Man Makes Himself Insulin Resistant/type Two Diabetic By Drinking Olive Oil

[tankasnowgod]

Seems we are on a "ray peat forum" but not on a forum of Ray Peat readers

Wait..... who is this mysterious "Ray Peat" you speak of?!?!?

 

[Such_Saturation]

Wait..... who is this mysterious "Ray Peat" you speak of?!?!?

I thought it was a kind of infrared ray to be honest

 

[tankasnowgod]

I thought it was a kind of infrared ray to be honest

I thought he was a character in that old children's joke-

Pete and Ray Peat were on a boat. Pete fell out, and Ray Peat said "That's sure to elevate the stress hormone adrenaline. Here, drink some of my sugared coffee to prevent the concomitant rise in cortisol, and be sure to supplement Progesterone, to oppose Estrogen."

 

[heaahde]

@Westside PUFAs what's your stance on wheat, oats, barley and rye? And also, how much fat (and sources) do you usually eat a day?

 

[SAFarmer]

There is no evidence excess blood sugar cause damage to cells, on the contrary Peat have written on numerous occasions and mentioned in interviews that very high blood glusose might even be helpful in situations of severe stress or poisoning. People don't take the time to properly read and do their own research anymore. So much confusion about what T2D and/or insulin resistance actually is, and also the difference between acute and chronic conditions. To more fully understand these concepts better, read all Peat's articles on the subjects (there are many, such as this one ), and then also this research paper below which describes the interaction of insulin, glucose and the role of the liver as well as other organs and cells.

Insulin: understanding its action in health and disease

 

[Matt1951]

People who have a gastric bypass for weight reduction, almost immediately improve their type 2 diabetes. It seems there are two primary factors that could cause this improvement - they are now severely calorie restricted, and most of the stomach and the upper part of the small intestine are bypassed.
People who have the lap band surgery have improved type 2 diabetes, but not as much as those who have the gastric bypass. This points to the bypassing of the stomach and upper intestine as being beneficial.

 

[haidut]

Are you aware of the difference between physiological insulin resistance and diabetic resistance? If not, I can recommend Peter at the Hyperlipid blog with dozen of articles explaining the difference between normal resistance (desirable and healthy in this context) and diabetic resistance.

The only difference is in terms of persistence. The temporary insulin resistance (even in lean person) after some types of meals, tends to clear away once fats are out of the bloodstream. The condition everybody likes to call "diabetes type II" is simply sustained systemic lipolysis, which both makes the cells insulin resistant and (if the floating fat is PUFA) poisons the liver, which is working overtime to excrete the excess. The human study with 6g aspirin daily found just that - you can stop diabetes type II in its tracks by strongly inhibiting lipolysis WITHOUT any actual weight loss. So, those people in the study continued to be morbidly obese but while on aspirin they are as insulin sensitive as a 20 year old college student. Weight loss cures diabetes through this mechansim - lowers fat store and this long term lipolysis. But if you are fasting or overexerting yourself to lose that extra weight you have a good chance of giving yourself diabetes type I as the floating PUFA from this excessive lipolysis can kill both your pancreas and liver...and maybe kidneys as well as lipolysis is well known to damage kidneys as shown by the studies I posted. There is nothing mysterious or complicated about "diabetes II". It is sustained lipolysis dominating the Randle cycle.

 

[Kyle M]

People who have a gastric bypass for weight reduction, almost immediately improve their type 2 diabetes. It seems there are two primary factors that could cause this improvement - they are now severely calorie restricted, and most of the stomach and the upper part of the small intestine are bypassed.
People who have the lap band surgery have improved type 2 diabetes, but not as much as those who have the gastric bypass. This points to the bypassing of the stomach and upper intestine as being beneficial.

Radical decrease in endotoxin absorption.

 

[schultz]

Obese people who get nerve damage from insulin resistance are proof that the repeated exposure to the extracellular glucose thats causing the damage.

This is not proof.

This is an extreme claim. Do you know where Peat said this specifically about glucose and nerve damage and FFA's?

Here are a few quotes from some of his articles.

"... glucose itself was found to protect the pancreatic beta-cells from poisons."

