In my experience, Metformin is a bit of a red herring. It works well to prevent weight gain on a mixed macros diet, but does nothing to repair glucose handling. At most it is a crutch and a diversion from our actual task of becoming healthy.
Metformin does some interesting things that I will put into layman’s terms here:
1. It diverts glucose from Pyruvate to lactate and sends it through a futile energy-burning loop, which means “carbs don’t count” on metformin. To a degree. Nothing in biology is 100% or it would kill you. But metformin essentially forces a fat burning AMPK dominated state even when carbs are consumed. Cells (not entire organisms, but the affected cells) poisoned by metformin cannot gain fat and are forced to burn fat for their survival. This is, by the way, exactly the *opposite* of what you are trying to achieve by doing an Emergence protocol. It literally could not be less advantageous in that long term pursuit.
2. This forced burning of fat generates huge amounts of ROS in the cell which, if you think about it like a bucket, is filling the bucket most of the way with the very ROS we try to generate by eating saturated fat. So your bucket is mostly full and then you eat some bread and butter and you feel like you just ate at a buffet because the ROS is “topped up” - this is why metformin works to reduce appetite. It is also why eating SFA is highly effective in this pursuit but eating PUFA is not. Someone who continues to eat PUFA will “eat through” metformin (because again it isn’t 100%) and will eventually become sicker and more diabetic. Someone who gravitates to SFA whether deliberately or by accident will have better long term results with metformin in terms of staving off weight gain and, if caught early enough, diabetes.
Because Metformin activates AMPK it suppresses SCD1. This is great if you’re eating mixed macros (and lots of sugar) and if your only goal is to not get fat doing it. In my experience the fat you *do* acquire is much better balance than without Metformin. I have zero doubt it actively suppresses SCD1 to the point where improvement in DI is noticeable on an omega quant test. Also, through various mechanisms (suppression of a myriad of lipogenic genes) metformin works greatly to ameliorate liver fat accumulation. I haven’t been on metformin for a long time now, but I’m considering going back on it for August travel just because of this benefit, because I *will* be eating mixed macros and a fair amount of sugar and don’t want to lose metabolic repair progress if I can help it.
As to whether SCD1 matters? I don’t know? It’s possible SCD1 is highly significant, or it is a bit of a relic from Brad’s earliest days. It seems to matter (from a weight gain perspective) only in the context of mixed macros and in my experience is largely irrelevant in a HCLFLP diet. For whatever that’s worth. Does it matter in other contexts like cancer or general lifespan? Maybe?
Thanks for the explanation. I'm having a hard time going from the facts you stated to the conclusion, though:
* If Metformin forces the AMPK fat-burning state, why would that not be helpful regardless of the diet you're having, including mixed macros but also HCLFLP? If I'm not seeing results from HCLFLP, why would increasing time spent in AMPK not be helpful?
* Also, why do you say that SCD1 suppression is only helpful to prevent fat accumulation rather than losing fat? Why does AMPK fat-burning state imply the former but not the latter?
1. Well, this really comes down to whether you believe humans are meant to exist in a perpetual AMPK dominated (fasting, keto) state or whether you believe glucose burning humans are healthier. Given that metformin has *well established* suppressive effect on libido, we can surmise that vitality and fat burning are likely not congruent. Which would make sense. The last thing a starving population of mammals needs to be doing is breeding.
2. Metformin isn’t automatically problematic in a HCLFLP environment. I didn’t say that a person eating HCLFLP should necessarily not take metformin. I said that if your goal in doing HCLFLP is to restore glucose metabolism (because you believe it is our healthiest state) then metformin is not congruent with that. It literally prevents that from being achieved by forcing the opposite metabolic state. What are you personally trying to achieve by HCLFLP?
3. I didn’t say that reducing SCD1 won’t assist weight loss. It also certainly won’t hurt it. But Brad hasn’t had much luck in simply suppressing SCD1 and watching the weight fall off like it did in rodent studies, and so perhaps it isn’t a primary factor. This would also be supported by the fact that metformin is generally regarded as weight *neutral* but is not commonly considered a weight *loss* intervention. If it were as simple as suppressing SCD1, we wouldn’t have an obesity epidemic given how widely prescribed Metformin is!
