1 Year Low Carb Intervention Cured 60% Of Patients From Diabetes

opethfeldt

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In people with poor health, insulin sensitivity and glucose handling are so poor that they can't really "handle" carbs. Naturally, they're gonna see improvements if they restrict carbs. However, that doesn't mean a low carb diet is optimal. It just means it's a good adaptive measure to address a specific problem in the short term. The better long term approach would be to balance hormones and improve insulin sensitivity so that carbs can be eaten freely. I don't think anyone here should need a refresher on the benefits of carbohydrates.
 

Whichway?

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I think the issue is when your body tries to use two substrates of energy in large amounts you run into issues. The major debate is whether or not we should be eating mostly fat or mostly carbohydrate.

I think this is a big part of it.

From what I’ve understood chronic inflammation seems to be major cause for diabetes and most other autoimmune disorders.

This too. Inflammation stops cells from working normally and they don’t continue to metabolise normally until the inflammation is resolved. Diets that drive inflammation, constantly stressful lifestyles and toxins means that our cells are under a constant barrage, and many of us begin to malfunction under these drivers.
 

TeaRex14

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The Hyperlipid has a very interesting idea on how this occurs using FADH2/NADH ratios. Basically, eating mixed diets (especially PUFA) can be bad and cause diabeetus.

If I recall, using the high carb low fat diet cured 60%, made 15% worse, and made no difference on the rest. Whereas on high fat low carb everyone improved in variable amounts. If I had the beetus, I would do low carb.

I don't agree that low carb will always cause low thyroid. I certainly believe it can but it depends on a bunch of other factors. Ketosis long term is a different story however.
I think it depends on what you consider "low carb". Anything under 100 grams habitually will end up depleting your liver glycogen, which in pretty much every case, lowers T3 production. Add this to the fact I'm talking about net carbs, some hardcore low carbers count all "carbs" as a carb. Green veggies should never be counted as carbohydrates because you almost always end up burning more glucose digesting them then you would actually take in. About 400-600 calories of digestible net carbohydrate would be mandatory on a daily basis to keep T3 production from declining. This would mean around 100-150 grams of carbs everyday not from low calorie veggies (i.e tubers, fruits, honey, maple syrup, sugarcane, etc.) is a necessity for long term support of thyroid. Most low carbers would think this isn't low carb at all. By the way, this is if we're talking about someone who's completely sedentary.
 

TeaRex14

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I agree with most of that report. The randle cycle is largely responsible for their findings. I am a stickler about certain details, I don't really like how they call lard a "saturated fat." It can be over 60% unsaturated in some examples when the hog was fed a bad diet. Pacific island hogs have the best lard, because coconut is part of their main diet. Bear in mind, any sort of randle response that's caused by a high fat, high carb, meal is much preferable to the randle response caused by adrenaline and stress. Adrenaline and stress cause free fatty acids to be raised indefinitely, until you find a way to terminate the stress cycle. In a non-stressful state, acute randle responses are less prone to cause issues.
 

dreamcatcher

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I agree with most of that report. The randle cycle is largely responsible for their findings. I am a stickler about certain details, I don't really like how they call lard a "saturated fat." It can be over 60% unsaturated in some examples when the hog was fed a bad diet. Pacific island hogs have the best lard, because coconut is part of their main diet. Bear in mind, any sort of randle response that's caused by a high fat, high carb, meal is much preferable to the randle response caused by adrenaline and stress. Adrenaline and stress cause free fatty acids to be raised indefinitely, until you find a way to terminate the stress cycle. In a non-stressful state, acute randle responses are less prone to cause issues.
Thank you for reading it. High fat in combination with high carb might be better than the randle response but neither are optimal for health.
 