"As information about the many physiological and biochemical events associated with diabetes has accumulated, the basic doctrine that "sugar causes diabetes" has extended itself to whatever the topic of discussion is: "Glucose causes" the death of beta-cells, glucose causes blood vessels to become leaky, glucose causes cells to be unable to absorb glucose, glucose causes the formation of free radicals, glucose impairs immunity and wound healing, but causes inflammation while preventing the "respiratory burst" in which free radicals are produced by cells that cause inflammation, it disturbs enzyme functions, impairs nerve conduction and muscle strength, etc., and it is also addictive, causing people to irrationally seek the very material that is poisoning them."

"Tens of thousands of publications describe the pathogenic effects of sugar. To prove their point, they grow cells in a culture dish, and find that when they are exposed to excess glucose, often 5 times the normal amount, they deteriorate. In the artificial conditions of cell culture, the oversupply of glucose causes lactic acid to accumulate, leading to toxic effects. But in the organism, the hyperglycemia is compensating for a sensed deficiency of glucose, a need for more energy."

"If diabetes means that cells can't absorb or metabolize glucose, then any cellular function that requires glucose will be impaired, despite the presence of glucose in the blood. It is the intracellular absence of glucose which is problematic, rather than its extracellular excess. Neuroglycopenia (or neuroglucopenia) or intracellular glycopenia refers to the deficit of glucose in cells. When the brain senses a lack of glucose, nerves are activated to increase the amount of glucose in the blood, to correct the problem. As long as the brain senses the need for more glucose, the regulatory systems will make the adjustments to the blood glucose level."

"While it's clear that it is the excessive oxidation of fat that damages cells in the "diabetic" state in which cells aren't able to use glucose, it's important to look at some of the situations in which so many researchers are blaming problems on hyperglycemia."

"Sugar can protect the beta-cells from the free fatty acids, apparently in the same ways that it protects the cells of blood vessels, restoring metabolic energy and preventing damage to the mitochondria. Glucose suppresses superoxide formation in beta-cells (Martens, et al., 2005) and apparently in other cells including brain cells.(Isaev, et al., 2008)."

"Some of the worst effects of “diabetes,” including retinal damage, are caused or exacerbated by insulin itself."

Regarding Glycation:::

"The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996). And the oxidation of fats rather than glucose means that the proteins won't have as much protective carbon dioxide combined with their reactive nitrogen atoms, so the real difference in the organism is likely to be greater than that seen by Fu, et al."


Here are some quotes from a podcast:

...it happens that in vitro, and in animal experiments, you can stimulate the growth of stem cells in the pancreas with glucose. So it isn't glucose that is responsible for killing those cells, it's an inflammation reaction. And the infammation causes breakdown of fatty acids which cause free radical injury to the tissue. And, because of that observation of the inflammation involving prostaglandins and fatty acids (unsaturated fatty acids), a few experimenters put lab animals on a totally fat-free diet, giving them only saturated fat or no fat at all. Just carbohydrates, and proteins, vitamins and minerals. And then tried to give them diabetes by all of the standard methods (poisoning the beta-cells of the pancreas in various ways) so they couldn't make insulin. And these fat-free animals didn't develop the experimental diabetes, the way all other animals do. So, experimentally it has been pretty well demonstrated that unsaturated fatty acids, breaking down, produce inflammation which activate many of the processes seen in diabetes. The degenerative processes in the retina and nerves for example, are where the damage starts very often before the blood sugar increases at all. So, if you're getting retinal degeneration and have normal blood sugar, or if you're getting numb and tingly hands and feet, and you have normal blood sugar, it's clearly not the sugar which is responsible for the degenerative changes.

Andrew: I understand that there are a lot of protective effects that sugar confers to the organism from the cellular energy standpoint. What other beneficial effects does sugar have when you look at it from a diabetic perspective?

