=png&auto=webp&s=dc7d150a0ab77151da89892d7a61e47ab855ae61
submitted by samuel_1000 to conspiracy [link] [comments]


2024.04.12 21:04 OnTheEdgeOfFreedom About Covid vaccination – history and observations

The post is locked because I know exactly what sort of response this will get from the deniers. I had to ban several people this week because I mentioned Covid in passing in a post and the deniers came charging out. How they find this sub I don’t know, but please note it’s an instant ban to post disinfo here, and nothing Annoys The Mod faster than vaccine disinfo. The lock here is just to save me from having to do a lot more bans. (If you find a problem in this post and can cite the issue, message me and I’ll fix it.)
Intro
Let’s do the history of Covid, in order to talk about the problems the US in particular has had managing it. Note I’m not going to cover origin – I have my suspicions but I don’t know, I think a few of the people who do are dead, and the US government itself never came to a conclusion.
So. Sometime early Dec 2019, it was becoming obvious that something bad was happening in China. Odd pneumonia deaths were spiking. The Chinese weren’t sharing a lot of information, but by the end of the month, flags were being raised everywhere. In January 2020, a mad scramble confirmed the worst: it was a novel coronavirus, and it was a killer.
Much of what follows is from https://www.cdc.gov/museum/timeline/covid19.html
A novel virus means, among other things, that people don’t have inherent immunity to it; the body has to start from scratch to generate a defense. This creates more problems than a simple variant of an existing disease and it put the WHO and all associated nations on high alert. What mattered now was two numbers: CFR (case fatality rate) and R0 (roughly, how easily it spreads). Both take large sample sizes to determine, so they were initially unknowns, but they are the most important things to determine for any disease. By 19 January it was obvious that R0 was going to be high: the disease was spreading rapidly and easily and had already reached 4 countries. The US started screening for it for flights from selected areas. Epidemiologists shifted from interest to concern to worry. It was too late… by 18 January it had reached the US (identified on the 20th). A few days later, a case popped up elsewhere in the US.
By 31 January, person to person spread had been confirmed in the US and quarantine measures began to be implemented.
Early testing for the virus was unreliable, but actual Covid-19 deaths were easy to count. By 10 February, Covid-19 had killed over 1,000 people worldwide, with some likely undercounting in China. People in epidemiological circles were openly predicting a pandemic. These were people who has studied the 1918 influenza pandemic and they knew how this could go. Governments started warning their population that lockdowns were coming. On 25 Feb, the CDC publicly announced the associated “disruptions may become severe.”
Yeah, no kidding.
By 11 March, there were over 4,200 Covid deaths worldwide. It was turning up everywhere, and the WHO formally declared a pandemic. By 13 March, it was declared a national emergency in the US.
The war against Covid was on.
---
Covid’s ascent
Ventilators were the primary defense against death in hospitals - there were no treatments - but they were in critically short supply from the start. Different US states established different criteria for who got ventilators. (Alabama, curiously enough, opted not to use them on mentally retarded people or folk with dementia, about as dark a decision as can be imagined. Other states chose criteria that tracked roughly with the odds of success.)
Work on a vaccine was in progress. The mRNA platform, originally intended for cancer research, had been shown in 2017 to be an effective antiviral platform, and work was begun to plan a phase 1 test on an mRNA nipah virus vaccine in 2019. The mRNA platform had ten years of development going for it and could be easily adapted to other viruses, but it was difficult to make it stable, and production and distribution would be a problem, even if it could be shown to be effective.
But Covid-19 was already taking off. A criteria was set: if the new vaccine could be shown to cut the hospitalization and death rate by 50%, it would be mass produced at government expense. 50% would have been considered good for a coronavirus vaccine. Influenza vaccines don’t always do that well.
In March, hydroxychlorquine was proposed as a possible mitigation. It would take a few months to determine if it helped, but standard antivirals were not working and a preliminary study with a small sample size indicated some effectiveness. (This turned out to be a mistake.) By 28 March, the FDA authorized an EUA stating that hydroxychlorquine could be attempted, but the CDC was demanding that it only be taken under a doctor’s supervision – unsupervised use of a form intended for fish had already killed someone. But the word has gotten out and people were trying it anyway.
In March, the CFR was estimated at around 3% - frighteningly high, but early estimates of CFR are notoriously unreliable and everyone in the field expected this to decline. It’s what got reported, though, without any caveats, a claim that came back to haunt epidemiologists, who were subsequently accused of fear mongering. R0 estimates were around 4 – also scary high, but also inaccurate.
Masks were in short supply everywhere and US agencies were trying to decide which doctors should get them (and got it wrong), while relegating the public to cloth masks. No one thought this was a great strategy but masks had to be reserved for doctors, because if we lost large numbers of doctors, the hospital system would crash and then the death toll would be enormous (and not just from Covid). No better solution was available, so the CDC suggested cloth masks be made at home. By April, cloth masks were a common sight. Hospitals were using freezer trucks as portable morgues in several cities.
By early April, the US opened a mass grave site for Covid deaths. As a chilling reminder of the 1918 pandemic, images of this were nightmare fuel for epidemiologists. Pressure increased to do something.
And the pandemic turned political. Then-president Trump declared he was cutting funding for the WHO because they hadn’t been clear about the threat (they had been); he did it mostly to deflect criticism away from himself - he’d been comparing Covid to the flu, even when he knew the situation was far worse. ( https://www.forbes.com/sites/tommybee2020/09/10/all-the-times-/trump-compared-covid-19-to-the-flu-even-after-he-knew-covid-19-was-far-more-deadly )
Meanwhile, stories that Covid wasn’t real started to flood the social media, almost exclusively on right wing sites. Masks were touted as ineffective, mostly by people with a business interest in tourism and entertainment. The war on Covid was barely a month old, but politics were starting to drown out the messaging. Right wing pundits started insisting it was just the flu.
Pressure to reopen businesses became extreme. There is unproven speculation that this may have been a cynical attempt to increase infection rates in cities and among Democratic voters, who are often more heavily represented in customer-facing roles. (Better off folk were already telecommuting, after all.) But the desire to keep the markets going - stocks were already plunging - was the public reason to push businesses to reopen. Unemployment was rising.
By early May, the US unemployment rate was over 14%. A lot of the losses were in entertainment and tourism, but people were also fleeing heathcare, due to burnout and a high death rate among workers. Trump was pushing harder for businesses to reopen, even as the NIH was warning the Covid death counts were probably conservative and it was too early to reopen everything. This went down poorly with business owners, who expected the lockdowns to be short and painless. For the US right wing, lead by business interests, Fauchi became public enemy number 1.
The CDC already knew that much worse was to come; early estimates of 240,000 dead even if everything went perfectly were already looking like a pipe dream. Some models were estimating a million dead in the US, some were estimating far lower. There wasn’t good data available. But it was obvious that it wasn’t going to go well.
And where were the vaccines?
Not available yet. In testing. The FDA was running through all three phases of testing in parallel, but even running tests in parallel, it takes time.
In the short term, antivirals and antibody treatments were tried. But Remdesivir, an anti-viral that showed promise, was available in late June. Unfortunately, Gilead Science, the developer, decided that despite being given quite a lot of public funding to develop it, that it needed to be sold for over $3000 per course. Backlash against pharma began.
By July, the CDC was screaming that people needed to wear cloth face masks when leaving the home, and the WHO was actively warning people that airborne transmission is the confirmed primary spread mechanism. But anti-mask sentiment in the US had been whipped into high gear and entire regions of the US viewed it as a mark of pride not to wear them. Active cases in the US hit 1% of the population – over 3 million people. Attempts to flatten the curve, initially successful, had collapsed. Too many people were ignoring mitigation advice, and too many people misunderstood the point – flattening the curve doesn’t prevent cases, it just pushes them to the right on the timeline, so there’s more time to ramp up hospital support. As deaths mounted, pundits claimed that flattening the curve “hadn’t worked.” It had – it pushed off the tsunami of cases a few months - but the tsunami eventually arrived.
In July, Herman Cain died of Covid. He'd been an active right wing denier of the disease's severity and had spread misinformation and mocked mitigations, including publicly attending a Trump rally in June without a mask. For reasons best described as unclear, his staff continued to post on his Twitter account after his death, and within a month "It looks like the virus is not as deadly as the mainstream media first made it out to be" appeared there. This made his name synonymous with the blind, rabid attempts of the MAGA crowd to dismiss Covid as a risk, and as of April 02024, HermanCainAward remains an active subreddit with 493,000 members. The number of right wing pundits who mocked Covid and then subsequently died of it became noteworthy; I kept a rough count early on and came up with 14 before I gave up. It was no real surprise - a lot of them were desk jockeys with health issues to begin with and they were avoiding masks and doing public gatherings.
By July 02020, hospitals were overloaded and people weren’t always able to get treatment; people were dying at home, sometimes uncounted, and spread was accelerating. But trolls were still claiming Covid victims were crisis actors and masks didn’t work. Stupidity, in short, became the second pandemic. https://www.gocomics.com/pearlsbeforeswine/2020/08/30
Vaccine testing was going well, but no one was going to suggest cutting any steps out of the testing process, so even as people were dying, it was not released. A little known fact: nowhere in the FDA phase test protocols is there any mention of how long the tests should take. It’s not based on time at all, it’s based on sample size and other factors. Finishing the phases can be slow because funding has to be raised for testing (testing is not cheap) and there’s often little incentive to do vaccines quickly – people get sick, so what – if it’s not going to make a lot of money. So verification often drags out pointlessly for months or years, waiting for the dollars to show up.
This time, though, governments were footing the bill for the testing, and they requested that all three phases of testing be run in parallel – a little riskier for the test volunteers, but there was no time to waste. With that, there were no delays left – just frantic attempts to get volunteers, monitoring for the few weeks needed to get results, rinse and repeat. Because in the end you need a big sample size to complete the protocol, and you only have so many people to collect and process results, it still takes time. But it never had to take years, and this time it wasn’t going to.
But it still takes months. And if the result wasn’t a 50%+ reduction in deaths, was all going to be for naught. That was the requirement for distribution.
By August, there were 5.4 million active cases and people were dying at a rate of 1,000 per day.
On 24 August , hopes that Covid was a one-and-done disease were shattered – a patient got his second case of Covid. There had never been much hope for Covid being a one shot disease, but this corrected it to no hope. Covid, epidemiologists wrote, was going to be with us forever.
By the end of September, the worldwide death count from Covid was over 1 million. It had happened in just ten months.
In October, New Zealand declared Covid beaten – they were Covid free, due to some truly impressive and draconian policies on quarantine and limiting travel into the country. They proved that if a nation was willing to do what it takes and come together, the disease could be controlled. (The downside was that locals who were outside of the country when the quarantine was enacted were often effectively exiles, as getting back in was difficult.) The US, meanwhile, was still seeing social media posts about how masks makes Covid worse, or how Covid doesn’t exist at all, how testing is a sham… I got asked by an overseas friend why the US was acting like the village idiot. I didn’t answer. I didn’t know what to say.
Also in October, the Delta variant of Covid was discovered in India. It got off to a slow start, but spelled trouble ahead.
On 4 November, the US recorded 100,000 new cases in 24 hours. Two weeks after Halloween, US cases spiked higher – evidence that indoor gatherings without masks are the primary vector of spread. And long Covid was finally being discussed.
Things could not have looked grimmer.
---
Counterstrike
16 November, 2020: Moderna’s COVID-19 vaccine is determined to be 95.4% effective in its clinical trial at preventing serious disease, hospitalization and death.
People had hopes, but no one expected this. The goal had been 50%. In the next week, Pfizer-BioNTech’s COVID-19 vaccine came in at 95% effective.
That week, the US caseload went past 11 million, but all eyes were on the vaccines. Manufacture and distribution were the next hurdles – the vaccines have to be kept cold or they degrade rapidly – but with the current rate of death, money was no object.
On 23 November, the FDA issued an EUA (Emergency Use Authorization) for a new antibody treatment. This helped, but antibody treatments tended to be specific to variants and much less effective when new variants appeared.
On 3 December, the recommendation came out that healthcare workers should be prioritized for vaccine distribution, the strongest signal yet that the vaccine was considered safe and release was imminent.
On 11 December, nearly a year after the disease had been identified, an EUA was given for the first Covid-19 vaccine, for people aged 16 and older. The first person in the US to receive vaccination (outside of the thousands who participated in clinical trials) was on 14 December. The EUA for Moderna’s version is on 18 December.
Then Tiffany Dover happened. She was a nurse who volunteered to get the vaccine during a livestream, to boost confidence in the vaccine. She was not a good choice. She was prone to fainting spells, and shortly after the vaccine was administered, she fainted on camera. It had nothing to do with the vaccine, but immediately it blew up social media. Trolls swarmed the story, demanding that she wasn’t prone to fainting spells because nurses weren’t… if you want to see the shitshow that followed, look at the comments on this video about the incident: https://www.youtube.com/watch?v=p9agUz5cQCk. It’s a troll zoo. What followed was worse – demands that she’d died immediately after. She was (and is) of course alive and well, but this became the basis of a fearmongering campaign driven by multiple sources trying to discredit American vaccines, the media, the government… for months. (She’s been interviewed since, and some trolls are still demanding she’s dead or even if she isn’t, it’s all lies anyway.)
It didn’t matter that the vaccine has been tested on over 43,000 people during phase 3 testing and the typical adverse effect was a headache. A pretty young girl was murdered by the vaccine is how this got spun.
Healthcare workers knew better. By 24 December, a million people in the US have been vaccinated, almost entirely healthcare workers. Production was still struggling to produce in bulk.
The timing could not have been closer. On 29 December, the first case of the more-contagious Alpha variant is detected in the US. The critical question became how effective the vaccine was in reducing spread – not the original goal, but with cases exploding, an important one.
22 January 2021, the Gamma variant was detected in the US. The R0 is unknown, but the speed at which variants are showing up confirms everyone’s worst fears. New variants might be able to dodge the vaccine, as happens yearly with influenza. On 28 January, Beta shows up in the US as well.
By the end of January, over 23 million vaccinations had been performed in the US. But the worldwide case count was over 100 million. The race was on.
On 27 February, the J&J one-shot vaccine is given an EUA. There was a lot of hope for this vaccine because it did not need to be boosted to be effective. It proves to be an ill-founded hope.
On 8 March, the CDC announces that fully vaccinated people can safely gather with other full vaccinated people without masking. They're accused of flip-flopping, and they’d come to regret that announcement as new variants show up.
Meanwhile, Europe was examining claims that one of the vaccines was causing blood clotting. This becomes a widely spread story, but on 18 March it was determined that they did not find a link between the vaccines and clotting, that any such risks were far outweigh by the benefits of vaccinations, and vaccinations proceeded again in most countries. (Something similar happened in the US in April – 6 reports of severe clotting were reported among users of the J&J vaccine, and distribution was briefly halted. On review, the distribution was continued.)
On 29 March the CDC announced announcement that the mRNA vaccines were highly effective at preventing infection. Unfortunately, on 2 April, the then-head of the CDC got carried away and announced that the vaccine stopped transmission. This was a serious overstatement – the best data at the time was that it was about 90% effective at stopping transmission of the original strain, which was wonderful, but it was not the absolute guarantee her words implied. Epidemiologists were enraged. No vaccine has ever completely prevented infection or transmission and the Covid vaccines were not an exception.
Worse, Delta was just starting to emerge as the dominant variant, and Delta had a higher R0. By 1 June it was well established as the dominant variant in the US, and the vaccine was not as effective at blocking transmission. (It would do even worse against Omicron.) It rapidly became obvious that the CDC had overpromised, and this became a huge talking point in right wing circles. This turns into a PR disaster for the CDC, and trust in the CDC declined as a result.
Delta was not to be trifled with. By April 30, India, which did not have effective vaccine distribution and had loosened restrictions, was seeing 3,500 deaths a day, and this is considered a severe undercount. Funeral pyre smoke was visible from space. (Trolls online claimed the photos of the pyres were faked and the deaths weren’t real.) When wood for the pyres ran out in some regions, bodies were dumped into rivers. The full death toll will never be known.
By 27 July, Delta’s surge causes the CDC to go back to recommending masking for everyone. This becomes another right wing talking point, as they point to the the fact that the CDC keeps “changing its mind”. The fact that different variants had different properties was left out of those talking points.
The head of the CDC received death threats, which continued until she resigned.
Meanwhile, a debate was raging about whether “natural immunity” – the incorrect name given to people who had had Covid-19 and were deemed relatively safe from reinfection – was better than protection offered by the vaccine. On 6 August, the CDC released data showing that vaccinated is more than twice as effective at preventing reinfection than infection itself – but it subsequently turns out that neither offers very long term protection.
Trolls were swarming youtube comments and other social media; the fact they are trolling is obvious, because while the vast majority of Americans are very much in favor of the new vaccines and are very aware of the risks of Covid, comments on youtube (by my own count in August) are disinformation over 96% of the time. The lies are so varied it's hard to keep track of them all. People were posting that Covid testing was unreliable and prone for false positives, masks were ineffective, Covid was a government plot, mitigations were a government plot to take away citizen freedoms (an idea stolen from a WEF paper warning that pandemics might be used an as excuse to limit freedoms, not a suggestion that it happen), that new Covid variants were being manufactured and deliberately released, the Covid vaccines contained demon blood, aborted baby blood, alien DNA, toxic mercury, or nanobots; that the ingredient list is a secret, that vaccinations shed mRNA to nearby people, that vaccines cause Covid, that vaccination records are the Mark of the Beast, that mRNA vaccines modify DNA... absolutely none of it true, but all of it is repeated endlesson on every news story and post about Covid. Some of these troll farms were eventually traced to China, Russia, and the Republican party. https://mediaengagement.org/research/social-media-influencers-and-the-2020-election/ There is no question that the trolls are coordinated - comments on stories followed very discernible waves where a certain disinfo topic would run everywhere for a week, then a another topic would replace it.
One of the most persistent disinfo claims was that the Covid vaccine isn't a vaccine at all because it doesn't "prevent disease." The trolls fail to mention that no vaccine has ever "prevented disease"; the best known vaccine is for measles and it's 96% effective if all three doses are given. Nothing has ever been 100%, but the trolls hammer the point repeatedly, which causes a split with anti-vaxxers who had been demanding that all vaccines are bad. This does make it easier to tell who's politically motivated vs who's just ignorant about science, but in the end it just encouraged vaccine hesitency in general, which subsequently causes a measles bloom.
On 24 September, the CDC announces that schools which required masking throughout the pandemic were a third as likely to have Covid outbreaks. This does nothing to silence the “masks are ineffective” trolls, who are dominating social media with disinformation about vaccine issues and mask ineffectiveness. Some are claiming the masks cause penumonia and that's what's really killing people. This is at variance with the fact that the majority of deaths are occurring in the unmasked population.
Zoonotic spread had been a question since the early days of the pandemic and the debate over how Covid was initially spread. The lab leak theory conpeted with the zoonotic transfer theory and no conclusion was ever reached. But on 3 November, the CDC released data showing that transmission between animals and humans was documented, and hundreds of animals had been infected. Subsequently, mink and deer were found to be disease reservoirs.
Bot generated downvotes on Covid stories and factual comments become so common that Youtube hides public downvote counts, causing howls of protest from trolls groups who were being paid to downvote.
And then came Omicron. On 19 November, the CDC recommended an additional booster shot for everyone, to head off the expected Omicron surge. The J&J vaccine is no longer one-and-done. The definition of “fully vaccinated” becomes blurry. By 1 December, omicron is in the US. By 16 December, omicron is determined to be about 1.6 times as transmissible as Delta. R0 is getting harder to measure because the vaccine knocks down transmission, but even so the R0 is judged to be about 3.4. Claims that it’s over 18, which would have made it more contagious than measles, are debunked, but still add to the confusion. But at 3.4, it’s wildly contagious and caused exponential growth.
By 3 Jan 02022, the US reports over a million new cases in one day. Omicron’s transmission advantage has overwhelmed containment attempts; just entering in a room after someone with Covid has left can be a risk factor.
The vaccine still holds up quite well at preventing death.
Meanwhile, ivermectrin has gained attention as the new quack cure. In early January, it’s determined that prisoners in an Arkansas jail have been fed ivermectrin and hydroxychloroquine without consent. It caused nausea and didn’t cure anyone’s Covid, but the news is a start reminder that some doctors don’t listen to medical guidance and are willing to roll the dice. Ivermectrin misuse caused a threefold increase in calls to poison control centers.
By early February, it’s shown that Omicron has gone from a 1% incidence rate to 99% in just six weeks in the US. It out-competes everything.
Reports surface that ivermectrin overdoses are stripping intestinal linings surface; people claim they are pooping out "rope worms" but it's actually often their own intestinal linings. As a testament to the ability of people to self-diagnose and self-medicate (a popular topic with preppers) this stands alone as a reason not to play doctor.
China has been instituting lockdowns since the beginning, and they add new ones on 14 March as Omicron makes the rounds there. Several manufacturers close up shop, causing worldwide supply chain issues.
On 24 March, the CDC reviews excess death numbers in the US. To no one’s surprise for 2019-2020, excess deaths rose 19% after the onset of the pandemic - the largest increase in over a century. Claims of crisis actors faking Covid deaths are finally gone; it’s nearly impossible to find anyone who doesn’t know someone dead of Covid in the US as the death toll approaches one million.
Florida – a source of copious amounts of faked Covid statistics and disinfo – strikes down a mask mandate involving public transportation on 18 April. Given Florida’s misreported data, it’s not possible to determine how much difference this made.
North Korea reports 3.27 million so-called “fever patients” in late May. Seeing as by April 2024 they only reported 74 Covid deaths, it’s safe to assume we’ll never see accurate numbers.
In May 02020, the US crossed 1 million dead to Covid.
---
Wrap up
We’ll skip ahead here.
In December of 2023, China suddenly opted to end all Covid restrictions. Numbers out of China are not to be believed, but it’s estimated they lost at least 2 million people in a few months as a result. They had their own vaccine which was believed not to be as effective as mRNA vaccines, and vaccine uptake may have been a problem in rural China. They simply decided to let it rip.
In 2023, trolls are trying to demand that long Covid is vaccine damage, not from Covid itself.
In 2024, it’s estimated that unvaccinated people have about 10-14 times the risk of death as vaccinated people, and this includes people who are not current on boosters. And despite claims, evidence of clotting is vanishingly rare (about 1 in 200000) and myocarditis is under 1 in 100000. Both conditions are far, far higher from Covid itself. But they remain right wing talking points.
The talking points kill people. By late 2021, Covid was becoming a red state problem. Vaccine and mask hesitancy in rural red state areas gave them increased hospital and death rates. Typically you’d expect cities to concentrate deaths of a pandemic, so most deaths would be in blue areas; and pre-vaccine, that was true. But by the end of 2021, vaccination and masking were widely adopted by left leaning folk and often avoided by right leaning folk, with hideous results: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10684792/ and specifically a graph here: https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=10684792_gr3.jpg
Attempts by the Republican party to curb anti-vaccination rhetoric fail; they discovered too late that they were disproportionally losing voters to Covid, but when Trump tries to take credit for the vaccine his audience boos him. The right has lost control of the Frankenstein they helped create, with the result that measles is making a resurgence in the US.
It’s not unreasonable to believe that Tucker Carlson’s “maybe the vaccines don’t work at all” comment killed a few hundred thousand people in the US alone. https://www.politifact.com/factchecks/2021/ap15/tucker-carlson/tucker-carlson-falsely-claims-covid-19-vaccines-mi/
Unfortunately, you can’t be tried in the US for deliberate lies that kill people. Which is a pity; we’d see less bullshit. In court, Carlson literally depended on “no reasonable person would believe what I say” as his defense.
It’s also worth noting that all the claims that were made in social media about the horrors of vaccination: it would modify DNA, you’d grow extra limbs, you’d become a puppet of the deep state/WEF via 5G, you’d end up possessed, you’d turn gay or become infertile, you’d get “turbo-cancer”, you’d drop dead after 1 years/2 years/3 years… none of it happened, and since there’s a 42 day window on vaccination side effects, none of it will. If you believed any of those claims… well, you’re a fool. And you should distrust your sources, because they told you all those things and none of it turned out to be real.
Disinfo is lethal. There’s a reason I ruthlessly ban people in this sub who do not present the reality of vaccine risk and effectiveness here. I don’t much like murderers.
So what is to be done?
On social media, block anti-vaccine people and people who post miniformation. If they are friends, let them know why you're cutting off contact; if they are strangers, just block silently. Many people are paid to do this and as their audience shrinks, they might lose revenue. The goal is to isolate and starve the beast.
If you cannot cut off contact, demand they cite every single claim. The weak point of disinfo is that there's never a creditable cite; it turns into "I heard from my cousin that his girlfriend" stories, or links to places like Newsmax or Telegram and people with no credentials. Ultimately the demand for cites backs them into a corner and they'll resort to "you can't trust scientists/media/government/doctors" at which point they've lost all credibility. It's not easy to defend the position that something their cousin heard from his girlfriend has more weight than an organization like Reuters or AP news, which has a reputation for accuracy to defend.
Keep in mind that, increasingly, online strangers are AI bots. This is a problem because they are cheap to run and well funded by state actors. We're already approaching 50% of all internet traffic being bot-generated. All you can do here is keep your circle of authors to known humans and friends and ignore anyone you don't recognize and can't verify.
Covid has been relegated to epidemic status. But stupidity and disinfo are raging world-wide pandemics. Your block function is your mask, posting actual verifiable data is vaccination, and your demand for cites are alcohol wipes. Do what you can to limit the spread.
submitted by OnTheEdgeOfFreedom to realWorldPrepping [link] [comments]


