Interaction between metformin and methotextrate

When it hurts just to look

2012.10.14 02:38 drumcowski When it hurts just to look

Pics and vids that make you go YIKES!
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2008.06.19 18:35 User Experience

A community where professionals, enthusiasts, and individuals interested in the field of user experience can share knowledge, ask questions, and engage in discussions about various UX-related topics.
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2010.08.16 05:33 GoodMusicTaste User Interface Design

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2024.05.30 21:38 BurgerSubPrincess Metformin and Inositol

I had a call with my naturopath today who suggested that Metformin and Inositol do not mix well and can lead to hypoglycaemia. My doctor never flagged me being on the Inositol and I see it suggested here all the time! I was wondering if anyone has any experience with this or has had any negative interactions between the two?
submitted by BurgerSubPrincess to PCOS [link] [comments]


2024.05.26 00:12 healthmedicinet Health Daily News May 24 2024

DAY: MAY 24 2024
5-24-2024

NEW STUDY OUTLINES THE WARNING SIGNS

Colon cancer is increasingly hitting Americans under the age of 50, and a new study outlines the warning signs that these young patients first encounter. The analysis was based on data from 80 different studies, involving almost 25 million patients under the age of 50. In nearly half (45%) of cases, blood in stools was an initial symptom, followed by abdominal cramps (40% of cases) and alterations in bowel habits (27% of
5-24-2024

STROKE RATES ARE RISING, ESPECIALLY AMONG THE YOUNG

The rate at which Americans under the age of 65 suffered a stroke rose by about 15% between 2011 and 2022, new government data shows. That was true even among the young: The rate of stroke jumped 14.6% among people ages 18 to 44 during the study period, researchers from the U.S. Centers for Disease Control and Prevention found. It’s not clear why stroke rates have risen so sharply, but rising rates of obesity and high blood
5-24-2024

THESE TIPS CAN HELP KEEP YOU SAFE DURING A POTENTIALLY SEVERE 2024 WILDFIRE SEASON

The 2023 wildfire season was worst on record. High temperatures and widespread drought fueled over 6,600 fires, burning a record-breaking 18.4 million hectares, an area more than double the size of New Brunswick. The fires emitted nearly 480 million tons of carbon, five times the emissions of an average season, turning the skies hazy and orange and blanketing much of North America in wildfire smoke for weeks. Many regions of Canada experienced over 40 days where air pollution concentrations exceeded the World Health Organization’s air quality guidelines, leading to
5-24-2024

SEMAGLUTIDE SIGNIFICANTLY REDUCES RISK OF COMPLICATIONS IN PATIENTS WITH TYPE 2 DIABETES, STUDY REVEALS

A pioneering study has demonstrated that semaglutide significantly reduces the risk of major kidney disease events, cardiovascular outcomes, and all-cause mortality in patients with type 2 diabetes and chronic kidney disease. will pave the way for new treatment strategies and offer hope to millions of patients globally. The study is also published in the New England Journal of Medicine. The FLOW (Evaluate Renal Function with Semaglutide Once Weekly) study is a double-blind, randomized, placebo-controlled international trial comprising 3,533 patients, with a
5-24-2024

STUDY FINDS HEAT PAIN PERCEPTION DECREASES WITH AGE

A. Experimental setup and conditions (created with BioRender.com); B. Correlation between age and pain thresholds; Significant difference in heat threshold; Pain ratings of heat stimuli across younger and older groups (**p < 0.01, ***p < 0.001); C. Significant difference in pain discriminability at various levels of heat stimuli; Correlations between pain discriminability and pain threshold; Correlations between age and discriminability of heat stimulation (**p < 0.01). Does pain perception change with age? In particular, is there a significant increase or decrease in perception between older and
5-24-2024

INTEGRATION OF PHARMACIES WITH PHYSICIAN PRACTICES HAS LITTLE IMPACT ON CANCER DRUG EXPENDITURES, STUDY FINDS

Integration of pharmacies with physician practices, where on-site pharmacies open at physician practice locations, is a growing trend in cancer treatment. However, little is known about how this integration affects drug utilization or expenditures, along with other aspects of the patient experience. Open compares the outcomes of patients treated by oncologists whose practices integrated with pharmacies, to those of oncologists that did not integrate. Researchers found a slight increase in utilization of oral oncology drugs,
5-24-2024

HOW AIR POLLUTION AFFECTS THE DIGESTIVE SYSTEM

The diseases caused by PM2.5 pollution in different systems are shown. CAD, cardiovascular disease; NASH, non-alcoholic steatohepatitis; HCC, hepatocellular carcinoma. Fine air particles, less than 2.5 micrometers in diameter (PM2.5), are a major air pollutant linked to various health problems. These particles can travel deep into the lungs and even enter the bloodstream when inhaled. Recent research suggests a major health concern: PM2.5 exposure can also damage the digestive system, including the liver, pancreas, and intestines.
5-24-2024

PEDIATRICIAN EXPLAINS HOW AI MAY AFFECT CHILDREN

Artificial intelligence is rapidly changing the way we work, play and communicate. While artificial intelligence has potential to help solve complex problems, you’ve likely also heard serious concerns about it—and especially, the ways AI might change the lives of children and teens. As child health experts at UNICEF have pointed out, kids around the world use AI almost daily. Most interactive toys, games and internet platforms made for children depend on AI technology. Even though AI is advancing faster than anyone expected, most nations have not considered how AI will
5-24-2024

AI MIGHT HELP SPOT BREAST CANCER’S SPREAD WITHOUT BIOPSY

New AI can help detect breast cancer that is spreading to other parts of the body, without the need for biopsies, a new study finds. The AI analyzes MRI scans to detect the presence of cancer cells in the lymph nodes under the arms, researchers said. In clinical practice, the AI could help avoid 51% of unnecessary surgical biopsies to test lymph nodes for cancer, while correctly identifying 95% of patients whose breast cancer had spread, results showed. Most breast cancer deaths are due to cancer that’s spread elsewhere, and
5-24-2024

HARNESSING THE POWER OF VIRUSES TO KILL CANCERS

A new research provides guidelines for the design, production and preclinical testing of viruses that infect and destroy cancer cells , while also promoting protective antitumour immunity. Credit: National Cancer Institute In the global hunt for both a cure and cancer treatments, researchers are finding it may be the very viruses we try to shield ourselves against that hold great promise in fighting the deadly disease. Pathogens—those bugs that routinely infect and sicken us, like the common cold or influenza—are being
5-24-2024

RESEARCH SHOWS NEW TREATMENT MAY ENABLE MORE PATIENTS WITH HIGH-RISK BLOOD CANCERS TO RECEIVE STEM CELL TRANSPLANTS

A new treatment approach using an older drug may enable more patients with high-risk blood cancers to receive transplanted stem cells from unrelated, partially matched donors, according to a study conducted by researchers at Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine and colleagues. Results to be presented at the annual meetings of the American Society of Clinical Oncology (ASCO) and the European Hematology Association suggest the new approach may expand the donor pool, with patients from underrepresented racial and ethnic groups standing to benefit
5-24-2024

DIGITAL INFANT FEATURES IN WORLD-FIRST PSYCHOLOGY RESEARCH

Early Learning Lab BabyX is a hyper-realistic computer-generated simulation of a human infant. In a world first, developmental psychology researchers at the University of Auckland will use the digital child to research adults’ interactions with babies. The infant on a computer screen responds to a social partner—including their voices, gestures, and expressions—just as a human infant would, smiling, laughing, crying, or getting cross and frustrated. The aim of the research is to look more closely at the nuances
5-24-2024

INTERNATIONALLY TRAINED FEMALE ONCOLOGISTS FACE MANY DISCRIMINATION CHALLENGES IN THE US, FIND RESEARCHERS

Coral Olazagasti expected a relatively smooth transition when she moved to New York to start her residency after graduating from medical school in her native Puerto Rico. But that proved wishful thinking. She not only experienced major culture shock, but also her superiors and colleagues often chastised her for speaking too loudly and joked about her accent. “Puerto Rico is a U.S. territory so when I moved to New York, I thought it wasn’t going to be a big change,”
5-24-2024

HOW COVID-19 ‘BREAKTHROUGH’ INFECTIONS ALTER YOUR IMMUNE CELLS

Colorized scanning electron micrograph of an apoptotic cell (green) heavily infected with SARS-COV-2 virus particles (yellow), isolated from a patient sample. New research from scientists suggests people who received COVID-19 vaccines and then experienced “breakthrough” infections are especially well armed against future SARS-CoV-2 infections. By analyzing blood samples from study volunteers, the LJI researchers discovered that people who experienced symptomatic breakthrough infections develop T cells that are better at recognizing and
5-24-2024

SCIENTISTS UNCOVER NEW TREATMENT PATHWAY FOR RARE ‘SPIDER WEB’ CHILDHOOD BRAIN TUMORS

Researchers have identified the unique features of an exceptionally rare set of childhood brain tumors—a discovery that could pave the way for more effective treatments. A decade-long study, carried out by a team from The Institute of Cancer Research, London, as part of a European working group, to comprehensively analyze a set of childhood tumors known as gliomatosis cerebri,
5-24-2024

TYPE 2 DIABETES TREATMENT FOUND TO IMPACT FUNGAL COMMUNITY IN HUMAN GUT

Metabolic diseases, such as type 2 diabetes, are associated with compositional shifts in the human gut microbiome, including the fungal fraction called the mycobiome. But research on the mycobiome and how type 2 diabetes or its common treatment, metformin, may interact remains relatively limited despite suggestions that these fungi can influence the overall health of the microbiome, according to a research team at Penn
5-24-2024

MORE MEDICAID NEEDED FOR INCARCERATED INDIVIDUALS WITH SUBSTANCE ABUSE DISORDERS, ACCORDING TO STUDY

A new study examining how state Medicaid programs are helping people with substance use disorders (SUD) uncovered the need to expand the programmatic features to assist individuals who are transitioning in and out of the criminal justice system. The study, “State Medicaid Initiatives Targeting Substance Use Disorder in Criminal Legal Settings, 2021,”
5-24-2024

SWEDEN ORDERS REVIEW AFTER ‘EXPLOSION’ OF ADHD CASES

Sweden is seeing “an explosion” of ADHD cases among children that has put it far above the global average, the government said Friday as it ordered a review to find out why. Around 10.5 percent of boys and six percent of girls in Sweden in 2022 had been diagnosed with Attention Deficit Hyperactivity Disorder (ADHD), Social Affairs Minister Jakob Forssmed told reporters, citing statistics from the Board of Health and Welfare. The figures were expected to rise to 15 and 11 percent respectively before leveling
5-24-2024

WALKABILITY IN NEIGHBORHOODS LINKED TO HEALTH, STUDY OF SIBLINGS SHOWS

When one family member looks out the window at sidewalks and green space and the other sees a multilane highway and power lines, the differences may contribute to more than just sibling rivalry. A new study by University of Maryland public health researchers has shown that those neighborhood characteristics correlate with different health outcomes.
5-24-2024