Ray: I've looked up what current journalists and doctors are saying are the mechanisms that cause nerve damage in diabetes and they have a standard 4 or 5 chemical or functional changes of nerve cells that they say are caused by excess glucose. They occur in the presence of excess glucose in the diabetic, but they also occur before or without the presence of glucose, and the deficiency of glucose is one of the things that can induce these same defensive reactions that are blamed on sugar. So you have to look at the evidence regarding the deficiency of glucose and compare it experiment by experiment with the kind of evidence they propose to explain glucose as the cause. And when you look at all of the events associated with diabetes and the symptoms you see that hormone changes typically go with it. Stress induces aromatase that increases estrogen production and also directly increases some of the pituitary hormones beside ACTH that drives the adrenals. Stress increases GH which provides fuel in an emergency by increasing FFA in the circulation. And the increased estrogen also increases the ACTH, prolactin, several of the stress hormones in the pituitary, but especially GH is very closely connected with estrogen. So females have higher, not only estrogen, but growth hormone and free fatty acids in circulation. And it happens that females have much more often problems with the nerve degenerative symptoms of diabetes, as well as being the ones that have the majority of type 1 diabetes during childhood. So, the effect of the free fatty acids on stress and glucoses, or any sugars protection against those stress reactions, is one of the basic things to look at. And avoiding hypoglycemic stress long before the problem reaches the stage of producing hyperglycemia. And in hyperglycemia, what you have is the bodies adjustment to the inability of cells to get enough energy, because they can't oxidize glucose, because the fats are blocking it. That's been known since the 60's, called the Randle Cycle...

 

[haidut]

It has everything to do with it. DNL - humans don't convert sugar into fat, even in excess.



95% of people who are T2D are overweight. But a lean person can also give themselves insulin resistance at any time. As I've said, it goes away within a few minutes to a few hours. Anyone can make themselves IR but the people who end up with nerve damage are overweight.



This is an extreme claim. Do you know where Peat said this specifically about glucose and nerve damage and FFA's? Obese people who get nerve damage from insulin resistance are proof that the repeated exposure to the extracellular glucose thats causing the damage. There is FFA's there too but thats why lean people don't get the nerve damage, because even if a lean person made themselves IR by eating a few slices of pizza, and then feels IR for the next few hours, it's likely not causing much nerve damage. It's the obese people with IR that get the damage.



The study says "Then after hibernation, they became sensitive to insulin again."

That's expected for humans too. How does that prove that fasting makes humans IR? The bears IR goes away and so does ours. During water only fasting in humans, we don't need much insulin because we are living mostly off of ketones. We still need a small amount of glucose because the brain and red blood cells still need a tiny amount of glucose during that time. But when we start to re-feed, like the bear, our insulin is fine.

This woman in this video didn't eat for 20 days and it cured the pain that she's been suffering with for 16 years. No insulin resistance afterwards. The reason you don't see much on water only fasting for humans is because True North in CA is the only place that does it in the US. There's one place in France too. Most of the people who do this are not a part of a study. They just come in and clean out for a few days or more. People who turn to WOF don't want to wait forever for studies to come out because the medical establishment thinks its quackery. Open minded people do it.

If a person is severely obese and most of the fat in their stores is PUFA, then fasting can do a lot of damage. Not only it lowers the basal metabolic rate (and possibly damages thyroid) but it can also trigger true type I diabetes due to FFA damaging the pancreas, liver and kidneys. As I mentioned in my other response above, losing weight is not a requirement for restoring insulin sensitivity. Lowering lipolysis is though, as that study with obese type II diabetic people taking 6g aspirin showed. So, if there was a way to get rid of all the fat without poisoning the other organs through lipolysis then I'd be all for it. Unfortunately, fasting is a dangerous way to do this. Look at the article on the Biggest Loser I posted a few months ago. These people did lose their weight through fasting and then regained it insanely fast afterwards due to their lowered metabolic rate AND induced insulin resistance through fasting. And mind you, after losing the weight many of them kept eatnig very consciously and stayed away from fried, high fat foods. The still regained their weight.
"Biggest Loser" Contestants Regained Weight. Peat Perspective

 

[SAFarmer]

This is not proof.