2024.04.10 03:18 thatdocman If PCT has failed you [Research and Options]

If PCT has failed you [Research and Options]
So guys, I thought I’d do a post about what the next options are if conventional PCT fails. I’ve heard from and spoken to many guys across the world on this, and I’d say in 70-75% of cases I can help get them relatively close to their pre-TRT or natural levels. Obviously, this is not a perfect science and this process can be complicated by a number of things: generally older guys and those who have used 19-nortestosterone derivatives/progestins (that are more suppressive than non-19-nortestosterone derivatives) are going to have a harder time to recover their HPT axis function. Another big variable is dosage and time on - obviously the guy who has been on 100mg TRT for 3 months and wants to come off is going to have a much easier time than the guy who has B&Ced for 10 years.
Now, in most cases, the big 3 usually suffice:

  • Time
  • Initial hCG stimulation (but removing this quickly - hCG is suppressive in its own right)
  • SERM to modulate estrogen receptors to increase T

However, men who have had significant suppression of their HPT axis over a long period of time for whatever reason just cannot seem to break past say 200-250 Total T levels, and may still feel terrible. I do have some theories around why this is the case, including damage to the Leydig and Sertoli cells (death, apoptosis) - however, what is interesting that even in these men, clomid or enclomiphene actually boosts their LH level to often double or triple reference range - and their body responds. Some men get some solid testosterone readings on enclomiphene, but here’s the issue: once the stimulus is removed, they often go right back down to hypogonadal levels of androgens. In other words, it’s almost as if the brain signalling just isn’t there (gonadotropin release: LH, FSH) to support their natural pre-anything baseline levels of testosterone.
In my opinion, with these men, if the fact that a SERM can raise their LH and they get a significant increase in testosterone as a result, only to go hypogonadal once removed, it’s not actually an issue at the Sertoli/Leydig cell level - this infrastructure is working well with the stimulus of enclomiphene. It’s actually, the brain isn’t pumping out enough gonadotropins. In other words, it’s a brain signalling issue higher up in the HPT axis.
So, there is another option for these kind of men. And it’s in the form of an analogue of GnRH called Triptorelin (acts in the same way that GnRH does). Now, way up in the cascade of the entire HPT axis, GnRH is released from the hypothalamus to stimulate your anterior pituitary to release LH/FSH. So the idea is this - if you can introduce a single, potent dose of GnRH, the idea is you can ‘kickstart’ your HPT axis back into life:

https://preview.redd.it/ckw32hdnzjtc1.png?width=644&format=png&auto=webp&s=d9968fe929eaee397349a3d05fd42cf105506e2b
Initially, you might be confused, because if you search Triptorelin online, you get the following:
“Triptorelin is a gonadotropin releasing hormone (GnRH) agonist that is a potent inhibitor of the synthesis of testosterone (in men) and estrogen (in women) and is used to treat advanced prostate cancer.”
A potent inhibitor of testosterone? Isn’t that the exact opposite of what we want? Well, triptorelin is a double-edged sword.

  1. Initially (first injection): Triptorelin, like other GnRH agonists, initially stimulates the pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This initial phase leads to a temporary increase in the production of sex hormones, like testosterone in men and estrogen in women.
  2. Continued Use: With continued administration, triptorelin downregulates GnRH receptors in the pituitary gland as the receptors are fully saturated, thus desensitised and downregulated. This downregulation leads to a significant reduction in the secretion of LH and FSH. As a result, the production of sex hormones (testosterone in men and estrogen in women) by the gonads is greatly reduced. In men, this effect is sometimes referred to as chemical castration. This is precisely why long-term and esterified triptorelin administration (to increase its half-life significantly) is used in men with prostate cancer to suppress androgens to basically castrate levels.
But, there is an opportunity to manipulate step 1 to try and kickstart your HPT axis. In fact, although its hard to find any evidence of this in the research (mainly because most studies are designed to investigate how well triptorelin suppresses androgens), there is some evidence that the first injection of triptorelin can significantly increase LH and androgens.
According to this study, which administered patients 11.25mg triptorelin pamoate Sub-Q, there was an initial increase in luteinizing hormone (LH) concentrations at week 1 after the first triptorelin injection. Specifically, the mean serum LH values increased by 37.6% at week 1 compared to baseline. However, from week 2 until the end of the study, LH levels were reduced (as expected with continued use). Now, regarding testosterone levels, there was a short-lived “flare-up” (not sure how that got passed as scientific language but anyway) of testosterone levels after the first injection of triptorelin, which is obviously an expected response with GnRH agonists. However again, as expected, after this initial increase, the testosterone levels decreased as intended by the treatment:

https://preview.redd.it/lqz4ybznzjtc1.png?width=1678&format=png&auto=webp&s=0053a24986c510c28d6e1ddd5dbe39a0b855a5f6
Now, to be completely honest, testosterone levels only rose around 50 ng/dL in the study above. Not exactly a great result. And you may be thinking, surely this isn’t going to fix my 10 year B&C-induced hypogonadism to any significant degree. Well, just wait.
In this next study, where rats were given intramuscular injections of triptorelin acetate biodegradable microspheres (0.6 mg/kg) every 28 days, for three rounds, there was a huge spike in total testosterone in the following fashion:

  • Initial Testosterone Spike: Following the first injection of triptorelin, there was an initial big surge in testosterone levels. The peak concentration of testosterone (Cmax) reached 22.8 ng/mL at 1 hour after the injection (graph below). This initial increase is consistent with an initial stimulation of the pituitary gland to produce LH and thus increase testosterone.
  • Subsequent Testosterone Suppression: After this initial spike, the testosterone levels showed a rapid and sustained decrease. The castration level of testosterone was reached within 5 days after the injection and was maintained below this level until day 28.
  • Repeated Doses: For the second and third injections (on days 28 and 56), there was a transient escape of testosterone above castration levels, with peak concentrations (Cmax) of 0.83 ng/mL and 1.27 ng/mL, respectively, observed on day 28 and day 56.
  • The second spike (0.83 ng/mL) was 22.8 ng/mL - 0.83 ng/mL = 21.97 ng/mL lower than the initial spike.
  • The third spike (1.27 ng/mL) was 22.8 ng/mL - 1.27 ng/mL = 21.53 ng/mL lower than the initial spike.

https://preview.redd.it/lrk7f5kozjtc1.png?width=1544&format=png&auto=webp&s=17960b0fd403b035cca63f3b794b2dacfc50dc14
But that first spike, the first dose was 27x higher than baseline levels. That’s a huge spike in testosterone and perhaps proof that if you could manipulate the pharmacokinetics of an initial dose of triptorelin, you could potentially ‘kickstart’ a sluggish HPT axis into life by forcing a concomitant increase in LH.
So, where does this leave us?
Well, the theoretical idea behind using triptorelin is as follows:

  1. Utilising the Initial Stimulatory Effect from known Phamacokinetic Studies: A single small dose of triptorelin may act as a powerful stimulant of the pituitary gland, leading to a surge in LH and FSH. This surge could, in theory, "kickstart" the testes into producing testosterone again.
  2. Cautions with Dosage: It's crucial to use a very small dose. A typical dose used for prostate cancer treatment would be far too high and could actually cause further suppression of the HPT axis. The dose intended to stimulate the HPT axis would be significantly lower, often referred to as a "micro-dose."
Take this with a grain of salt and obviously not medical advice, but something like a once off 100mcg shot of triptorelin could be an option here, as a micro-dose to kickstart the HPT axis again.
In summary, this post was mainly for the guys where conventional PCT has failed or they have had such an aggressive and sustained suppression of their HPT axis for such a long time that once the stimulatory effect of a SERM/PCT is removed their HPT axis just cannot return to their natural baseline levels. Using triptorelin is highly controversial and there really is limited information on using it in the context of HPT restarts (as opposed to androgen suppression), but my goal is to get as much information out there as possible so you can be informed in the fitness industry. Groundbreaking research and new theories are often deemed crazy and unrealistic at the start, but can lead to some interesting scientific discoveries.
To have men out there going to their doctor, complaining about low/borderline-low testosterone levels to only be brushed aside and told “you’re fine”, or worse shamed for their usage, is unacceptable to me - these men need help just as much as anyone else.
Thanks so much for reading guys, I’ll see you in the next one! Social links are on my profile if interested in more.
submitted by thatdocman to Testosterone [link] [comments]


2024.04.10 03:16 thatdocman If PCT has failed you [Research 2024]

If PCT has failed you [Research 2024]
So guys, I thought I’d do a post about what the next options are if conventional PCT fails. I’ve heard from and spoken to many guys across the world on this, and I’d say in 70-75% of cases I can help get them relatively close to their pre-TRT levels. Obviously, this is not a perfect science and this process can be complicated by a number of things: generally older guys and those who have used 19-nortestosterone derivatives/progestins (that are more suppressive than non-19-nortestosterone derivatives) are going to have a harder time to recover their HPT axis function. Another big variable is dosage and time on - obviously the guy who has been on 100mg TRT for 3 months and wants to come off is going to have a much easier time than the guy who has B&Ced for 10 years.
Now, in most cases, the big 3 usually suffice:

  • Time
  • Initial hCG stimulation (but removing this quickly - hCG is suppressive in its own right)
  • SERM to modulate estrogen receptors to increase T

However, men who have had significant suppression of their HPT axis over a long period of time for whatever reason just cannot seem to break past say 200-250 Total T levels, and may still feel terrible. I do have some theories around why this is the case, including damage to the Leydig and Sertoli cells (death, apoptosis) - however, what is interesting that even in these men, clomid or enclomiphene actually boosts their LH level to often double or triple reference range - and their body responds. Some men get some solid testosterone readings on enclomiphene, but here’s the issue: once the stimulus is removed, they often go right back down to hypogonadal levels of androgens. In other words, it’s almost as if the brain signalling just isn’t there (gonadotropin release: LH, FSH) to support their natural pre-anything baseline levels of testosterone.
In my opinion, with these men, if the fact that a SERM can raise their LH and they get a significant increase in testosterone as a result, only to go hypogonadal once removed, it’s not actually an issue at the Sertoli/Leydig cell level - this infrastructure is working well with the stimulus of enclomiphene. It’s actually, the brain isn’t pumping out enough gonadotropins. In other words, it’s a brain signalling issue higher up in the HPT axis.
So, there is another option for these kind of men. And it’s in the form of an analogue of GnRH called Triptorelin (acts in the same way that GnRH does). Now, way up in the cascade of the entire HPT axis, GnRH is released from the hypothalamus to stimulate your anterior pituitary to release LH/FSH. So the idea is this - if you can introduce a single, potent dose of GnRH, the idea is you can ‘kickstart’ your HPT axis back into life:

https://preview.redd.it/z9vfw405zjtc1.png?width=644&format=png&auto=webp&s=db1d0dbfe38bb415811d7a272f4337b46b3744ed
Initially, you might be confused, because if you search Triptorelin online, you get the following:
“Triptorelin is a gonadotropin releasing hormone (GnRH) agonist that is a potent inhibitor of the synthesis of testosterone (in men) and estrogen (in women) and is used to treat advanced prostate cancer.”
A potent inhibitor of testosterone? Isn’t that the exact opposite of what we want? Well, triptorelin is a double-edged sword.

  1. Initially (first injection): Triptorelin, like other GnRH agonists, initially stimulates the pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This initial phase leads to a temporary increase in the production of sex hormones, like testosterone in men and estrogen in women.
  2. Continued Use: With continued administration, triptorelin downregulates GnRH receptors in the pituitary gland as the receptors are fully saturated, thus desensitised and downregulated. This downregulation leads to a significant reduction in the secretion of LH and FSH. As a result, the production of sex hormones (testosterone in men and estrogen in women) by the gonads is greatly reduced. In men, this effect is sometimes referred to as chemical castration. This is precisely why long-term and esterified triptorelin administration (to increase its half-life significantly) is used in men with prostate cancer to suppress androgens to basically castrate levels.
But, there is an opportunity to manipulate step 1 to try and kickstart your HPT axis. In fact, although its hard to find any evidence of this in the research (mainly because most studies are designed to investigate how well triptorelin suppresses androgens), there is some evidence that the first injection of triptorelin can significantly increase LH and androgens.
According to this study, which administered patients 11.25mg triptorelin pamoate Sub-Q, there was an initial increase in luteinizing hormone (LH) concentrations at week 1 after the first triptorelin injection. Specifically, the mean serum LH values increased by 37.6% at week 1 compared to baseline. However, from week 2 until the end of the study, LH levels were reduced (as expected with continued use). Now, regarding testosterone levels, there was a short-lived “flare-up” (not sure how that got passed as scientific language but anyway) of testosterone levels after the first injection of triptorelin, which is obviously an expected response with GnRH agonists. However again, as expected, after this initial increase, the testosterone levels decreased as intended by the treatment:

https://preview.redd.it/1ogjyhl5zjtc1.png?width=1678&format=png&auto=webp&s=7f3f255bda9c6c92ee136414f08875cddbb89916
Now, to be completely honest, testosterone levels only rose around 50 ng/dL in the study above. Not exactly a great result. And you may be thinking, surely this isn’t going to fix my 10 year B&C-induced hypogonadism to any significant degree. Well, just wait.
In this next study, where rats were given intramuscular injections of triptorelin acetate biodegradable microspheres (0.6 mg/kg) every 28 days, for three rounds, there was a huge spike in total testosterone in the following fashion:

  • Initial Testosterone Spike: Following the first injection of triptorelin, there was an initial big surge in testosterone levels. The peak concentration of testosterone (Cmax) reached 22.8 ng/mL at 1 hour after the injection (graph below). This initial increase is consistent with an initial stimulation of the pituitary gland to produce LH and thus increase testosterone.
  • Subsequent Testosterone Suppression: After this initial spike, the testosterone levels showed a rapid and sustained decrease. The castration level of testosterone was reached within 5 days after the injection and was maintained below this level until day 28.
  • Repeated Doses: For the second and third injections (on days 28 and 56), there was a transient escape of testosterone above castration levels, with peak concentrations (Cmax) of 0.83 ng/mL and 1.27 ng/mL, respectively, observed on day 28 and day 56.
  • The second spike (0.83 ng/mL) was 22.8 ng/mL - 0.83 ng/mL = 21.97 ng/mL lower than the initial spike.
  • The third spike (1.27 ng/mL) was 22.8 ng/mL - 1.27 ng/mL = 21.53 ng/mL lower than the initial spike.

https://preview.redd.it/bat3uv56zjtc1.png?width=1544&format=png&auto=webp&s=f365c778b2a9fac5373c9b14d1935295b69f56f2
But that first spike, the first dose was 27x higher than baseline levels. That’s a huge spike in testosterone and perhaps proof that if you could manipulate the pharmacokinetics of an initial dose of triptorelin, you could potentially ‘kickstart’ a sluggish HPT axis into life by forcing a concomitant increase in LH.
So, where does this leave us?
Well, the theoretical idea behind using triptorelin is as follows:

  1. Utilising the Initial Stimulatory Effect from known Phamacokinetic Studies: A single small dose of triptorelin may act as a powerful stimulant of the pituitary gland, leading to a surge in LH and FSH. This surge could, in theory, "kickstart" the testes into producing testosterone again.
  2. Cautions with Dosage: It's crucial to use a very small dose. A typical dose used for prostate cancer treatment would be far too high and could actually cause further suppression of the HPT axis. The dose intended to stimulate the HPT axis would be significantly lower, often referred to as a "micro-dose."
Take this with a grain of salt and obviously not medical advice, but something like a once off 100mcg shot of triptorelin could be an option here, as a micro-dose to kickstart the HPT axis again.
In summary, this post was mainly for the guys where conventional PCT has failed or they have had such an aggressive and sustained suppression of their HPT axis for such a long time that once the stimulatory effect of a SERM/PCT is removed their HPT axis just cannot return to their natural baseline levels. Using triptorelin is highly controversial and there really is limited information on using it in the context of HPT restarts (as opposed to androgen suppression), but my goal is to get as much information out there as possible so you can be informed in the fitness industry. Groundbreaking research and new theories are often deemed crazy and unrealistic at the start, but can lead to some interesting scientific discoveries.
To have men out there going to their doctor, complaining about low/borderline-low testosterone levels to only be brushed aside and told “you’re fine”, or worse shamed for their usage, is unacceptable to me - these men need help just as much as anyone else.

Thanks so much for reading guys, I’ll see you in the next one! Social links are on my profile if you are interested in more.
submitted by thatdocman to trt [link] [comments]


2024.03.28 19:24 Money_Molasses3210 A levels Guide (CJC Edition)

Hello! This is an A level guide for CJCians (but I'll try my best to talk about things which can apply to redditors from other JCs). Mainly, through this post, I will talk about the basic rules and mindset u have to follow to do well in As, followed by how u can boost portfolio, and lastly how to study for the subjects I have studied in As.
Do note that following this doesn't necessarily mean that you will 100% gaurantee + chope you will do well in As; I'm merely stating observations based on what I see and what I have done.
P.S. If u have any questions down the road, do comment! I'll answer ASAP.
I honestly didn't feel like doing it since I am very very unqualified (I see an A levels guide by 2 90RPers with H3 dist???) and I don't want to talk about my grades, cos it feels like flexing sometimes. However, my junior wants me to finish it, so here I am! ;-;
I'll lay down my grades so you can assess my credibility when I start my yap fest later on: Subjects Prelims A Levels
H2 Math: A A
H2 Physics: A A
H2 Economics: B A
H1 Chemistry: A A
H1 GP: B B
H1 PW: -- A
H1 Chinese (Does that even matter?): From E to C
If you are lazy like me and don't want to do the math, I had a small RP jump from Prelims- 86.25RP to A levels- 88.75RP! And another minor side note, I had H3 Game Theory Pass, but not like it matters here.
And for Ppl who wanna know my O levels for the relevant subjects, A1 for pure physics, A2 for E math, A1 for A math, and C5 for English LOL.
Now that I've covered the groundwork, I will go on to talk about the main topic ya'll are visiting for. Even starting off writing this godforsaken essay, I know I am going to yap harder than our master waffler Principal Woo Soo Min (Seriously, how does she yap better than Phyllis?), so I will be inserting as many tacky CJ jokes as possible to keep ya'll entertained while you scroll. So sit back and watch, let me cook; better than Sedap Auntie's Popcorn Chicken and our BUSSIN milo (my chicago fr).