Broken man

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From what I’ve understood chronic inflammation seems to be major cause for diabetes and most other autoimmune disorders. There’s several different reasons for chronic inflammation and metabolic problems. I think inflammation can interfere with the bodies metabolic processes and dysfunction of metabolic processes can cause inflammation. It’s a vicious cycle of eating wrong foods, high PUFA, low nutrient and also eating opposite of what you need depending on the state your body is in. Everyone has different foundations and the route to better health ain’t always the same. But look at india and diabetes. Even though they eat lots of healthy spices that’s supposed to lower blood glucose and control diabetes their diabetes and dementia aswell are skyrocketing. They consume high PUFA now a days. Specially since they switched out GHEE butter in cooking to cheaper vegetable oils they cook over high heat. On top of that fast food consumption is growing quickly in india. And sugar has never been a staple in their diet so can’t be the sugar. It’s the inflammation. Eating anti-metabolic inflammatory foods. In general 100 years ago or more autoimmune disease was quite rare. Now it’s very common since we invented pressing canola for the oil. We’re making oil from flowers and their small seeds. Thats very unnatural to find or ingest even a tablespoon of canola oil in nature. How many rapeseed seeds would you have to eat naturally? And would they even be digestable? Probably meant to be pooped out like other seeds to spread the plant. Not press them and consume their oil content. Its so obvious since our health went to the crapper after we started putting it in everything.
Good one.
 

haidut

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A fairly recent study demonstrating how low carb can cure diabetes in 60% of patients.

Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. - PubMed - NCBI

This + the fasting study showing the same in my opinion prove it is not the FFA that cause insulin resistance and diabetes, it is overstimulation of insulin that does. Like all neurotransmitters and hormones, also insulin obeys the same rules of resistance when overactivated.

You know, I like your posts and contrarianism in general...but couldn't you find a better study?? This is absolute trash and it pretty much says so right in the abstract. All they did was measure HbA1C at 70 days and at the end of the intervention (1 year). How does that show they "cured" diabetes?? As you well know HbA1c is a long term indicator of past blood sugar levels, approximately an average of the last 6 months. So, all this study showed is that when you restrict sugar and put people into ketosis their blood sugar levels will drop over the course of the intervention. Astounding finding! /s
It says nothing about their insulin sensitivity/resistance AFTER the intervention stops. This study would have been good if it measured HbA1c, fasting blood glucose and did a glucose challenge test say 1 year after the intervention ended. The HbA1C at that point would show their blood sugar levels about 6 months after the intervention ended, and the fasting blood sugar and glucose challenge test would show their insulin sensitivity/resistance a full year after the intervention ended. If all of these are good then you can say there was probably a curative effect. As it stands now, this study should not have even made it past peer review. It has about the same validity as the Biggest Loser show, and guess what - those people rapidly regained weight after the show even on a lower calorie diets than before entering the show!
"Biggest Loser" Contestants Regained Weight. Peat Perspective

So, again, showing that blood sugar drops when you enter ketosis and also restrict sugar for a year is about the same as saying that you will lose weight when you starve. Why is this even a study deserving funding is simply beyound me...
It says nothing about what happens after, which is the true definition of cure. When chemotherapy, surgery and radiation eradicate cancer in some person the doctors do not call it a "cure", they call it remission. Only after 5 years of no cancer sign they will call it a cure, and even then very carefully so. In this case, I am not even asking for 5 years, I am asking for only 1. And judging from the Biggest Loser study the results are pretty obvious - people got worse.

Even the study you posted does not call it a cure, but a remission. So, why are you calling it a cure?? Also, the study says that only 25% of the participants achieved remission yet you say 60%. Why is that?! And last but not least, 24% of the 1-year biomarker values ended up missing. So, the conclusions about remission (and certainly NOT a cure) are even more suspect in light of that missing data.

Finally, as far as the insulin agonism causing resistance - if this were true then administering AAS would be causing androgen resistance, and progesterone would be causing progesterone resistance. Well, they don't. The primary factors in diabetes II is excess lipolysis blocking sugar oxidation (Randle Cycle), high estrogen which increases fat oxidation and this also blocks sugar oxidation (Randle Cycle), and last but not least high cortisol, which increases gluconeogenesis and blocks insulin's effects. It is not coincidence that glucocortcoid antagonists are approved for diabetes II, and more than 170 inhibitors of 11b-HSD1 (cortisol synthesis) are also in clinical trials for the same condition.
11β-HSD1 inhibitors for the treatment of type 2 diabetes and cardiovascular disease. - PubMed - NCBI
https://csrf.net/doctors-articles/m...ation-for-the-treatment-of-cushings-syndrome/
"...On February 17, 2012, the Food and Drug Administration (FDA) approved mifepristone (Korlym) as a once daily oral medication to treat patients with Cushing’s syndrome. The specific indication was for the treatment of elevated blood sugar in patients with Cushing’s syndrome and type 2 diabetes mellitus. Mifepristone was approved for patients who had failed or were not candidates for surgical treatment of their Cushing’s syndrome."