STUDY REVEALS RIGHT ATRIUM CHANGES IN CARDIOVASCULAR DISEASES

Cardiovascular disease has profound effects on the structure and function of the heart. While past research has mainly focused on the left ventricle and the coronary arteries, the effects of the disease on the right atrium remain largely unexplored. The right atrium functions as the entryway to the heart, pushing blood towards the right ventricle and the lungs. It also houses the pacemaker of the heart, the sinoatrial node, that initiates and maintains the heartbeat. For this reason, pathological remodeling of the site
5-24-2024

RATES OF SEVERE MULTIPLE DRUG INTOLERANCE SYNDROME UP IN FIBROMYALGIA, IBS

Patients with fibromyalgia and irritable bowel syndrome (IBS) have increased rates of severe multiple drug intolerance syndrome (MDIS), according to a study published in the May issue of the Journal of Allergy and Clinical Immunology: In Practice. Alicia A. Alvarez, M.D., from Sarasota Memorial Hospital in Florida, and colleagues conducted a retrospective chart review to examine the prevalence of MDIS in patients diagnosed with fibromyalgia or IBS. Patients who had been seen at a large academic center were identified and matched to controls seen within the same timeframe by exact
5-24-2024

COMBINING HUMAN OLFACTORY RECEPTORS WITH ARTIFICIAL ORGANIC SYNAPSES AND A NEURAL NETWORK TO SNIFF OUT CANCER

Researchers have developed an artificial olfactory system that discriminates odorants at the molecular chain length level. The olfactory system has been developed through the integration of human olfactory receptors and organic synaptic devices. The system generates distinct conductance patterns for odorants and mixtures. This approach enables precise odorant recognition via training and inference simulations.
5-24-2024

SCIENTISTS PROPOSE THERAPEUTIC APPROACH FOR INFLAMMATORY BOWEL DISEASE

. In a study published in Cell Host & Microbe, a research team has demonstrated the causal link between microbial factors and dysfunction of intestinal stem cells (ISCs) in colitis. On the basis of this mechanism, they proposed a possible approach to restore ISC function in colitis. Inflammatory bowel disease (IBD) is a chronic disease characterized by microbial dysbiosis and dysfunction of ISCs in the gut. However, how these two factors are directly communicated remains poorly understood. In this study, researchers first revealed that ?
5-24-2024

NEW BIOMARKER PREDICTS SUCCESS OF IMMUNOTHERAPY IN KIDNEY CANCER

Immunotherapy increases survival rates in kidney cancer, but does not work for everyone. A Leuven research team has developed a new method to predict which patients will benefit from it. The team of Francesca Finotello (Computational Biomedicine Group) from the University of Innsbruck also contributed. Their study also opens new avenues to even more effective treatments. Every year, roughly 1,300 people in Austria are diagnosed with kidney cancer. Thanks to
5-24-2024

PATIENT CARE TAKES CENTER STAGE

The 2024 American Society of Clinical Oncology (ASCO) Annual Meeting is being held May 31 to June 4, 2024, in Chicago and online. The theme of this year’s meeting is “The Art and Science of Cancer Care: From Comfort to Cure.” Attendees will share and discuss the latest clinical cancer research impacting patient care. “Treatment advances involving targeted therapies, immunotherapy, and new uses of technology, as well as research on improving patient quality of life and outcomes are among the topics that will be highlighted in the meeting’s official Press
5-24-2024

PARENTAL LEGAL SYSTEM INVOLVEMENT LINKED TO ADVERSE CHILD MENTAL HEALTH

Parental legal system involvement may negatively impact child mental health, according to a study published online May 23 in Pediatrics. Lilian G. Bravo, Ph.D., R.N., from the David Geffen School of Medicine at the University of California in Los Angeles, and colleagues used two-year follow-up data from the Adolescent Brain Cognitive Development Study when children were 11 to 12 years of age to examine whether adverse parental legal system involvement (incarceration, arrest) was associated with suicide risk. Of the 10,532 children included in the study, 6.5 percent reported parent incarceration
5-24-2024

SCIENTISTS LEVERAGE MACHINE LEARNING TO DECODE GENE REGULATION IN THE DEVELOPING HUMAN BRAIN

Massively parallel characterization and prediction of gene regulatory activity in the developing brain. In a scientific feat that broadens our knowledge of genetic changes that shape brain development or lead to psychiatric disorders, a team of researchers combined high-throughput experiments and machine learning to analyze more than 100,000 sequences in human brain cells—and identify over 150 variants that likely cause disease. The study, from scientists at Gladstone Institutes and University of California, San Francisco (UCSF), establishes a comprehensive catalog of genetic sequences involved in brain
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2024.05.23 18:03 xzRe56 WEEK 1 KIT 2: REVIEW

I completed my first week on Kit 2 yesterday and, as so many of the posts on here have been helpful for me in my "Hims journey," I thought I'd reflect on my week and offer tips that I've found helpful. I'll try to keep this up weekly. Feel free to let me know your thoughts and experiences.

ABOUT ME

MEDICATIONS

For Week 1, Kit 2 contains the following medications:
a) Naltrexone (14 mg 1/2 tab per day)
b) Metformin XR (750 mg 1x per morning with food)
c) Bupropion XL (150 mg 1x per day)

DISCOVERY

On Day 1, I did something that really helped later on, looking back on it. Before beginning the program, I had read horror stories on this sub-Reddit about people's interactions with these medications, so I decided to take each by itself on the first day in order to isolate their effects on me.
NALTREXONE: I took the half tab of Naltrexone first thing in the morning and went about my routine: doing daily puzzles, completing Duolingo exercises, trying some brain games and, of course, browsing Reddit. At about the two hour point, I began to feel fuzzy-headed (a dull cloudiness in the brain that reminded me of just waking up in the morning, or of being mildly stoned). I also felt a bit tingly around my hands and face, with a slight but not debilitating nausea. Luckily, I am retired, so I lay down and took a short 20- or 30-minute nap, from which I awoke feeling refreshed and ready for the day.
METFORMIN XL: Many Reddit users reported having difficulty with Metformin, specifically with diarrhea issues if they didn't take it with food (which HIMS definitely advises). On Day 1, I took Metformin after a decent-sized lunch, about four hours after the Naltrexone. As it turned out, I had no side effects whatsoever with this drug. Had I not taken this separately from the Naltrexone, I would not have known which of the two affected me, or would have thought they both negatively affected me.
BUPROPION XL: I administered this medication about four hours after the Metformin, with just water, and felt no symptoms whatsoever.
WATER: I found drinking plenty of water to be an important part of the program. HIMS conveniently provides a water bottle to help with this. Drink at least two bottles per day!

TWEAKS TO MY ORIGINAL PLAN

After the initial "discovery" phase on Day 1, I decided for the remainder of the first week to administer Naltrexone and Metformin together in the morning with sufficient food: generally yogurt and fruit, a protein bar and milk, a protein shake, or egg and toast. I never experienced diarrhea, but the effects of the Naltrexone remained, curiously decreasing in intensity as the week progressed, I would then take the Bupropion at some point after noon, generally around 2:00 pm. Again, I experienced no effects from this medication.

RESULTS

At the end of Week 1, had lost 6.7 lbs. I honestly was surprised, because I didn't really feel any different. I'm sure a lot of it was water, but I'll take it. I noticed at times this week that I felt quite euphoric, happy and generally positive. I tend to be a "let it flow" kind of guy, but this was next level. (For example, yesterday I stood in line at the County Assessor's Office for over an hour and wasn't phased by the wait or off-put by the experience. I just queued up as though I were an Englishmen and endured the wait and was even cheerful to the person who eventually assisted me). I've read from several on here that this program robs you of your sex drive, love for food and drink, exercise drive (if there is such a thing) and joie de vivre, which I found to be partially true and partially false (for me).
Sex drive? Well, I'm 68 and gay, so what can I say? In our community, 68 is ancient and you're something of an invisible entity. My husband tends to have a much less prominent libido than me, but I found that this program kind of evened us out. I definitely felt less inclined towards (or interested in) porn or even sexual fantasizing: it just wasn't that important. Not that, when the moment presented itself, I couldn't perform; it was just that I had a blasé attitude about sex, in general, something that I've NEVER experienced. It might have been off-putting if I were 25, but I'm not. Ha! (Interestingly, I found that other potential addictive areas of my personality, such as doom-scrolling through political posts on Twitter, weren't even enticing. It's not that I don't care; I just realize that I can't control anything beyond voting and donating to my candidate/party of choice. My angry edges are warm and fuzzier now).
Food and drink? I've never been a foodie per se, but I like staple, carby, comfort foods. I grew up in the Southwest and Mexican/Tex-Mex has always been my favorite food -- the spicier the better. I found I still craved Mexican food, but that I could only eat a few chips and maybe one taco before I felt completely full. Later, I discovered that only fajitas without the chips and tortillas satisfied me. Curiously, I felt ambivalent to spice. Where I live, Mexican food is quite bland (I always ask for the special salsa they have in the kitchen, for the workers, because it's more authentic). Usually, I'm scrambling to find enough spicy things to add (jalapeños, etc.) to make it palatable, but with the meds cocktail I could take or leave salsa. It's not that spicy foods revolted me, as some have written on here. I just really didn't care one way or the other. This program definitely has curbed my appetite for carbs: I didn't have French fries this week, for example, and I used to have fries with every meal. Bread (which never interested me much anyway) didn't even look appetizing. Beer? No way. I've been to three Cubs games this week (I live nearby, and can walk) and have had no beers, no hotdogs, no popcorn or peanuts. The only alcohol that has been even remotely palatable are hard seltzers, and then only a couple. White wine is meh; red wine is yuck. I can't explain it, but there is a noticeable lessening of interest in food or drink altogether. You eat for sustenance, not pleasure. You drink water for hydration and to help the kidneys, and nothing else is satisfying -- plus you're always full from water. It's a win-win, I guess. Someone on here advised to always eat something lean, green and raw with every meal -- great advice! Another said that if you look down on your plate and nothing even looks appetizing, at least eat the protein (you'll crave protein anyway) and leave the rest. Put your fork down: the meds are working. Again, great advice! I find that I am sleeping better and worrying less. I still enjoy a couple THC edibles in the evening, with a hard seltzer, and I'm out like a lamp. It used to take two bottles of wine and a ball peen hammer!
Exercise? Huh? Of course, like most of us, I have never been a regular gym rat. I tend to avoid it like the plague (Mark Twain said, and I concur, that every time he felt the urge to exercise he lay down and let it pass). That's me. However, I plan to work more activity into my routine, including working out. I think it's important as you lose weight to hit the dumbbells to tighten the flabby skin that will remain when we are all at zero body fat like good Roman gods and goddesses -- ha! Yesterday (another baseball game) I was surprised to find that I'd walked 11,000 steps! I probably didn't walk 11,000 steps last month! I was amazed. I plan to walk more as the program continues. I also find I have more energy to do chores around the house, with less fuss and drama. I believe I'm altogether a better human being, which feeds into the joie de vivre that I'm feeling. I hope this part of the program will remain with me for the rest of my life.
I hope some of this has helped. My advice is to take the pills separately on your Day 1 so you know for sure which drugs interact with you -- and how. Drink plenty of water, try to exercise and go about your day knowing that all is well, the pounds will come off and you will be a better person at the end. So far, I'm very satisfied and excited to see where this journey takes me.
More next week. Cheers!
submitted by xzRe56 to HimsWeightloss [link] [comments]


