55 replies to this topic

[misterE]

One of the modern misconceptions about diabetes prominent among doctors, nutritionists and laymen alike, is that eating carbohydrates turns into blood-sugar, raises insulin levels and causes diabetes. This flawed logic has led to mass "carbophobia" and leads people to eat more fat and protein calories, the exact wrong type of fuel for the human body, the type of fuel that keeps people diabetic and keeps the pharmaceutical industry profitable.

 

One of the very first studies ever done on diabetes was conducted back in 1920's by a fellow named Shirley Sweeney [1]. The study he did was a very simple study and is considered a "classic" in the medical-literature. What Sweeney wanted to find out, is what aspects of the diet caused elevated blood-sugar. So what he did was got four groups of young college students and put them on four different diets; a high-carbohydrate diet (consisting of bananas, potatoes, oatmeal, flour, syrup and juice), a high-protein diet (consisting of lean-fish, lean-meat and egg-whites), a high-fat diet (consisting of egg-yolks, mayonnaise, butter, cream and olive-oil), and the forth group ate nothing at all as a control group.

 

Sweeney then tested their blood-sugar and what he found was that all the groups were diabetic...except the high-carbohydrate group! He was so baffled by these results that he took one student from the high-carbohydrate group and switched him over to the high-fat group and found that his blood-sugar rose to diabetic-levels. He took the same student and starved him and yet his blood-sugar was still considered in the diabetic range, but once he went back to eating liberal amounts of starch and sugar... his blood-sugar came within the normal healthy range.

 

The study was considered a strange paradox and confused the researchers very much. The implication and understandings of these results were not realized for about another 30 to 40 years later.

 

Starting in the late 1940's came a researcher from Duke University named Walter Kempner and he made an observation that cultures around the world that seemed to be the thinnest, the healthiest and resisted diabetes lived mostly on starchy foods. These cultures relied on grains to fuel their populations and simply didn't have access to high-protein and fatty-foods that wealthy Americans were use to eating on a daily basis. He created a diet called: The Rice Diet, which consisted exclusively of white-rice, fruit, juice and table-sugar.

 

The Rice Diet was given to diabetics who were on the verge of death due to sever diabetic complications. These folks were going blind, losing their kidney-function, developing atherosclerosis and becoming obese. Once put on the Rice Diet, their diabetes was quickly reversed along with all of the other complications of diabetes. These results were published in the medical-literature and was (and still is) considered the "ultimate diet therapy" [2-4].

 

Research in the 1970's began to clearly show the anti-diabetic effects of dietary carbohydrates. Researcher James Anderson conducted dozens of studies showing that diabetics improved when put on a high-fiber/high-starch diet [5-7].

 

In 1971 Brunzell et al conducted controversial research showing that feeding simple-sugar to people with diabetes produced beneficial metabolic effects and that all aspects of diabetes was improved by feeding them sucrose [8]. Brunzell stated in the report: "This data suggests that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin".

 

Then came the researcher Nathan Pritikin, who changed his diet once he developed severe heart-disease. He noted the same observation that Kempner noticed; all population of people who were free from diabetes and atherosclerosis ate primarily a high-carbohydrate diet. The Pritikin Diet consisted of unrefined starches like beans, whole-grains and potatoes, along with fruits, vegetables and lean meats in limited amounts. The diet quickly reversed diabetes and this was also published [9]. Nearly 30 studies have been conducted out of the Pritikin Longevity Center over the next thirty years, showing reversal of diabetes with this type of diet.

 

 Nathan Pritikin bragged about these results so much that when he died, researchers wanted to see if he was correct. They autopsied his corpse and were surprised to find that he was free of atherosclerosis [10]. His veins were nearly crystal-clean. The report says: "The coronary arteries were soft and pliable, no scars were visible. In a man 69 years old, the near absence of atherosclerosis and the complete absence of its complications are remarkable."

 

I was so surprised when I realized the vast treasure trove of research showing the protective effects of carbohydrates against diabetes and the migration studies, showing that when populations of people who traditionally eat high-carbohydrate diets migrate to western-countries and eat less carbohydrates (and more fat and protein) they quickly develop diabetes [11]. I wanted to challenge myself and solve the seemingly strange paradox that Sweeny documented early on.  