Some excerpts from the study.

"... Secondary aims were (1) to determine if a difference in primary outcomes existed between participants who self-selected on-site versus web-based education delivery and (2) explore the time course of biomarker change at 70 days and 1 year into the CCI. Primary endpoints to assess effectiveness of the intervention were change in glycosylated hemoglobin (HbA1c), body weight, and medication prescription after 1 year. Secondary outcomes, including clinical biomarkers of associated physiological systems and adverse events, were assessed to determine safety of the intervention."

"...A recent primary care-led weight management intervention utilizing a 3–5 month VLCD resulted in a 10 mmol mol−1(0.9%) reduction in HbA1c and 10% weight loss at 1 year; 46% of participants achieved HbA1c below 48 mmol mol−1 (< 6.5%) while taking no medications [27]. While only 25% of participants in the present investigation achieved this measure of diabetes remission, the protocol for the present investigation discontinued metformin prescription only because of contraindication, intolerance, or patient request given its efficacy for T2D prevention and recommended use in certain populations "

"...Across all biomarkers, 4% of baseline values and 24% of 1-year values were missing (due to dropout, incalculable values, or inability to procure timely samples) and thus imputed to conduct the intention-to-treat analysis. Two-sample t tests were used to test whether baseline differences and differences between 1-year biomarker changes were significant. "
 
J

jb116

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You know, I like your posts and contrarianism in general...but couldn't you find a better study?? This is absolute trash and it pretty much says so right in the abstract. All they did was measure HbA1C at 70 days and at the end of the intervention (1 year). How does that show they "cured" diabetes?? As you well know HbA1c is a long term indicator of past blood sugar levels, approximately an average of the last 6 months. So, all this study showed is that when you restrict sugar and put people into ketosis their blood sugar levels will drop over the course of the intervention. Astounding finding! /s
It says nothing about their insulin sensitivity/resistance AFTER the intervention stops. This study would have been good if it measured HbA1c, fasting blood glucose and did a glucose challenge test say 1 year after the intervention ended. The HbA1C at that point would show their blood sugar levels about 6 months after the intervention ended, and the fasting blood sugar and glucose challenge test would show their insulin sensitivity/resistance a full year after the intervention ended. If all of these are good then you can say there was probably a curative effect. As it stands now, this study should not have even made it past peer review. It has about the same validity as the Biggest Loser show, and guess what - those people rapidly regained weight after the show even on a lower calorie diets than before entering the show!
"Biggest Loser" Contestants Regained Weight. Peat Perspective

So, again, showing that blood sugar drops when you enter ketosis and also restrict sugar for a year is about the same as saying that you will lose weight when you starve. Why is this even a study deserving funding is simply beyound me...
It says nothing about what happens after, which is the true definition of cure. When chemotherapy, surgery and radiation eradicate cancer in some person the doctors do not call it a "cure", they call it remission. Only after 5 years of no cancer sign they will call it a cure, and even then very carefully so. In this case, I am not even asking for 5 years, I am asking for only 1. And judging from the Biggest Loser study the results are pretty obvious - people got worse.

Even the study you posted does not call it a cure, but a remission. So, why are you calling it a cure?? Also, the study says that only 25% of the participants achieved remission yet you say 60%. Why is that?! And last but not least, 24% of the 1-year biomarker values ended up missing. So, the conclusions about remission (and certainly NOT a cure) are even more suspect in light of that missing data.