Basic Advice (Applies to All JCs):

Surprisingly, there is a lot of things to talk about for CJ than other JCs, because Science stream students (Includes arts ppl too!) are an abomination to behold. So i will list down common mistakes CJCians/Other JC ppl do that does them no good + harms their grades, in order of ranking.

1. Mugging Revenge Arc (Fueled by your inner darkness):

Ok, if you are one of these people who started hardcore mugging at January and February, pardon me if I am breaking community guidelines, but are you acoustic? You are mugging at the start of your JC syllabus, a time where they are easing you into the curriculum. So, you are quite literally maxxing out your fundamentals (which, prob like 5% will come out in As) and hitting the AS vertical range with little LRAS, cos you are trading huge amounts of effort for little gain in skills and content.
This is usually a huge red flag for burnout, and often times I see the foyer tables packed with J1s at the start of J2, only for that emo (i need my academic comeback arc) craze to end by March/early April.
I understand that you regret underperforming, I did too. I wanted to go EJC (COP: L1R5 6) but I got 14 raw, which honestly hit me like a truck. I studied from afternoon to morning (4am), grappling with covid to what end (I had to go to hospital, even until today idk why :p). Thus, it is good to remember that revenge is slow and sweet, so take your learning slow when you kickstart your JC journey. Matriculation is a time for exploration; make new friends, and prioritise productivity over time studied. We are not competing with KPIs uk. I will talk about how i study later on. Take baby steps alright? A levels isnt a 100m sprint, it is a marathon.
Remember: Alex Wong had to walk first in order to cycle, and had to roll first before he could walk (I feel so bad for saying this now alamak)

2. Hold pen, not hold hand:

Like come on man, time is so tight in JC and you still want a girlfriend?? I can tell you with confidence that 90% of the relationships formed in CJC usually die out quickly and end out with you going depresso and not motivated to study. Prior experience: I saw a PW group get all B cos of relationship issues.
Second point is, why CJ??? You can find a much better guy/girl anywhere else, so it must be because of desperation. There is a reason why pregnancy rates are not what it used to be 10 yrs ago, and it is not because we are any less horny. All in all, there's no point pursuing love during JC; it is high maintenance, and low chance of success at the cost of your grades.
My advice is to step up your game, bro. If you really want to go out with a girl/guy and have the physical touch of a woman/guy (like me fr ;-;), perhaps stay good friends and confess after A levels? In the meantime, you 2 can go on study dates. Make your relationship mutual; help each other in building your work ethic, and teach each other valuable skillsets which would ultimately help both of you on D day (i.e. A levels).
Just, don't think with your Neil Armstrong Jet Cannon as first priority ok? Focus on delayed gratification first... (YES! WE GET IT DAWN ANG!!!)

3. Drama & Hype:

I put them together since they are not that bad but still impactful to your studying
Drama is definitely inevitable in any JC, even between teachers (I heard a couple back when I was in J1, it would surprise you). ESPECIALLY in PW AHEM AHEM, it can cost you your A if drama ruins the rapport between your grp mates or their productivity. More relevant to 70RPers is that it can also affect your mentality as well. If you feel worthless, you would be worthless.
So my advice would be to steer clear of drama as much as possible, but I know it can be hard to avoid; I have had my own share of ppl trashtalking me, some for stupid and some for good reason. My take is to ignore them, and if it really directly affects you (e.g. PW), do not sound out to the teacher, it is so useless. Just strategise and find a way to make all parties happy and productive.
(I feel like I need to point this out, but when I mean do not tell cher, it means do not ask your cher to tell slackers to buck up or face a penalty. U r going to sabo ur team rapport unintentionally. If you want to seek counselling due to issues like bullying, then it is a good idea. You can also reach out to your school counsellor as well)
On the other side of the spectrum, you are high after the orientation craze (can't blame you, it is hype). The times where you glorify staircase 6 as our holiest (ironically) tourist attraction should be over, and you should lock in already. If you don't, you mind may be oriented towards getting the most out of your JC experience instead of studying, which could lead to your work snowballing and you would definitely suffer later on in J2. If you reach that stage, CJ will not be burning hot for you anymore (CJ is burning hot cheer fr).

How I study (Brief Overview but it's not brief):

There are many different ways to study and manage your time, but I will talk about mine here. If this is as boring as morning sharing, deal with it, just like how you have to stand in the piazza to wait for their yapping to cease.
It is quite simple. Just think up a simple checklist to do for the day. Always prioritise your homework/assignments first. It doesn't have to be as long as the queues during recess (apart from Oishii food stall. Poor Oishii, the food is not bad...)
This is an example of what I would usually do in a day (J1):
  1. Do SLS assignment (Physics Kinematics) + take notes + do tutorial qns
Yeah. Its literally just that. But do note that some physics assignments actually take damn long to complete, with like 4 sections (A,B,C,D) and school physics notes are very difficult to simplify and conceptualise (I will talk about it later on).
I have to emphasize that you should finish assignments ahead of time (like quite literally, finish your SLS assignments and notes at least 1-4 days after they are released in the portal. I usually check it regularly) , because especially in J1 block test, you won't have time to finish assignments while studying for the papers.
I often try to give myself more things than I can chew in a day. This is so that I can max out my time. If I do finish my work, I either give myself more if I don't feel like I have done enough or take a break for the day. Honestly, my point is to do however much you can do without feeling like shit everyday. A levels is just as much of a battle with the mind as it is a battle against time and grades, so make sure you do not go insane grinding; make it your first priority.
I was also in that academic comeback arc, so I started my JC journey with asking seniors how to study as a J1. I will list them down here.
  1. "Use Mid Year Hols to make sure J1 subject concepts are all strong, because content in J2 would move very fast." I cannot emphasize how this saved my entire JC journey, because that is the only time you can actually catch up before everything goes lightspeed, and this is probably the only reason why I was ahead of everyone.
  2. "If the first test (i.e. Block Test) in J2 is bad, do not be demoralised, since marking is stricter." This is true, and its CJ's way of saying WAKE UP BOYYYY. They will also do it again for prelims
  3. "Make sure practical should be strong. Practical would be like 10-20% of your grades"
  4. "J2 would be a lot busier, so enjoy J1 life first." Please do, otherwise you would burn out for sure in J2. Try to keep your UAS within the threshold of at least 65RP/80RP to ensure you are on the right track for science students. For arts, 50RP/80RP, considering the strict marking of arts stream.
I just want to thank the guy who gave me this god tier advice when I randomly met him in an ASTAR talk on AI in CJ. Honestly, bro was the reason why I had such a good start in JC, so I wish him the best!
Before the hols, you would be given revision packages from your subject tutors (Except for physics. Another L for physics dpt). I emphasize that these are a godsend and is definitely the best way for you to get an academic comeback. You should try to complete all of them during the hols. But ofc, it is a lot, so I will talk about how to manage that further down.
This is an example of what I would do in the hols (both J2 and J1):
  1. Do math revision package
You would start to realise that my checklist is very simple. You don't need so much effort to plan a timetable for what to do for the day; it can be distracting when you keep checking the time (like how I start my stopwatch whenever Phyllis Lim starts her speech). But if it suits you very well, then that is good too! Fundamentally, stick to your style.
During the holidays, I would start finishing my assignments first (which would take like 2-4 days), and then start grinding practices in the revision packages. Ranking the workload for each revision package... definitely math is the hardest to complete, it would take up half of my holidays. After that, it would be economics, and then GP (it is just doing SAQ, how bad can it be? Boy was I wrong HAHAAHA).
I would make sure that Math rev package is finished, because every question given tests a unique concept/nuance that must not be overlooked if uw that A. Afterwards, there may be a time crunch for economics, since they would give you tons of essays and CSQs to do. For J1 mid year hols, I would analyse the essays and do qn interpretation instead of doing the full essays since I have yet to know how to craft my Reqs (I will explain how later for each subject). Then, for CSQ, I would do full ans for short qns and summary for the essay qns (i.e. 8m and 10m). Then for GP, I would do like 5-10 qns for each qn type in SAQ and then yeah thats pretty much it. If u got time, you can do summary practices ig.
If you are in J2, your workload would be much higher, since concepts are going to come faster than the light shining from Mr Sandanam's bald head (Shit's a flashbang I tell you). Thus, your checklist is gnna be a bit more than usual.
An example would be this on a normal sch day (this actually happened btw):
  1. Do 1 full economics essays timed practice on topic ______ and 1 CSQ (do planning for essay qns)
  2. Do 1 full math paper 1 from prelim paper _____ (e.g. RJ, VJ, etc)
Another example during the break before As:
  1. Do 5 full economics essays
  2. Do 2 full math prelim papers
  3. Do 1 Physics Paper 2 and Paper 3
Just make sure it is within your workload threshold. Otherwise, it would be joever for u before A levels (like Mark Li's BMI, buuuuut not like he minds).
And I must EMPHASIZE THIS WITH ALL MY BEING. TAKE A BREAK. You ain't batman; you can't survive on 4hrs of sleep everyday fighting crime (aka your assignments). Take a break day on a/the weekend to unwind, and go out to eat with family/friends. Personally, I would do it on a sunday, but whichever floats ur boat. This is to ensure you are productive and not studying blindly. Even if you do 1000 practices of math qns, you are not going to beat a guy who does 50 qns and actively reads the answers and his working to analyse and rectify his mistakes. It also helps in the battle of attrition; you need to make sure you are in tip top condition for As.
CJC also has a late night study programme. I advise you go for all of them, because you are going to do a lot more work than you would at home as you are under supervision of teachers (wow, shocker amirite). Just don't come for the food, like my god can yall at least register for the dates where PSG is coming pleaaaaseee? Point aside, it would definitely be productive, and if you study with friends, you can discuss topics and ask questions about topics you are weaker at in the canteen (unless uw to do alone and silent, library is the place to go). Round table next to the stairs was my favourite spot.
Lastly, there is a way to gauge your ability for science stream ppl. Always gauge based on percentile. Once you are top 5% for the subject in the exam, you are likely to get A in A levels ( to put into retrospect, Physics distinction rate last yr is ~15%). If you can do it consistently, it is pretty much gauranteed. However, being principal honours roll does not gaurantee that you are good enough to get 90RP; it is only a good chance, albeit better than anyone else.
P.S. I am only scratching the surface. If you need more clarifications, feel free to ask!

Portfolio Boost:

Portfolio is pretty impt because it can help with ABA to unis if your RP is slightly below cutoff, scholarships and admission into highly competitive universities/courses. And, it can also help you fill up your Holistic Student Development Form, which is a godsend for uni/scholarship apps.
I gotta be fr; as a person with no leadership, a lot of extra curriculars are gated by grades/leadership.
I will cover them one by one. (leadership is very subjective, since I am not a leader, so take my words with a grain of salt)
There are different kinds of leadership in CJ; CCA exco, Student Council, SL and class committee.
What is common between all leadership types is that its admission is pretty much a popularity fest, and that applies for all JCs; you need to make yourself out to be a good leader, make new friends, etc to get elected these positions, while also making a good pitch through speeches. You can be an absolute menace to society but if you make urself out to be a good leader, boom leadership attained!
Moreover, the involvement you have in school events varies with each kind of leadership. While HTC/AHTC are both tier 1 leadership iirc, they have less (but still quite a lot) involvement in school events than SC. It would be another essay on its own to explain how CCA exco helps boost portfolio, so tldr is involvement is less than HTC/AHTC, although they tend to have similar or higher workloads, esp if we are talking about CCA presidents. Imo, SLs definitely has the highest involvement in school events, like sports carnival, etc. HTC/AHTCs generally look at class welfare and sch ceremonies, while SC organises events like teachers day, easter, etc.
If you are not in leadership, you are kind of missing out on these involvement, which can actually noticeably boost your co curriculars.
Moreover, grades can also influence your extra curriculars, albeit to a lesser extent. If you get honours roll, you would be in this talent development programme (TDP), where they would share events/activities which you can take part in to boost your portfolio. To list a few examples, outside of nomination for scholarships, there is the SUTD SEED Programme and the Halogen Programme (this one i took part in). It is reasonable why it is gated by grades; it requires quite the time commitment during school curriculum btw, so it is not suited for you if you are already struggling with studies.
I emphasize that I say all of this not to say your portfolio is joever once you don't take leadership/have good grades, but it is more like you can get all of these resources once you hit certain thresholds. Outside of these 2 areas, there are also other events to take part in to make your co curricular records look sweet.
Closer to Mid Year Hols, the school would give a couple of presentations regarding 4 programmes (u can only take part in 1 of the 4 but can apply for all), namely Work Attachment Shadowing Programme (WASP), STEM STRETCH Programme, and a law programme (i.e. JCLP) and an overseas immersion trip iirc. All of these programmes have their own prerequisites, based on MYE grades (much more lenient than TDP), which I will elaborate later on.
WASP is probably the closest thing to an internship out of all events in CJC. There is a range of different work attachments offered, and it varies from law (again, but only 1 slot) to like tech. I speculate that it is based on MYE grades, while following a class based quota of maybe 1-2 per class. people with like 40RP can get inside. you have to write an essay of application for the slot you want. I wanted the law one but was brought to CISCO LOL. Outclassed by a person who wanna go there to wear suit for fun gg. (If I am not wrong, It is headed by Ms Valerie at my time?) It takes place close to the start of hols (varies across diff attachments).
STEM STRETCH programme is what it sounds, and it should also be based on MYE grades oso. (it would be headed by Math HOD Lim Chye Fook, the NPC who walks around with his backpack like he is gearing up for a learning journey). You would be exploring science projects iirc (e.g. bottle rockets), if that tickles your fancy.
I am not too sure about the Law programme (JCLP) and the overseas immersion trip, but i am pretty sure the trip is mainly targetted towards VIA hours.
And I saved you 1hr of yapping in morn assembly/CCE which you can spend on playing brawl stars. You're welcome.
That is probably a pretty high key event for you to take part in, and a pretty impt one at that, since it is low risk on grades and high return.
Another one would be to sign up for OGL. That one is more strict on grades since you are competing with the cohort LOL. They gauge based on grades (I am quite sure above 50/80RP UAS should be fine), and then they shortlist you for an interview, which would then decide whether u r in. Iirc, the questions would be something cliche, along the lines of relations between OG ppl and you as an OGL, and how to break up conflict within ur OG.
There is also activities offered by various departments. The math department offers quite a few competitions and activities to take part in. If I am not wrong, Australian Math Competition, Math Olympiad and GC drawing competitions are some of the things the math dpt offers. Moreover, I am pretty sure the arts department also offers trips to certain areas for cultural immersion(I could be wrong tho). The school may also invite you to talks and dialogue sessions with ministers (e.g. Maliki Osman and CPDD (Economics)).
Lastly, you can also search for events to take part in online/friends can invite you to take part with them. I am talking bootcamps, competitions and programmes by universities. I heard people can also take up mentorships as well. So there is a wide range of activities to take part in, as long as you search for it. Not that it matters too much though, if you are selectively searching for local uni courses only.

How to study (Specific subjects):

I have already written 3.8k words and on the brink of insanity. So if you are still reading, congrats! You probably can survive Mark Li's grandmother stories without sleeping. Truly a pillar of pure focus.
I will cover how to study each subject here. Essentially, how to approach the subject, how to do your questions and how to ace the paper on D day. I'll start with the most boring ones.
In the general sense, I try my best to max out/finish every practice given to me, I actually finish almost all of them, so ig thats what u have to do to be decent uk
Fun fact: I only took GP tuition, so you can actually make it with just CJ stuff

H2 Physics:

You take this subject either because you are good at it, or you are a chronic gambler (like me). The quality of your learning development is sizeably dependent on your teachers (albeit more so on you), and your odds are pretty much 2/13 when getting a good cher to teach the subject, ever since our holy god Mr Nordin left the school (you guys don't know him anyways). Your best shot at As is our favourite pokemon trainer Zachary Kok, or should i say Ash Kok, if you get what I mean :) (I hate my life rn). Lim Seow Thong is also quite good and will give you the resources (and his own videos!) to help you ace your exams. If you are ignite, don't need to worry man, all your chers should be decent at worst.
The way to approach physics questions is to ground your answers in concept. In calculation qns, try your hardest to stick the the equation used in the qn and sub in values to get the answer. "Close Enough" answers won't work anymore, that was the biggest mistake I made in physics. It needs to be accurate, and based on logic. For long response qns, you need to follow cause and effect thought processes when answering questions (i.e. this happens, causing this and then finally this happens), while ensuring all logic gaps are filled, so that you hit all the keywords cambridge markers are looking for. My point is, it is alright doing grandmother stories if it means jamming in as much concepts as possible; thats what i usually do LOL.
All the chers in physics dpt definitely know their stuff, but when it comes to teaching... jesus its like listening to 18 morning sharings in a row. I can't listen like at all, like I have turned into lobotomized sand. So I can feel yall when you say science stream is pretty much a death sentence. But, you can still do well with CJ resources!
The order of which I recommend studying for the subject is:
SLS + tutorial Qns + notes Assignment Qns A level Topical TYS Promo/Prelim Papers A level Papers
What I did was:
SLS + tutorial Qns + notes Assignment Qns Supplementary Qns Promo/Prelim Papers A level Papers
Why I recommend Topical TYS instead of Supplementary qns is cos while supplementary qns use older A levels qns which help with content building, Topical TYS is more relevant in terms of application while also achieving content thresholds.
The reason why I put SLS, tutorial Qns and notes together is because I do SLS while writing notes, and the SLS gives u assignments in the form of tutorial qns to do. So in finishing SLS, I also finish notes and tutorials.
Physics Dpt also give this revision package nearer to MYE (which is a LITTLE TOOOOO LATE) but I honestly didnt even use it. If it works for you, then continue using it! I can't really testify its effectiveness though.
How I write notes for physics is really simple. Plug in definitions, and add concepts which may be impt in exams (you can use the learning outcomes to see if it is useful). Make sure that these concepts are displayed as simple as possible, without burning your eyes and making it hard to revise in. Leave some space to add special notes to certain concepts so that you can add them when you make mistakes i practice.
All of this advice applies to Papers 1,2 and 3. As for Paper 4, I have to write another essay again (fml).
Practical is pretty limited when it comes to practice, since you can only really practice during prac sessions in the lab, so do make full use of it. However, there are many things you can practice, like table values being in what sf, how to estimate uncertainty, etc. (I am not going into detail for my sanity, but if you wanna know, just comment and ask!)
Hop onto holy grail, and look for practical papers to practice. Some prac papers answer keys already have values keyed in, so write those answers into foolscap (or your qn paper, if u printed it), with the exception of uncertainty values, tables, graphs, linearization, calculation of gradients and constants, and the short and long planning (sounds like a mouthful, but it rly isnt). Do these questions on your own, practising how sf and decimal places work in calculation of values in tables, best fit line, and how the structure works in long and short planning.
You can practise like this digitally before prac exams, but on the day of exams, please print some papers beforehand to practise before/during your shift to get a feel of actual exam scenario.
Generally speaking, all prelim papers (referring to Papers 1,2,3) are generally about the same standard, so you can legit try out any paper you feel like doing and it should be fine.

H2 Math:

Home of the most NPC teachers you would meet. Clearly, being slammed with algebra and finding the normal distribution for their students actually being normal has taken a toll on their personality. Huge side note, but math teachers would dominate a game of Old Maid with their god tier poker faces. But they are the most meme dpt in the school; they made a sequel of Ginseng Impact questions from MYE to Promos ( I am not kidding.)
As a clapback, I made my own question on Ginseng Impact and answered it at the back of my paper 2 qn paper during prelim exams. They did not take too kindly to it HAHAAHAHAHA (I still got 79% overall LMAOO)
The way you need to approach it is always very structured, even for stats. As long as you understand the meaning behind each step to finding the answer to the question and apply it with equal mastery, you are Gucci.
Even the work sequence isn't really that hard. It is just:
Read notes + Watch lecture Videos + Make notes (Do at the same time) Do tutorial qns Do supplementary qns Do revision package do prelim/promo papers A level papers
Because the revision packages by the math dpt is so good, if u just finish it during the hols, you can definitely score A in the exams (at least for me it did). However, you should only be doing it during the hols. Beyond that, you should start doing prelim/A level papers
I make notes to internalise the info rather than to revise it (this applies to all my subjects, but especially for math), so I only plug in the basic eqns and structures (applies to hypothesis testing)
If you really have no time, focus more on pure math than stats. Pure math has a higher proportion of marks, and even if you have gotten the method to solve stats qns, you can still get it wrong (AHEM PNC). But only do this if u legit have no time.

