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A new study explores anti-aging properties of metformin
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<blockquote data-quote="dickielongate" data-source="post: 152992" data-attributes="member: 38930"><p>Old thread I know, but I think there is room to question the story of the article. If it was all true, shouldn't we expect more evidence of real world outcomes with all the millions taking it? At least she begins by declaring her preemptive distrust.</p><p></p><p>I find it misleading to mix together known issues with supposition and unproven conclusion, which is present more than once. But worse than that there is some either careless or wilful misrepresentation of some of the data in the studies referenced. </p><p></p><p>On <strong>B12</strong>, there are some valid concerns, but you could argue the fact that people taking metformin are not being given the information is the problem.</p><p></p><p>Leeching is a poor description. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874129/" target="_blank">Blocking aborption </a>would have been better. It would have been more informative to point out the degree of blocking, the typical rate of depletion, and that with <a href="https://www.ncbi.nlm.nih.gov/pubmed/19846797" target="_blank">screening and supplementation</a> it's really not problem if you're informed. </p><p></p><p>The statement about <strong>ATP </strong>production seems misleading if you actually read what she's referenced:</p><p></p><p>"<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100525" target="_blank">Metformin reduces mitochondrial ATP production in skeletal muscle by as much as 48%</a>. Sit with that one for a moment, a 48% reduction in cell fuel. Imagine functioning at only half capacity. This would make basic activities difficult at best and exercising to lose weight a very unlikely proposition"</p><p></p><p><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100525" target="_blank">To achieve a 48%</a> drop according to the study (if I was a 100kg rat) I would need to consume 30g (30,000mg) of metformin. Note also that an equivalent of 3g per day, no ATP reduction effects were produced. </p><p></p><p>"..the types of disturbances we might see become quite clear: neurocognitive decline, psychiatric instability, neuropathy, heart rate, rhythm and blood pressure abnormalities, along with gastrointestinal distress to name but a few. Underlying all of these symptoms, and indeed, all mitochondrial dysfunction, is an overwhelming sense of <a href="http://www.hormonesmatter.com/?s=fatigue&submit=" target="_blank">fatigue</a> and malaise."</p><p></p><p>On associating metformin with <strong>neurocognitive decline</strong>, which suggests to the casual reader a causal relationship, a quick search turns up stuff which <a href="https://www.ncbi.nlm.nih.gov/pubmed/24577463" target="_blank">reports the opposite</a>.</p><p></p><p><strong>GI distress</strong> is well documented, but <a href="http://www.alliedacademies.org/articles/metformin-and-its-gastrointestinal-problems-a-review-10324.html" target="_blank">not concretely tied to mitochondrial function</a>. It seems <a href="https://www.ncbi.nlm.nih.gov/pubmed/9408071" target="_blank">doubtful metformin affects blood pressure</a> in a meaningful way. Likewise, there is no obvious evidence I have found that points to metformin causing fatigue, unless lactic acidosis is about to kill you.</p><p></p><p><a href="https://www.ncbi.nlm.nih.gov/pubmed/20071560" target="_blank">The study referenced</a> describes measuring short term insulin sensitivity changes after one bout of <strong>exercise</strong>. Reading further on this, I think it would be wrong to draw conclusions <a href="https://care.diabetesjournals.org/content/35/1/131" target="_blank"> This study</a> makes the picture clearer, and notes:</p><p></p><p>"Although acute bouts of exercise can increase insulin sensitivity for up to 48 h, the time-course effects of the combined treatment remain unclear. Despite the lack of additive effects on insulin sensitivity, combining metformin with training, as described in the recent American Diabetes Association clinical recommendations (<a href="https://care.diabetesjournals.org/content/35/1/131#ref-9" target="_blank">9</a>), may still be a potentially useful strategy to prevent the transition from prediabetes to diabetes. "</p><p></p><p>Regarding <strong>aerobic capacity</strong>, Marrs states:</p><p></p><p>"<a href="http://www.ncbi.nlm.nih.gov/pubmed/18347654" target="_blank">Metformin also reduces peak aerobic capacity, </a>reducing performance and making exercise more difficult."</p><p></p><p>Again it's not such a clear picture or black and white story on cardio. There is evidence that perceived exertion has increased, but changes to vo2 max were not significant. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4906084/" target="_blank">This study</a> suggests metformin can play a role in improving <strong>cardiovascular function</strong> in insulin resistant subjects.</p><p></p><p>Marrs doesn't touch on this, but regarding resistance training and <strong>muscle synthesis</strong>, it seems likely that there is a positive effect from metformin<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5405504/" target="_blank"> at least in older people.</a></p><p></p><p>Regarding the<strong> immune system</strong> impact of metformin, with all the convincing theory you would expect to easily find evidence if rates of disease and infection to be impacted by metformin users. But it's easy to find <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6162822/" target="_blank">evidence </a>of the <a href="https://www.nature.com/articles/s41598-018-21612-6" target="_blank">opposite</a>.</p><p></p><p>I would argue it's irresponsible for someone presenting things as facts to mix in statements like:</p><p></p><p>"I would suspect predisposes those who take Metformin to more infections "</p><p></p><p>Because readers will believe it, even though it really does seem like a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5013429/" target="_blank">baseless suspicion</a></p><p></p><p>In all the studies I've linked, I promise there has been no cherry picking or digging. In almost every case I've taken the first Google results looking for the subject matter. Try for yourself, and don't believe everyone with a PhD who throws out lots of big words and study references.</p></blockquote><p></p>