2024.05.23 17:26 AlricaNeshama PCOS Information

Hello everyone.
I have been seeing a lot of questions concerning PCOS and their confusion. So many are lost and it seems like doctors are not telling you what you need to know. They seem to be leaving you in limbo.
A little about me.
I am almost 46 years old (one month away). I developed this disease at 16 but did not get a formal diagnosis until I was 33. Yes, it took me 17 years to be taken seriously. I had a full hysterectomy and a bilateral salpingo-oophorectomy at 34. What is that? In short: The uterus, ovaries, fallopian tubes, and cervix are removed. You retain nothing! Now, that was because of how bad mine was.
Now, onto the information. It is going to be a lot and it is going to be scary. But you all NEED to have this information.
You cannot make actual choices and decisions and come to any understanding if you do not have all of the facts.
I know about it because I have been fighting it for almost 30 years. I have studied, researched, and dug into information I could get my hands on to know about this disease.
Understand, the information just barely existed when I started.
A lot has changed and now it's widely available, the problem is doctors don't bother to explain it to you, so you understand and know what you need to do. The choices you make do impact your body.
PCOS:
Polycystic ovary syndrome (PCOS) is a lifelong condition that affects women, with symptoms like irregular periods and male-pattern facial or body hair, that often emerge during puberty or early adulthood. Up to 6 to12% of women in the U.S. have PCOS, according to the Centers for Disease Control and Prevention (CDC).
In PCOS the ovaries produce an abnormal amount of androgens, male sex hormones that are usually present in women in small amounts. The name polycystic ovary syndrome describes the numerous small cysts (fluid-filled sacs) that form in the ovaries. However, some women with this disorder do not have cysts, while some women without the disorder do develop cysts.
Ovulation occurs when a mature egg is released from an ovary. This happens so it can be fertilized by a male sperm. If the egg is not fertilized, it is sent out of the body during your period.
In some cases, a woman doesn’t make enough of the hormones needed to ovulate. When ovulation doesn’t happen, the ovaries can develop many small cysts. These cysts make hormones called androgens. Women with PCOS often have high levels of androgens. This can cause more problems with a woman’s menstrual cycle. And it can cause many of the symptoms of PCOS.
Treatment for PCOS is often done with medication. This can’t cure PCOS, but it helps reduce symptoms and prevent some health problems.
our hormones interact with many different systems in your body, like your immune system and your central nervous system, and can cause myriad symptoms that are not yet well understood, such as insomnia.
PCOS raises your risk for many other conditions including:
Endometrial polyps or cancer, due to the thickening of your endometrial lining caused by infrequent menstruation
Diabetes
Depression, anxiety, bipolar disorder and obsessive compulsive disorder
Sleep apnea
High blood pressure and cardiovascular conditions
Thyroid problems
What causes PCOS?
The exact cause of PCOS is not clear. Many women with PCOS have insulin resistance. This means the body can't use insulin well. Insulin levels build up in the body and may cause higher androgen levels. Obesity can also increase insulin levels and make PCOS symptoms worse.
PCOS may also run in families. It's common for sisters or a mother and daughter to have PCOS.
How is PCOS diagnosed?
Your health care provider will ask about your medical history and your symptoms. You will also have a physical exam. This will likely include a pelvic exam. This exam checks the health of your reproductive organs, both inside and outside your body.
How is PCOS treated?
Treatment for PCOS depends on a number of factors. These may include your age, how severe your symptoms are, and your overall health. The type of treatment may also depend on whether you want to become pregnant in the future.
What are the complications of PCOS?
Women with PCOS are more likely to develop certain serious health problems. These include type 2 diabetes, high blood pressure, problems with the heart and blood vessels, and uterine cancer. Women with PCOS often have problems with their ability to get pregnant (fertility).
Insulin Resistance:
Insulin resistance is a condition where cells in the body don't respond properly to insulin, a hormone that moves glucose from the blood into cells. This prevents the cells from easily absorbing glucose from the blood, so the pancreas produces more insulin to help glucose enter the cells. As long as the pancreas can produce enough insulin, blood glucose levels will remain healthy. However, over time, the pancreas can become worn out and unable to produce enough insulin, which can lead to high blood sugar levels.
National Institute of Diabetes and Digestive and Kidney ...
Insulin Resistance & Prediabetes - NIDDK
What is insulin resistance? Insulin resistance is when cells in your muscles, fat, and liver don't respond well to insulin and can't easily take up glucose from your blood. As a result, your pancreas makes more insulin to help glucose enter your cells. As long as your pancreas can make enough insulin to overcome your cells' weak response to insulin, your blood glucose levels will stay in the healthy range.
Mayo Clinic Explains Insulin Resistance
Aug 17, 2022 — let's first talk about what insulin does when you eat food your body converts the food into dietary sugars insulin is a hormone released by the pancreas that tells your cells to open up to that sugar and convert it into energy with insulin resistance the cell don't react. and don't open up resulting in excess sugar in the blood. over time the pancreas keeps trying to regulate the blood sugar producing more and more insulin until it wears out. and can produce large amount of insulin anymore as a result blood sugar levels increase to the point of being in the diabetic. range. anyone can become insulin resistant. in particular people with excess weight at a higher risk compared to the general population.
Cancer:
Every single human on this planet has cancer cells. They are called antigens.
Cancer cells can evade the immune system by changing their ability to process and present antigens. For example, cancer cells can:
Downregulate MHC molecules: This makes them invisible to the immune system
Interfere with proteasome activity: This prevents the degradation of cancer cell-associated antigens.
Antigens on cancer cells are targets for the immune system, but many are not cancer-specific and can also be found on normal tissues. These antigens are often products of mutated cellular genes, aberrantly expressed normal genes, or genes encoding viral proteins.
Every cancer antigen has a marker.
Uterine cancer is CA 125. The normal range is in te 30's.
Mine is 177.
Which puts you at higher risk for every type of cancer that exists.
Food Intolerances:
These can vary from person to person.
Fruit for many will be an issue because of the natural sugars.
Such, as I can have fruit once a month as a treat. Otherwise, I'd turn into the Goodyear Blimp in a manner of a short time.
Breads, high fat, high sugar, fried foods, etc. All tend not to be good for us.
What you NEED to do. Talk to your Dr. Have them get you in touch with a dietician and a Nutritionist.
Because what your body will and will not allow varies.
Sleep Apnea:
Sleep apnea is a common sleep disorder that causes people to stop breathing or breathe shallowly during sleep. These interruptions can last from a few seconds to minutes and can occur up to 100 times an hour. When a person stops breathing, their brain is briefly awakened, which prevents them from getting the deepest, most restful sleep. People with sleep apnea often wake up feeling tired, even after a full night's rest.
There are three types of sleep apnea:
Obstructive sleep apnea (OSA): The most common type, caused by soft tissue in the back of the throat relaxing and blocking the airway
Central sleep apnea (CSA): Caused by irregularities in the brain's signals to breathe
Complex sleep apnea: A third type of sleep apnea
The biggest problem with this disease is that it leads to heart issues.
Especially if sleep apnea isn't treated.
A part of my heart has already started slowing down because I can't wear the masks.
I went for my overnight study and nearly caused a 60 pile up crash because I kept nearly passing out as I drove.
I was beyond exhausted.
Hair Loss:
Polycystic ovary syndrome (PCOS) can cause hair loss in 20–30% of patients. PCOS is a hormone disorder that can cause hormonal imbalances, which can lead to excess androgens, or male hormones, like testosterone. These imbalances can cause hair to become dry, brittle, and damaged, and can lead to female pattern hair loss, also known as female pattern alopecia.
Facial Hair Growth:
Polycystic ovary syndrome (PCOS) can cause excessive hair growth on the face, chest, back, or buttocks, a condition known as hirsutism. This is caused by high levels of androgens, or male hormones, which can disrupt the menstrual cycle and prevent ovulation. This cycle can lead to more androgens, which are responsible for masculine physical characteristics like facial hair.
WHAT DOCTORS ARE NOT TELLING YOU:
Dental Diseases:
Women with PCOS tend to manifest poor periodontal conditions, such as positive bleeding on probing (BOP), deep PD, and high plaque index (PI). Interestingly, controlling PCOS with oral contraceptives and metformin mitigates periodontal inflammation.
It destroys dentin.
Bone Density:
(PCOS) can impair bone metabolism, which may increase the risk of fractures. Studies have shown that women with PCOS have lower levels of bone formation markers in their serum, which could negatively impact bone mineral density (BMD)
It's a Bone Degenerative Disease!
In short, it's a SLOW DEATH SENTANCE!
Polycystic ovary syndrome (PCOS) is a lifelong condition that can increase the risk of early death. A June 2023 study presented at the Endocrine Society's annual meeting found that women with PCOS have a 47% higher risk of overall mortality than women without PCOS, and die about one year earlier. The study also found that women with PCOS have:
A 67% higher risk of death from cardiovascular diseases
A 38% higher risk of death from tumors
Triple the risk of death from diabetes and lung infection
Understand ladies, everything you do...Carries a greater significant risk to your life.
Gentlemen, you too need to understand that carrying your children, is a higher risk for both mom's and child's lives.
Polycystic ovary syndrome (PCOS) can cause reproductive issues that can affect pregnancy, including:
How does PCOS age the body:
Women with PCOS differ in reproductive hormones past menopause. Hirsutism symptoms such as unwanted hair growth and balding worsen with age. The most important findings are that metabolic parameters worsen in overweight women with PCOS, increasing their risk for life-long health issues beyond menopause.
How does PCOS lead to any early death:
Polycystic ovary syndrome (PCOS) is a chronic condition that can increase the risk of early death by almost 50% for women. This is due to the link between PCOS and an increased likelihood of developing diabetes, cardiovascular disease, and bronchitis. According to a study presented at ENDO 2023, women with PCOS have a higher risk of death from: Diabetes (aHR = 3.07), Other circulatory system diseases (aHR = 2.07), and Bronchitis (aHR = 3.61).
What is the life expectancy of a woman with PCOS?
The group with PCOS had been diagnosed at a mean age of 27 years. The mean follow-up time was 13.1 years in both groups, during which 1,003 controls and 177 women with PCOS died. The mean age at death was 51.4 years for the PCOS group versus 52.6 years for the control women, a significant difference
Everything you do matters, and has effects, and consequences to you and your body!
I hope this helps because you NEED to be aware of the dangers of this disease.
Medication:
For weight management and keeping the insulin resistance in check.
Metformin.
To keep the facial hair growth down
Spironolactone
They are the medications most likely to be prescribed for women with PCOS. However, you need to understand that medications work on everyone differently
Speak to your OBGYN!
submitted by AlricaNeshama to PCOS [link] [comments]