H2 Econs:

Goated department. Notes are lengthy but pretty good, lectures are fun and informative. Ok, that second point can be argued for depending on the teacher. If you survive the 10.0 Magnitude Earthquake which is Mark Li and Alex Wong entering the LT, you would be in for a treat since the info they give you is pretty much liquid gold (maybe if we filter out Mark Li's story, but it adds to the fun). If its our Halimah Yacob doppelganger Marhaini, hahaha. Good luck.
So the way to approach this subject is via causal links. Every mechanism, every concept and every answer always follow a cause and effect, and the highest top notch answers have done causal links to the max, closing all logic gaps like crazy. (Causal link: ______ causes _____, which leads to ______, causing __(End goal)__) E.g. Rise in supply PAP fall in price
A huge misunderstanding is that Econs is like an arts subjects means memorise a shit ton. Nawwww. Econs is a social science, it follows the logic structure of a science subject, but is tested in a fashion similar to an arts subject.
The work sequence goes like this:
SLS + Read notes + Make notes Do planning for selected essay qns in tutorial Do revision packages Do assignments Prelim/Promo Papers A level papers
You should definitely make notes for econs, cos it is preeetty long. You can compress their 100pg notes to 20 pgs. My way of writing notes is to write a header (e.g. Chapter 1 -- PPC) and draw lines to create 2 columns on the left and right to write your notes. Leave space in the middle for special notes when the econs dpt gives u additional information in lectures, when you make mistakes in essay writing and when you see interesting points made in answer keys.
Always make sure you write your notes in causal links (e.g. AD rise real GDP rise unplanned fall in inventory stock rise in demand for factor inputs, including labor cyclical UNN falls) Pardon if my concept wrong, its been 5 months already ;-;
Other than all of this, it should be fine. Your chers should be able to carry you

H1 Chem:

Mrs Tie is going to have a field day with H1 being a pass/fail. For those who is still under the normal grading system, you still need to invest some effort into getting that A.
I need to emphasize that the bell curve for H1 Chem is rly cancerous, coupled with the fact that CJ exam papers is so much easier than other JCs. Make sure you don't just aim for excellence; aim for perfection instead. Approach H1 Chem like a memory and "common sense" subject;
As for work sequence, I am not very sure for the future 70RPers, but Mrs Tie should have planned for ya'll to not work so hard, so this is for the 90RPers;
Read notes + do practice questions make notes Do RAP (During lesson) Do practice papers given by Mrs Tie
It's pretty simple! (Coming from top in cohort) Make sure you do notes for chapters ahead of what Mrs Tie is teaching, so that you have more time for other subjects. Also, I use answers from other prelim answer schemes to beef up my answers, since Mrs Tie's answers are oversimplified (aims to help ppl pass, not score well)
Also, again, leave space for additional notes in your notes when you make mistakes when doing practices.

H1 GP:

Jeez, this is probably the most flexible one out of all subjects. My only emphasis is that one should not see GP as a subject which cannot be studied, but one which can be grinded. And yes, I am aware of the syllabus change.
Approach GP like a formula. There is a strict format to answering SAQs and essays, and with the right investment, you can actually ace the exam.
I won't give a work sequence for this, but rather things you have to do.
For SAQ and Summary writing, use the revision packages. My only mistake was underestimating how useful it is in developing skillsets essential to scoring well. And you know how impt SAQ is in paper 2. For summary writing, unless u r an arts student or really good at english, just paraphrase word for word man. At least you are accurate, and not missing out on marks because of vocab errors.
Follow the format ur cher gives you, because each GP cher teaches differently from each other, unless that cher is really horrible.
With a greater mark proportion into AQ, content is much more impt to acing GP. But, we do have to note that sometimes, the topic given is just unreasonable (like who knows photography???). When you do not have any content for AQ, draw from personal observation. Like even the most common of practices like HDB void deck marriages and Prayer sessions can be used in AQ if relevant. At the end of the day, it matters just as much to know how to plug in content than to know content.
For essay writing, specialise in preferably 8 topics (5 at min) and make sure these topics aren't so ulu. I prefer topics like SG contemporary issues and maybe tech and AI.
Study content on the topics you chose using straits times, or podcasts (just search __(topic)__ podcast) and you can probably find it. Moreover, CJ also gives content packs on certain topics which you can use too.

It has been 6k words and I am on my final marbles. Just note that all my jokes are in good fun. All the teachers i made fun of are extremely nice and approachable, so if u need help can always ask them.
As my final words, the real challenge imo isn't As, but after it. All that pent up stress built towards A levels would be gone and you would feel confused. Despondent even. After all, you conditioned yourself to work like a machine, to the point where when you are free to make choices, you would be a bit overwhelmed (a bit of an exaggeration but u get me). If you need help, do voice out to me! I can help.
That said, this is all from me. Good luck, and all the best for As!
submitted by Money_Molasses3210 to SGExams [link] [comments]


2024.03.26 04:15 EmergencyAccount9668 Omega-6 fatty acids: the alternative hypothesis for diseases of civilization

https://web.archive.org/web/20210419222349/https://breaknutrition.com/omega-6-fatty-acids-alternative-hypothesis-diseases-civilization/

Omega-6 fatty acids: the alternative hypothesis for diseases of civilization

by breaknutrition Aug 25, 2017

Diseases of civilization

The world is facing a health crisis of unprecedented proportions. What have become known as chronic diseases, Western Diseases, or Diseases of Civilization (DC), have become pandemic as populations around the world adopt the lifestyle that first became prevalent in the country that perfected industrialization, the United States.

What are they?

The DCs revolve around the Metabolic Syndrome (MetSyn), a set of signs of disease that include central obesity, excess fats (or fatty acids) in the blood, high blood pressure and excess blood sugar. The diseases that associate with the MetSyn include the biggest killers in the industrial nations: heart disease, cancer, diabetes, neurological illnesses such as Alzheimer’s and host of seemingly unrelated autoimmune conditions.
Many causes have been blamed for the spread of the DCs; including lack of exercise, wheat consumption, excess consumption of calories, carbohydrates, sugar, animal fats, meat, environmental toxins such as pollutants or pesticides, genetics (most implausibly) and any cluster of associations dreadfully referred to as ‘multi-factorial’.
Each of these proposed causal factors fails, in my view, to explain the pandemic. What I’d like to introduce is an alternative hypothesis, one that better fits the observed epidemiology and that has clearly-described mechanisms that explain much of the pathology for the DCs.
Since it started in America, we’ll start with America. In the late 1800s and early 1900s three events occurred almost simultaneously. First, a method of detoxifying cottonseed oil, which had been an industrial waste product of the cotton industry, was discovered . Next came a method to ‘hydrogenate’ cottonseed oil, or make it into a solid-at-room-temperature edible fat . Thus cottonseed oil and the hydrogenated derivative known as Crisco—introduced in 1911—entered the food supply in large quantities for the first time .
Simultaneously, America began to experience heart disease in large quantities. Previously a very rare condition, heart disease quickly became an epidemic, and the relatively new modern medical profession began to track it, and attempt to devise treatments . Similarly, cancer “control” became a concern, with the forerunner of the American Cancer Society being founded in 1913 .
The single biggest change in the American diet over the 20th century was the increase in seed oils, which increased 1000-fold

What changed?

America, a massive agricultural exporting nation, exported the fruits of the industrial revolution, which included new foodstuffs, including white wheat flour, sugar and vegetable fatty acids— so called to distinguish them from the traditional animal fatty acids that had been used as food since human evolution.
I will refer to vegetable fats (or fatty acids) as seed oils, to distinguish fats made from seeds such as cotton, corn, soy, rape and others from fatty acids made from fruit like olives or palm fruit. This will become important later on.
Wherever American industrially-produced foods were introduced, DCs soon followed. Although not generally well known now, a number of doctors and scientists recognized the impact of industrial foods on populations abandoning their traditional diets for what has become known as the Standard American Diet (SAD) . I prefer the acronym MAD, Modern American Diet, as the American diet prior to industrialization was a largely meat-based one, and did not produce the same diseases, and will use that throughout . Original graph is from Teicholz, N., The Big Fat Surprise, Simon & Schuster: New York, 2014.
![chart representing meat consumption in the United States from 1800-2007](https://web.archive.org/web/20210419222349im_/https://i0.wp.com/breaknutrition.com/wp-content/uploads/2017/08/America-meat-trend-1.png?resize=1080%2C697&ssl=1)

Japan as the canary in the coal-mine

While there are many cases we could examine, perhaps the most telling was the MAD being introduced to post-WWII Japan. After the Japanese surrender, America took over the southern Japanese island of Okinawa, and used it for their base of operations. Unlike most other traditional cultures into which the MAD was introduced, Japan was a highly industrialized country. Yet Okinawans still ate a traditional diet that revolved around pork, yams, and fresh vegetables, and made them famous as one of the “Blue Zones”, a population with exceptionally long lifespans—in fact, the longest in the world .
What is less known is what happened after America took control. The first American fast-food restaurant opened in Okinawa, 9 years before Tokyo, to meet the American soldiers’ appetite. Okinawans also enjoyed American fast food and rapidly adopted it as their own . In that one generation, DCs exploded into Okinawa. Fathers attending the deaths of their sons became a common occurrence, with obesity, heart disease and cancer becoming common.
Hirome Okuyama, a Japanese scientist exploring the dramatic change in longevity in Okinawa, in 1996 published a paper pointing the finger clearly :
Dietary fatty acids – the N-6/N-3 balance and chronic elderly diseases. Excess linoleic acid and relative n-3 deficiency syndrome seen in Japan
“The age distribution of the survival rates of male Okinawans in 1990 is also interesting. The mortalities from all causes for the generations over 70 years of age were the lowest, whereas for those males less than 50 years old they were the highest among the 47 prefectures…”
In a single generation, Okinawa went from the lowest mortality in Japan to the highest

Seed-oils and refined flours brought DCs to Japan

This one incident clearly disproves a number of leading hypotheses on the emergence of DC. It’s clearly not genetic (although that’s a factor, especially in Japan), as gene networks underlying complex adaptations don’t change that quickly. It’s not just caused by total carbohydrates per se, as the Okinawans had a high carb diet with tubers, rice and fruit prior to Americans arriving .
![survey showing okinawan people dietary lifestyle ](https://web.archive.org/web/20210419222349im_/https://i2.wp.com/breaknutrition.com/wp-content/uploads/2017/08/okinawa-diet-table.png?resize=1080%2C225&ssl=1)
Americans introduced much larger quantities of cheap refined flours which replaced the Okinawan carb sources. It’s not caused by meat, as the rest of Japan had a huge increase in meat consumption after WWII, and longevity increased, unlike in Okinawa. It’s not caused by animal fatty acids, as they were rapidly replaced by cheap seed oils imported from America—which introduced a program to ‘Americanize’ the Japanese diet.
It’s unlikely to be caused by saturated fatty acids, as consumption of saturated fat was and remains lower in Japan than it was or is in America, and there are no mechanisms to explain how natural saturated fatty acids causes disease. Environmental toxins are an unlikely explanation too, as, while Japan was industrialized, Okinawa didn’t experience a major change in that regard.
There’s also no possibility of a local environmental factor in Okinawa, as Japanese who moved to America saw a similar increase in DCs. And just to throw it out there, this also disproves the cholesterol-heart disease hypothesis, as cholesterol is not associated with heart disease in Japan, but with increased longevity .

Excess Linoleic Acid Syndrome (ELAS)

In my reading, the diseases that surround the MetSyn share common traits. Inflammation and insulin resistance are oft-cited, but perhaps more significant traits include mitochondrial dysfunction, apoptosis (cell death), necrosis (tissue death) and genetic damage.
These point to the common mechanism, named ELAS by Okuyama . I think it’s the best candidate for cause and best explanation of the MetSyn and related, chronic DCs.

What’s Linoleic acid?

Linoleic acid (LA) is an Omega 6 fatty acid (n-6 PUFA) fat which is considered essential to human and animal function. To head folks off at the pass, n-6 fatty acids are found in all natural foods, plants and animals, so this isn’t something you need to avoid entirely – it’s not possible, nor necessary.
There are three major kinds of fatty acids. LA is a polyunsaturated fatty acid (PUFA) . It’s joined by monounsaturated fatty acids (MUFA) such as oleic acid (named for olive oil) and saturated fatty acids (SFA) such as stearic acid (named for steers, beef) or palmitic acid (named for palm oil). Fish oil is also a PUFA, but of the omega-3 variety (n-3 PUFA).
Omega 6 fatty acids are primarily made by plants, as are the similar n-3 PUFAs, and are concentrated up the food chain by animals eating those plants. The major sources of Omega 6 fatty acids in the MAD are oils refined from seeds and animals fed a high proportion of seeds.
PUFAs have traits which make them of interest: they’re highly susceptible to oxidation (rancidity), unlike MUFA or SFA, and they’re used throughout the body as building blocks for tissues and for various signaling functions, after being converted into other chemicals.
The rancidity of PUFAs is the root of the problem
When food goes rancid, it usually smells and taste bad because the MUFAs and PUFAs have decomposed into peroxides . Both n-6 and n-3 PUFAs are highly likely to go rancid. Humans don’t detect the rancidity of Omega 6 fatty acids particularly well, they smell slightly stale and people actually prefer the taste.
Contrast this to rancid n-3 PUFAs and imagine eating a rotten fish. No thanks! This is likely because concentrated n-6 foods were rare until the modern era .

The problems with rancid PUFAs

Both n-3 and n-6 PUFAs going rancid produce toxins, but the n-6 fatty acids produce worse toxins. Most notable of these—and best studied—are acrolein, HNE, and MDA; although there are many others. Collectively, they’re called oxidized linoleic acid metabolites (OxLAMs). Acrolein is the acute toxin found in cigarette smoke. HNE is the best marker of effects of ELAS, as it is only produced from n-6 fatty acids. All three are both produced in cooking or heating n-6 fatty acids, but are also produced in the body. How toxic are these products? Cooking with seed oils is the leading cause of lung cancer in non-smoking women in China .
The list of toxicities of these three chemicals is most impressive. Acrolein is a biocide, meaning toxic to all life. HNE and MDA are less bad than that but are cytotoxic (kill living cells), mutagenic (induce mutations in DNA) and genotoxic (destroy DNA). OxLAMs are also highly reactive, which means they can combine with other molecules in the body, inducing and stimulating malfunction .

A primary mechanism of ELAS

An increase in Omega 6 fatty acids consumption rapidly remodels the tissues in the body, as the fats are replaced throughout. In some tissues it happens within weeks, in others, like the human brain, it appears to take much longer . Increased n-6 consumption rapidly remodels cartilage, for instance, in all species studied, driving out the more stable omega-9 fatty acids (Oleic acid is a n-9 MUFA) . The same happens in mitochondria . As mentioned, mitochondrial dysfunction and DNA damage is a signature of the MetSyn and all related diseases. It’s seen in the fat cells in obesity, in the pancreas in diabetes and in the lining of the vessels of the heart in atherosclerosis, as well as in conditions of heart failure, fatty liver disease, neurological diseases such as Alzheimer’s and Parkinson’s, and, most notably, cancer.

OxLAMs trigger destructive chain reaction events

The mechanism for this is well-described, although not well-recognized. Excess n-6 linoleic acid (LA) consumption causes a remodeling of a molecule called cardiolipin in the mitochondria, the key energy-producing part of cells in all higher life forms. Cardiolipin comprised of LA is uniquely susceptible to oxidation compared to n-3 PUFAs, MUFAs or SFAs and this can happen spontaneously, as LA oxidation can be catalyzed by iron and cardiolipin is in constant contact with iron atoms in mitochondria. When cardiolipin oxidizes, a chain reaction can start. In vitro, so on the lab bench, this reaction continues until all cardiolipin is consumed, but luckily our body has countermeasures .
In this process OxLAMs are produced. HNE, for instance, causes other cardiolipin molecules to oxidize, thus potentially causing a self-sustaining chain reaction. Reactive Oxygen Species (ROS) are produced in the reaction, which can also cause adjacent cardiolipin to oxidize .
However, OxLAMs are several orders of magnitude more damaging to the bodies than simple ROS . HNE itself can induce the production of ROS. Oxidized cardiolipin causes mitochondrial dysfunction, as mitochondria are impaired with oxidized cardiolipin .
What follows is mitochondria either collapsing, inducing apoptosis or necrosis . Apoptosis is seen throughout DCs—in cancer the cells are essentially ignoring the apoptotic signal and going rogue. The Warburg Effect noted in cancers is thought to be a cellular reaction to mitochondrial dysfunction in which the cells adopt an alternative energy pathway to better suit their uncontrolled proliferation.
Thomas Seyfried, who has contributed much to the field of cancer metabolism, notes that dysfunctional cardiolipin has always been observed in cancer cells so far . Necrosis is seen in late-stage DCs, such as atherosclerosis, cirrhosis of the liver, heart failure and Alzheimer’s.
Once loose in the cells, the OxLAMs rapidly propagate, in a process known as Oxidative Stress (OxStr). HNE and MDA are the primary markers used to measure OxStr. ROS cannot leave mitochondria which are well prepared for them, but OxLAMs, being water-soluble, rapidly distribute throughout the cells and beyond. OxLAMs are also a regular part of mitochondrial function: HNE induces mitochondria to downregulate as a basic negative-feedback mechanism.
Presumably this is to limit HNE creation and the spare the important antioxidant glutathione (GSH), as well as the aldehyde dehydrogenase enzyme (ALDH). GSH and ALDH are both important in protecting the body against evolutionarily-expected levels of HNE. Unfortunately for us, excess HNE can impair the function of both GSH and ALDH, thus allowing propagation of a runaway chain-reaction.
Decreased levels of GSH are a typical sign of excess production of HNE, and a dietarily induced deficiency in GSH production predisposes to the DCs . A genetic deficiency in ALDH, which is highly prevalent in Japan and China, predisposes to all DCs .

Tissue health as a function of levels of different fatty acids

Confusingly, assays of n-6 status in pathological tissues often show a lower level of n-6 than other fatty acids, and in these cases, addition of n-6 can actually improve function. This appears to be due to the chain reaction depleting LA or arachidonic acid (AA). The latter is a long-chain n-6 fatty acid produced in the body from LA. N-6 levels are lower, but HNE levels have risen as N-6 is converted into OxLAMs .
OxLAMs can bind to and alter the function of DNA, both in the mitochondrion and cell nucleus. In fact, they appear to be the leading cause of genetic damage, as the markers used for genetic damage are those generated by OxLAMs . Widespread generation of mutagenic and genotoxic chemicals in a live organism (in vivo) would go a long way towards explaining the genetic damage common in DCs.

OxLAMs are inflammatory

OxLAMs such as HNE directly induce inflammation, increasing inflammatory markers. Excess levels of LA-derived AA also induces inflammation, as it is used to build chemicals that send pro-inflammatory messages to the body. The mechanism of anti-inflammatory drugs such as aspirin, NSAIDs and Cox-2 inhibitors partially impairs this pathway.
It appears that a fundamental job of macrophages, an immune-system cell that attacks foreign cells, is to remove toxic OxLAMs from the tissues. Macrophage infiltration into tissue is seen in various DCs other than atherosclerosis, including obesity . One explanation is that the modifications made by OxLAMs to molecules cause those molecules to resemble Pathogen-Associated Molecular Patterns (PAMPs)—the molecules appear the same to macrophages as those on bacteria.
Antibodies for oxidized LDL cholesterol (OxLDL) exist and development of these antibodies for therapy against atherosclerosis has revealed the antibodies to be equally sensitive to bacteria-derived lipopolysaccharides and OxLDL .
Anti-cardiolipin antibodies are seen in several severe autoimmune diseases and are only sensitive to oxidized cardiolipin. Thus excess n-6 is a known cause of autoimmunity. It may be the fundamental cause of the increase in allergic diseases seen in Okinawa and around the world .

Specific disease pathologies

Cardiovascular Disease (CVD)

Goldstein and Brown received a Nobel Prize for discovering the LDL receptor . The next thing they tried to do was to induce the first stage of atherosclerosis, the conversion of macrophages into foam cells, which form the core of the atherosclerotic plaques that are thought to cause heart disease. They failed . Steinberg and Witztum then discovered that LDL must be modified through oxidation to cause macrophages to become foam cells
The nature of the substrate for lipid peroxidation, mainly the in lipid esters and cholesterol, is a dominant influence in determining susceptibility. As noted by Esterbauer et al. (52), there is a vast excess of in LDL, in relationship to the content of natural, endogenous antioxidants. The importance of the fatty acid composition was impressively demonstrated by our recent studies of rabbits fed a diet high in linoleic acid (18:2) or in oleic acid (18:1) for a period of 10 wk. LDL isolated from the animals on oleic acid-rich diet were greatly enriched in oleate and low in linoleate. This LDL was remarkably resistant to oxidative modification, measured either by direct parameters of lipid peroxidation
Esterbauer discovered HNE which is always present in atherosclerotic lesions in all species. Oxidized n-6 PUFAs comprise a large proportion of the fatty acids found in these plaques . OxLDL is the second-best known predictor of myocardial infarction, exceeded only by the OxLDL/HDL ratio (HDL is high-density lipoprotein) .
Other aspects of circulatory disease, such as varicose veins and erectile dysfunction, also display increased rates of OxStr, as determined by the presence of OxLAMs. HNE and oxLDL are active throughout the pathological process to create foam cells, induce macrophage entrance into the lining of the vessels and spur apoptosis, necrosis as well as DNA damage seen in atherosclerosis.
Steinberg and Witztum followed up their rabbit study with a human study, which confirmed the importance of LA in creating OxLDL . Other studies have confirmed the effect. The most successful CVD prevention trial ever, the Lyon Diet Heart Study, which produced a 70% reduction in CVD rates, specifically reduced the consumption of LA and increased the consumption of n-3 and n-9 fats.
It adds validation to the mechanism in humans but should be noted that the metabolites were not measured . Clearing HNE reduces atherosclerotic lesions in an animal model .
Similarly, oxidative activities of OxLAMs are seen in varicose veins, with these markers always being present at affected areas . Erectile dysfunction also appears to be a consequence of this process. Erectile dysfunction drugs, aside from the obvious effects, also have an antioxidant effect, and appear to prolong life in those with vascular diseases .