+ 1

 

[SAFarmer]

Look at the article on the Biggest Loser I posted a few months ago. These people did lose their weight through fasting and then regained it insanely fast afterwards due to their lowered metabolic rate AND induced insulin resistance through fasting. And mind you, after losing the weight many of them kept eatnig very consciously and stayed away from fried, high fat foods. The still regained their weight.
"Biggest Loser" Contestants Regained Weight. Peat Perspective

Evelyn over at Carbsane made the point well that there is not proof that these people had lower meatbolic rates for the same weight and age groups in the population. (The Carb-Sane Asylum: Are the Super-Obese the Ones Who Are Metabolically Adapted? )
Do you have any other data that supports your argument that they had lowered metabolic rates after dieting?

 

[Westside PUFAs]

@Westside PUFAs what's your stance on wheat, oats, barley and rye? And also, how much fat (and sources) do you usually eat a day?

I think all three are perfectly fine sources of sugar. I do fine with gluten. Some don't. My fat sources right now are fresh coconut meat, red palm oil, green olives, and sprouted pumpkin seeds. I eat lean animal meats and eggs weekly so there are some fat in those.

very high blood glusose might even be helpful in situations of severe stress or poisoning.

I think it's supposed to be stored as glycogen and then released as a constant stream and then that same stream is supposed to be metabolized by the cells right away. But it's an interesting concept.

People don't take the time to properly read and do their own research anymore.

Just because you disagree doesn't mean you have to make projections about what I do or don't read. I can easily say back "speak for yourself" but that gets us nowhere.

So much confusion about what T2D and/or insulin resistance actually is, and also the difference between acute and chronic conditions.

I agree, which is why I wrote this: Diabetes Needs To Be Renamed

To more fully understand these concepts better, read all Peat's articles on the subjects

I've read those years ago. I don't agree with Peat on everything. Again, this thread was posted in the "lounge."

It is the intracellular absence of glucose which is problematic, rather than its extracellular excess.

Either way, the problem is still insulin resistance.

The degenerative processes in the retina and nerves for example, are where the damage starts very often before the blood sugar increases at all. So, if you're getting retinal degeneration and have normal blood sugar, or if you're getting numb and tingly hands and feet, and you have normal blood sugar, it's clearly not the sugar which is responsible for the degenerative changes.

That's interesting and I'll look into it more but again, the problem is insulin resistance, which is caused by fat, free fatty acids and intramyocellular lipids. So it looks like it's not all the "toxic" starch that turns into "toxic" glucose is the problem. So what's the solution? Eat more fat? I don't think so. Speaking of free fatty acids, what about this quote?:

"Just about everything that goes wrong involves FFA increase. If they are totally saturated fatty acids, such as from coconut oil and butter, those are less harmful, but they still tend to shift the mitochondrial cellular metabolism away from using glucose and fructose and turning on various stress related things; By lowering the carbon dioxide production I think is the main mechanism."-RP

many of them kept eatnig very consciously and stayed away from fried, high fat foods.

I don't believe they did. I know my fellow obese Americans. I was one of them. I know what we like to eat. I know what makes us fat. I don't believe for one millisecond that they didn't eat high fat again, both pufa and dairy fat. And they are also ignorant to what a "healthy" diet is. They weren't eating a starch based diet for satiation and glycogen. No way. They ate salads with oil then when they got hungry from not being satiated they stuffed their faces with pizza, burgers, french fries and ice cream.

 

[schultz]

@Westside PUFAs

I was strictly talking about elevated sugar in the blood. I don't think elevated sugar in the blood is harmful (even though the elevated sugar is a sign something is wrong). The general belief is that elevated glucose in the blood causes damage, like this definition from wiktionary:::

glucotoxicity ‎(plural glucotoxicities)

1. (pathology) The toxic effects of excessive levels of glucose in the blood (as in diabetes)

I am agreeing with you that fat is the problem. Though it's possible the fat breakdown is not the only thing causing damage. Lactic acid, loss of protective CO2, excess insulin could be direct contributors, but I haven't look deeply into this topic so I am not well versed in its intricacies.

 

[haidut]

Evelyn over at Carbsane made the point well that there is not proof that these people had lower meatbolic rates for the same weight and age groups in the population. (The Carb-Sane Asylum: Are the Super-Obese the Ones Who Are Metabolically Adapted? )
Do you have any other data that supports your argument that they had lowered metabolic rates after dieting?