2024.05.18 00:44 N8V_Link Anxiety out of control following ozempic

Just a warning, this maybe a bit disorganized and or have poor grammar at times.
Hello everyone, I'm at a bit of a bad place right now and I've been looking for information / support / acknowledgement that this exists from strangers. I don't really know what good it will do me, but I hope by getting myself out there it can help my mental health a bit.
Bit of a back story. I'm 36 now and I've had anxiety all my life. It started when I was 9 and I chocked on a tortilla from taco johns. From there I remember infrequent times where I was hungry I would shake uncontrollably. I didnt always have the best food options growing up but I learned to live with it. As an adult I would have panic attacks if I went to long without eating. The symptoms were essentially copy and pasted what hypoglycemia would look like. However my blood sugar during these times was fine.
I've been on lexapro for about a decade now and my anxiety was under control with the trigger listed above as the only thing I had to actively manage. With needing to eat to avoid panic attacks, you can imagine it was hard to control my weight.
Cue last september, I had a burning sensation when taking a pee. Turns out I was passing sugar in my urine. It's type 2 diabetes time! I immediately took control the best I could with dietary changes. I lost about 25 lbs in a few months on my own adding victoza about 6 weeks after my diagnosis. I had wanted ozempic as many of my friends were on it. I was also scared of metformin because of its rare interaction with alcohol.
Late january we had a shortage of victoza here. At the same time I conveniently got a letter in the mail that my insurance would now cover ozempic. I had been stable and doing quite well. My weight had plateaued but my blood sugar was under control. Now it's time to restart the process but hopefully lose more weight! Around 2/23 I started my first dose of ozempic.
April 10th was my first episode. officially I was diagnosed with fainting. I was sleeping in bed and I woke up and something felt off. I was overwhelmed with panic and rushed out and immediately fainted. I went to the ER and after a battery of tests nothing was found to be wrong with me.
May 1st it happened again. This time my primary started my on buspar to help with the anxiety. I had high hopes that this was just my anxiety and this would fix it. It lasted all of 2 weeks.
May 15th was just a few days ago now. I've had some normal and some not so normal days between my last 2 dr visits but something broke for me this morning. I was looking at something and had a feeling of nostalgia and it triggered a panic attack. I was stuck in that moment and everything I did to look forwards felt hopeless. I woke my wife and tried to have her help calm me down. After talking to her I was feeling numb and felt like doing things to feel again. I wanted to hit the walls, bite myself, or anything to feel real. Thats when I decided to go in again, these thoughts were not my own.
In the ER they have me ativan which calmed me down. I made an appointment with my primary and saw her that afternoon. We agreed to stop the buspar and the ozempic as well. We feel as if the ozempic nausea is triggering my anxiety and the buspar seems to have exasperated it rather than help. It's been 8 days since my last shot of ozempic. I'm taking hydroxyzine for the anxiety episodes. It helps but makes me sleepy. Last night I had nightmares and when I woke up i couldnt stay awake long enough to get away from them due to the sedative effect. I think I'll try and ride out the day without them.
For now I'm trying to take it a minute at a time, an hour at a time, a day at a time. Each time I have a slight bit of nausea its sugar coated with anxiety. We are hoping that once the ozempic leaves my body ill return to how I was before and able to manage my anxiety.
If youve made it this far thanks for reading. There is no tldr if you skipped to get here.
submitted by N8V_Link to mentalhealth [link] [comments]


2024.05.18 00:43 N8V_Link Ozempic / anxiety

Just a warning, this maybe a bit disorganized and or have poor grammar at times.
Hello everyone, I'm at a bit of a bad place right now and I've been looking for information / support / acknowledgement that this exists from strangers. I don't really know what good it will do me, but I hope by getting myself out there it can help my mental health a bit.
Bit of a back story. I'm 36 now and I've had anxiety all my life. It started when I was 9 and I chocked on a tortilla from taco johns. From there I remember infrequent times where I was hungry I would shake uncontrollably. I didnt always have the best food options growing up but I learned to live with it. As an adult I would have panic attacks if I went to long without eating. The symptoms were essentially copy and pasted what hypoglycemia would look like. However my blood sugar during these times was fine.
I've been on lexapro for about a decade now and my anxiety was under control with the trigger listed above as the only thing I had to actively manage. With needing to eat to avoid panic attacks, you can imagine it was hard to control my weight.
Cue last september, I had a burning sensation when taking a pee. Turns out I was passing sugar in my urine. It's type 2 diabetes time! I immediately took control the best I could with dietary changes. I lost about 25 lbs in a few months on my own adding victoza about 6 weeks after my diagnosis. I had wanted ozempic as many of my friends were on it. I was also scared of metformin because of its rare interaction with alcohol.
Late january we had a shortage of victoza here. At the same time I conveniently got a letter in the mail that my insurance would now cover ozempic. I had been stable and doing quite well. My weight had plateaued but my blood sugar was under control. Now it's time to restart the process but hopefully lose more weight! Around 2/23 I started my first dose of ozempic.
April 10th was my first episode. officially I was diagnosed with fainting. I was sleeping in bed and I woke up and something felt off. I was overwhelmed with panic and rushed out and immediately fainted. I went to the ER and after a battery of tests nothing was found to be wrong with me.
May 1st it happened again. This time my primary started my on buspar to help with the anxiety. I had high hopes that this was just my anxiety and this would fix it. It lasted all of 2 weeks.
May 15th was just a few days ago now. I've had some normal and some not so normal days between my last 2 dr visits but something broke for me this morning. I was looking at something and had a feeling of nostalgia and it triggered a panic attack. I was stuck in that moment and everything I did to look forwards felt hopeless. I woke my wife and tried to have her help calm me down. After talking to her I was feeling numb and felt like doing things to feel again. I wanted to hit the walls, bite myself, or anything to feel real. Thats when I decided to go in again, these thoughts were not my own.
In the ER they have me ativan which calmed me down. I made an appointment with my primary and saw her that afternoon. We agreed to stop the buspar and the ozempic as well. We feel as if the ozempic nausea is triggering my anxiety and the buspar seems to have exasperated it rather than help. It's been 8 days since my last shot of ozempic. I'm taking hydroxyzine for the anxiety episodes. It helps but makes me sleepy. Last night I had nightmares and when I woke up i couldnt stay awake long enough to get away from them due to the sedative effect. I think I'll try and ride out the day without them.
For now I'm trying to take it a minute at a time, an hour at a time, a day at a time. Each time I have a slight bit of nausea its sugar coated with anxiety. We are hoping that once the ozempic leaves my body ill return to how I was before and able to manage my anxiety.
If youve made it this far thanks for reading. There is no tldr if you skipped to get here.
submitted by N8V_Link to Ozempic [link] [comments]


2024.05.08 02:26 _Cherryfairy_ Questions about medication interactions

I'm a 19 y/o female. I'm on lansoprazole, aripiprizole, Metformin, fluoxetine, Lisdexamfetamine, and the pill. I have a quick question about my medications. I want to ask as I won't be seeing my psychiatrist for a while. So basically whilst I was doing my research on new medications I came across a few interactions between my meds one being the lansoprazole and the Lisdexamfetamine and the other being the latter and the fluoxetine. I also saw aripiprizole and the lisdexamfetamine.I'm wondering if I should reach out to my doctor and raise these concerns or if they're even worth raising.
submitted by _Cherryfairy_ to AskPsychiatry [link] [comments]


2024.05.07 23:48 _Cherryfairy_ Question about Medication interactions

19F, 5'4. I'm on lansoprazole, aripiprizole, Metformin, fluoxetine, Lisdexamfetamine, and the pill. I know I just posted but I have a quick question about my medications. I want to ask as I won't be seeing my psychiatrist for a while. So basically whilst I was doing my research on new medications I came across a few interactions between my meds one being the lansoprazole and the Lisdexamfetamine and the other being the latter and the fluoxetine. I also saw aripiprizole and the lisdexamfetamine.I'm wondering if I should reach out to my doctor and raise these concerns or if they're even worth raising.
submitted by _Cherryfairy_ to AskDocs [link] [comments]


2024.05.03 05:08 thatdocman Balancing Bodybuilding and Death [A 2024 Guide to Aging]

Hey guys, so I thought I’d do a post on aging and how to combat aging on a biological level. This post isn’t just “to live to 120, eat healthy” - instead, I want to delve into the specific biological targets that are going to help you live even 3-4 years longer if the benefits are reaped whilst young and you accumulate these biological benefits throughout the course of your life.
Why am I posting here? See the thing is, that a lot of us guys who train heavy, eat a lot and are in a constant state of anabolism with high protein loads, well, the science is pretty strong on this being a good way to shorten our lives. Initially you may be thinking, but I exercise, how can that possibly be bad? The thing is, heavy resistance training turns on mTOR which is a protein kinase (enzyme) in nearly all of our cells that controls a lot, including cell growth and metabolism (it is responsible for sensing when the body needs to lay down new muscle tissue after hypertrophy training for example). But, heavy training, anabolic load, protein, excess eating and so on… all these things stimulate mTOR to a significant degree, which has been implicated in the science as being pretty bad for longevity. So in this post, I’m not going to recommend “just don’t train” or “just cut protein” as that’s just unrealistic. Could you technically just not train and not eat any protein and live an extra 15 years? Quite possibly, yes. But what kind of life is that?
This post instead is going to be targeted at creating a balance between longevity and bodybuilding/resistance training, whilst also understanding a little bit more about the processes behind aging and what’s actually going on. I think it’s a kind of cool idea to try and balance getting jacked and living a long life - and finding a balance somewhere in between these 2 extremes.
I also recommend supplements and foods to combat these vectors once I describe them.

The Process Itself: How do we Age?

Most scientists are now in agreement that aging is a combination of complex processes, and have pretty much narrowed the biological aging process down to the following general categories:

  1. Dysregulation of anti-aging or pro-longevity signalling pathways
  2. Loss of mitochondrial function
  3. Reduced proteostasis (building and turnover of proteins)
  4. Lack of stem cell regenerative capacity
  5. Persistent and uncontrolled production of proinflammatory and free radicals that lead to cellular senescence (cells stop dividing)
  6. Telomere (protective cap for our DNA) erosion
  7. Loss of quality control in DNA/RNA
  8. Chromatin (DNA) and epigenetic alterations (environmental, lifestyle factors)

Firstly, I’ll break down each of these and then describe ways to combat this through dietary, lifestyle or supplemental intervention.
Please note: the research in this field is constantly shifting. Even next month, some of these concepts may be added to or out of date entirely. But as of May 2024, this guide encompasses quite a bit of the current research on aging. I do hope you enjoy - I do this all for free because I enjoy it, but if you are interested in more - my social links are on my Reddit profile. There’s a reason I’m doing this too for you guys who train either bodybuilding or strength training a lot - I’ll touch on this point later.