Cancer

Cancer is considered by many to not be a single disease but a wide array of diseases with, so far as we know, different causes. Viruses are a well-known cause of certain cancers, so it is safe to say that there is no single causal agent of cancer, however appealing that prospect would be.
Much of the pathological behavior of cancer cells can be explained by the effects of OxStr: mitochondrial dysfunction, genetic damage, and a shift to glycolysis despite the presence of oxygen. HNE damages and impairs the function of pyruvate dehydrogenase, the enzyme that allows substrates produced by glycolysis to enter the mitochondria .
This loss, combined with malfunctioning mitochondria emitting high rates of ROS and OxLAMs, may explain the metabolic dysregulation and anti-oxidant upregulation often seen in cancer cells.
Epidemiological work has shown low rates of cancer in populations eating traditional diets. In Asians, migration to industrialized countries increases breast cancer rates many-fold to the point where they reach Western levels .
LA in the diet is in fact required to induce cancer in animals experimentally. The cancer-promoting effects of LA increase as it increases in the diet. This effect plateaus at around 4.4% of total energy, well below levels of consumptions seen in industrial civilizations .
![chart showing level of cancer tumors in rat consuming high levels of EFA in their diet.](https://web.archive.org/web/20210419222349im_/https://i2.wp.com/breaknutrition.com/wp-content/uploads/2017/08/4-LA-cancer-rats-1.png?resize=870%2C1052&ssl=1)
One of the hallmark traits of cancer cells is the seemingly random mutations pervading unstable and disorganized nuclear genomes. There can be tens of thousands of mutations, much fewer than that and sometimes none at all . For many cancers, the theory of it resulting from a single mutation doesn’t hold for most cancers. HNE and MDA both damage DNA in vivo and HNE preferentially damages the p53 gene. The latter is part of the body’s natural cancer-control mechanism and is defective in colorectal and hepatocellular cancers .

Obesity

Omega 6 fatty acids consumption appears to be involved in obesity through several pathways. HNE, which is elevated in obesity, directly induces fat-storage across species at an intra-cellular molecular level by inducing pathological behavior in adipose tissue. The latter then fails to differentiate normally, leading to engorged adipose cells typical of obesity . As LA converts to AA, AA upregulation leads to increased production of endocannabinoids anandamide and 2-AG.
Anandamide and 2-AG are the cannabinoids our body’s produce themselves and are so-called mimetics of trans-Δ⁹-tetrahydrocannabinol (THC) found in marijuana. Injection of endocannabinoids in animal models induces overeating, regardless of how full they feel . Elevated 2-AG is a typical feature in human obesity.
Several studies by a group at the NIH have shown that dietary LA modulates production and levels of 2-AG and can directly induce obesity . Blocking the endocannabinoid receptor using a drug prevents obesity and metabolic syndrome, in animals and humans; however the side-effects like increased rates of suicide are unacceptable, leading to withdrawal of the drug .

Diabetes

One long-observed medical observation is that insulin resistance (IR) accompanies sepsis, a condition caused by infection. OxStr precedes IR in humans and OxLDL antibodies acutely reduce IR in a primate model of atherosclerosis . So the PAMPs found in OxLDL appear to be preoccupy by the immune system, with IR maybe being a reaction to a perceived infection.
A reduced LA diet has been shown to reduce IR in two human studies; one measured OxLAMs, which were also reduced .
HNE injected into skeletal muscle cells directly induces IR in those cells . Mitochondrial dysfunction is a common feature of diabetes and the resulting shift in energy production may play a role in IR. LA directly induces hyperinsulinemia in vivo in animal models of beta cells (which produce insulin in the pancreas) and OxLDL directly causes beta-cell death.
High levels of blood sugar (hyperglycemia) is a central feature of type 2 diabetes. Shulman et al. argue an adipose-centric theory whereby hyperglycemia in type 2 diabetes results from uncontrolled adipose tissue lipolysis which feeds into liver metabolism as an excess of acetyl-CoA that will go on to spur further gluconeogenesis (the creation of new glucose).
Others postulate a liver-centric theory where insulin directly changes the liver’s insulin-to-glucagon ratio, lowering it and thus leading to further gluconeogenesis .
Regardless of the explanation one subscribes to about why type 2 diabetics have high blood sugars, high levels of HNE accompany dysregulation of gluconeogenesis. However, I’ve not seen a mechanism to explain it.
The relation between the food you eat and insulin secretion is represented by the food insulin index, an interesting metrics to watch if you are diabetic.

Neurological diseases

OxStr has become recognized as a major pathological factor in several severe neurological conditions, the incidence of which has been increasing along with increasing n-6 consumption, as seen with Alzheimer’s, Parkinson’s and Lou Gehrig’s disease (ALS). As opposed to rat brains, human brains appear to have a rate-limiter for uptake of LA. AA however, which is only produced in small quantities from LA but concentrates in tissues, does pass the blood-brain barrier.
It’s been observed that AA increases prior to the onset of Alzheimer’s but decreases after its onset . AA is more subject to oxidation to HNE than LA is. HNE and other OxLAMs increase as AA decreases, perhaps indicating the self-perpetuating reaction is underway.
HNE is always found in the pathological areas of the brain. Injecting HNE in an animal model induces the formation of beta-amyloid plaques , the signature of Alzheimer’s disease.
People suffering from epilepsy have been prescribed high-fat ketogenic diets and often benefited from them immensely .
This is possibly because of direct neuronal effects of the diet on “ATP-sensitive potassium (KATP) channel modulation, enhanced purinergic (i.e., adenosine) and GABAergic neurotransmission, increased brain-derived neurotrophic factor (BDNF) expression consequent to glycolytic restriction, attenuation of neuroinflammation, as well as an expansion in bioenergetic reserves and stabilization of the neuronal membrane potential through improved mitochondrial function” .
However, these ‘clinical’ or ‘classical’ ketogenic diets have used highly inflammatory fats like hydrogenated soybean oil and have even been given as replacement shakes instead of a meal . This likely renders the treatment much less effective given how triggering (epileptogenic) inflammatory factors can be for epilepsy . This is why more modern incarnations of the diet tend to use a variety of non-inflammatory fats like butter, lard, coconut oil and olive oil which also happen to taste better.

Liver Disease

Non-Alcoholic Fatty Liver Disease (NAFLD) is a new disease which only appeared when n-6 consumption levels reached the current high levels.
It mimics the effects of alcohol-induced Fatty Liver Disease (FLD). Like cancer, LA is required to induce FLD in animals. Very low levels of LA in the diet allows animals to consume up to 30% of energy as alcohol without pathology .
Total Parenteral Nutrition (TNP) is a feeding strategy in humans with damaged or malformed guts. Fatty liver is a common consequence in TNP and replacing LA-rich oils with fish oils cures the condition in human infants .
A small pilot study from Poland examining NAFLD in humans reduced the dietary levels of n-6 while providing the bulk of calories as carbohydrates.
OxLAMs were reduced, as was insulin, HOMA-IR, weight and NAFLD resolved in 100% of subjects . HNE directly induces the fibrosis seen in advanced liver disease and in other DCs.

Blindness

The leading cause of the blindness in the United States is Age-related Macular Degeneration (AMD). This is probably the only condition where the causal role of n-6 has not only been established but is becoming widely recognized. It’s illustrative of principles that should likely be informative for treating other DCs. The retina of the eye is rich in PUFAs and like other tissues is affected by diet.
N-3 supplementation does not affect the progression of AMD unless it’s accompanied by low n-6 intake . That combination is preventative—an evolutionarily-appropriate balance of the fats appears to be crucial. N-6 fatty acids are very susceptible to oxidation by radiation, even visible light; blue light will induce retinal n-6 PUFAs to oxidize to highly toxic HNE.
This may also be the causal pathway behind sunburn and skin cancer.

And more!

Osteoporosis, osteoarthritis, asthma, diabetic side-effects such as kidney failure, chronic pain and my personal favorite, sunburn, all have pathological roots in ELAS. Even high rates of violence have been compellingly linked to ELAS.

Pathological cofactors

Several cofactors induce worsened OxStr is humans. In vitro, mixing LA, glucose and water at physiological concentrations induces peroxidation of LA into OxLAMs; the same has been shown in an in vivo animal model where increased n-6 feeding induced cardiolipin breakdown with subsequent induction of hyperglycemia causing mitochondrial collapse and cardiac necrosis .
This is seen in heart failure, now epidemic amongst humans. Alcohol, fructose, smoking, radiation and infection all increased levels of OxStr and as in FLD, the effects of OxLAMs may play a role in the pathology associated with those factors. If two factors contribute to a disease but the disease only appears when one is present, it’s logical to conclude that the required factor is causal.

A final note on epidemiology

The epidemiology around n-6 consumption and DCs reminds me of an old joke. A policeman sees a drunk crawling around under a street light.
“What are you doing?”
“I’m looking for my keys!”
“You lost them here?”
“No, I lost them over there.”
“Why are you looking here, then?”
“Because this is where the light is!”
Applying epidemiology to nutrition is a very daunting task. Conducting it in a modern, industrial society is much easier than going to a traditional society with no government statistics or wealthy research institutions.
So most of the epidemiology looking at food consumption is done in the industrial nations, which have mostly had high incidences of seed oils for a very long time, before nutritional epidemiology became a science
Seed oils appear to cease increasing rates of cancer appearance after they comprise 4.4% of energy, and saturate tissues at 5% .
Most industrial populations get more than 5% of energy from seed oils , so comparing one to another is to compare high to high, when what one wants to see is high vs low.
Nevertheless, there are a number of studies looking at DCs in populations with differing food patterns, and they strongly support the hypothesis, with the incidence of DCs in populations consuming fewer seed oils being either fractional or non-existent . This likely explains the rapid increase in DCs seen in countries eating MAD-type diets.

What’s missing?

According to several scientists I’ve read the work of or listened to lately, funding is missing. This is highlighted by Dr. Ron Krauss who works at the National Institutes of Health (NIH). According to him, the NIH have largely stopped funding clinical nutrition research.
That, combined with the pro-n-6 PUFA bias in the American nutrition establishment, means that it’s unlikely much research will be done in the U.S. Much of the research seems to be done in either second-tier US institutions or in Europe and Asia.
There’s a lot of lab work looking at mechanisms but not a lot of human interventional studies. The few that do exist however, like the Lyon Diet Heart Study, Christopher Ramsden’s work and the pilot LA metabolite intervention from Poland are all very compelling .
Research I would like to see on this question is an examination of PUFA status and OxLAM load in those few people still eating a traditional diet free from DCs, as well as interventional studies lowering n-6 PUFA.
Most such studies make no attempt to lower n-6, but just add n-3 on top of it. Due to competition between the two types of fatty acids and as seen in AMD, this is unlikely to be a successful strategy
It’s essentially the modern Japanese diet: excess n-6 but good n-3. This has not prevented DC in Japan, but they do have lower rates of some diseases, like cardiovascular diseases.

Conclusion

HNE was discovered in the early 1980s, many decades after seed oils were introduced. The relationship between n-6 and endogenous production of signaling molecules was discovered later. N-3 fatty acids became recognized as important after that.
Research into this topic was in the 10s of papers in the 1970s and has increased by 135-fold today. It’s a burgeoning field but one that appears to be very much under the radar. In reading through the literature, I have come to the conclusion that the case for ELAS as the root cause of Diseases of Civilization is overwhelming.
Personally, I came to this topic through Stephan Guyenet and his excellent Whole Health Source blog. After months of reading his posts and reading the papers he linked to, I decided to cut seed oils from my diet on the spur of the moment, standing in front of the salad dressings in a cafeteria.
My irritable bowel syndrome of 16 years disappeared in two days. My carb cravings disappeared as quickly, allowing me to discover an underlying wheat sensitivity. Sunburn became a thing of the past and as a pale blonde who had always assumed I was ill-adapted to life under the sun, this was revolutionary.
My excess weight dropped off, along with my now too-large pants one morning, never to return. And after six broken bones in two years, I haven’t broken one since.
I started reading on the topic because I wanted to understand what had caused my personal health recovery – and I guess because I like puzzles.

What to do about excessive n-6 consumption?

Avoid eating seed oils, foods containing seed oils—junk food and animals fed high levels of grains and seed oils, like pork and chicken. Don’t go crazy with the nuts. Eat some fish. But no, you can’t fix ELAS with extra n-3 fatty acids like fish oil, as the Japanese case demonstrates.
Except for fasting, this is the simplest health intervention ever, as it’s impossible to become deficient in n-6 fatty acids when eating whole foods. Even if a fraction of the diseases with pathological signs pointing to n-6 are proven, you’ll still be far better off.
William E.M. “Bill” Lands spent his scientific career studying the role of n-6 and n-3 fatty acids in the body. His conclusion, the title of an article written during his retirement, deserves to be the note to end on here :
Prevent the cause, not just the symptoms
submitted by EmergencyAccount9668 to StopEatingSeedOils [link] [comments]


2024.03.16 19:36 LongVsShortToenails What's in the dark shall come to light.