Yes, there is a lot of evidence going back at least 50 years but the topic is not very popular with the medical crowd as it suggests dieting and exercise are bad in the long run as downregulations of the metabolic rate are well known to be causally related to quite a few diseases, including diabetes. Actually, it is not the BMR that matters so much for health as the Non-Exercise Activity Thermogenesis (NEAT) - i.e. how much heat you generate without forcing yourself. NEAT is of course strongly tied to thyroid function and proper hormone balance.
Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss. - PubMed - NCBI
Study shows metabolic adaptation in calorie restriction
"...Researchers at the Pennington Biomedical Research Center in Baton Rouge, LA, have shown that when people significantly reduce their calorie intake, they undergo a metabolic adaptation that results in a slower metabolic rate. The slower metabolic rate results in a behavioral adaptation in which individuals become less physically active. The researchers examined data from 48 overweight people who followed 1 of 4 diet regimens for 6 months: a 25-percent calorie restriction (CR) diet, a low-calorie diet, a 12.5-percent CR diet plus 12.5-percent aerobic exercise program, or a normal diet. While the first three groups lost weight, after 6 months, the CR and low-calorie diet groups showed a reduction in their basal metabolic rate, accompanied by reduced physical activity. The CR plus physical activity group also lost weight but did not undergo a metabolic adaptation. This is the first study to measure metabolic rate and energy expenditure precisely through the use of doubly labeled water and indirect calorimetry. The study also shows that long-term calorie reduction without increased exercise can result in a lower metabolic rate. The researchers note that the data “suggest potential mechanisms by which CR causes large inter-individual variability in the rates of weight loss and how exercise may influence weight loss and weight loss maintenance.”

Another study with the same message.
Impact of energy intake and exercise on resting metabolic rate. - PubMed - NCBI
"...Resting metabolic rate is modulated by the amount of calories consumed in the diet relative to energy expenditure. Excessive consumption of energy appears to increase resting metabolic rate while fasting and very low calorie dieting causes resting metabolic rate to decrease. Since the metabolic rate at rest is the primary component of daily energy expenditure, its reduction with caloric restriction makes it difficult for obese individuals to lose weight and to maintain weight that is lost. Whether exercise has a carry-over effect on resting metabolic rate remains controversial, even though this question has been studied extensively during the last 90 years. Reasons for contradictory results include variations in control of prior diet and exercise patterns, inadequate exercise frequency, intensity and duration, and the possibility of response to exercise varying between individuals. Several lines of evidence suggest exercise may modulate resting metabolic rate. Bed rest in sedentary individuals leads to a reduction in resting metabolic rate. Similarly, in highly trained runners, cessation of daily exercise training lowers resting metabolic rate by about 7 to 10%. Resting metabolic rate is depressed in previously sedentary obese individuals on a very low calorie diet, but it quickly returns to the predieting level when exercise of sufficient frequency, intensity and duration is undertaken while dieting. These findings suggest caloric intake and daily exercise can modulate resting metabolic rate. Exercise of adequate intensity and duration may also enhance resting metabolic rate."

I hate to quote WP, but it is decent article and sums it up rather well.
Basal metabolic rate changes as you age
"...Going on a crash diet to shed the pounds fast? Think again. Although the pounds will dwindle, so will your metabolic rate and most likely your lean body mass — which in the end is exactly what you don’t want. “If you go on, say, a 900-calorie-a-day diet, you will have a hard time getting the nutrients you need,” says Rebecca Mohning, a D.C. nutritionist. “Without the daily requirement of protein, you will break down your lean muscle mass.” “Basically, the body will make sure it gets what it needs to function — and if it doesn’t get what it needs from food, it will take what it needs from the muscles,” says Fairfax-based nutritionist Danielle Omar, who owns Foodconfidence.com. “It’s not that smart when you consider that you are in essence eating away at your own muscle mass.” And less lean muscle mass means you burn fewer calories — probably not what you were going for. You will also lower the body’s basal metabolic rate (BMR) — the minimum amount of energy you need to keep the basic functions going (such as liver and brain function and breathing; breaking down food requires about 10 percent of the total BMR). "