Finally, as far as the insulin agonism causing resistance - if this were true then administering AAS would be causing androgen resistance, and progesterone would be causing progesterone resistance. Well, they don't. The primary factors in diabetes II is excess lipolysis blocking sugar oxidation (Randle Cycle), high estrogen which increases fat oxidation and this also blocks sugar oxidation (Randle Cycle), and last but not least high cortisol, which increases gluconeogenesis and blocks insulin's effects. It is not coincidence that glucocortcoid antagonists are approved for diabetes II, and more than 170 inhibitors of 11b-HSD1 (cortisol synthesis) are also in clinical trials for the same condition.
11β-HSD1 inhibitors for the treatment of type 2 diabetes and cardiovascular disease. - PubMed - NCBI
https://csrf.net/doctors-articles/m...ation-for-the-treatment-of-cushings-syndrome/
"...On February 17, 2012, the Food and Drug Administration (FDA) approved mifepristone (Korlym) as a once daily oral medication to treat patients with Cushing’s syndrome. The specific indication was for the treatment of elevated blood sugar in patients with Cushing’s syndrome and type 2 diabetes mellitus. Mifepristone was approved for patients who had failed or were not candidates for surgical treatment of their Cushing’s syndrome."


Some excerpts from the study.

"... Secondary aims were (1) to determine if a difference in primary outcomes existed between participants who self-selected on-site versus web-based education delivery and (2) explore the time course of biomarker change at 70 days and 1 year into the CCI. Primary endpoints to assess effectiveness of the intervention were change in glycosylated hemoglobin (HbA1c), body weight, and medication prescription after 1 year. Secondary outcomes, including clinical biomarkers of associated physiological systems and adverse events, were assessed to determine safety of the intervention."

"...A recent primary care-led weight management intervention utilizing a 3–5 month VLCD resulted in a 10 mmol mol−1(0.9%) reduction in HbA1c and 10% weight loss at 1 year; 46% of participants achieved HbA1c below 48 mmol mol−1 (< 6.5%) while taking no medications [27]. While only 25% of participants in the present investigation achieved this measure of diabetes remission, the protocol for the present investigation discontinued metformin prescription only because of contraindication, intolerance, or patient request given its efficacy for T2D prevention and recommended use in certain populations "

"...Across all biomarkers, 4% of baseline values and 24% of 1-year values were missing (due to dropout, incalculable values, or inability to procure timely samples) and thus imputed to conduct the intention-to-treat analysis. Two-sample t tests were used to test whether baseline differences and differences between 1-year biomarker changes were significant. "
 
OP
R

rei

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Haidut the 60% came from this presentation:

edit: sorry, it was this presentation:

I called it cure because i assumed so as the presentation said "reversed diabetes". The IDM clinic uses fasting to cure diabetes which means patients can eat carbs after the fasting intervention without needing insulin. Same mechanism and also they call it remission because of legalese.

This is how i see diabetes: when you eat carbs they are absorbed and have to be quickly dealt with or coma results. Insulin forces the sugar into insulin sensitive cells. Once glycogen stores are full the rest of the cells need to work harder to take care of the sugar. If excess carbs keep on coming in the fat cells get overworked and become insulin resistant. Now the last defense line is working overtime (liver and visceral adipose) and once they cannot cope any longer you become diabetic.

Fasting primarily burns visceral fat and fat from the liver and only secondarily from elsewhere. This restores the ability to cope with the next sugar onslaught. Low carb is a much slower way to achieve the same.

Endotoxin plays a role here as it burdens the liver and prevents it from taking care of the sugar effectively.
 
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TeaRex14

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Thank you for reading it. High fat in combination with high carb might be better than the randle response but neither are optimal for health.
I eat a lowfat diet for this very reason. The US diet people, various organizations, consider a diet to be low in fat when around 30%. This is still kind of high if the goal is to prevent a randle response, at least for most people. I find around 20% and under is a good goal to hit, 10-15% being the sweet spot for most people. Limiting dietary fat is probably the best way to prevent increases in free fatty acids, but you could also experiment with niacinamide which can lower FFA as well.
 

Cirion

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I believe the biggest problem is bread, pasta and rice which has 2x the insulin index of glucose. A 150g medium portion of white rice makes same problem as 300g sugar

Nah. I mean yes, but no at the same time. Yes because most people have poor glucose handling, and this effect will be even more pronounced from starches. Basically, it just exposes a problem with someone. But no, because in the long run, someone with properly functioning sugar metabolisms will be able to handle carbs of all sources. Peat says starches are not necessarily incompatible with health, but also that for those with digestion problems, starch should be zero. In the long run though, starches are not "Bad" per-se, but most people can not handle them, so it is bad for THEM.

All that said... I do avoid starches because I certainly can't handle them at the present time in any quantities and I don't see myself bringing them back either.
 