Dysregulation of anti-aging or pro-longevity signalling pathways:

The big players here are the main components of metabolic signalling pathways: AMPK (AMP-activated protein kinase), SIRT1 (Sirtuin 1), mTOR (mammalian target of rapamycin) and the IIS (insulin/insulin-like growth factor signaling) pathway.
AMPK:
The central modulator of metabolic homeostasis in our cells is AMPK, which regulates the cellular balance of ATP (our energy). AMPK is activated when ATP levels are low (for example during endurance exercise) and promotes catabolic pathways to generate more ATP, inhibiting anabolic pathways. Studies are pretty strong now that increasing activation of AMPK increases longevity and lifespan. How do you activate AMPK to reap these pro-longevity benefits? The following are known activators of AMPK:


AMPK is our cell’s way of sensing when energy levels are low (intracellular energy sensor).


AMPK itself.

SIRT1:

https://preview.redd.it/5epjsforn4yc1.png?width=1280&format=png&auto=webp&s=37bb6f29e16903fd43c4d732f60a27b8fcba001b
SIRT1 is another protein that regulates glucose and lipid metabolism. SIRT1 activation is incredibly pro-longevity, with it being shown to reduce inflammation, DNA damage, oxidative stress and it can also lower the generation of reactive oxygen species that can damage our tissues and cells. It can also help reduce mitochondrial dysfunction. Increased SIRT1 activity is linked with increased NAD+ levels and they seem to have a harmony with each other in the research. NAD+ can directly boost the activity of SIRT1, so this seems to be a promising target for longevity purposes.
To increase NAD+:


https://preview.redd.it/48xl5zcsn4yc1.png?width=830&format=png&auto=webp&s=d16fc196d84a9388ba7312ff90458ffc0f432640
mTOR:
As I touched on earlier, chronic activation of mTOR is anti-longevity (bodybuilding for example). The entire mTOR complex includes mTORC1 and mTORC2, and it is activation of mTORC1 (which promotes muscle protein synthesis and what is activated strongly when we train and ingest protein) that is the issue. Prolonged activation of mTORC1 contributes to aging by basically promoting dysfunctional protein quality control: basically overwhelming the capacity of our body’s usual inbuilt defensive mechanism to recognise and destroy mis-folded proteins. And here, you can imagine that a bodybuilder on compounds, taking high amounts of protein and training heavily will have an almost chronic activation of mTOR to be laying down new muscle. Yet, inhibition of mTOR enhances the lifespan of almost every organism studied.

https://preview.redd.it/y54kf9xsn4yc1.png?width=692&format=png&auto=webp&s=095e171f802d1ff51cdc34ea1cc713818854ebc8
Insulin/IGF-1 pathway:
Both insulin and IGF-1 stimulate mTOR and contribute to aging by turning on mTOR and inhibiting AMPK.

Loss of Mitochondrial Function

Mitochondrial dysfunction can lead to the production of ROS (reactive oxygen species), thereby increasing cellular damage - and it is this process that is linked to the development of atherosclerosis (for example) once ROS interact with LDL and neuronal damage by ROS damage to neurons themselves.

https://preview.redd.it/xyl2hdmtn4yc1.png?width=689&format=png&auto=webp&s=7f95eee91234b8067e827000efb995c6c2d275c3

Loss of Proteostasis

As we age we lose the ability to correctly fold proteins: proteostasis basically ensures the renewal of proteins and prevents the accumulation of damaged proteins, but losing this ability is common in age-related disorders like Alzheimer’s and Parkinsons, as well as cancer. For example in the image below, you can see how loss of proper folding of muscle proteins can lead to significantly dysfunctional muscle bellies in older populations:

https://preview.redd.it/ftoqog5un4yc1.png?width=560&format=png&auto=webp&s=e4d8176fcb9a79ef1471bba351ba41bea1dffd00

Loss of stem cell regenerative capacity

Age-related changes in stem cells are those that contribute to the lack of tissue regeneration and therefore poorer cellular outcomes.

Increased cellular senescence

Organisms have programmed mechanisms to eliminate damaged cells and induce cell replacement, improving tissue functionality and preventing the appearance of aberrant cellular alterations that could induce tumour growth. However, these mechanisms can fail with age and produce an accumulation of senescent cells in the remaining defective tissue, contributing to overall dysfunction.

https://preview.redd.it/p17b0irun4yc1.png?width=834&format=png&auto=webp&s=dbbb1d427def85f9d25073038e5520e95932eb64

Telomere (protective cap for our DNA) erosion

Telomeres are repetitive nucleotide sequences found at the ends of chromosomes that protect them from deterioration or fusion with neighboring chromosomes. In humans and most other eukaryotes, telomeres consist of a simple repeating sequence of DNA building blocks (nucleotides), typically TTAGGG, which is repeated thousands of times. The primary function of telomeres is to cap the ends of chromosomes, essentially serving as protective buffers that keep the chromosome ends safe from sticking to each other or breaking down, which could lead to genetic instability.

https://preview.redd.it/dtcidyavn4yc1.png?width=300&format=png&auto=webp&s=fb8022a2b07d3a221910a06c9f316c5c0adcaa2d
Each time a cell divides, the telomeres get a bit shorter. This shortening is due to the fact that DNA polymerase, the enzyme responsible for copying DNA, cannot replicate the very end of a linear DNA molecule. Over time, as a cell continues to divide, its telomeres can become critically short. When telomeres reach a critical length, cells typically stop dividing or die, which is a mechanism associated with aging. This telomere shortening can be somewhat counteracted by an enzyme called telomerase, which can extend the length of telomeres in certain cells.
Telomeres and telomerase play crucial roles in aging, cellular senescence, and cancer. Telomerase activity is present in stem cells and some white blood cells, and it is also reactivated in many cancer cells, allowing them to multiply indefinitely, which contributes to cancer progression. Understanding telomeres and telomerase has provided scientists insights into the biological processes of aging and aided development of new treatments for cancer and age-related diseases.

Loss of quality control in DNA/RNA

The term "loss of quality control in DNA/RNA” is referring to failures or inefficiencies in the cellular mechanisms that ensure the accuracy and stability of genetic information. This can involve various processes including DNA replication, RNA transcription, and the repair of DNA damage. When these processes are compromised, it can lead to mutations, transcription errors, and overall genomic instability.

Chromatin (DNA) and epigenetic alterations (environmental, lifestyle factors)

Chromatin is the complex of DNA, RNA, and proteins that makes up chromosomes within the nuclei of our cells. The primary function of chromatin is to efficiently package DNA into a small volume to fit in the cell nucleus and protect the DNA structure and sequence. Chromatin also plays an essential role in regulating gene expression and DNA replication and repair. Dysfunction in these processes leads to aging via cell death. Epigenetic alterations meanwhile refer to heritable changes in gene expression that do not involve changes to the underlying DNA sequence. These changes can be influenced by various environmental and lifestyle factors, such as diet, stress, exposure to chemicals, and aging. Bodybuilding may be one of these stressors.
With all of that - how do we actually combat these processes to try and live slightly longer whilst also maintaining muscle mass and not just becoming a bamboo stick that lives to 90 years old…

Well the research right now is promising on the following areas to target given these biological pathways I just spoke about above:
AMPK manipulation:


https://preview.redd.it/h64f743wn4yc1.png?width=1252&format=png&auto=webp&s=8d825e4ccbd9f647af7194ad0f6ccdb01b1624e3
mTOR inhibition:
Now technically, you can turn off mTOR with a compound called rapamycin (discovered in 1972) - this is an extreme option and will turn off muscle protein synthesis to a significant degree: studies have shown even short term rapamycin usage to have a number of benefits. However, this unrealistic and part of this guide is actually balancing longevity with bodybuilding too, so just completely shutting off the primary driver behind new muscle growth is a pretty dumb and unrealistic thing to do. So, it’s better to do either a lower carb diet or reduce protein intake slightly. There’s no real reason to be chowing down 300g protein per day for most people. In particular, reducing the following amino acids seem to have the most impact in terms of not stimulating mTOR chronically:

There is a potential to reduce the intake of those slightly whilst still being able to build muscle.
Utilising phenolic compounds to combat aging and activate SIRT1:
Pheno-what compounds? Well, phenolic compounds seem to be a promising third tier of compounds to combat cellular aging. Phenolic compounds are secondary metabolites synthesized by plants to carry out various functions such as reproduction, protection against predators, or even ultraviolet (UV) radiation. There are 8000 different phenolic compounds, including for example, flavonoids.

https://preview.redd.it/izlc9ynwn4yc1.png?width=800&format=png&auto=webp&s=bf4af77c1bfc0f0066621d2622851deb54f07a36
Resveratrol is a phenolic compound present in high amounts in grapes, and has been shown to activate sirtuins (by up to 2.4x above baseline), with evidence showing it can also reduce reactive oxygen species generation (ROS cause tissue injury) and reduce mitochondrial dysfunction. Other flavonoids have been implicated in activating this pathway and reducing ROS, such as quercetin.

https://preview.redd.it/jtmknc7xn4yc1.png?width=558&format=png&auto=webp&s=c9169d3ac0c8ac1985419ef345f8d556dcd76be8
Resveratrol dosing can be up to 5g/daily in humans, but more realistically somewhere around 1-2.5g can exert similar benefits whilst also being cost effective if buying resveratrol as an OTC supplement.
Utilising curcumin as an anti-oxidant:
Chronic oxidative stress and related systemic inflammation play important roles in cellular senescence and aging. These conditions result from an imbalance between the generation of reactive oxygen species (ROS) in mitochondria and their elimination by endogenous systems of antioxidant defence. Damage to vital biomolecules such as lipids, proteins and nucleic acids caused by ROS has been implicated as a main driver of aging. Given this, supplementation with bioactive phytochemicals has emerged as an attractive alternative to the intake of synthesized antioxidants. Phytochemicals are secondary metabolites produced by plants to protect them from environmental stresses and pathogenic invasions. Evidence was obtained that these compounds can promote the health and life spans of heterotrophic organisms, including humans.
So, the idea here is that reducing oxidative stress with the intake of biologically active antioxidant substances seems to have a lot of promise. One of these is curcumin at around 80mg/day (found in tumeric).