So, bottom line is this - if you diet you will most likely end up lowering your BMR. This is due to both general thyroid function adaptations (inhbition) and also loss of muscle mass (which is the primary fat-burning tissue). So, once you lose your fat (and muscle) the only way to keep BMR going is through exercise (stress). That is an arguably worse state than being sedentary with higher BMR (and BMI) as studies have shown that health is possitively correlated with resting BMR and negatively correlated with "forced" BMR (i.e. through exercise). Basically, you have to keep exercising to cover the reduction in BMR and even if you manage to keep the BMR higher it is through stress (adrenaline/cortisol/prolactin/etc). Exercise is the replacement for the lost thyroid function but it is a self-defeating strategy - not only you have to keep doing it indefinitely but it also ends up lowering your BMR in the long run.

 

[superhuman]

@haidut very cool to see you follow the latest in regards to fitness/exercise and fat loss as well. These last 1-2 years there has been allot of researched done from many credible PHD people in the bodybuilding/weight lifting industry and it really seems to be that RMR does not get effected at all when dieting, even very hard. Exept if you loose muscle during that time with like eating little protein and not moving or doing any resistance training.

But like haidut mentions the results show that the harder you diet and longer the NEAT/BMR plummet like crazy. I can attest to this myself since i have dieted down to very low bodyfat levels and when your in that state and restricting calories you avoid anything that spontaneous or require energy unless you force yourself to do it. Just walking around something vs walking straight ahead annoys you because it costs energy and will to go around something.

It also just comes to general NEAT, fidgeting etc just allot of small things that adds up to allot of calories each day.

 

[Westside PUFAs]

I hate to quote WP, but it is decent article and sums it up rather well.

That WP article is just clickbait for people who think "carbs" are pizza, ice cream and french fries.

Going on a crash diet to shed the pounds fast? Think again.

Of course that doesn't work because you don't "cure" obesity or excess fat. You get rid of it and you maintain leanness. There is no "cure." There's only maintenance. Of course it doesn't work because leanness is achieved by eating a satisfying and nutritious diet long term, day after day, week after week, month after month, year after year among other lifestyle factors.

So, bottom line is this - if you diet you will most likely end up lowering your BMR.

Where are the controlled clinical trials proving this with extensive blood markers and extensive daily food logs?

Ray Cronise summed it up well:

"Penn's transformation challenges status quo and suggests we can all make a change. Like much of his advice, Presto centers on breaking away from accepting mass mediocrity and instead seeking the best. Our struggles are real, but laughing at our mistakes brings us much closer to success than living a life driven by fear. We hear a lot of exaggerated claims about slowing metabolisms (the latest biggest loser distraction) and warnings against losing weight too quickly. Of course none of this will apply to the 196,000 people that had some form of bariatric surgery last year or the 703,000 in the 4 years prior."

on Penn Jillette's transformation. His BMR didn't slow after dieting. And Cronise hits a home run when he says "Of course none of this will apply to the 196,000 people that had some form of bariatric surgery last year or the 703,000 in the 4 years prior." Game. Set. Match. Where's all of their slowed BMR's?

.

 

[tankasnowgod]

on Penn Jillette's transformation. His BMR didn't slow after dieting. And Cronise hits a home run when he says "Of course none of this will apply to the 196,000 people that had some form of bariatric surgery last year or the 703,000 in the 4 years prior." Game. Set. Match. Where's all of their slowed BMR's?

.

I could possibly see Ray and Penn being an exemption, through the use of cold thermogenisis and mechanisms like brown fat, but slowed BMRs are the rule when it comes to weight loss, not the exception. It will absolutely apply to the people that had bariatric surgery. It's simple physics. All mass, even white fat, burns some calories at rest. Mass goes down, BMR goes down. It also applies to activity, as it takes more energy to move say, 250 pounds than it does 200. If Ray and Penn have indirect calorimity readings that show that BMR goes up (or holds steady) as weight goes down, that is amazingly impressive.