Hello, I've recently made an account on reddit because I wanted to inform others, especially other women, on the state of disinformation of HPV, pap smears/ cervical cancer and womens overall health. I will also include a short segment on men and HPV. My goal is to better inform women about things in our health that doctors routinely fail to tell us, and/or outright lie about. ** There may be some spelling mistakes throughout.** There's a lot of fear mongering, dismissiveness and dishonesty pertaining to womens healthcare, and I want to encourage other's to think for themselves and ask hard questions whenever we go in for care. Now, I am not anti getting screened or anti-vax. I have my testing and all up-to-date vaccinations. I simply want women to know the risks, benefits and statistics of cervical screening. I will include further links below in a list. Please read EVERYTHING (or at least majority) before commenting. ** The more women are informed, the better chance we have of improving our healthcare. Women are told that if we've ever had sex, then we're at risk of cervical cancer. This is not the entire story. There are many risks factors for development of cervical cancer. How many are you aware of aside from smoking? Hormonal birth control (3-5 yrs of usage), infection with an STD (Chlamydia etc), HIV status, being immunosuppressed, having had an organ transplant, multiple parity (at least 3+ children), multiple sex partners (although what's the real issue if even virgins are told they're at risk), diet and yes, even family history https://www.imperial.ac.uk/news/218633/genes-associated-with-increased-risk-cervical/. According to https://thamesvalleycanceralliance.nhs.uk/our-work/patient-engagement-patient-experience/campaigns/cervical-cance?utm\_source=SM&utm\_medium=T034&utm\_campaign=CervPjan23, 1/10 cases of cervical cancer in the UK are caused by birth control with at least 5yrs of use. Your risk remains heightened for up to 10 yrs after stopping. I wonder what the figure would be like in America. I would wager your gyno has not made you aware of any of these risks factors other than smoking. 1. Women should also know that it is not enough to simply be infected with HPV to develop cervical cancer, although cancer can develop regardless of personal risk. HPV causes 98-99% of cervical cancers, but it is not SUFFICIENT enough to cause cancer. This is developing information, but multiple cancer organizations/ studies have backed up this claim. I personally believe that women are not naturally prone to HPV related cancers as opposed to men (even before screening and the vaccine), and the incidence has been blown out of proportion. It does NOT mean that you or I would NOT develop these cancers at any time, so please don't take this as me saying "Don't screen". That's not what im getting at. https://www.hpv.org.nz/about-hpv/hpv-and-cancer https://www.cancercenter.com/cancer-types/cervical-cancerisk-factors HPV, cervical cancer and women 2. Cervical cancer (in America) was much higher in the 1900's, with estimates hovering around an average 30 cases per 100,000 (white women). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958036/#:\~:text=While%20evidence%20from%20the%201950s,the%2030s%20per%20100%2C000%20women. 3. (Although, cervical cancer was never common but relative to the female population back then, it could be considered frequent). However, its hard to find any other papers citing cervical cancer incidence and death rates over the years, sans screening (I suppose this is deliberate). Rates were far higher for black women, although information is lacking. I will say, that it has always been observed that cervical cancer in black women was always highest. Figures hovered around "30-40% more likely to develop cervical". When you look at official numbers, black women make up a little over 2000 cases each year, out of 11,500-14,000 cases https://jacksonhealth.org/blog/2018-01-15-african-american-cervical-cance. 4. ^^^ This is a graph showing the incidence/death rate of cervical cancer before the invention of the Pap in 1941. We can see that there was a slight, natural decline in rates before the pap was introduced in America. Total hysterectomies also increased during the period between 1935-1975. Smoking began to decrease at a rapid rate in the 1960’s. How can we confidently declare falling rates of CC are a direct result of pap smears, and not because of natural decline and increase of hysterectomies/decrease in smoking? Also note the combination of cervical cancer, AND uterine cancer to make the rates appear higher. We've been told that cervical cancer was once "the #1 cancer killer of women". However, if you try searching for sources and studies on this claim, you will find nothing other than this baseless claim with no reputable sources to back it up. Cervical cancer was never a major killer of women in the developed world https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153831/. In fact, in order to save a few lives from cervical cancer, thousands of women would have to be screened over decades to prevent these few deaths. Despite many cancer organizations and studies claiming that pap smears save lives and are largely the reason for a decrease in cervical cancer, paps have never been clinically studied in randomized trials to test their effectiveness, nor have they been proven to save lives. A few lives may be saved from the development of cervical cancer, but the vast majority of women do not benefit from testing. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1125803/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153831/ 5. You may have also heard or read that cervical cancer is increasing among women in their 30's and 40's. The real story is that a rarer type of cervical cancer( adenocarcinoma), is increasing in white women. Adenocarcinomas are tougher to detect on pap smears and usually go unnoticed until cancer has developed. The increase in this cancer is usually blamed on lack of screening or women being "too old" to have gotten the HPV vaccination. Now that we know there are many risk factors to cervical cancer development, it feels a bit biased and inaccurate to say that an increase in cervical cancer is solely due to these factors. This same sentiment is shared concerning cervical cancer in the developing nations, where doctors/scientists will claim that the lack of screening is the reason why cervix cancer is so high. What they are failing to address is the increased rates of smoking, high prevalence of HIV and other STD's and lack of proper nutrients. Screening will not help much if the underlying risk factors are still there. https://ascopubs.org/doi/10.1200/GO.20.00079 https://ijgc.bmj.com/content/33/4/592.long https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(22)00148-X/fulltext#:\~:text=Findings,observed%20between%202007%20and%202018. https://publichealth.jmir.org/2022/12/e40657 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521146/#:\~:text=Consistent%20with%20other%20studies%2C%20our,cervical%20cancer%20by%20histologic%20type.&text=Although%20squamous%20cell%20carcinoma%20incidence,increased%2C%20especially%20among%20white%20women. https://www.medscape.com/viewarticle/986408?form=fpf 6. Pap smears give women false clearance that "everything is good down there". A clear pap smear usually won't detect your stage 3 adenocarcinoma. You are never "safe" from cancer. This is common sense. How many times have you read on Reddit that a woman's pap smear was clear, only for it to be CIN2 (which isn't cancer), the following year? Getting our cervixes scraped on the outside once yearly, to every 3-5 yrs will not stop cells inside of the cervix from proliferating and becoming cancerous. I believe the changes from a normal pap smear to highly abnormal within a year reflect that. I suggest y'all take a look at this site, which includes women who have had cervical cancer or are currently batting it https://cervivor.org/. The large majority of these women went for a gyn exam (with pap) every year, and still ended up with cervical cancer. Some of these women were vaccinated, many maintained healthy lifestyles and still, they were diagnosed with cervical cancer. 7. Quite a few women stated they had never heard of HPV, or they weren't aware of cervical cancer. The more I read these stories, the more it seems obvious that cervix cancer cannot be prevented. Cancer is completely random, so I am suspicious that pap smears do much to prevent this cancer. Take into account many stories where the woman's abnormal cells actually WERE cancerous, and they had to have continuous pap smears. Some came back normal, others continuously were abnormal and others flipped between normal and abnormal. Now, this ties back into my previous comments that, 1. Pap smears are inaccurate, and 2. getting our cervixes scrapped on the outside will not prevent cells inside from mutating and becoming cancerous. If up to 90% of abnormal lesions regress on their own, then we know at least 10% of women will develop cervical cancer even with yearly testing. A pap smear will not stop you from getting cancer, and rather just tell you if you have it or not. 8. HPV may remain on speculums and transvaginal probes even after intense cleansing. When you get a pap smear, there is the brush that lightly scrapes the outer part of the cervix to collect a sample. It takes a few weeks/ couple months for the cervix to fully heal from the scraping. While your cervix is healing, there is a small chance that your pap was done with an HPV infected speculum, thus infecting you or re-infecting you with the virus. Granted, the sample sizes in these studies were very small, but this is very concerning: https://serval.unil.ch/resource/serval:BIB\_F744117D937B.P001/REF.pdf https://pubmed.ncbi.nlm.nih.gov/26071392/ https://pubmed.ncbi.nlm.nih.gov/22761513/. Additionally, pap smears DO NOT test for any type of cancer. A pap smear's sole responsibility is to test for "abnormal" cells. But because they are highly inaccurate, it cannot tell between actual precancers and benign dysplasias that would heal on their own. What gynos fail to tell women is that 70-80%, up to 90% of "abnormal" lesions regress without treatment. But instead of calling lesions "abnormal", gynos will call them "precancerous". Many things can cause an abnormal pap smear. Having sex within the past 24 hrs, getting off your period or about to start, having a yeast or BV infection, heightened stress, beginning menopause and localized, vaginal inflammation. 9. By telling women the lesions are "precancerous and need to be removed immediately, this gives the false impression that you were just about to get cancer, when in reality, your gyno cannot tell which lesions are cancerous vs benign. If up to 90% of lesions regress, it is false to call them precancerous as they would never turn into cancer. Im sure you've read of women posting on Reddit that "if I hadn't gotten the "precancerous" lesions removed, I would have gotten cancer and died!!" Because of the continued misinformation from gynos about what an "abnormal" result really is, women are thinking the pap smear saved their life when they were never in danger. This is why there's such a fuss over the change to 3-5 years for cervical screening and why women and doctors alike think its too "long" between testing. This example of a petition in Australia to keep 2 yearly pap smears is a direct consequence of women not being told the entire truth of cervical cancer and HPV. They believe their health is at risk due to misinformation https://bmjopen.bmj.com/content/8/2/e019171.You either get cancer or you dont. We have been lied to for so long about abnormal results https://theconversation.com/doctors-must-stop-misleading-women-about-cervical-screening-90496. This leads me into the state of overtesting and overdiagnosis, excess colposcopies, cone biopsies as the result of an abnormal pap. I've seen many a story of women complaining about the extreme pain of cervical biopsies/colposcopies without anesthesia and how doctors dismiss their pain, even after pleads to stop the process (I've personally haven't had to have a biopsy...yet). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423652/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6086061/. I believe gynos/doctors receive reimbursements for every pap smear and following colposcopy or biopsy. There is wayyy too much to write about, therefore all links discussing the blatant overuse of these procedures will also be included below. However, this is NOT a call to stop screening. 10. I would also like everyone to take a look at a proposed, updated method for prostate screening. This was based in the UK and im in America, but prostate cancer affects men worldwide. Have a look at the comments.... notice the reoccuring theme of not having a prostate and/or PSA exam due to overdiagnosis and overtreatment https://www.bmj.com/content/381/bmj.p1062/rapid-responses 📷? In this other article, it says in the UK that they are trying to find the "best way" to create a test for prostate cancer https://prostatecanceruk.org/about-us/news-and-views/2023/11/introducing-transform. No such consideration given to womens cervical screening until recently. Other organizations have also noted that annual prostate screening isnt beneficial for mean due to the risks of harms, even in light of increasing cases of prostate cancer in younger men https://mariekeating.ie/cancer-information/prostate-cancescreening-for-prostate-cance#:\~:text=Currently%2C%20there%20is%20no%20test,of%20a%20national%20screening%20programme. !! Men are given the luxury of having everything tested and trialed for them to reduce risk of harms, while women have to "wait and see" if something is effective. Another example of men being given an easier way to test rather than an invasive exam https://www.sciencedaily.com/releases/2023/02/230207191546.htm. If a full proof blood test was created for cervical cancer, the first criticism would be how its probably "innacurate" and "it makes women believe they dont need a pap smear" I can already imagine that. The disfiguration and brutalization of womens' bodies in the medical field is normalized. Men are given a choice. Women are given a demand. Hpv and Men Where are men getting this false information that HPV doesn't cause issues for them? I work in dermatology and men come in for HPV related genital warts and biopsies on the penis or scrotum in droves. It is extremely common, and even the dermatologists say so. But when you look online, sources state that hpv warts are "uncommon" in men. Completely false and another example of dishonesty in the medical field. No, HPV does not *naturally* affect women more. Everything must only affect women huh? What I find fascinating is that women who come in for warts (on the hands and feet) were usually over the age to have gotten the original HPV vaccine, and yet despite being unvaccinated, it was not women coming in with genital warts, but the men. Additionally, men should know that not only can HPV cause anal and penile cancers for men, but also head, neck and throat cancers which have surpassed cervical cancer in the US, UK and Germany (so far). It was first reported back in 2010/2011 that head/neck cancers in men would upsurge cervical cancer in women- https://ascopubs.org/doi/10.1200/JCO.2011.36.4596. As of 2020, head and neck cancers in men are the most common related HPV related malignancy. It also (on a causative basis) causes prostate cancer. It's been found that between 17-32% of all diagnosed prostate cancers in the US are attributable to HPV. The link between HPV and prostate cancer was noted back in 1970! Unfortunately, I cannot find the study where I originally read that. There's also an ongoing investigation if it also causes testicular cancer. Both of these cancers are increasing rapidly among younger men worldwide. It's odd to me given the information, that there is no rush to create a test for mens' genitals and throats given they are far more at risk. Men are given the option to discuss risk, benefits, pros and cons when it comes to any intimate testing. Women are told "get it done or you'll get cancer". The narratives are clearly different. Links for Men https://www.fredhutch.org/en/news/center-news/2017/01/hpv-infection-half-american-men-study.html#:\~:text=HPV%20infection%20in%20men%20is,old%20they%20are%2C%20said%20Dr. https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.32498 https://www.sttammanyurology.com/posts/prostate-canceprostate-cancer-in-young-men-what-young-men-should-know/ https://www.sttammanyurology.com/posts/prostate-canceprostate-cancer-in-young-men-what-young-men-should-know/ https://cancerquest.org/newsroom/2020/09/does-hpv-cause-prostate-cancer https://www.healthline.com/health/prostate-cancecan-hpv-cause-prostate-cancer#are-they-connected https://abcnews.go.com/Health/men-higher-rates-hpv-compared-women-cdc/story?id=46620419 https://www.nature.com/articles/s41571-022-00603-7#:\~:text=In%20both%20the%20UK%20and,1). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221528/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191828/#:\~:text=Specifically%2C%20the%20incidence%20of%20prostate,per%20100%2C000%20person%20years2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10132363/#:\~:text=HPV%2Drelated%20oropharyngeal%20SCCa%20has,yearly%20cases%20of%20cervical%20cancer. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871537/ https://www.newscientist.com/article/2115987-viruses-may-have-evolved-to-hit-men-hard-but-go-easy-on-women/ https://www.karmanos.org/karmanos/news/throat-cancer-now-surpasses-cervical-cancer-as-the-3289 Final thoughts I aint got nothing else to say. All further links will be included in the list below, including several links to go along with the claims in this post. Most are peer-reviewed articles, there are some blog posts about womens experiences with gynecology. There's also links to cervical cancer organization websites. Some BMJ journals are paywalled and sorry, but the cost is too expensive for me, so if anyone would take the honors of purchasing the articles go right ahead... Please, stay informed everyone. Listen to your doctors, but also do some research and ask questions! This is absolute proof that we are purposely kept in the dark. Sources/Links/Statistics 1. Causes of CC (having HPV not sufficient for cancer): https://www.cancercenter.com/cancer-types/cervical-cancerisk-factors https://publichealth.jmir.org/2022/12/e40657 https://www.hpv.org.nz/about-hpv/hpv-and-cancer https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.33841 :HIV causing CC Africa 2. Risk of abnormal pap progressing to cancer : https://www.uptodate.com/contents/follow-up-of-low-grade-abnormal-pap-tests-beyond-the-basics/print#:\~:text=Atypical%20squamous%20cells%20of%20undetermined%20significance%20(ASC%2DUS)%20%E2%80%94,percent%20%5B1%2C2%5D. https://healthtalk.org/experiences/cervical-abnormalities-cin3-and-cgin/what-is-cin/#:\~:text=CIN3%20is%20an%20abnormality%20in,It%20isn't%20cancer. 3. Screening not saving lives: https://forwomenseyesonly.com/2020/05/04/covid-19-helps-underscore-non-urgency-of-pap-tests/ https://pubmed.ncbi.nlm.nih.gov/12714468/ https://www.bmj.com/content/315/7113/953.full https://jech.bmj.com/content/62/4/284 https://www.bmj.com/content/352/bmj.h6080.full (scroll down to 'Article Tools' then click on '34 responses') https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1377516/ (Scroll down to 'Full Text', then click on and read pages 151-157. I know the twxt is from 1998 in the UK, but the information remains revelant to women anywhere) 4. Screenings overused: https://www.kevinmd.com/2009/11/informed-consent-missing-pap-smears-cervical-cancer-screening.html (After reading the article, scroll down and read the comments) https://pubmed.ncbi.nlm.nih.gov/13678510/#:\~:text=Our%20findings%20raise%20the%20possibility,low%20risk%20of%20cervical%20malignancies. https://www.cuimc.columbia.edu/news/cervical-cancer-screening-tests-often-overused-study-finds https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085723/ https://theconversation.com/doctors-must-stop-misleading-women-about-cervical-screening-90496 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423652/ 5. Cancers that *could* be prevented : https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02178-4/abstract (if we know cc is extremely rare under age 30, the vaccination results aren't spectacular) https://seer.cancer.gov/statfacts/html/cervix.html https://jech.bmj.com/content/62/4/284 6. Women's experiences with gynecology: https://forwomenseyesonly.com/ https://www.reddit.com/Wedeservebette https://www.reddit.com/WomensHealth/comments/1bepzel/my\_obgyn\_told\_me\_any\_pain\_i\_experienced\_is\_in\_my/ https://www.reddit.com/TwoXChromosomes/comments/1berdr0/i\_have\_hpv\_and\_im\_so\_mad\_about\_it/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447652/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6086061/ https://healthunlocked.com/nhsengland/posts/130374741/abolish-screening-programmes-for-the-worried-well-and-start-treating-the-sick https://www.medhelp.org/posts/Womens-Health/Fear-of-Gynecological-Exam/show/25440 https://patient.info/forums/discuss/avoiding-smear-test-372917 https://www.bmj.com/content/383/bmj.p2772 https://patient.info/forums/discuss/not-sexually-active-but-nurse-tells-me-i-need-a-smear-296950 https://plasticdollheads.wordpress.com/2017/01/14/the-fear-mongering-of-the-smea 7. Incidence of gynecological vs urologic cancers: https://www.cdc.gov/canceuscs/about/data-briefs/no11-gynecologic-cancer-incidence-UnitedStates-2012-2016.htm https://www.cdc.gov/canceuscs/about/data-briefs/no21-male-urologic-cancers.htm#:\~:text=in%20the%20testis.-,Incidence,or%20renal%20pelvis%2C%20and%20testis.
submitted by LongVsShortToenails to WomensHealth [link] [comments]


2024.03.15 19:21 LongVsShortToenails What's in the dark shall come to light.

What's in the dark shall come to light.
Hello,
I've recently made an account on reddit because I wanted to inform others, especially other women, on the state of disinformation of HPV, pap smears/ cervical cancer and womens overall health. I will also include a short segment on men and HPV. My goal is to better inform women about things in our health that doctors routinely fail to tell us, and/or outright lie about. ** There may be some spelling mistakes throughout.**
There's a lot of fear mongering, dismissiveness and dishonesty pertaining to womens healthcare, and I want to encourage other's to think for themselves and ask hard questions whenever we go in for care. Now, I am not anti getting screened or anti-vax. I have my testing and all up-to-date vaccinations. I simply want women to know the risks, benefits and statistics of cervical screening. I will include further links below in a list. Please read EVERYTHING (or at least majority) before commenting.
  1. Women are told that if we've ever had sex, then we're at risk of cervical cancer. This is not the entire story. There are many risks factors for development of cervical cancer. How many are you aware of aside from smoking? Hormonal birth control (3-5 yrs of usage), infection with an STD (Chlamydia etc), HIV status, being immunosuppressed, having had an organ transplant, multiple parity (at least 3+ children), multiple sex partners (although what's the real issue if even virgins are told they're at risk), diet and yes, even family history https://www.imperial.ac.uk/news/218633/genes-associated-with-increased-risk-cervical/. According to https://thamesvalleycanceralliance.nhs.uk/our-work/patient-engagement-patient-experience/campaigns/cervical-cance?utm_source=SM&utm_medium=T034&utm_campaign=CervPjan23, 1/10 cases of cervical cancer in the UK are caused by birth control with at least 5yrs of use. Your risk remains heightened for up to 10 yrs after stopping. I wonder what the figure would be like in America. I would wager your gyno has not made you aware of any of these risks factors other than smoking.
  2. Women should also know that it is not enough to simply be infected with HPV to develop cervical cancer, although cancer can develop regardless of personal risk. HPV causes 98-99% of cervical cancers, but it is not SUFFICIENT enough to cause cancer. This is developing information, but multiple cancer organizations/ studies have backed up this claim. I personally believe that women are not naturally prone to HPV related cancers as opposed to men (even before screening and the vaccine), and the incidence has been blown out of proportion. It does NOT mean that you or I would NOT develop these cancers at any time, so please don't take this as me saying "Don't screen". That's not what im getting at.
https://www.hpv.org.nz/about-hpv/hpv-and-cancer https://www.cancercenter.com/cancer-types/cervical-cancerisk-factors
HPV, cervical cancer and women
  1. Cervical cancer (in America) was much higher in the 1900's, with estimates hovering around an average 30 cases per 100,000 (white women). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958036/#:~:text=While%20evidence%20from%20the%201950s,the%2030s%20per%20100%2C000%20women.
(Although, cervical cancer was never common but relative to the female population back then, it could be considered frequent). However, its hard to find any other papers citing cervical cancer incidence and death rates over the years, sans screening (I suppose this is deliberate). Rates were far higher for black women, although information is lacking. I will say, that it has always been observed that cervical cancer in black women was always highest. Figures hovered around "30-40% more likely to develop cervical". When you look at official numbers, black women make up a little over 2000 cases each year, out of 11,500-14,000 cases https://jacksonhealth.org/blog/2018-01-15-african-american-cervical-cance.

https://preview.redd.it/r1ykzyn6hjoc1.png?width=1280&format=png&auto=webp&s=de2eec8eff150d69a09f197abb7d5aa378cf7390
4. ^^^ This is a graph showing the incidence/death rate of cervical cancer before the invention of the Pap in 1941. We can see that there was a slight, natural decline in rates before the pap was introduced in America. Total hysterectomies also increased during the period between 1935-1975. Smoking began to decrease at a rapid rate in the 1960’s. How can we confidently declare falling rates of CC are a direct result of pap smears, and not because of natural decline and increase of hysterectomies/decrease in smoking? Also note the combination of cervical cancer, AND uterine cancer to make the rates appear higher. We've been told that cervical cancer was once "the #1 cancer killer of women". However, if you try searching for sources and studies on this claim, you will find nothing other than this baseless claim with no reputable sources to back it up. Cervical cancer was never a major killer of women in the developed world https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153831/. In fact, in order to save a few lives from cervical cancer, thousands of women would have to be screened over decades to prevent these few deaths. Despite many cancer organizations and studies claiming that pap smears save lives and are largely the reason for a decrease in cervical cancer, paps have never been clinically studied in randomized trials to test their effectiveness, nor have they been proven to save lives. A few lives may be saved from the development of cervical cancer, but the vast majority of women do not benefit from testing.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1125803/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC153831/
*** In this pdf link "Vital Statistics of the United States form 1942": https://www.cdc.gov/nchs/data/vsus/VSUS_1942_1.pdf , scroll down to page 31. Here, we are shown the number of deaths for multiple causes of death, including deaths from cervical cancer in 1941/1942. Notice how it says 16,393 deaths for Cancer of the Uterus? And underneath, cancer of the cervix with 6,493 deaths? Unspecified deaths concerning the uterus were at 9,900 deaths. This is where the "cervical cancer used to be the #1 cause of death" statistic comes from. The data were intentionally misinterpreted by combining all deaths from uterine cancer to make it seem as these deaths were all from cervical cancer. This agrees with the graph I showed you earlier. The true #1 cause of death for women at the time was breast cancer, with over 15k deaths. #2 would be unspecified uterine cancers at 9k, then cervical cancer at 6k, which would make it the 3rd cause of death. Interesting enough, we see that prostate cancer caused 8k deaths in men, more than deaths from cervical cancer. We are being lied to.
5. You may have also heard or read that cervical cancer is increasing among women in their 30's and 40's. The real story is that a rarer type of cervical cancer( adenocarcinoma), is increasing in white women. Adenocarcinomas are tougher to detect on pap smears and usually go unnoticed until cancer has developed. The increase in this cancer is usually blamed on lack of screening or women being "too old" to have gotten the HPV vaccination. Now that we know there are many risk factors to cervical cancer development, it feels a bit biased and inaccurate to say that an increase in cervical cancer is solely due to these factors. This same sentiment is shared concerning cervical cancer in the developing nations, where doctors/scientists will claim that the lack of screening is the reason why cervix cancer is so high. What they are failing to address is the increased rates of smoking, high prevalence of HIV and other STD's and lack of proper nutrients. Screening will not help much if the underlying risk factors are still there.
https://ascopubs.org/doi/10.1200/GO.20.00079
https://ijgc.bmj.com/content/33/4/592.long
https://www.thelancet.com/journals/lanepe/article/PIIS2666-7762(22)00148-X/fulltext#:~:text=Findings,observed%20between%202007%20and%20201800148-X/fulltext#:~:text=Findings,observed%20between%202007%20and%202018). https://publichealth.jmir.org/2022/12/e40657
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521146/#:~:text=Consistent%20with%20other%20studies%2C%20our,cervical%20cancer%20by%20histologic%20type.&text=Although%20squamous%20cell%20carcinoma%20incidence,increased%2C%20especially%20among%20white%20women.
https://www.medscape.com/viewarticle/986408?form=fpf
6. Pap smears give women false clearance that "everything is good down there". A clear pap smear usually won't detect your stage 3 adenocarcinoma. You are never "safe" from cancer. This is common sense. How many times have you read on Reddit that a woman's pap smear was clear, only for it to be CIN2 (which isn't cancer), the following year? Getting our cervixes scraped on the outside once yearly, to every 3-5 yrs will not stop cells inside of the cervix from proliferating and becoming cancerous. I believe the changes from a normal pap smear to highly abnormal within a year reflect that. I suggest y'all take a look at this site, which includes women who have had cervical cancer or are currently batting it https://cervivor.org/. The large majority of these women went for a gyn exam (with pap) every year, and still ended up with cervical cancer. Some of these women were vaccinated, many maintained healthy lifestyles and still, they were diagnosed with cervical cancer.
7. Quite a few women stated they had never heard of HPV, or they weren't aware of cervical cancer. The more I read these stories, the more it seems obvious that cervix cancer cannot be prevented. Cancer is completely random, so I am suspicious that pap smears do much to prevent this cancer. Take into account many stories where the woman's abnormal cells actually WERE cancerous, and they had to have continuous pap smears. Some came back normal, others continuously were abnormal and others flipped between normal and abnormal. Now, this ties back into my previous comments that, 1. Pap smears are inaccurate, and 2. getting our cervixes scrapped on the outside will not prevent cells inside from mutating and becoming cancerous. If up to 90% of abnormal lesions regress on their own, then we know at least 10% of women will develop cervical cancer even with yearly testing. A pap smear will not stop you from getting cancer, and rather just tell you if you have it or not.
8. HPV may remain on speculums and transvaginal probes even after intense cleansing. When you get a pap smear, there is the brush that lightly scrapes the outer part of the cervix to collect a sample. It takes a few weeks/ couple months for the cervix to fully heal from the scraping. While your cervix is healing, there is a small chance that your pap was done with an HPV infected speculum, thus infecting you or re-infecting you with the virus. Granted, the sample sizes in these studies were very small, but this is very concerning:
https://serval.unil.ch/resource/serval:BIB_F744117D937B.P001/REF.pdf
https://pubmed.ncbi.nlm.nih.gov/26071392/
https://pubmed.ncbi.nlm.nih.gov/22761513/. Additionally, pap smears DO NOT test for any type of cancer. A pap smear's sole responsibility is to test for "abnormal" cells. But because they are highly inaccurate, it cannot tell between actual precancers and benign dysplasias that would heal on their own. What gynos fail to tell women is that 70-80%, up to 90% of "abnormal" lesions regress without treatment. But instead of calling lesions "abnormal", gynos will call them "precancerous". Many things can cause an abnormal pap smear. Having sex within the past 24 hrs, getting off your period or about to start, having a yeast or BV infection, heightened stress, beginning menopause and localized, vaginal inflammation.
9. By telling women the lesions are "precancerous and need to be removed immediately, this gives the false impression that you were just about to get cancer, when in reality, your gyno cannot tell which lesions are cancerous vs benign. If up to 90% of lesions regress, it is false to call them precancerous as they would never turn into cancer. Im sure you've read of women posting on Reddit that "if I hadn't gotten the "precancerous" lesions removed, I would have gotten cancer and died!!" Because of the continued misinformation from gynos about what an "abnormal" result really is, women are thinking the pap smear saved their life when they were never in danger. This is why there's such a fuss over the change to 3-5 years for cervical screening and why women and doctors alike think its too "long" between testing. This example of a petition in Australia to keep 2 yearly pap smears is a direct consequence of women not being told the entire truth of cervical cancer and HPV. They believe their health is at risk due to misinformation https://bmjopen.bmj.com/content/8/2/e019171.You either get cancer or you dont. We have been lied to for so long about abnormal results https://theconversation.com/doctors-must-stop-misleading-women-about-cervical-screening-90496. This leads me into the state of overtesting and overdiagnosis, excess colposcopies, cone biopsies as the result of an abnormal pap. I've seen many a story of women complaining about the extreme pain of cervical biopsies/colposcopies without anesthesia and how doctors dismiss their pain, even after pleads to stop the process (I've personally haven't had to have a biopsy...yet). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423652/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6086061/. I believe gynos/doctors receive reimbursements for every pap smear and following colposcopy or biopsy. There is wayyy too much to write about, therefore all links discussing the blatant overuse of these procedures will also be included below.
However, this is NOT a call to stop screening.
10. I would also like everyone to take a look at a proposed, updated method for prostate screening. This was based in the UK and im in America, but prostate cancer affects men worldwide. Have a look at the comments.... notice the reoccuring theme of not having a prostate and/or PSA exam due to overdiagnosis and overtreatment https://www.bmj.com/content/381/bmj.p1062/rapid-responses 📷? In this other article, it says in the UK that they are trying to find the "best way" to create a test for prostate cancer https://prostatecanceruk.org/about-us/news-and-views/2023/11/introducing-transform. No such consideration given to womens cervical screening until recently. Other organizations have also noted that annual prostate screening isnt beneficial for mean due to the risks of harms, even in light of increasing cases of prostate cancer in younger men https://mariekeating.ie/cancer-information/prostate-cancescreening-for-prostate-cance#:~:text=Currently%2C%20there%20is%20no%20test,of%20a%20national%20screening%20programme. !! Men are given the luxury of having everything tested and trialed for them to reduce risk of harms, while women have to "wait and see" if something is effective. Another example of men being given an easier way to test rather than an invasive exam https://www.sciencedaily.com/releases/2023/02/230207191546.htm. If a full proof blood test was created for cervical cancer, the first criticism would be how its probably "innacurate" and "it makes women believe they dont need a pap smear" I can already imagine that. The disfiguration and brutalization of womens' bodies in the medical field is normalized. Men are given a choice. Women are given a demand.
Hpv and Men
  1. Where are men getting this false information that HPV doesn't cause issues for them? I work in dermatology and men come in for HPV related genital warts and biopsies on the penis or scrotum in droves. It is extremely common, and even the dermatologists say so. But when you look online, sources state that hpv warts are "uncommon" in men. Completely false and another example of dishonesty in the medical field. No, HPV does not *naturally* affect women more. Everything must only affect women huh? What I find fascinating is that women who come in for warts (on the hands and feet) were usually over the age to have gotten the original HPV vaccine, and yet despite being unvaccinated, it was not women coming in with genital warts, but the men.
  2. Additionally, men should know that not only can HPV cause anal and penile cancers for men, but also head, neck and throat cancers which have surpassed cervical cancer in the US, UK and Germany (so far). It was first reported back in 2010/2011 that head/neck cancers in men would upsurge cervical cancer in women- https://ascopubs.org/doi/10.1200/JCO.2011.36.4596. As of 2020, head and neck cancers in men are the most common related HPV related malignancy. It also (on a causative basis) causes prostate cancer. It's been found that between 17-32% of all diagnosed prostate cancers in the US are attributable to HPV. The link between HPV and prostate cancer was noted back in 1970! Unfortunately, I cannot find the study where I originally read that. There's also an ongoing investigation if it also causes testicular cancer. Both of these cancers are increasing rapidly among younger men worldwide. It's odd to me given the information, that there is no rush to create a test for mens' genitals and throats given they are far more at risk. Men are given the option to discuss risk, benefits, pros and cons when it comes to any intimate testing. Women are told "get it done or you'll get cancer". The narratives are clearly different.
Links for Men
https://www.fredhutch.org/en/news/center-news/2017/01/hpv-infection-half-american-men-study.html#:~:text=HPV%20infection%20in%20men%20is,old%20they%20are%2C%20said%20Dr.
https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.32498
https://www.sttammanyurology.com/posts/prostate-canceprostate-cancer-in-young-men-what-young-men-should-know/
https://www.sttammanyurology.com/posts/prostate-canceprostate-cancer-in-young-men-what-young-men-should-know/
https://cancerquest.org/newsroom/2020/09/does-hpv-cause-prostate-cancer
https://www.healthline.com/health/prostate-cancecan-hpv-cause-prostate-cancer#are-they-connected
https://abcnews.go.com/Health/men-higher-rates-hpv-compared-women-cdc/story?id=46620419
https://www.nature.com/articles/s41571-022-00603-7#:~:text=In%20both%20the%20UK%20and,1).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221528/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191828/#:~:text=Specifically%2C%20the%20incidence%20of%20prostate,per%20100%2C000%20person%20years2.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10132363/#:~:text=HPV%2Drelated%20oropharyngeal%20SCCa%20has,yearly%20cases%20of%20cervical%20cancer.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871537/
https://www.newscientist.com/article/2115987-viruses-may-have-evolved-to-hit-men-hard-but-go-easy-on-women/
https://www.karmanos.org/karmanos/news/throat-cancer-now-surpasses-cervical-cancer-as-the-3289
Final thoughts
I aint got nothing else to say. All further links will be included in the list below, including several links to go along with the claims in this post. Most are peer-reviewed articles, there are some blog posts about womens experiences with gynecology. There's also links to cervical cancer organization websites.
Some BMJ journals are paywalled and sorry, but the cost is too expensive for me, so if anyone would take the honors of purchasing the articles go right ahead... Please, stay informed everyone. Listen to your doctors, but also do some research and ask questions! This is absolute proof that we are purposely kept in the dark.
Sources/Links/Statistics
1. Causes of CC (having HPV not sufficient for cancer): https://www.cancercenter.com/cancer-types/cervical-cancerisk-factors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1122763/
https://publichealth.jmir.org/2022/12/e40657
https://www.hpv.org.nz/about-hpv/hpv-and-cancer
https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.33841 :HIV causing CC Africa
2. Risk of abnormal pap progressing to cancer : https://www.uptodate.com/contents/follow-up-of-low-grade-abnormal-pap-tests-beyond-the-basics/print#:~:text=Atypical%20squamous%20cells%20of%20undetermined%20significance%20(ASC%2DUS)%20%E2%80%94,percent%20%5B1%2C2%5D%20%E2%80%94,percent%20%5B1%2C2%5D).
https://healthtalk.org/experiences/cervical-abnormalities-cin3-and-cgin/what-is-cin/#:~:text=CIN3%20is%20an%20abnormality%20in,It%20isn't%20cancer.
3. Screening not saving lives:
https://forwomenseyesonly.com/2020/05/04/covid-19-helps-underscore-non-urgency-of-pap-tests/
https://pubmed.ncbi.nlm.nih.gov/12714468/
https://www.bmj.com/content/315/7113/953.full
https://jech.bmj.com/content/62/4/284
https://www.bmj.com/content/352/bmj.h6080.full (scroll down to 'Article Tools' then click on '34 responses')
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1377516/ (Scroll down to 'Full Text', then click on and read pages 151-157. I know the twxt is from 1998 in the UK, but the information remains revelant to women anywhere)
4. Screenings overused:
https://www.kevinmd.com/2009/11/informed-consent-missing-pap-smears-cervical-cancer-screening.html (After reading the article, scroll down and read the comments)
https://pubmed.ncbi.nlm.nih.gov/13678510/#:~:text=Our%20findings%20raise%20the%20possibility,low%20risk%20of%20cervical%20malignancies.
https://www.cuimc.columbia.edu/news/cervical-cancer-screening-tests-often-overused-study-finds
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085723/
https://theconversation.com/doctors-must-stop-misleading-women-about-cervical-screening-90496
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5423652/
5. Cancers that *could* be prevented :
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02178-4/abstract02178-4/abstract) (if we know cc is extremely rare under age 30, the vaccination results aren't spectacular)
https://seer.cancer.gov/statfacts/html/cervix.html
https://jech.bmj.com/content/62/4/284
6. Women's experiences with gynecology:
https://forwomenseyesonly.com/
https://www.reddit.com/Wedeservebette
https://www.reddit.com/WomensHealth/comments/1bepzel/my_obgyn_told_me_any_pain_i_experienced_is_in_my/
https://www.reddit.com/TwoXChromosomes/comments/1berdr0/i_have_hpv_and_im_so_mad_about_it/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447652/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6086061/
https://healthunlocked.com/nhsengland/posts/130374741/abolish-screening-programmes-for-the-worried-well-and-start-treating-the-sick
https://www.medhelp.org/posts/Womens-Health/Fear-of-Gynecological-Exam/show/25440
https://patient.info/forums/discuss/avoiding-smear-test-372917
https://www.bmj.com/content/383/bmj.p2772
https://patient.info/forums/discuss/not-sexually-active-but-nurse-tells-me-i-need-a-smear-296950
https://plasticdollheads.wordpress.com/2017/01/14/the-fear-mongering-of-the-smea
7. Incidence of gynecological vs urologic cancers:
https://www.cdc.gov/canceuscs/about/data-briefs/no11-gynecologic-cancer-incidence-UnitedStates-2012-2016.htm
https://www.cdc.gov/canceuscs/about/data-briefs/no21-male-urologic-cancers.htm#:~:text=in%20the%20testis.-,Incidence,or%20renal%20pelvis%2C%20and%20testis.
submitted by LongVsShortToenails to Wedeservebetter [link] [comments]