https://preview.redd.it/9mvbep1yn4yc1.png?width=750&format=png&auto=webp&s=92af0be0ee60136b3193f12efc6407eb9919107b

https://preview.redd.it/z755csnyn4yc1.png?width=832&format=png&auto=webp&s=8c8f0d044ef3c979683b0db2665945886428cdc1
NAD+ and SIRT1 relationship:
NAD+ keep sirtuins going by activating them and providing them ‘fuel’. Indeed, it is supplementation with NAD+ and its precursors that represent a potential therapeutic target to slow down aging-related diseases - especially seeing as NAD+ can activate SIRT1, a pathway you want to keep activated for longevity purposes. NAD+ is also a very important substrate molecule for DNA repair, immunomodulation and gene expression.
However, can you just take NADH - the reduced form of NAD+ and hope that it will raise blood levels enough? Not really - due to inefficient metabolism and poor absorption of NAD+ through the gastrointestinal system, oral bioavailability of NAD+ is low. Intravenous infusions can be better, yet are expensive, so:
Other supplements:
Niacin: shown to increase NAD+ levels, but flushing is an issue (niacin also elicits good HDL improvements and LDL lowering effects too, I’ve spoken about this in other videos)
NMN (Nicotinamide Mononucleotide): can raise NAD+ levels. Dose: well-tolerated at doses up to 1000mg/day.
Nicotinamide riboside: can raise NAD+ levels without skin flushing
A note about NAD+ kinetics: Importantly, in some studies, NAD+ levels were downregulated following chronic consumption. It was unclear whether this phenomenon was due to either saturation of uptake mechanisms, impaired conversion of nicotinic acid to nicotinamide or impaired NAD+ metabolism in bone marrow. Therefore, long-term supplementation with NAD+ precursors may have a deleterious impact on cellular function, inducing an unwanted adaptive response. This may be evidence that coming on and off NAD+ precursors may potentially be more beneficial than chronic supplementation.
Interestingly, caloric restriction increases NAD+ levels and CR has been shown to increase lifespan by up to 50% over control animals, most likely due to how caloric restriction significantly turns on SIRT1.
Mitochondrial modulation:
The basic idea here is that mitochondria have an important role in cellular health and lifespan, cross-talking to a number of the pathways I spoke about earlier (mTOR, AMPK and the insulin/insulin-like growth factor signaling (IIS) pathway). Mitochondrial dysfunction also can shorten telomeres (a common feature of the aging process).
With that information, there is convincing evidence that mitochondria play crucial roles in key cellular processes and contribute to many aspects of the aging process and aging-associated pathology. Consistent evidence was obtained that manipulation of mitochondria-related pathways may substantially affect both life span and health span in various animal models and that the life-extending effects of many pro-longevity compounds are significantly mediated by manipulating mitochondrial function (i.e. improving it).
So, what are some mitochondria-modulating pro-longevity compounds? Some of these are ones we’ve already gone over, again evidence that these pathways don’t just exist in isolation and that certain compounds can hit multiple ‘vectors’ in the whole longevity puzzle:

Anti-oxidant defence:
The final piece of the puzzle is using antioxidants to prevent the formation of oxygen radicals and free radical oxidation processes in cells and tissues (that damage them). Free radicals damage tissues and inhibit SIRT1, so compounds that can offset this damage by protecting tissues is going to be helpful in terms of cellular aging and dysfunction.
Antioxidants in chemistry, by definition, are compounds capable of terminating radical chemical reactions. The good news is, natural antioxidants include a lot of the compounds I’ve already detailed:

So in conclusion, there is a balance between bodybuilding and training hard and also thinking about longevity. The main takeaways:

The final thing I will say is this…
How aggressively you pursue these pathways is totally up to you. You could take a human from birth and just completely turn off mTOR and any muscle protein synthesis, activate their AMPK, keep their SIRT1 activity high and yes, that human could probably live to 120. But what quality of life would that be? To never train, never have any significant muscle mass, never be able to eat much. The other side of the coin (the other extreme) is take that same human from birth, chronically have mTOR turned on 24/7 through training, protein intake, 3000-4000 calories a day, AAS etc. and that human would probably have a significantly reduced quality of life. I do believe there is a balance in between those 2 extremes, and honestly where you decide to lie between those 2 extremes is up to you. I just wanted to present the science so you can think about these things and be a little bit more informed about aging and some of the biological processes at play.

https://preview.redd.it/ixcj7702o4yc1.jpg?width=1024&format=pjpg&auto=webp&s=966d8f55ac8479210492416369a755b367846ffd
Thank you very much for reading, social links on my Reddit profile if interested, it helps out a lot.
See you in the next post!
submitted by thatdocman to Supplements [link] [comments]


2024.04.26 20:54 hana_fuyu Metformin and Fertility?

I just recently started taking Metformin for my insulin resistance and triglycerides. I have seen that it increases fertility in us with PCOS. I am currently taking a hormonal BC pill for my symptoms, but I also do not want to get pregnant at all. My husband and I haven't used protection in the years we've been together because we haven't needed to. Should we start now? I know there's no interactions between Met and my pill, but I am worried about the general increase in fertility rates. Anyone have any experience in this and if there were actually any changes?
submitted by hana_fuyu to PCOS [link] [comments]


2024.04.18 17:13 Opening_Confidence52 My essay on Zepbound and Tirzepatide during these trying times

My essay on Zepbound and Tirzepatide during these trying times
Hey, everyone. I started with Mounjaro for weight loss July 5 and nearly immediately MJ went into shortage. I couldn’t handle the monthly drama of “Will I or won’t I have the medicine this month” so I went alternative with knowing I could always go back to the name brand with the coupon when supply shortages cleared up.
Supply shortages never cleared up.
Here are the issues with waiting the supply out:
  1. you have a metabolic/endocrine/hormone medical condition and are taking what is basically a hormone treatment medicine to treat your condition.
Ozempic/Wegovy = one hormone (receptor agonist). Mounjaro/zepbound= two hormones (receptor agonists). In phase 3 clinical trials, Retatrutide= three hormones (receptor agonists).
2) once you are off the shots for 2 weeks, you have to start back at 2.5mg
3) In the JAMA studies and in podcasts and YouTube videos with the researchers, this is what they say: (my paraphrases)
A) Chronic obesity is a disease. It is a disease of a malfunctioning set point. The reasons it malfunctions are varied— look at the graphic I posted below. These are all the things Zepbound works on. There is nothing except the medicine that will fix all of this.
This is a quote from the New England Journal of Medicine study I posted below. ***Initially, obesity was thought to result from an imbalance between caloric intake and energy expenditure. However, current understanding recognizes that the development of obesity is influenced by complex interactions of biological and psychosocial factors.**** (CICO doesn’t work for many people, and really might only work for people who haven’t damaged their bodies through dieting)
B) Your body fights back. Once you start losing weight, your body will make it so that you get hungrier and you crave sugar more. The medicine fixes this.
C) Exercise is good for you and your body but it has relatively little to do with weight loss.
D) Because the medicine is working with your hormones, it’s a bad idea for the majority of people to just go off for a while. Your hormones will be left hanging and you will start to gain weight back.
E) If you find a Tirzepatide half life calculator online, you will see that depending on how long you have been on it and what dose you are on, it could take as much as 8 weeks for the drug to leave your system. So if you stop, you might do ok for a while but then you will most likely have issues with food noise, weight gain etc.
The bottom line is: you have to find Tirzepatide any way you can get it. Alternative sources are a real thing right now, and let me tell you, the freedom and peace of mind when you don’t have to worry about supply is such a nice change of pace. Even if you use alternatives to bridge your supply issues, that is better IMO than going without.
You arent on a diet really. Sure, maybe you cleaned up your food choices and are taking better care of yourself, but the medicine is what is working and why we are all here. Also, the appetite suppression etc are basically side effects of the shots; there have been many weeks where I felt nothing at all and still lost weight. This includes the weeks where I did eat more because appetite suppression wasn’t the main thing I felt that week.
There are no tips and tricks for you to get through this shortage. You need to keep taking Tirzepatide or try a different med your doc recommends (but they are all in and out of shortage also aside from metformin).
https://preview.redd.it/51i125rz89vc1.jpg?width=1137&format=pjpg&auto=webp&s=8f97eb957050c588c7308a740b44ce14f641f308
submitted by Opening_Confidence52 to Zepbound [link] [comments]


2024.04.13 09:15 healthmedicinet Health Daily News April 12 2024

DAY: APRIL 12 2024


submitted by healthmedicinet to u/healthmedicinet [link] [comments]


2024.04.13 00:21 Torso_McTeague Curious to start inositol, had interesting/not great experience with Metformin

Hello all, very happy to have found this sub! My doctors have been flip-flopping on whether or not I have PCOS (painful and heavy periods, facial hair growth, obesity, but all my bloodwork is in normal ranges except for the LDL is getting higher), so I have been prescribed spironolactone (ages ago, have not taken for over a decade) and recently Metformin.
I am a huge fan of beer, but I do try to limit my drinking both for weight control and PCOS. However, on Metformin I felt like I was instantly thrown into lactic acidosis; my entire body felt heavy and like I was moving through sludge with every step. (And to clarify, the amount I was having was basically a couple of taster pours on a Friday after work, so not even a half-pint's amount.) I didn't notice drastic weight loss, but since stopping Met about a month ago, I feel like I've put weight on (even though my energy is better).
I was weighed for the first time in awhile at the doctor's this week, and it spiraled me into tears; highest I've ever been in my life. I'm desperate to try something different, and I've stopped drinking alcohol entirely until I can get some kind of handle on this. I'm curious if anyone else has had such a severe reaction from (what appears to be) an interaction between Met and alcohol, and (regardless of my not drinking now) if you all think I might see better results from the myo-inositol.
submitted by Torso_McTeague to PCOS [link] [comments]


2024.04.05 20:25 pebblebypebble Only got from 7.5 to 7.2 this past A1C test... Any tips for lowering blood sugar for a multi-year diabetic who is just struggling to keep up with it all?

A couple of years ago I took a medication that didn't work out well and ever since my blood sugar levels have been a lot harder to control and I need a lot more diabetes medication. Has anyone found anything that has helped reduce their blood sugar levels post a bad medication reaction without adding more meds? Had a PA appt this morning and she tried to put me on insulin... NO!!!!! Plus I can't handle any more side effects than I already have... Fatigue and brain fog on the meds are awful. My daily AM sugar is around 160 and I need to get it below 130 before my next nurse visit. I also need to lose about 65lbs still, even though I've lost A LOT already. 46/F. Perimenopause
I have a list here of what I need to do and changes I can make... If you can help me prioritize what changes I should work on first, I would deeply appreciate it!!!

Things I currently do (and how reliably I do them):

Things I try to do and did before the bad medication but now consistently fail at pulling off (so I'm basically not doing them):

Things I would have a hard time doing at all:

TLDR: My AM blood sugar level needs to be lower by 50 points to get below 130 and avoid additional medication. What changes should I make to either tighten up what I am doing or try something new to get to that goal the fastest?
Thank you all! (edited for typos)
submitted by pebblebypebble to diabetes_t2 [link] [comments]


2024.03.12 06:19 FromReelingToHealing Warfarin + Metformin?