 

Type-2 diabetes is a disease where the blood-sugar is increased and the insulin-receptors have become "resistant" to insulin, meaning even thou the pancreas is making plenty of insulin, none of the insulin being made is having an effect in the body, leading to an insulin-deficiency at the cellular level.

 

In normal healthy people, insulin lowers blood-sugar by promoting the uptake of blood-sugar into the muscles and liver to be stored as glycogen. Or in other words... insulin takes sugar out of the bloodstream and into the cells, where it is stored as glycogen and used for energy.

 

The body is very resilient and if carbohydrates are not eaten, the body will actually produce its own glucose. The reason why the body produces its own glucose is to supply glucose for the brain, which must have glucose to function. Without glucose, the brain will shut down and begin to die (like what is seen with Alzheimer's disease). The process of making glucose is called gluconeogenesis and this happens by converting amino-acids (protein) into glucose. The body also makes glucose from glycerol, which comes from the body-fat reserves.

 

The body has a very tightly controlled negative feedback loop installed in the body; a counter regulatory process if you will. When you are not eating carbohydrates, gluconeogenesis increases to supply glucose for the brain. When you are eating plenty of carbohydrates, gluconeogenesis is decreased because you have plenty of carbohydrates coming in to feed the brain and the body has no need or obligation to create its own glucose when you are supplying plenty of glucose from the diet.

 

There is a class of hormones called glucocorticoids, which are secreted when the brain demands more glucose. These glucocorticoids increase blood-sugar by stimulating and upregulating gluconeogenesis. Cortisol and glucagon are two important glucocorticoids that increase blood-sugar and diabetics have extremely high levels of these hormones [12-18]. Diabetics also have high rates of gluconeogenesis occurring as a result of these elevated glucocorticoids [19-21].

 

Insulin lowers blood-sugar by not only transporting glucose out of the blood, but also by inhibiting gluconeogenesis, whereas glucocorticoids raises blood-sugar by liberating glucose out of the cells and into the bloodstream and by stimulating gluconeogenesis. So in essence, the elevated blood-sugar found in diabetics is not the result of carbohydrate consumption... but rather from excessive gluconeogenesis.

 

Knowing this is crucial to understanding the paradox of Sweeney's results. The reason why the high-carbohydrate group had normal blood-sugar was because they were increasing their insulin-secretion, suppressing their glucocorticoids and lowering gluconeogenesis, while the other groups (the high-protein, the high-fat and the starvation groups) were increasing their glucocorticoids and suppressing their insulin-secretion.

 

The consumption of starch and sugar stimulates insulin and suppresses glucocorticoids, which lowers blood-sugar... while low-carbohydrate diets (and even overt starvation) stimulates glucocorticoids and suppresses insulin, which leads to elevated blood-sugar. I believe this is why diabetics crave sweets and sugar so much. Their craving for sugar is exactly what their body needs to shut down the excessive levels of glucocorticoids that are in turn making them diabetic.

 

The underlying cause of type-2 diabetes is not the overconsumption of carbohydrates... the cause of type-2 diabetes is an elevation of glucocorticoids; brought about by a lack of carbohydrate intake. This explains why the rates of diabetes in America has increased dramatically over the years, as Americans eat less carbohydrates and more fat, like what they have been doing since the beginning of the 20^th century [22].

 

     

[1] Arch Intern Med (Chic). 1927;40(6):818-830. Dietary Factors That Influence The Dextrose Tolerance Test. Sweeney S.

 

[2] Am J Med. 1948 Apr;4(4):545-77. Treatment of hypertensive vascular disease with rice diet. KEMPNER W.

[3] Postgrad Med. 1958 Oct;24(4):359-71. Effect of rice diet on diabetes mellitus associated with vascular disease. KEMPNER W, PESCHEL RL, SCHLAYER C.

[4] Z Klin Med. 1954;152(4):328-45. Effect of rice diet in experimental hypertension and in patients with heart, kidney and vascular diseases. KEMPNER W.