2024.03.15 18:28 Hot-Spite-2162 Low MCAT High GPA stat - where do I stand? & help with school list

Hi! I'm an ORM (Asian, female) attending a T20 and will be graduating this year. I'm planning to apply this cycle with a gap year and I was wondering if my MCAT(&retake) was a major red flag to my application.
state of residency: OH (permanent resident)
cGPA and sGPA: 3.99/3.98 (transferred into a T20 after sophomore - red flag?)
MCAT score(s) and breakdown: 513 (129/125/130/129) -> 513 (131/125/130/127)
I was getting FLs around 519 so I planned to retake it but the day before the test, I caught a flu which completely wrecked the test. I should've voided the test but I paid A LOT & studied so long that I just wanted to see my score. Idk if I should do a third retake at this point. I am exhausted with this exam tbh. (also for the CARS, English is my second language) I know most schools look down upon you when you take more than three MCATs :( Should I go for a third retake?
Clinical experience: ~200 hours as a hospice volunteer, ~1000 hours as a caregiver for my grandma with dementia
Non Clinical experience:
Hobbies: volunteered to record audiobooks for children in both my native language & English since high school.
Shadowing experience and specialties represented: 15 hours in NICU and 50 hours in oncology/hematology
Research experience and productivity:
Goals: I want to learn more about epigenetics in human populations & genotype-phenotype relationships which could be translated clinically.
School List (not done): OSU, Cincinnati, Case Western, Wayne State, Virginia, Emory, Yale (I'm not saying that I could go here but it has been my dream school for years)
I would love some recommendations on school lists that have strong genetic backgrounds in MSTP. I know my MCAT is a red flag as an ORM :/ Any help would be greatly appreciated. Good luck to y'all applying this cycle!!
submitted by Hot-Spite-2162 to mdphd [link] [comments]


2024.03.12 06:07 CappedMLM I am designing an ethical labour hire system derived from MLMs. AMA

Seriously. No bullshit. Ask me anything.
I know this is Click-baity, I know. But I absolutely believe it.
In fact, I’m not selling you anything. I am asking you to poke holes in my idea - be constructive but critical. I am asking for constructive ideas to maybe change this to a popular opinion.
This is not a gimmick, this is a concept that I believe can work.
The basic concept.
Create an MLN that is designed using a DAG network instead of a tree network. This allows a multi-parent / multi-child system instead of single-parent / multi-child system.
The basic money creation is not from selling products, it is providing services. This decentralizes the revenue creation from being supplied by a single source (product supplier / creator) to all the individuals that provides the service.
MLNs use a commission system that all commissions flow up. My system allows/needs commissions to flowback down as well. If an individual has too much commission flowing into them, the system creates a back flow commission to the individual's downline.
When you create a graph to show the wealth spread of a standard MLM network, it will show a very pointy, very high, very skinny, high-point. This system takes a graph of an ideal wealth spread and applies the commission rates to try and match the graph.
And that's the guts of it.
Why would people sign up for this? Where's the incentive?
Why work for any system? Whether as an employee, self employed, or any other type of personal fundraising, we all provide value and get something in return. Usually something like money else we value. It's a transaction.
Whether that's "That's now clean enough to eat off" or "So now done, the you won't have to worry about them ever again" or "You can pick it up in the morning, I'll be finished by then.", you still want to be paid for doing the job.
I know that currently there is a load of labour hire companies that make a shit load of money off the backs of others. People pay XYZ company $$$ to get individuals to do tasks 1, 2, & 3. The individuals get paid 60% of $$$ to complete the tasks 1, 2, & 3. The other %40 goes to paying for the business to keep the lights and the Sales Manager's hookers & blow. They're the only expenses to a business, right?
So instead of company XYZ, they get work through cMLM, the capped MLM labour hire company. You still have %60 of what the customer pays, but beyond system costs to run the company, profits mostly go to commissions.
Like other MLMs, marketing & hands on administration gets handled through your upline, hence commissions.
Commission upflow and downflow.
Commissions flow up like a normal MLM. If someone's commissions are spiking up a lot more than others, you can get commission backwash that flows commissions back down your downline.
This does not stop or reverses your commissions, it takes the top off to make things more even.
This is not about killing the incentive to grow, its about not making it too extreme.
Everybody doesn't get the same, but it discourages extreme individual growth. We want good, health growth, not cancerous growth.

This a capitalist system design.
It is designed to encourage growth. It's how it grows that really matters.
A normal MLM participant wants as many sales as possible attributed to them, whether directly or indirectly through their downline.
This cMLM encourages growth of the system by making the commission growth not linear. The higher you get, the slower the commissions grow. They still increase, just the rate of increase that slows. There is a point of diminishing returns for self wealth. You can still make money off commissions, but it's not endless individual growth.
Here's the thing. If your extreme growth causes commission back flow down your downline, that would make you very popular with your downline.
This is what can stop it from being an evil entity. This is how it can fix wealth inequality.
submitted by CappedMLM to AMA [link] [comments]


2024.03.08 16:00 Any_Car5127 Zonal training and Cancer risk

The other day a 68 year old buddy and I were talking about our exercise. He posted a graph of his HR during a run. It hovered around 154, which for old men like us almost certainly puts it in the region between AeT (the aerobic threshold) and AnT (the anaerobic threshold) which means that his training is likely causing his body to favor burning glycogen rather than fat. Intensities between AeT and AnT are generally considered a bad place to train and are called "no man's land".
The top of Zone 2 in the standard 5 zone model that Attia uses is AeT. I don't recall him discussing the reason for "Zone 2" training but it is to get your body to rely on burning fat more than glycogen. This increases endurance because your body stores a hell of a lot more calories in fat than it does in glycogen. People who train in no man's land tend to have "aerobic deficiency syndrome" (aka ADS).
Anyway my friend has fought off cancer his entire life. He had a kidney removed as a child because of cancer and has had lots of skin cancers removed and had other major surgeries to remove cancers too. He said that he wanted to be in no man's land to burn glycogen because glycogen fuels cancer. I told him I thought that was a really interesting idea. I have no idea if it's the right thing to do or not but it's interesting. He said he got the idea from a book called "Anticancer Living" . I haven't read it and don't plan to but if you're in the same boat as my friend it's worth thinking about. Just because Deepak Chopra endorses it on Amazon doesn't mean everything in the whole book is wrong. :-)
submitted by Any_Car5127 to PeterAttia [link] [comments]


2024.03.04 17:40 SeeCrew106 Why I don't like Trump - and you shouldn't either

Donald J. Trump is the worst President the United States has ever had.[1][2][3] He's a sexist[4][5][6], a rapist[7], a peeping tom[8][9] and a sexual molester who fucked drugged-up children like a "total fucking beast"[10][11][12][13] and who openly endorses pedophiles[14].
He's a pathological liar[15][16], a mentally ill narcissist[17a][17b], a lazy[18] slob[19][20], an irredeemable dumbass[21][22][23][24][25], a racist[26][27][28][29][30][31][32] and a Jew hater[33][34][35].
He's a traitor and an insurrectionist[36][37][38][39][40][41][42][43] slavishly devoted to a foreign enemy dictator[44][45][46][47][48][49][50][51][52][53][54] who wants to destroy the U.S. and Europe.
He's a criminal[55], a terrible businessman[56] and a fraud[57][58][59] who even shafts money out of charity events for kids with cancer together with his butthead son[60], a conspiracy theorist[61] in serious cognitive decline[62][63], a deadbeat[64a][64b], a homophobe[65][66][67][68][69][70], a self-proclaimed war lover[71][72], an authoritarian[73][74][75][76], an attention-starved[77] megalomaniac[78] unqualified[79][80] and unfit[17a] for office and a fascist. He's a shameless grifter and a sociopath without empathy. He's a vindictive, childish loser addicted to cable television and social media slapfights. He's also a habitual backstabber. And he stinks. And he paints his face with brown shit. And he incites violence.
[1] NY Times - How Does Trump Stack Up Against the Best — and Worst — Presidents?
[2] Siena College Presidential Ranking Poll 2022 (PDF)
[3] Axios - Read: Historians rank Trump as worst president
[4] ETS - A final response to the "Tell me why Trump is Sexist"
[5] Time - Our President Has Always Degraded Women — And We’ve Always Let Him
[6] Rolling Stone - A Timeline of Donald Trump’s Creepiness While He Owned Miss Universe
[7] The New Republic - Judge in E. Jean Carroll Case: Yes, Donald Trump Is a Rapist
[8] BuzzFeed News - Teen Beauty Queens Say Trump Walked In On Them Changing
[9] CNN Politics - Donald Trump to Howard Stern: It’s okay to call my daughter a ‘piece of ass’
[10] Daily Beast - Inside Donald Trump’s One-Stop Parties: Attendees Recall Cocaine and Very Young Models
[11] news.com.au - Shocking claims of Donald Trump’s wild parties
[12] Times of Israel - Report: Trump hosted cocaine-fueled parties with underage girls
[13] NY Daily News - Donald Trump hosted wild parties with sex, cocaine and underage models: report
[14] NPR - RNC Restores Financial Support For Roy Moore As Trump Gives Full Endorsement
[15] JPDU - Graph of Trump's Lies
[16] Washington Post - Trump is hardly the first serial liar in the White House. But his deceptions are different
[17a] KDHX - 'Unfit: The Psychology of Donald Trump' Diagnoses The President
[17b] MeidasTouch - Top Psychiatrist SOUNDS ALARM on Trump’s Deteriorating Mental State Burn the Boats
[18] Trump Research Book - Trump is too lazy to be an effective president
[19] Daily Beast - Trump’s Roach-Infested Restaurants Are Vile Compared to the Red Hen
[20] FastCompany - What Trump’s Messy Office Reveals About His Leadership Style
[21] Daily Kos - Former Wharton Professor: "Donald Trump Was the Dumbest Goddam Student I Ever Had."
[22] The Young Turks - The 7 DUMBEST Trump Statements
[23] Vanity Fair - A Brief History of Trump’s Allies Calling Him an Idiot
[24] Quartz - All the ways Trump’s closest confidants insult his intelligence
[25] Politico - ‘Idiot,’ ‘Dope,’ ‘Moron’: How Trump’s aides have insulted the boss
[26] ETS - A final response to the "Tell me why Trump is racist"
[27] Vox - Donald Trump’s long history of racism, from the 1970s to 2020
[28] NY Times - Looking Back 1973 Meet Donald Trump
[29] New Yorker - The Death and Life of Atlantic City ("When Donald and Ivana came to the casino, the bosses would order all the black people off the floor")
[30] NY Times - Trump Will Not Apologize for Calling for Death Penalty Over Central Park Five
[31] Washington Post - ‘They’re rapists.’ President Trump’s campaign launch speech two years later, annotated
[32] Wikipedia - Barack Obama citizenship conspiracy theories - Campaigners and proponents - Donald Trump
[33] Washington Post - Trump’s long history of trafficking in antisemitic tropes
[34] NY1 - Trump attacks 'liberal Jews' amid Rosh Hashanah holiday
[35] Vanity Fair - Donald Trump Celebrated Rosh Hashanah by Going Full Antisemite (Again)
[36] HuffPost - Ex-Senior Trump Official: He’s A ‘Traitor’ And ‘A Clear And Present Danger’
[37] MSNBC - 'A traitor': Anonymous former senior Trump official speaks out in new book
[38] NPR - Reports: Trump Gave Classified Info To Russians During White House Visit
[39] The Conversation - Why treason is a key topic in Trump’s 14th Amendment appeal to the Supreme Court
[40] Ohio Capitol Journal - The Trump indictment tells the disturbing story of a traitor working to overthrow American democracy
[41] Department of Justice - United States of America v. Trump
[42] NPR - Read the Jan. 6 committee's report and recommendations for preventing another riot
[43] GovInfo - Select January 6th Committee Final Report and Supporting Materials Collection
[44] Politico - Manafort’s man in Kyiv
[45] Politico - Is Putin playing Trump like he did Berlusconi?
[46] The Sydney Morning Herald and The Age - Donald Trump shoves Montenegro Prime Minister
[47] The Guardian - 'Very aggressive': Trump suggests Montenegro could cause world war three
[48] CBC - Trump, standing with Putin, sided with him over U.S. intel. Is this the dawn of 'America's surrender'?
[49] RFE/RL - Trump Faces Tidal Wave Of Criticism Over Handling Of Summit With Putin
[50] Time - How Trump Ended Up Looking Weak in Front of Putin
[51] Business Insider - Trump told Putin ‘I’m a big fan of yours’ and asked him to be the guest of honor at a Miss Universe pageant, in a series of fawning letters
[52] Politico - Trump calls Putin ‘genius’ and ‘savvy’ for Ukraine invasion
[53] NY Times - The Untold Story of ‘Russiagate’ and the Road to War in Ukraine
[54] NY Mag - Trump Blurts Out ‘Peace’ Plan to Hand Russia Chunks of Ukraine
[55] ETS - A final response to the "Tell me why Trump is a criminal"
[56] ETS - A final response to the "Tell me why Trump is a terrible businessman"
[57] Le Monde - Trump is dealt new legal blow with heavy conviction in financial fraud trial
[58] ABC News - Judge finalizes $25 million settlement for 'victims of Donald Trump's fraudulent university'
[59] American Progress - Trump University: A Look at an Enduring Education Scandal
[60] ABC7 Chicago - Eric Trump funneled cancer charity money to his business: Report
[61] Wikipedia - List of conspiracy theories promoted by Donald Trump
[62] The Daily Show - Trump's Best Words: 2019 Edition
[63] The Standard - Donald Trump is showing signs of mental incapacity like Joe Biden — and his opponents are delighted
[64a] The Atlantic - 'In Financial Circles, It's Pretty Well Known That Trump Is a Deadbeat'
[64b] USA Today - exclusive: Hundreds allege Donald Trump doesn’t pay his bills
[65] LGBTQ Nation - The top ten worst comments Donald Trump has made about LGBTQ people
[66] HuffPost - Trump Signs Law Quietly Undercutting Obama's Protections For LGBTQ Workers
[67] NY Times - Justice Department Says Rights Law Doesn’t Protect Gays
[68] Washington Post - Proposed HHS rule would strip Obama-era protections for LGBTQ individuals
[69] CBC - New Trump policy defines gender as a person's biological sex (Editorialized subtitle used for clarity)
[70] ABC News - State Dept. fighting to deny US citizenship to gay couple's child
[71] JPDU - Donald J. Trump anti-war? BULLSHIT.
[72] HuffPost - Actually, Donald Trump Loves War
[73] USA Today - Donald Trump repeats comment he would be a dictator 'for one day' if reelected in 2024
[74] Associated Press - Trump’s vow to only be a dictator on ‘day one’ follows growing worry over his authoritarian rhetoric
[75] The Hill - Trump called for ‘termination’ of parts of Constitution in December
[76] The Washington Post - Trump calls political enemies ‘vermin,’ echoing dictators Hitler, Mussolini
[77] Rolling Stone - Attention-Starved Trump May Start 2024 Campaign During Biden’s Inauguration, Report Says
[78] The Nation - Trump Is a Cornered Megalomaniac—and That’s a Grave Danger to the Country
[79] France24 - Republican security experts say Trump 'not qualified to be president'
[80] Deutsche Welle - 'Donald Trump is manifestly unqualified to be president' (Yes, this and the previous source are from 2016, but they were prescient about Trump, and all of their objections still apply today)
submitted by SeeCrew106 to JamiePullDatUp [link] [comments]