[QUOTE="dickielongate, post: 152992, member: 38930"] Old thread I know, but I think there is room to question the story of the article. If it was all true, shouldn't we expect more evidence of real world outcomes with all the millions taking it? At least she begins by declaring her preemptive distrust. I find it misleading to mix together known issues with supposition and unproven conclusion, which is present more than once. But worse than that there is some either careless or wilful misrepresentation of some of the data in the studies referenced. On [B]B12[/B], there are some valid concerns, but you could argue the fact that people taking metformin are not being given the information is the problem. Leeching is a poor description. [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874129/']Blocking aborption [/URL]would have been better. It would have been more informative to point out the degree of blocking, the typical rate of depletion, and that with [URL='https://www.ncbi.nlm.nih.gov/pubmed/19846797']screening and supplementation[/URL] it's really not problem if you're informed. The statement about [B]ATP [/B]production seems misleading if you actually read what she's referenced: "[URL='http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100525']Metformin reduces mitochondrial ATP production in skeletal muscle by as much as 48%[/URL]. Sit with that one for a moment, a 48% reduction in cell fuel. Imagine functioning at only half capacity. This would make basic activities difficult at best and exercising to lose weight a very unlikely proposition" [URL='https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100525']To achieve a 48%[/URL] drop according to the study (if I was a 100kg rat) I would need to consume 30g (30,000mg) of metformin. Note also that an equivalent of 3g per day, no ATP reduction effects were produced. "..the types of disturbances we might see become quite clear: neurocognitive decline, psychiatric instability, neuropathy, heart rate, rhythm and blood pressure abnormalities, along with gastrointestinal distress to name but a few. Underlying all of these symptoms, and indeed, all mitochondrial dysfunction, is an overwhelming sense of [URL='http://www.hormonesmatter.com/?s=fatigue&submit=']fatigue[/URL] and malaise." On associating metformin with [B]neurocognitive decline[/B], which suggests to the casual reader a causal relationship, a quick search turns up stuff which [URL='https://www.ncbi.nlm.nih.gov/pubmed/24577463']reports the opposite[/URL]. [B]GI distress[/B] is well documented, but [URL='http://www.alliedacademies.org/articles/metformin-and-its-gastrointestinal-problems-a-review-10324.html']not concretely tied to mitochondrial function[/URL]. It seems [URL='https://www.ncbi.nlm.nih.gov/pubmed/9408071']doubtful metformin affects blood pressure[/URL] in a meaningful way. Likewise, there is no obvious evidence I have found that points to metformin causing fatigue, unless lactic acidosis is about to kill you. [URL='https://www.ncbi.nlm.nih.gov/pubmed/20071560']The study referenced[/URL] describes measuring short term insulin sensitivity changes after one bout of [B]exercise[/B]. Reading further on this, I think it would be wrong to draw conclusions [URL='https://care.diabetesjournals.org/content/35/1/131'] This study[/URL] makes the picture clearer, and notes: "Although acute bouts of exercise can increase insulin sensitivity for up to 48 h, the time-course effects of the combined treatment remain unclear. Despite the lack of additive effects on insulin sensitivity, combining metformin with training, as described in the recent American Diabetes Association clinical recommendations ([URL='https://care.diabetesjournals.org/content/35/1/131#ref-9']9[/URL]), may still be a potentially useful strategy to prevent the transition from prediabetes to diabetes. " Regarding [B]aerobic capacity[/B], Marrs states: "[URL='http://www.ncbi.nlm.nih.gov/pubmed/18347654']Metformin also reduces peak aerobic capacity, [/URL]reducing performance and making exercise more difficult." Again it's not such a clear picture or black and white story on cardio. There is evidence that perceived exertion has increased, but changes to vo2 max were not significant. [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4906084/']This study[/URL] suggests metformin can play a role in improving [B]cardiovascular function[/B] in insulin resistant subjects. Marrs doesn't touch on this, but regarding resistance training and [B]muscle synthesis[/B], it seems likely that there is a positive effect from metformin[URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5405504/'] at least in older people.[/URL] Regarding the[B] immune system[/B] impact of metformin, with all the convincing theory you would expect to easily find evidence if rates of disease and infection to be impacted by metformin users. But it's easy to find [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6162822/']evidence [/URL]of the [URL='https://www.nature.com/articles/s41598-018-21612-6']opposite[/URL]. I would argue it's irresponsible for someone presenting things as facts to mix in statements like: "I would suspect predisposes those who take Metformin to more infections " Because readers will believe it, even though it really does seem like a [URL='https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5013429/']baseless suspicion[/URL] In all the studies I've linked, I promise there has been no cherry picking or digging. In almost every case I've taken the first Google results looking for the subject matter. Try for yourself, and don't believe everyone with a PhD who throws out lots of big words and study references. [/QUOTE]
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A new study explores anti-aging properties of metformin
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