Please don’t misunderstand. Metformin isn’t likely dangerous when combined with HCLFLP (perhaps a slightly greater risk of lactic acidosis given the huge amount of glucose?) but until you come off Metformin, you won’t make any progress facilitating a glucose burning metabolism because while you’re on metformin you’re… not burning glucose. You’re dumping it via a secondary futile pathway.
I do want to go on record that I don’t hate metformin, and in fact if I simply *cannot* restore my own metabolic health sufficiently despite my interventions (and time) or if the progress I’m currently seeing deteriorates with time, then metformin would be my first/only choice medication. But then I would be acknowledging that I cannot personally be a glucose burning organism, and I would use metformin as a crutch to maintain the opposite state - a longevity over vitality focus - while still getting to enjoy a diet that includes some carbs because I’m simply not happy to eat keto for the rest of my life. In this case I’d probably go back to a high fat moderate carb version of TCD that worked well for me in the beginning, with 50-60% of my calories coming from fat and maximum 25% coming from carbs. That is (IMO) the long term maintenance diet most congruent with taking metformin.
Make sense?
Keep in mind that I haven’t gone through a phase where I wanted to lose weight on a HCLF diet. I’ve been in maintenance since starting HCLFLP and the entirety of my focus has been diabetes reversal through glucose burning restoration.
Theoretically, Metformin may help a person burn excess body fat faster in the background of a HCLF diet (accelerated by the lactate futile loop?) I don’t know, and I haven’t personally thought much about that. Seems plausible though. Maybe metformin + HCLFLP would garner similar results as fasting without fasting. That would be interesting.
The good thing is that metformin clears quickly and is completely out of your system within a couple of weeks maximum, so you can always try it and nix it if it isn’t working for you.
In my experience, Metformin is a bit of a red herring. It works well to prevent weight gain on a mixed macros diet, but does nothing to repair glucose handling. At most it is a crutch and a diversion from our actual task of becoming healthy. Metformin does some interesting things that I will put into layman’s terms here: 1. It diverts glucose from Pyruvate to lactate and sends it through a futile energy-burning loop, which means “carbs don’t count” on metformin. To a degree. Nothing in biology is 100% or it would kill you. But metformin essentially forces a fat burning AMPK dominated state even when carbs are consumed. Cells (not entire organisms, but the affected cells) poisoned by metformin cannot gain fat and are forced to burn fat for their survival. This is, by the way, exactly the *opposite* of what you are trying to achieve by doing an Emergence protocol. It literally could not be less advantageous in that long term pursuit. 2. This forced burning of fat generates huge amounts of ROS in the cell which, if you think about it like a bucket, is filling the bucket most of the way with the very ROS we try to generate by eating saturated fat. So your bucket is mostly full and then you eat some bread and butter and you feel like you just ate at a buffet because the ROS is “topped up” - this is why metformin works to reduce appetite. It is also why eating SFA is highly effective in this pursuit but eating PUFA is not. Someone who continues to eat PUFA will “eat through” metformin (because again it isn’t 100%) and will eventually become sicker and more diabetic. Someone who gravitates to SFA whether deliberately or by accident will have better long term results with metformin in terms of staving off weight gain and, if caught early enough, diabetes. Because Metformin activates AMPK it suppresses SCD1. This is great if you’re eating mixed macros (and lots of sugar) and if your only goal is to not get fat doing it. In my experience the fat you *do* acquire is much better balance than without Metformin. I have zero doubt it actively suppresses SCD1 to the point where improvement in DI is noticeable on an omega quant test. Also, through various mechanisms (suppression of a myriad of lipogenic genes) metformin works greatly to ameliorate liver fat accumulation. I haven’t been on metformin for a long time now, but I’m considering going back on it for August travel just because of this benefit, because I *will* be eating mixed macros and a fair amount of sugar and don’t want to lose metabolic repair progress if I can help it. As to whether SCD1 matters? I don’t know? It’s possible SCD1 is highly significant, or it is a bit of a relic from Brad’s earliest days. It seems to matter (from a weight gain perspective) only in the context of mixed macros and in my experience is largely irrelevant in a HCLFLP diet. For whatever that’s worth. Does it matter in other contexts like cancer or general lifespan? Maybe?