2024.03.04 14:28 Crinkez [Magnum Opus] A clash of titans: The most cancerous competition bibite

Mid-2022 we saw the first bibite competition. It was an incredible month or two, where we saw bibite cultivators from all over gathering together for the same purpose: To make the best, and submit it, becoming the ultimate super competitor.
This was perhaps the hottest topic in the old (since defunct) fan discord server, where we saw posts from the creators of Magnus Terra, and later, Nubbi Competitor.
After the submission deadline, all bets were off, and bb8 files of vicious specimens were being shared and tested. I initially struggled vs Magnus Terra, but after finally defeating it, moved on to more dangerous opponents. It quickly became obvious that the Nubbi species was the final to-beat benchmark.
Then the video released, and Luscus xHybridus emerged victor over Nubbi Competitor. It was a momentus occasion, and most people sighed with relief that the ordeal was over, and went back to resting on their laurels. But it wasn't over. It's never over.
A few, myself included, started asking the question: Can I create the most powerful competition bibite, despite the competition being over? And - what is the most powerful threshold a bibite can attain, given unlimited time; unlimited generations?
A new, slower, but much more perilous arms race began. One that was years in the making. This is my side of that story.
I've been meaning to do this writeup for months. Originally inspired by SkarixO's excellent essay on the creation of Apophis Apocalysis. https://www.reddit.com/TheBibites/comments/x46fhb/how_i_created_apophis_apocalypsis_full_document/ Unfortunately I don't have fancy graphs.
Regrettably, I started experimenting with the bibites rather casually when I discovered it halfway through 2022, and messed around a lot from around June 2022 starting with v0.41, so when the tournament was announced, I did not immediately take it seriously. A few days prior to the submission date, I pitted all the best mini-bibites I had adapted thus far from various worlds against each other.
The winner: a generation 209 specimen aptly named 2022-07-19a - I renamed it 'Rat Chomper', and submitted it the day before the cutoff date. Unfortunately it did not have avoidance behavior.
Post-submission I renamed RatChompter to 'Racho', in order to be stealthy on the discord servers.
2022-07-21 Racho Stopper: Generation 460, I adapted this one at 11x speed, and named it stopper as it had now developed an avoidance behavior. I tested it against the original gen 209 and this one was clearly superior. This advancement was done in a single day, but I foolishly did not switch my computer on on the final day of submission to do further optimization, as I believed only one submission per person was permitted.
2022-09-08 Racho Layer: Generation 950. I had been doing a routine adaption of the previous 'Stopper' subspecies, and quite by chance, I spotted a single individual around gen 950 laying eggs extremely swiftly. I watched this individual for a while, twice saving it from swimming off into the void, then decided to save it to file. On a whim, I pitted it against the 'Stopper' subspecies. The results were immediately obvious: Racho Layer was significantly more powerful.
Incidentally, Racho Layer is the subspecies I pitted against Magnus Terra in the original bibite fan discord. They defeated Magnus Terra after a legendary 50 hour battle, the populations of both species alternatingly exploding. I witnessed for the first time competition results that I had never imagined could occur. Several times over their 50 hour battle, one species would almost strangle the other into submission. Racho Layer at one stage had over 500 individuals, and Magnus Terra dropped to around 10 individuals. However Magnus Terra bounced back into the hundreds, causing a drop in Racho Layer numbers. The same occurred the other way around, where Racho Layer would almost go extinct, only to make a huge comeback against Magnus Terra. It is important to note that mutations had not been disabled for this particular matchup. Testing was done with 0.42
What I discovered is both species were so powerful that they altered the very nature of the simulation. A population explosion of either species would cause pellet count to drop, and a mass die-off, resulting in the underdog having a counter population explosion and regaining the upper hand. Prior to this, I had not had the opportunity to test bibites powerful enough to do this.
Interesting to note, Racho Layer did not always fare so well against Apophis Apocalypsis, despite Magnus Terra managing to defeat Apophis Apocalypsis in private tests I ran. In some tests, Apophis wins, in others, Racho Layer wins. There can be wide variation here.
2022-09-10 Racho Pink: A direct descendent of the Racho Layer lineage. Nothing special, color naturally became pink.
It was around this time I started to take note of a significant effect on competition results based on the maturity of the initially placed bibites in the tournament. This was tested extensively against both the Magnus lineage and the Didymus lineage, primarily Didymus Phoenix, and an even stronger descendent, Didymus DW (later renamed Didymus Neoplasma)
As v0.42 did not have a maturity equalization function, all following experimental local tournaments were done by manually normalizing maturity to 1.5 Originally I started normalizing to 1.0, but someone in the fan discord suggested that not all bibites can lay eggs immediately at 1.0 maturity due to energy requirements, hence my adjustment to 1.5 maturity as a standard, at the time.
This process has been made redundant with 0.5x as this version now has a function to normalize maturity upon placement.
2022-09-12 Racho Aurora: Generation 2600. Code name during the selection phase was 'Racho Pink 2600a'. Racho Aurora was the first descendent of Racho Layer that was a significant improvement. Aurora was convincingly stronger across the board. Capable of decimating all Magnus and Didymus species at that point, the strongest being Magnus Summum and Didymus Neoplasma. Aurora was even stronger than my own side project, DestaToss, the strongest of which was DestaTossPlatinum.
There were many failed projects in my attempts to improve the lineage's competition strength: RachoLayerTriHex, RachoSteel, RachoPink3600 (gen 3600), RachoBlade, etc. some of which were ran concurrently.
2022-09-14 Racho Blade Ultimate: Generation 3500. This specimen must be highly noted, as it was the pinnacle and final result of all the Steel/Blade tests, and remained my most powerful bibite for well over a month. It was convincingly stronger than Aurora, although in tournaments the initial population explosion phase is somewhat slower than Aurora, it wins in sheer capability of surviving very sparse pellet conditions. This specimen was capable of defeating Nubbi Rex (a Nubbi Competitor descendent) in some conditions, although it did not fare quite as well when tested later against the original Nubbi Competitor or Luscus xHybridus.
2022-10-06 Racho Kala, Magna, Ingens, Citius and Parvus experiments: This was an experiment to attempt to finally increase the strength beyond Racho Blade Ultimate. The test ultimately failed, as the final winner ended up being slightly weaker than Racho Blade Ultimate. This is where I started using Latin for naming schemes to make my bibite saves sound more interesting.
A couple of months passed while I waited for the official tournament results.
2022-12-18 to 2022-12-23 Latin Colors test: Aurum (Latin gold) Caeruleum (Latin blue) Flavum (Latin yellow) Fuscus (Latin brown) Purpura (Latin purple) Rubrum (Latin red) Viridis (Latin green)
I ran this test in response to the tournament outcome announcement video, where Luscux xHybridus was announced the winner. My original assumption that Racho Blade Ultimate was undefeatable was mistaken, as both Nubbi and Luscus could defeat it under specific conditions, though interestingly if I lowered the biomass significantly, Racho Blade Ultimate would still come out on top.
2022-12-23 Racho Aurum (gen 5349) (not to be confused with its ancestor Aurora) proved to be the first succesful adaption of Racho Blade Ultimate.
2023-03-25 On this date I advanced the methodology of adapting highly competitive bibites, achieving nearly an order of magnitude in strength over the original 'Aurum', something which I previously hadn't believed possible. At the time of writing (March 2024) I shall now reveal the secret I used to do this, as by now it is a secret that several other people have discovered:
Turn off mutations and wait. That's it. That's the secret. Pretty anticlimatic, but it is hugely helpful in discovering some of the most powerful bibites in your tidepool.
Racho Aurum 1.1 (gen 5376) was the first result, which I'll tentatively dub Racho Uritur. Uritur is Latin for 'refined', and I think 'refined gold' is an apt name. If I recall, this is the first adaption I've developed using the official 1v1 tournament settings, and as such, it fares much better now in those conditions. I suspect this is due to pellet sparsity, more than sim size.
My first test with this specimen vs Luscus xHybridus in the official 1v1 settings led to a crushing victory. Luscus was left with a single individual (vs hundreds of Racho's) by the 1 hour mark, a clear victory.
A test vs Nubbi Competitor showed Nubbi was far more resilient against a stronger opponent than Luscus. Nubbi lasted just over 4 hours before being driven to extinction; it should be noted that the Racho had an advantage in biomass at the 1 hour point. A reasonable victory.
2023-03-26 Racho Aurum 1.2a (gen 5421) was the next success story. A direct descendant of Racho Aurum 1.1, I tested the two against each other, and at the 1 hour point, 1.2a had over 300 individuals vs 1.1's 60 or so. We'll call this one Racho Uritur Infan, meaning child of the original Racho Uritur. Something notable about these bibites is that they're very good at splitting pellets.
2023-03-27 Racho Aurum 1.3c, (gen 5517) code for test subject which we'll dub Racho Albu. Albu/Album is Latin for white; short for 'white gold'. It's difficult to give a % improvement from 1.2a to 1.3c but in the first test, at the 1 hour point, 1.3c had 433 individuals vs 1.2a's 85 individuals. A significant improvement. Albu also occasionally tosses pellets. In a 1v1 test against Luscus, Racho Albu caused Luscus to go extinct in under 35 minutes.
Beyond this point the generation numbers become increasingly inaccurate, to the point where there's not much use in keeping track of them. The mutations disabled phase can take most of a day to run (at 1x speed), and of course generation counters going up during mutations disabled are of little importance.
Aurum 1.4, 1.5, and 1.6 tests failed to make headroom over 1.3c (Albu)
2023-04-24 Nubbi Icosi (gen 20,000) becomes the most powerful 1v1 mini-bibite. At time of writing, the only one capable of defeating Albu. Nubbi Icosi set a new benchmark, probably an order of magnitude more powerful than the original Nubbi Competitor & Luscus.
I switched to a new naming scheme, using Orian instead of Aurum going forwards:
2023-05-04 Racho Orian (A1 & A2) more powerful than Albu.
2023-05-11 Racho Orian B3 (generation 6830) defeats all previous Racho specimens comfortably. In a test vs Racho Albu, OrianB3 won at 1 hour with numbers 519 vs 137
OrianC, OrianD, OrianE - all failed to make an improvement over B3.
2023-09-26 OrianF2.3 tested victorious against OrianB3
2023-11-06 OrianGe identified as stronger than F2.3
2023-11-07 OrianH project, methodology used is identical to the OrianG project, where I ran 3 sims simultaneously at 1x speed for a full day, and at the end of the day only save the sim with the most bibites. Load 3 copies of that "best" sim the following day and repeat etc.
2023-12-03 finished the OrianH project; Unfortunately Ge is about 30% better performing than H1, very disappointing.
2023-12-06 Started the OrianI project. Same as previous project but ran over less time. Overall failure.
2023-12-20 Starting the OrianJ project, running for the first time on the FFA settings to see if we can get better results.
2023-12-29 Identified RachoOrianJ1 as superior to Ge.
And that ends my experiments on the Racho lineage (so far). RachoOrianJ1 is currently the most powerful descendant. In my testing it defeats all other mini-bibites, including Nubbi Icosi.
--- TL;DR conclusion: I don't know if RachoOrianJ1 is the strongest competition herbivore mini-bibite, but it defeated all others in tests I ran. It is perhaps the most cancerous however. It's very small, splits pellets, and cranks out eggs far faster than the 2022 top competitors.
Fun facts:
My final secret: Pellet splitting. It's a very powerful technique for competition bibites. Try it. I suggest linking Tic to want2eat.
In the original mid-2022 tournament there were two or three bibites that were actually more powerful than Luscus xHybridus. Minima Spinner was the most powerful submission, but evidently failed in the sole FFA world to make a top-16 spot.
Racho, Nubbi, and Imperator are currently the most powerful competitor mini-bibites that I'm aware of.
Robm has created whales that crush any competition minibibite due to the large sweeping paths the whales take.
nigct has created a predator that can cause competition mini-bibite herbivores to go extinct generally within a few minutes.
I found a (near) zero drag specimen I must have adapted in Dec 2022.
Obligatory: this is for the most part all v0.51 - the soon to be released v0.6 greatly changes the behavior of bibites adapted in earlier versions.
All relevant Racho bb8 files: https://uploadnow.io/f/pQtYzZn
Discord: https://discord.gg/7TVF8X3X9H
submitted by Crinkez to TheBibites [link] [comments]


2024.02.22 16:18 Swag369 Question about Interpreting a Meta Analysis

Hey guys, I was doing some research for a school paper, and I and I was using a paper that was mentioned in a jeff nippard video, about weightlifting and health.

In the attatched graph, the J curve of risk seems to go OVER 1 for everything except diabetes, around 130 min of exercise.

I'm not used to reinterpreting study results, but isn't this literally saying that if I lift for more than 2 hours, that I'm INCREASING my cancer risk and such?
I'm sure there is some confounding with steroids at that lengths of working out, i'm not sure how much that is realvent here...

Wondering what a more developed take of interpreting this would be?
https://preview.redd.it/vtwzkjfyl5kc1.png?width=1275&format=png&auto=webp&s=c526dbac175c703da6f2aca5fabf3eb053f0b17b
submitted by Swag369 to exercisescience [link] [comments]


2024.02.22 07:57 EntropicEctacy Had an NDE, year later astral travelled back and went through the white light

Some years ago when I was still doing drugs, I overdosed and was clinically dead for some 15-20 minutes. A year later a religious friend of mine asked if I could use my rapport of promising astral travelling / gateway experience, to visit it again. I spoke with someone who felt like Jesus / my guide, who told me my friends’ dead fathers last words they told them. Let’s get into it.
The NDE: I remember feeling weightless, I had no body, everything was black, as if I was consciousness floating in a special void. I remember feeling calm, not sad and not happy, but yet I’d say amazing? Perhaps it was my consciousness not feeling weighed down my it’s earth dimensions issues. Not sure. I felt to every essence of the words, ‘At peace’.
I remember being curious about where my nose was (in my vision) and my hands are body. It felt like an eternity in there, but also felt like 2 minutes. Time was surely illusory.
The last moments there, I recall seeing an old wooden door, with a faint glow behind it, leaking out the sides.
The Revisit / Astral Travel: a year later, sober, a friend of mine was curious of my experience and had known I’d been practising deep meditation and the gateway experience for astral travelling. I had a couple ‘successful’ connections by that point, and they asked if I could try and go through that door.
Usually my travels take me about 3 hours from start to finish to do a mixed method of Dr Monroe / Bineural Beats / gateway tapes / Eastern Yogi etc. goes by quick, but this time did not disappoint; it did however, leave me with more questions than answers.
Going Through the light: Once I had gotten back to the ‘Void’ as many NDE’rs call it, I tried to find the door, but struggled. Months prior, a lady who when she’d 8-12 was used by a local cult for her ‘visions’ had taught me a trick she was taught. Placing a stark familiar object- in my case my great grandmothers’ grandfather clock- and look for something that doesn’t fit. I saw an old wooden chair next to it, and then a bright white light shimmering out to the side, and there was the door.
My friend had asked if I could move in the NDE, I said I never tried. I didn’t have legs here, I remember thinking that I wanted to move forward, and then I did. Instead of going through the door, I had to open it. Only now after seeing this theory, am I curious if that holds more context than I thought.
Opening this olden wooden door, was a bright white light, typical to what you’d all imagine. Going through it, I saw marble floors inside a multi story circular building, with bookshelves going around, and a huge white marble desk in front of me, with a big tree behind them in the middle of this building.
A man stood behind it in a white robe, there were some 10-15 people in normal clothes looking at the books however. The rear of this somewhat small/medium sized building, was a white marble arch of sorts, leading out to green fields of hills, almost exactly like The Emporers New Groove movie.
People were sprawled out on the grass and hills, with a sparingly big beautiful tree some distance from the archway. The people out here were clothed in white robes of sorts however. Hills went on as long as the eye could see.
I remember a presence to my left, and it was a guide that resembled Jesus. I asked what this place was, and he asked me to follow him down a hallway, which was white walled, white marble floor, leading to a white marble bench used for sitting.
We sat down, and reassured me that I had made mistakes in life and were needing to amend them. He never said that this was heaven, but I didn’t seem to ask him what it was. I asked some personal questions about my life, and If they’d come to fruition, it felt like I was sitting and talking so intimately in that it was the moment before you orgasm. It was pure, I also felt comfortable, like it was truly Jesus / a Holy Spirit.
Before going into this travel, my friend had asked me if I could bring him proof, or to speak to someone that he’d know.
This guide told me to reassure my friend, and that he’ll have difficult choices moving forward and is at a crossroads. That my friend had hurt people, but it would be okay.
He then told me this;
”Tell (my friend) that his father loves him, he is proud of him, he forgives him, and to tend to his garden.”
I remember saying okay, I thanked him, and said I was going to go, that I would see him when my time comes and I would try my best to keep turning my life around.
Upon telling my friend what I heard, he thanks me profusely. He went silent on messages after that for a month or so.
He ran a small tech company, but upon his reply some time later, he had sold everything and was running an online theology / church blog. He messaged and asked how I was, and sent me a link to a post he made about that day.
It read that he was skeptical of my ‘talents’, as he called them, and after hearing what I told him, he had broken down into tears. It read that He was a closeted homosexual and his father never approved of it, kicked him out and eventually got cancer whilst apart. Reconnecting on his deathbed, his father had told him he wished he was a good Christian, and to ”tend to his garden’.
As a kid, when his father would tuck him into bed at night, or at any occasion when he asked for advice, he would tell him to ”tend to his garden in the morning”.
Now, His company he ran, was growing quite parabolic online, I’ve seen the graphs, it was nearly unmanageable. He felt burnt out and was straying away from his faith, and after reading the blog post, I think in part it was his battle of his sexual orientation and how it fits with religion, at least to him.
My thoughts now, and questions:
Relating back to the prison planet and soul catcher theory etc., I’m curious as to why I always had an old wooden door? I am a life path 33 (for those into numerology) but essentially I am on my last reincarnation / or have lived lots of lives, I’m not sure. Could this have something to do with it? I love meditation, mindfulness, Buddhism etc. and try to live in that way in person.
I find it interesting that he shared some final words and memories of a friend, that turned out to be true. I find it also interesting that they now have doubled down on religion and are recruiting others to the dubious ‘white light’.
I have never gone back there since, but I’ve always felt so strongly that whatever that was, is real and I will go there again.
This prison planet, soul catcher theory, really makes me try and think about everything I saw then and the NDE, curiously.
I’d love to hear what you think happened, why something like a door was used to block the light? And why my guide told me those things? I’d love some answers…
Thankyou
submitted by EntropicEctacy to EscapingPrisonPlanet [link] [comments]


2024.02.21 03:15 -apophenia- Blinding in cancer research - how far to go?

I am planning out a mouse experiment where we will be testing a potential cancer treatment against a negative control. The main readout of effectiveness will be tumour size change over time (monitored by bioluminescent imaging), and 'survival' curves (Kaplan-Meier graphs) based on time to reach a humane endpoint. I will be doing the welfare monitoring and imaging analysis that the endpoint decisions are based on, so it's obviously important that I be blind to whether the mice are receiving the treatment or the control.
I have two potential plans for how to go about blinding myself and I'm interested in opinions from other scientists about which of these is the better experimental design. I'd especially appreciate opinions from people experienced in cancer research and animal studies because the logistics here are quite tricky. I am currently the only person in the lab able to do the imaging data analysis, so having somebody else do this is not an option even though it would solve a lot of problems.
Plan A: Somebody else aliquots the drug and vehicle into vials labelled 'X' and 'Y', without telling me which is which. I do all of the injections and imaging, and make endpoint decisions, knowing which mice are in group 'X' and which are in group 'Y'. The major advantages are that it's hard to screw it up, and I could do the simultaneous imaging/injection steps without needing an assistant, which is good given that I'm anticipating weekend work (I signed up for this, but I really don't want to require it of my students). The major disadvantage is that if the drug works really well, I might be able to tell which group is getting the treatment.
Plan B: Another lab member keeps the records of which mouse is on which drug, and that person does the injections but has no involvement with data analysis or endpoint decisions. I do those things, without knowing which treatment each individual mouse is receiving. The major advantage is that I think it's stronger blinding/it wound be almost impossible for me to guess what treatment an animal is getting. The major disadvantages are that every injection day will require 2 people for multiple hours, and I think it's much more likely that a drug mixup could happen / a mouse could get the wrong drug with this design.
Whew long post - opinions would be appreciated!
submitted by -apophenia- to labrats [link] [comments]


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