CLASH

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@cinderella
@TeaRex14
The elevated blood glucose and insulin following the high fat, high carb meal is a good thing. It means stable energy between meals without or with less crashes. With an elevated or maintained blood sugar in conjunction with a slow decline and matching insulin levels I would venture to guess that the cortisol and adrenaline levels of these people were significantly lower. Meaning that they had to rely less on the adaptive hormones to function. Also, for the articles to say that the participants were whole body insulin resistant is a jump, I would venture to guess some tissues such as the CNS remain insulin sensitive while other tissues such as the muscles rely more on fatty acids; an intelligent nutrient partitioning system.

——————————————————————

In my opinion this forum is loaded with low fat dogma. Its almost a religion here, maintained by the echo chamber that are the community members. To be fair though, i once believed in/followed the paradigm, of course to my own physical detriment. Time after time i see people recommending others to lower thier fat when theyre not feeling well or they keep having adrenaline rushes or anxiety/ panic attacks. I think this advice is questionable and I think that many issues on thie forum are a product of eating too low fat. Especially in the context of people gaining massive amounts of weight, developing gut issues and eating large quantities of sugar/ carbs every hour just to avoid getting a stress reaction. If you go to fruitarian forums, you will see that many people require endless amounts of fruit and sugar every hour to avoid getting crashes. They describe being hungry all the time. I think this is due to the lack of fat in thier diet leading to essentially roller coaster blood sugar levels. I believe people on this forum are experiencing the same issues. For the weight gain, i would say it most likely comes down to bacterial issues in the intestine from ingesting too many carbs in the absence of fats and hormonal issues from the dairy. I highly doubt the validity of the calories in/ calories out model and would be so bold as to say most weight issues are hormonal/ inflammatory in nature. This is especially apparent to me considering that people on this forum tend to gain weight specifically around the belly with rare reports of excess whole body subcutaneous fat gain. Dairy hormones and gut issues from excessive carbs in the absence of fat/ types of carbs (starch) consumed seem to be easy targets as causes in my mind. As for the gut issues specifically, fat is a stimulator of bile and the intestine. The bile and the fatty acids both protect from endotoxin and function as antiseptics. They also both stimulate peristalsis, so if anyone is having constipation here, I’d recommend trying to increase your consumption of long chain fatty acids. This mirrors peoples reports of fixing constipation with bile acids on this forum.

Furthermore, I’ve put this out multiple times on this forum; almost all large mammals eat about 40-50% of thier calories from fat. This is from whales to the great apes. I dont think humans would be any different, except for maybe an increase in carbs by a small percentage due to our increased brain function. Many people discuss how muscular chimps/ gorillas are, yet they have a low protein diet. I dont think it has as much to do with the protein content as it does the fat content. Chimps/ gorillas diets are mostly fat due to fermentation of fibers in the colon to short chain fatty acids by bacteria which are then processed by the chimps/ gorillas liver if I’m not mistaken to longer chain fats. These fats serve to increase anabolic hormones, provide fuel for the musculature and spare sugars for the CNS. I think the large musculature is mainly a hormonal component determined by fat intake as opposed to a protein component, as long a certain threshold of protein is eaten. If you would like proof of this take a look at bodybuilders/ fitness enthusiasts using trenbolone or any other anabolic androgen/ steroid, muscularity is drastically increased regardless of dietary intake for many people and especially in people in which protein is adequate. Again I think the hormonal component is the most important for weight/ muscularity. This component, in my experience is largely dependent on adequate fat and carb intake after a threshold of protein is met and subsequently hormone/ gut health. So for young men on this forum struggling with thier androgen levels (another issue I see here alot in conjunction with the aformentioned issues above), which thier seems to be quite a few of, as opposed to taking exogenous hormones, perhaps increasing fat to appropriate levels to allow for adequate steroid production would be a better first option.

——————————————————————

@Cirion
I dont think this starch issue has much to do with glucose handling, that seems to be secondary at most. I think its almost entirely an issue of bacterial growth in the intestine which starch seems to reliably induce. Some ethnicities of human seem to do better than others at handling starch but in the long run it seems the outcome is pot bellies in old age.