My endo recommended I start meds for my borderline diabetes, as it been unresponsive to diet. Of all the options, metformin seems the safest. I found some potential interactions between warfarin (I'm a lifer) and metformin, but also a few posts from people who were on both without incident.
Am waiting for a call back from my hematologist, would love to hear from others who have been on warfarin and metformin.
Or anyone who's anticoagulated for life and on diabetes meds - what worked for you? I keep seeing potential drug interactions between all the diabetes meds and oral anticoagulants.
Thank you in advance!
submitted by FromReelingToHealing to ClotSurvivors [link] [comments]


2024.03.05 02:30 VitaminTed Birth story (long) - planned homebirth turned induction for pre-eclampsia - positive experience

Birth story (long) - planned homebirth turned induction for pre-eclampsia - positive experience
CW episiotomy, minor PPH. I’m nonbinary and use they/he pronouns
I had a relatively uncomplicated pregnancy and most of my prenatal care was managed through a private homebirth midwife. I was diagnosed with gestational diabetes at 24 weeks and it was mainly diet controlled. I went on metformin around 32 weeks because fasting numbers were a bit higher than I was comfortable with. I managed my GD with a continuous sensor rather than finger pricks as it gave me a better idea of how my body responded to foods. My GD was pretty well managed the whole way along (I include that bit because my baby turned out huge)
36-40 weeks: absolutely no signs of labour. I was physically and mentally comfy and happy to wait for baby.
41 weeks: I had an appointment at 41+2 where I was pretty ready to not be pregnant anymore. We were looking at my partner potentially not being able to get time off work after New Years so the longer we waited the more likely it was that I’d be without support after the birth. We decided to try castor oil in a “midwives brew” as a method of induction. I’m aware there’s some discourse around this being unsafe but my midwife and the team she works closely with have used it many times with good results, and there is no evidence that it makes baby pass meconium.
The next day I made and took a dose of the smoothie in the morning. I started having some mild cramping soon after but not a lot. Our midwife recommended a second dose 6 hours after the first when nothing much was happening. I did that, went for a long walk, and started getting some fairly intense contractions. We set up the birth space and prepared for things to get intense, but the contractions fizzled out later in the evening and I was hoping they’d ramp up while I was asleep, but instead I woke up to absolutely nothing.
I took that as a sign from the universe that maybe baby just needed us to wait, and so I decided to go into the hospital for some monitoring at 41+4 just to make sure everything was all good and it was okay to keep waiting for baby, particularly considering I had GD. CTG was perfect, and ultrasound showed good blood flow to and from the placenta.
The doctor who did the ultrasound was awful. He was confrontational and tried to scare me into induction, saying things like my baby was probably huge and I’d end up with a c-section if I tried to birth at home, that my fluid levels were low and if I ran out of fluid the placenta and my baby would die. He said that me being overdue (not even over 42 weeks!!) was “downright dangerous”. I told him as long as monitoring was fine I was happy to continue waiting for now. I also refused a growth scan and he was clearly unhappy with that.
I booked some more monitoring privately through an ultrasound place for 42w. Again everything was fine with blood flow, though interestingly my fluid levels were high, not low like the hospital doctor said.
At my 42w appointment with my midwife, we did a stretch and sweep to try to get things moving. Unfortunately at this appointment my blood pressure was a little high and there was protein in my urine, so I went into hospital for further assessment.
I had another awful encounter with the doctor from Saturday who again tried to pressure me into induction before the blood test results were even back. He was incredulous that I wouldn’t make a decision around induction until the blood test results came in. He was also incredibly aggressive on a phone call with my midwife, accusing her of “supporting an overdue, diabetic, hypertensive (even though my blood pressure readings in hospital were normal) person to birth at home”. It was clear that wasn’t what was happening, considering that I’d willingly gone to hospital to confirm the diagnosis and for further assessment. I was so shaky and dysregulated after this interaction with him and I asked for him to be removed from anything regarding my care. His demeanour was almost enough to scare me off of any further interaction with the hospital system, and if I’d encountered him earlier in pregnancy, I would have been incredibly reluctant to engage in any further care with the hospital, even if it was strongly recommended.
Ultimately the hospital confirmed diagnosis of pre-eclampsia and I had to come to terms with no longer being safe to birth at home. They weren’t able to induce me that night, so I checked out of the hospital against medical advice. It was my son’s birthday the next day and I really wanted to finish making his cake, and I had an acupuncture appointment as well that I was hoping might help induce labour. I figured if it was an urgent situation they would have made room for me to be induced immediately. I returned to hospital the next evening for an induction, and my private midwife met us at the hospital and helped to brief them on my pregnancy and situation. I set the room up with fairy lights, pregnancy art, and pride flags/pronoun signs.
The midwife on shift accidentally broke my water while attempting to insert the balloon catheter. Contractions started fairly quickly after that. Water was completely clear with no meconium, which was a bit of a surprise considering how overdue I was and that I’d had some castor oil to try to induce labour.
I was able to get about 3 hours of sleep before the contractions got too intense to sleep through. Once I was awake, the night shift midwife had a chat to me about putting a cannula in just in case I needed medication to manage the blood pressure. I wasn’t keen on a cannula unless I needed the pitocin, but agreed to this rationale. I wish I hadn’t…it took three different people 5 attempts to try to put one in and it was unsuccessful. I have very difficult veins and I had to point blank tell a doctor I’m not having any more attempts unless an anaesthetist comes and tries. Even with an ultrasound machine the anaesthetist wasn’t able to. At this point my contractions had disappeared and I told everyone to leave me alone so I could try to reestablish labour. I decided to try to rest again and see if that would help.
I woke up in the morning to no contractions at all. Tried walking, pumping, everything I could think of to get it started again with no luck. I asked my midwife to come in to help and together we decided that pitocin was the next thing to try.
This was a big change to my birth plan and it meant that a lot of the interventions I didn’t originally want, I did decide to consent to. However, I didn’t feel pressured into it at all and genuinely felt like I’d exhausted all other options to help my body labour naturally. Maybe my only regret was agreeing to the cannula in the middle of the night, because maybe labour would’ve kept ramping up, but there’s no way to know. It may have worked if they’d listened to me when I said I had difficult veins and got the anaesthetist straight away, instead of trying so many times. It also might not have.
I met the doctor and the midwife team before starting the pitocin and was immediately reassured. The doctor was so respectful and said straight up that she thought my birth plan was completely reasonable. She asked about my previous birth experiences and talked about her birth philosophy and I was happy to hear it aligned with mine. I didn’t get the sense that she was motivated by fear or risk aversion and that made it so much easier for me to trust her.
I started the drip at 11.30am (after it took the consultant anaesthetist two attempts for a successful cannula), and turned it up at 12.30pm. From there, labour established quickly and I moved between sitting on the ball, in the shower, and kneeling on the bed. I asked my friend who was going to take photos for us to come soon. Things felt pretty intense pretty quickly, and within a few hours I felt the urge to vomit and then had some involuntary pushing on the toilet. I remember feeling excited as I’d heard that the fetal ejection reflex can just take over and get baby out quickly.
That didn’t happen. For the next two hours, I continued to experience involuntary pushing and at some point the contractions were back to back with no rest. By this point I was so done. I was begging for an epidural, a c section, a break. I was genuinely overwhelmed and couldn’t believe the baby was still not out yet. I think a big part of this was that I was expecting involuntary pushing to lead to the fetal ejection reflex, and it didn’t. They ended up turning the drip off and also giving me an injection to slow down the contractions. Somewhere in all that, they asked about putting the scalp electrode on as the CTG kept losing trace. I was so sick of them getting in my space to try to reposition the monitors that I was happy for that.
Everything while I was pushing was a blur and I vaguely remember thinking that it was taking far too long. I heard the doctor say she was very keen for baby to be born soon. Doctor explained that she’d like to try to stretch my perineum a little around baby’s head to help it move through. When that was unsuccessful, she explained that she thought it was necessary to cut a small episiotomy to give baby’s head some room. At this point I would’ve agreed to them chopping me straight down the middle like a rotisserie chicken 😂 I was so so done and so exhausted, and I thought that there was no way baby was coming out on his own.
Once the episiotomy was done, birthing the rest of the head was still incredibly slow. I remember them saying 20% out, 30% out, 40% out with each contraction. Once the head was fully out, they got me to shift positions to put my leg up just in case of shoulder dystocia, but it wasn’t an issue. I expected baby to shoot right out with the next contraction but it still took a couple of pushes and the midwives pulling him out of the birth canal for him to come out after the shoulders were born. He was in there pretty tight 😂
I had a huge sense of relief and pride once he was born. He was alert straight away and it didn’t take long before he was rooting around for food. I birthed the placenta with no issues with just a pitocin injection.
A couple of hours later I did end up passing a whole bunch of clots and ended up being classified as a minor haemorrhage. We were in hospital an extra couple of days for a blood transfusion and iron infusion because I felt quite wibbly.
He was born at 42+2 weeks gestation after 6 hours of active labour. He weighed 5.7kg (12lb 10oz) with a 38cm head. We all thought by looking at him that he was maybe 4.5-4.8kg, I distinctly remember my midwife saying “oh fuck off” when he weighed in at 5.7kg 😂😂
Even though the whole experience didn’t go to plan, it was an incredibly positive experience and in a way, how difficult the birth was made it easier to manage the disappointment of not being able to birth physiologically at home. Debriefing afterwards with my midwife, she shared that she doesn’t see too many episiotomies that are genuinely necessary, but she absolutely felt that mine was. She also said that they were all quite worried about baby’s heart rate and it seemed he wasn’t coping with the back to back contractions (thanks pitocin). Despite this, there was no sense of fear, panic, or coercion in the room and the doctor was so incredibly respectful and calm when speaking to me.
I’m really glad I didn’t get any growth scans. It was already so hard to power through, it would’ve been impossible if we’d had an inkling of how big he was. I’m also so so grateful for the individualised prenatal care and the ability to work with my private midwife to manage my risk factors in a way that I felt comfy with.
It was difficult to come to terms with not being able to have the homebirth I planned. One thing that has helped is to frame it that my original goal around birthing at home was to have an experience where I was respected and was able to make decisions about my own care. Ultimately I got that, even if it wasn’t in the setting I wanted, and it felt so much better than my traumatic first birth.
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2024.03.01 06:19 neurogod00 Metformin

Anyone aware of any interactions between metformin and raspberry leaf tea? Any anecdotes and/or scientific papers?
submitted by neurogod00 to PCOS [link] [comments]


2024.03.01 06:13 neurogod00 Metformin researchers?