The issue with the Biggest Loser phenomenon is the matter of degree. Instead of BMRs going down as would be predicted, they absolutely crash. So an expected drop from say, 1900 to 1700 calories a day goes more like from 1900 to 1000.

But there could be a number of factors to this. The Biggest Loser diet is probably the most radical diet ever designed. Daily caloric deficits of 4,000-7,000 calories are common. Bariatric surgery patients are in bad shape, but contestants on The Biggest Loser are in far worse shape at baseline than the average bariatric patient, at baseline or even after 12 months of forced caloric restriction. BL contestants also lose more weight in a period of 7 months than bariatic patients do over the course of their first year. The massively out of shape people go from completely sedentary to working out 4-6 hours a day in less than a week. On top of that, some use water manipulation techniques for big weekly weight losses, and stimulants like Adderall are used by some contestants.

Here is the study comparing the two -https://www.ncbi.nlm.nih.gov/pubmed/25236175

 

[Westside PUFAs]

Starch, and it's potential persorption, could be involved in the cell aggregation.

What do you think about this take on persorption?:

"I researched this awhile back and thought I would share my notes, in case this actually were to concern anybody…

Volkheimer used 200g of potato starch to cause embolisms in his subjects. Think about that for a moment. That’s an enormous dose of starch granules. Even people who eat raw potato starch—for the resistant starch—rarely consume more than 40-50g per day. And it would be a challenge to eat more than 8-12g of starch granules in a day from food.

Volkheimer believed that persorption was some kind of flaw in the gut that allowed starch granules to leak through. And if starch granules that were larger than a red blood cell (6-8 microns in diameter) could get stuck in the blood vessels and cause blockages and embolisms. This was theorized because some blood vessels are so tiny that the red blood cells must travel single-file to pass through. However, it’s highly unlikely that the lymph and blood vessels are not prepared to handle such intrusions. If not, I doubt our species would have been able to tolerate Underground Storage Organs (USOs). Furthermore, it’s well recognized that the liver is specifically designed to filter such particles from the blood.

If we are going to worry about starch granules—which are often larger than the diameter of a red blood cell—then we must also worry about anything else that fits this criteria:

Activated charcoal, has a particle size range of 1-150 microns, and seems to have the ability to detoxify the blood. These are surely persorbed as Volkheimer specifically mentions “charcoal” being persorbed in his subjects.

As pointed out, above, carrots have a starch granule size of 4-26 microns, and should therefore cause embolisms according to Volkheimer.

Raw unfiltered honey, contains pollen that range from 2.5 to 1,000 microns! Most honey producers will filter the pollen out their honey with sieves that range from 50 microns (heavily filtered) to 600 microns (lightly filtered). But, as we know, Hunter Gatherer populations tend to eat a lot of honey and they didn’t filter their honey with modern sieves. So, I can imagine lots of large and small pollen getting persorbed by Hunter Gatherers every day.

It would seem that persorption probably isn’t some kind of design flaw in our bodies. Combine that with the practice of geophagy (eating dirts and clays) and you get the picture that these particles are probably supposed to temporarily roam through our blood vessels. Persorption appears to be an intentional mechanism with a purpose.

Obligate carnivores consume raw meat, which is rich in glycans (glycolipids, glycoproteins, etc.), which is what we know of as animal fiber. Animal fiber is persorbed as well, and likely has a very wide range. Some of these glycans are probably used throughout the body. In fact, any fiber particle that is eaten from any food will surely become persorbed in the same manner.

Glycosaminoglycans (GAGs) from blueberries literally get transported to your blood vessels and play a role in maintaining their health. Without persorption, there would be no way for GAGs to contribute to the health of blood vessels...."

Radical decrease in endotoxin absorption.

Do you think most people have impaired digestion?



.

 

[Peater Piper]

Here is the study comparing the two -https://www.ncbi.nlm.nih.gov/pubmed/25236175

What's surprising about this is that The Biggest Loser group kept significantly more lean mass, yet still had double the metabolic adaption at six months. Also, the bariatric group showed no metabolic adaption by 12 months according to the second image?