————————————————————————

EDIT: I’d like to stipulate I’m not in favor of low carb or low protein. I’m in favor of adequate fat, adequate protein, adequate carb. I myself consme 300g of sugar a day from fruit/ juice, 120-140g of protein a day from
Animal sources (seafood and ruminants) and 160-200g of a fat a day from beef tallow and refined coconut oil.
 
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SB4

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@CLASH I have to agree that there is perhaps a too heavy bias towards low fat here. I think enviroment and genetics both play a huge role in what diet is best for you.
 

TeaRex14

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@cinderella
@TeaRex14
The elevated blood glucose and insulin following the high fat, high carb meal is a good thing. It means stable energy between meals without or with less crashes. With an elevated or maintained blood sugar in conjunction with a slow decline and matching insulin levels I would venture to guess that the cortisol and adrenaline levels of these people were significantly lower. Meaning that they had to rely less on the adaptive hormones to function. Also, for the articles to say that the participants were whole body insulin resistant is a jump, I would venture to guess some tissues such as the CNS remain insulin sensitive while other tissues such as the muscles rely more on fatty acids; an intelligent nutrient partitioning system.

——————————————————————

In my opinion this forum is loaded with low fat dogma. Its almost a religion here, maintained by the echo chamber that are the community members. To be fair though, i once believed in/followed the paradigm, of course to my own physical detriment. Time after time i see people recommending others to lower thier fat when theyre not feeling well or they keep having adrenaline rushes or anxiety/ panic attacks. I think this advice is questionable and I think that many issues on thie forum are a product of eating too low fat. Especially in the context of people gaining massive amounts of weight, developing gut issues and eating large quantities of sugar/ carbs every hour just to avoid getting a stress reaction. If you go to fruitarian forums, you will see that many people require endless amounts of fruit and sugar every hour to avoid getting crashes. They describe being hungry all the time. I think this is due to the lack of fat in thier diet leading to essentially roller coaster blood sugar levels. I believe people on this forum are experiencing the same issues. For the weight gain, i would say it most likely comes down to bacterial issues in the intestine from ingesting too many carbs in the absence of fats and hormonal issues from the dairy. I highly doubt the validity of the calories in/ calories out model and would be so bold as to say most weight issues are hormonal/ inflammatory in nature. This is especially apparent to me considering that people on this forum tend to gain weight specifically around the belly with rare reports of excess whole body subcutaneous fat gain. Dairy hormones and gut issues from excessive carbs in the absence of fat/ types of carbs (starch) consumed seem to be easy targets as causes in my mind. As for the gut issues specifically, fat is a stimulator of bile and the intestine. The bile and the fatty acids both protect from endotoxin and function as antiseptics. They also both stimulate peristalsis, so if anyone is having constipation here, I’d recommend trying to increase your consumption of long chain fatty acids. This mirrors peoples reports of fixing constipation with bile acids on this forum.

Furthermore, I’ve put this out multiple times on this forum; almost all large mammals eat about 40-50% of thier calories from fat. This is from whales to the great apes. I dont think humans would be any different, except for maybe an increase in carbs by a small percentage due to our increased brain function. Many people discuss how muscular chimps/ gorillas are, yet they have a low protein diet. I dont think it has as much to do with the protein content as it does the fat content. Chimps/ gorillas diets are mostly fat due to fermentation of fibers in the colon to short chain fatty acids by bacteria which are then processed by the chimps/ gorillas liver if I’m not mistaken to longer chain fats. These fats serve to increase anabolic hormones, provide fuel for the musculature and spare sugars for the CNS. I think the large musculature is mainly a hormonal component determined by fat intake as opposed to a protein component, as long a certain threshold of protein is eaten. If you would like proof of this take a look at bodybuilders/ fitness enthusiasts using trenbolone or any other anabolic androgen/ steroid, muscularity is drastically increased regardless of dietary intake for many people and especially in people in which protein is adequate. Again I think the hormonal component is the most important for weight/ muscularity. This component, in my experience is largely dependent on adequate fat and carb intake after a threshold of protein is met and subsequently hormone/ gut health. So for young men on this forum struggling with thier androgen levels (another issue I see here alot in conjunction with the aformentioned issues above), which thier seems to be quite a few of, as opposed to taking exogenous hormones, perhaps increasing fat to appropriate levels to allow for adequate steroid production would be a better first option.