Hi friends, does anyone know of any literature indicating the interaction between meformin and raspberry leaf tea? I’m curious because I can’t find much, wondering in anyone has any insight or works in the field and can comment on the mechanistic actions of metformin.
submitted by neurogod00 to labrats [link] [comments]


2024.02.21 21:17 DictatorD Recently put on Metformin and on pre-existing BC -- PLEASE help with side affects

Hi there!
I have recently been put on metformin for pre-diabetes, and have been on birth control for over a year to treat my PCOS. It's been just under three weeks, but I've started feeling immense levels of anxiety and overthinking. When I overthink, it's to the point where my chest starts physically hurting because it feels like my thoughts are beating me up. I have cried nearly every single night for about a week and I'm just about fed up.
The only time I've ever felt this way in the past is when I very, very first started birth control after my PCOS diagnoses about a year and a half ago. I switched birth control and the anxiety went away, and have been on that same BC since. I am starting to believe that maybe my Metformin is doing something to interact with my hormones that my BC gives me, which is prompting this intense emotional response.
At this point, I'm torn between deciding whether I need to immediately stop taking my birth control or my metformin. Personally, i am leaning towards stopping Birth Control because I fear diabetes more than I fear my PCOS, but i very much want to hear thoughts from others who may know more than me.
Please do share with me your thoughts. My gyno's office is incredibly hard to reach and I am looking for advice that can help me alleviate this near debilitating level of overthinking and anxiety until I can make an appointment with my gyno, which probably won't be until mid to late march.
submitted by DictatorD to PCOS [link] [comments]


2024.02.16 02:32 Appropriate_Idea_185 My mom has a concerning amount of medication

My mom (45f) (5ft) (200lbs) is starting to concern me because between her psychiatrist and her primary doctor she has a very very long prescription list. These mainly include, amlodipine(10mg), metoprolol(2x a day)(50mg), lamotrigine(100mg), hydroxyzine(2x a day)(50mg), lorazepam(1mg)(2x a day), venlafaxine(225mg), naproxen (2x a day)(500mg), atorvastatin (10mg), Ambien(10mg), flexiril (10mg), Omeprazole(20mg), imitrex (50 mg)(when needed) She survived breast cancer been in remission for about a year or so now. Also diagnosed with bipolar, just got her a1c (6.7) is down and is still taking the medication for diabetes (metformin(50 mg 4x a day) and rybelsus(14mg) Should she be downsizing why does she have so much I just feel like she has too much and she's seems to have these weird airhead moments she didn't used to have 6 months ago. I'm fearing medications interacting etc.
submitted by Appropriate_Idea_185 to AskDocs [link] [comments]


2024.02.04 12:34 Utter_Choice Long COVID and at risk

I have Long COVID starting in 2020 because of CDC and their cloth masks. I was bedridden for a year with excruciating headaches, PEM and fatigue so bad I had to rest after showering. I had to move back in which my parents, which is rough because it turns out my mom hates me.
I've been to over 50 different doctors and I am getting better but even just a few weeks ago they found a CSF leak that they patched and found myself unable to get up for more than 15 minutes without developing an excruciating headache (think it was an interaction between contrast and the metformin I was taking). I am almost fully recovered but have now been referred to a spinal surgeon.
My Mom had a plumber come over. I apologized and asked the plumber and his assistant to wear masks and I brought him some. He was very gracious about it. While we were chatting I noticed it was pulling on his ear. My mom has more comfortable masks that she refused to get for him.
I came out an hour later and he wasn't wearing any mask. I'm fairly certain that she told him it was fine to take it off.
I already wear a mask any time I leave my room and run a hepa filter in the room because she constantly lies to me about masking. I've literally seen her after she told me she was going to be masked and she wasn't. The part where I am really struggling is that her looking good for this rando is more important than my ability to work, provide for myself or live. I am currently taking a bootcamp and volunteer with women who code in hopes of getting a job in tech so I can work at home and not get another round of COVID.
I was so much healthier before I got sick. I'm terrified that the next infection will leave me bedridden for the rest of my life. That idea terrifies me, I don't think I'll make through another round. I don't know that I can live like that. I've told her this a few times.
If I get sick, I may never be able to return to work. I'm terrified shell expose me and I'll never be able to leave. Which doesn't make any sense to me because if she hates me so much, why would she make it hard for me to leave? I'm so distraught by how little regard she has for my future and health on top of being terrified. It breaks my heart that she's basically willing to cripple me to make someone else comfortable.
submitted by Utter_Choice to ZeroCovidCommunity [link] [comments]


2024.01.20 05:45 CombinatonProud The Pharmacology of Myricetin, The Endurance-Doubling Polyphenol

The Pharmacology of Myricetin, The Endurance-Doubling Polyphenol
This post will look into the many interesting mechanisms of the polyphenol, Myricetin. It is not to be understated, and it transcends most similar polyphenols through being a potent endurance-enhancer and nootropic. Just for reference, this is a repost to this sub, with a few updates for accuracy.

Introduction to Myricetin

Myricetin is a natural product found in many plants/fruits, most notably bayberries/strawberries. However, the flavonoid content of foods is extremely variable [1] and is influenced by both location, soil quality, and other factors.
As mentioned, myricetin is prominantly found in bayberry extract [22] alongside other polyphenols (such as myricitrin and quercetin). Consuming bayberry is one way to intake Myricetin, but it requires a high dose, and is combined with many other polyphenols that may increase the cytotoxic potential.
Most people intake only about 20mg of myricetin per day through diet (on average) [6], while the performance-enhancing/nootropic doses are about 10-20x higher. Myricetin's oral bioavailability is only about 10%, meaning dosages required for pychoactive/enhancing effects range between 250-600mg [2].
Most polyphenols/flavonoids are pretty weak in terms of efficacy, however myricetin stands out from the rest in multiple ways. It's most notable effects are that it enhances physical endurance, is a potent antidepressant, and directly inhibits SARS-COV-2 and HIV.

Performance-Enhancing Effects of Myricetin

https://preview.redd.it/5clvcu6owidc1.png?width=480&format=png&auto=webp&s=6311641516ff1c899a33a0e53e93adbab4efa576
Myricetin is a potent endurance enhancer, doubling physical endurance in rodents after 4 weeks (in multiple studies) [17][18] at the human equivilant dose of 250-300mg. This effect is mediated through multiple mechanisms, however Myricetin does this most notabley through increasing the expression of the following (directly/indirectly) in muscle fiber: PGC-1b, PGC-1α, ERRa, PPAR-a/b/d/γ, Sirt1, Foxo1, and more.
Myricetin most notably enhances PGC-1b, which is associated with performance in endurance athletes [15], and is associated with endurance in animal models [16]. Myricetin also promotes the conversion of fast-to-slow twitch fiber in muscle [18], and this would create an expected increase in endurance and decrease in strength. However, in the studies provided, Myricetin enhanced grip strength in mice, showing a modest strength-enhancing capability of the compound on top of endurance enhancement.
Myricetin also enhances GLP-1 [26], which means it is likely an exercise mimetic through it and also it is likely to induce some degree of fat loss as seen with other GLP-1 agonists.

Antidepressant Effect

https://preview.redd.it/7ie1ezjpwidc1.png?width=309&format=png&auto=webp&s=658de367fdfe89b1a23d7d74f1721d2e3d1c9707
In multiple studies, myricetin ameriolated symptoms of depression and increased stress resilience [19]. This antidepressant effect has also been seen in anecdotal reports using the pure powder form of this compound. This is potentially through anti-inflammitory effects, CAMKII/BDNF/NGF/TrkB/COMT modulation, or other mechanisms.
Myricetin is also a MAO inhibitor, but seems to be less potent than quercetin in that regard [27], so most of its antidepressant effects may be due to other mechanisms.
In one study [19], chronic administration of myricetin restored hippocampal BDNF protein levels in mice subjected to repeated restraint stress.

Anxiolytic & Anti-PTSD Effect

Myricetin exerts antidepressant and anxiolytic effects through regulation of HPA axis and activation of the BDNF-ERK signaling pathway [20].
Myricetin inhibits stress-induced changes in 5-HT, BDNF, TrkB, NE, ACTH and more. It has been shown to be most anxiolytic at the human equivilant dose of 200-300mg, with a slightly lower efficacy at 500mg equivilant human dose. [21]
https://preview.redd.it/q7wqsqk3xidc1.png?width=386&format=png&auto=webp&s=47bf89c5d918e625b0715a09a63409f56112a665

Protective Effect in Alzheimer's/Parkinson's Disease

Myricetin improved learning and memory in rodent models of Alzheimer's. It reduced oxidative stress, inhibited AChE, decreased iron accumulation, and suppressed Aβ aggregation. It also has protective mechanisms through increased phosphorylation of CREB, a transcription factor that regulates BDNF and NGF expression. [2][4]. Myricetin also reversed motor deficits and dopamine depletion in Parkinson's models. It suppressed oxidative stress, prevented α-synuclein aggregation, and inhibited iron accumulation. Mechanisms involve tyrosine hydroxylase, BDNF, and COMT inhibition (which is almost exclusively located in the PFC, meaning inhibition enhances PFC function [10]) [2][5].

Protective Effect in Epilepsy

Myricetin reduced seizure rates in a mouse model, potentially by enhancing GABA-A activity (contextually) and inhibiting MMP-9. It activated CaMKII signaling and potassium currents to calm hypothalamic PVN neurons [8].

Protective Against CVD

Myricetin exhibits cardioprotective, anti-hypertensive, anti-atherosclerotic, anti-hyperglycemic, and anti-hyperlipidemic effects. In addition, myricetin may alleviate some of the complications caused by adult-onset diabetes. The combined functions of myricetin allow for the prevention of CVD [9].

Oxidant Interactions

Myricetin can act as a pro-oxidant compound when it interacts with DNA [6]. Studies involving in vitro models have shown that myricetin causes the degradation of DNA. This may make myricetin seem bad at a glance, however at higher and higher concentrations of myricetin, the rate of DNA damage has been shown to decrease [7]. Therefore, adding additional myricetin through supplementation would actully reduce existing pro-oxidation caused through low-quantity myricetin intake through standard diets. Myricetin is also anti-inflammatory through its ability to inhibit the amplified production of cytokines that occurs during inflammation.

Antidiabetic Effect

Several in vitro and animal studies have indicated the antidiabetic capabilities of myricetin [6], however, myricetin's close relative myricitrin seems to have a larger potential for anti-diabetic actions, showing as effective (and even more effective) as metformin, with less side effects [11].

Protective Against COVID-19 / Antiviral

Myricetin inhibits the viral replication of SARS-COV-2 [12][13], with very potent inhibitory effects shown in multiple studies. It does this through binding directly to SARS-COV-2, through targeting Mpro. Myricetin was identified to have potent inhibitory activity with an IC50 of 3.684μM in the enzyme assay [13].
Using Myricetin, alongside GCP-II/KAT-II inhibition, currently seems like the best way to ameriolate COVID-19 symptoms, through the literature currently available.
Myricetin also inhibits other viruses, including HIV [14], which has been shown in multiple studies using rodent models.

ROA For Best Metabolism

The best hypothetical Route of Administration based on literature available is 250-600mg early in the morning on an empty stomach. This is probably the best ROA as myricetin does seem to have some interaction with liver enzymes, meaning food or drink could potentially effect metabolism.

Discussion

Myricetin has a lot of different beneficial effects, and it is definitely an interesting compound to say the least. It has proven effective in preliminary human testing, especially for its antidepressant and pro-endurance effects.
If you want a source for Myricetin, it can be found on penchant.bio
Thank you for reading. If you found this post useful, share this (or crosspost) to those who you think would be interested. Also consider joining the sub.
submitted by CombinatonProud to prefrontal [link] [comments]


http://rodzice.org/