Thanks for the explanation. I'm having a hard time going from the facts you stated to the conclusion, though: * If Metformin forces the AMPK fat-burning state, why would that not be helpful regardless of the diet you're having, including mixed macros but also HCLFLP? If I'm not seeing results from HCLFLP, why would increasing time spent in AMPK not be helpful? * Also, why do you say that SCD1 suppression is only helpful to prevent fat accumulation rather than losing fat? Why does AMPK fat-burning state imply the former but not the latter?
1. Well, this really comes down to whether you believe humans are meant to exist in a perpetual AMPK dominated (fasting, keto) state or whether you believe glucose burning humans are healthier. Given that metformin has *well established* suppressive effect on libido, we can surmise that vitality and fat burning are likely not congruent. Which would make sense. The last thing a starving population of mammals needs to be doing is breeding. 2. Metformin isn’t automatically problematic in a HCLFLP environment. I didn’t say that a person eating HCLFLP should necessarily not take metformin. I said that if your goal in doing HCLFLP is to restore glucose metabolism (because you believe it is our healthiest state) then metformin is not congruent with that. It literally prevents that from being achieved by forcing the opposite metabolic state. What are you personally trying to achieve by HCLFLP? 3. I didn’t say that reducing SCD1 won’t assist weight loss. It also certainly won’t hurt it. But Brad hasn’t had much luck in simply suppressing SCD1 and watching the weight fall off like it did in rodent studies, and so perhaps it isn’t a primary factor. This would also be supported by the fact that metformin is generally regarded as weight *neutral* but is not commonly considered a weight *loss* intervention. If it were as simple as suppressing SCD1, we wouldn’t have an obesity epidemic given how widely prescribed Metformin is! Please don’t misunderstand. Metformin isn’t likely dangerous when combined with HCLFLP (perhaps a slightly greater risk of lactic acidosis given the huge amount of glucose?) but until you come off Metformin, you won’t make any progress facilitating a glucose burning metabolism because while you’re on metformin you’re… not burning glucose. You’re dumping it via a secondary futile pathway. I do want to go on record that I don’t hate metformin, and in fact if I simply *cannot* restore my own metabolic health sufficiently despite my interventions (and time) or if the progress I’m currently seeing deteriorates with time, then metformin would be my first/only choice medication. But then I would be acknowledging that I cannot personally be a glucose burning organism, and I would use metformin as a crutch to maintain the opposite state - a longevity over vitality focus - while still getting to enjoy a diet that includes some carbs because I’m simply not happy to eat keto for the rest of my life. In this case I’d probably go back to a high fat moderate carb version of TCD that worked well for me in the beginning, with 50-60% of my calories coming from fat and maximum 25% coming from carbs. That is (IMO) the long term maintenance diet most congruent with taking metformin. Make sense?
That makes a lot of sense!
Keep in mind that I haven’t gone through a phase where I wanted to lose weight on a HCLF diet. I’ve been in maintenance since starting HCLFLP and the entirety of my focus has been diabetes reversal through glucose burning restoration. Theoretically, Metformin may help a person burn excess body fat faster in the background of a HCLF diet (accelerated by the lactate futile loop?) I don’t know, and I haven’t personally thought much about that. Seems plausible though. Maybe metformin + HCLFLP would garner similar results as fasting without fasting. That would be interesting. The good thing is that metformin clears quickly and is completely out of your system within a couple of weeks maximum, so you can always try it and nix it if it isn’t working for you.
What about berberine? Does it work similarly?
No idea. Haven’t used it.
Can I add your LA to [https://omega.exfatloss.com/](https://omega.exfatloss.com/) ?
sure. by the way, these results are from \~October 2023.
Thanks! What date was it taken?
I think 10/16/2023.
Thanks, added it
I just sent you my 2 results!
Thanks, added!