——————————————————————

@Cirion
I dont think this starch issue has much to do with glucose handling, that seems to be secondary at most. I think its almost entirely an issue of bacterial growth in the intestine which starch seems to reliably induce. Some ethnicities of human seem to do better than others at handling starch but in the long run it seems the outcome is pot bellies in old age.

————————————————————————

EDIT: I’d like to stipulate I’m not in favor of low carb or low protein. I’m in favor of adequate fat, adequate protein, adequate carb. I myself consme 300g of sugar a day from fruit/ juice, 120-140g of protein a day from
Animal sources (seafood and ruminants) and 160-200g of a fat a day from beef tallow and refined coconut oil.
I think the issues people deal with in everyday life are vastly different from each other, therefore not everyone is going to benefit from the same protocol. However when someone is vastly overweight, metabolic syndrome, etc. they already have some level of insulin resistance. It would make sense, from a physiological point of view, for them to restrict fat intake to some degree so they can start metabolizing the glucose better. When the other route is taken, and you lower carbs instead of fat, you just exacerbate the preexisting condition. It can also eat away your muscle tissue, there's a reason why cutting bodybuilders typically reduce dietary fat the most, it has no protein sparing effect. If you cut mostly carbs, you'll end up losing a lot of lean mass with your bodyfat. Likewise having to eat literally every hour isn't healthy either, but I wouldn't be so quick as to blame a lack of dietary fat. If your liver holds glycogen well you won't be crashing like that, so it's likely a liver issue. Fruitarians are notorious for not eating enough protein, which can definitely impact the liver negatively. I somewhat agree with you on the calorie in calorie out thing. However habitually taking in more calories then you burn will cause you to grow, the difference is someone who's hormonally healthy will grow bigger (muscle). Someone hormonally unhealthy will just get fatter. Cortisol, along with estrogen, are the main contributors to excess belly fat. Reducing free fatty acids is one of the best ways to reduce cortisol. It's well known in low carb circles that cortisol is the "fat burning hormone." Everywhere else cortisol is simply referred to as a stress hormone. Stating the obvious, inactivity plays a crucial role as well, so does lack of quality sleep.
 

Peater Piper

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Low blood sugar, doesn't mean there isn't insulin resistance.
They had a reduction in HOMA though, which indicates increased insulin sensitivity. High fat diets in themselves do decrease insulin sensitivity, at least temporarily, but significant weight loss tends to counteract this completely. I've seen a number of cases of people performing better on OGTTs after doing low-carb paleo. If we think of type 2 diabetes at a hormonal level, then it shouldn't be a surprise that lowering inflammation and estrogen will benefit insulin sensitivity, regardless of the diet type. I'm not advocating a particular diet, I've seen people benefit from both very low fat/high carb and high fat/low carb as well. Some people try both types of diets and still struggle.
 

Cirion

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edit - nvm... realized I read out of context
 
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Tarmander

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"I could not stand the heat, and would be very uncomfortable in the heat. My BP would rise and I would lose all energy. After moving to Siberia, my heat intolerance has been cured."
 

TeaRex14

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They had a reduction in HOMA though, which indicates increased insulin sensitivity. High fat diets in themselves do decrease insulin sensitivity, at least temporarily, but significant weight loss tends to counteract this completely. I've seen a number of cases of people performing better on OGTTs after doing low-carb paleo. If we think of type 2 diabetes at a hormonal level, then it shouldn't be a surprise that lowering inflammation and estrogen will benefit insulin sensitivity, regardless of the diet type. I'm not advocating a particular diet, I've seen people benefit from both very low fat/high carb and high fat/low carb as well. Some people try both types of diets and still struggle.
Well it's really hard to say that low carb is 0% effective, because if it were, it wouldn't exist. However the entire idea of low carbing your way out of diabetes seems like a diametrically opposed protocol when you take into account various hormonal responses. Insulin is trying to lower your blood sugar, while cortisol is trying to raise your blood sugar. When you take this into account, it doesn't make logical sense to use a dietary plan that's going to chronically raise cortisol. Cirion brought up a good point too. Weight loss on a low carb diet is simply result of restricted calories. If you go from eating 350 carbs in a single day, to only eating 50 carbs in a single day, that a 1,000 calorie reduction.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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