 

[5] Diabetes Care. 1978 Mar-Apr;1(2):77-82. Long-term effects of high-carbohydrate, high-fiber diets on glucose and lipid metabolism: a preliminary report on patients with diabetes. Anderson JW, Ward K.

 

[6] Am J Clin Nutr. 1979 Nov;32(11):2312-21. High-carbohydrate, high-fiber diets for insulin-treated men with diabetes mellitus. Anderson JW, Ward K.

 

[7] Adv Exp Med Biol. 1979;119:263-73. High carbohydrate, high fiber diets for patients with diabetes. Anderson JW.

 

[8]  N Engl J Med. 1971 Mar 11;284(10):521-4. Improved glucose tolerance with high carbohydrate feeding in mild diabetes. Brunzell JD, Lerner RL, Hazzard WR.

 

[9]  Diabetes Care. 1983 May-Jun;6(3):268-73. Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and exercise in the treatment of NIDDM patients. Barnard RJ, Massey MR, Cherny S.

 

[10] N Engl J Med. 1985 Jul 4;313(1):52. Nathan Pritikin's heart. Hubbard JD, Inkeles S, Barnard RJ.

 

[11] Food Nutr Res. 2012;56. Changes in dietary habits after migration and consequences for health: a focus on South Asians in Europe. Holmboe-Ottesen G, Wandel M.

 

[12] Eur J Endocrinol. 2006 Feb;154(2):325-31. Cortisol correlates with metabolic disturbances in a population study of type 2 diabetic patients. Oltmanns KM¹, Dodt B, Schultes B.

 

[13] Diabetes Care. 2007 Jan;30(1):83-8. Cortisol secretion in patients with type 2 diabetes: relationship with chronic complications. Chiodini I, Adda G, Scillitani A.

 

[14] Eur J Endocrinol. 2005 Dec;153(6):837-44. Association of subclinical hypercortisolism with type 2 diabetes mellitus: a case-control study in hospitalized patients. Chiodini I, Torlontano M, Scillitani A.

 

[15] Clin Endocrinol (Oxf). 2006 Sep;65(3):301-9. Insulin resistance, endocrine function and adipokines in type 2 diabetes patients at different glycaemic levels: potential impact for glucotoxicity in vivo. Lindmark S, Burén J, Eriksson JW.

 

[16] Diabetes Obes Metab. 2011 Oct;13 Suppl 1:126-32. The role of dysregulated glucagon secretion in type 2 diabetes. D'Alessio D.

 

[17] Am J Physiol Endocrinol Metab. 2003 Apr;284(4):E671-8. Glucagon and regulation of glucose metabolism. Jiang G, Zhang BB.

 

[18] J Clin Endocrinol Metab. 2000 Nov;85(11):4053-9. Lack of suppression of glucagon contributes to postprandial hyperglycemia in subjects with type 2 diabetes mellitus. Shah P, Vella A, Basu A.

 

[19] J Clin Invest. Oct 1992; 90(4): 1323–1327.  Increased rate of gluconeogenesis in type II diabetes mellitus. A 13C nuclear magnetic resonance study. I Magnusson, D L Rothman, L D Katz.

 

[20] Am J Physiol Endocrinol Metab. 2001 Jan;280(1):E23-30. Gluconeogenesis in moderately and severely hyperglycemic patients with type 2 diabetes mellitus. Boden G, Chen X, Stein TP.

 

[21] Diabetes. 1997 Jun;46(6):1010-6. Evidence of increased systemic glucose production and gluconeogenesis in an early stage of NIDDM. Perriello G, Pampanelli S, Del Sindaco P.

 

[22] J Am Diet Assoc. 1982 Aug;81(2):120-8. Review of trends in food use in the United States, 1909 to 1980. Welsh SO, Marston RM.

Edited by misterE, 08 June 2014 - 07:07 PM.

[Eruditus]

Shit my mom got rid of her prediabetic bloodsuger levels by going on an atkins diet. Must have been a fluke, better bring back all the redbull and potato chips now that we have been informed of the truth

[Dolph]

If you think that red bull and potato chips are the only plausible alternative to Atkins all my honest pity is with you...

[Eruditus]

If you think that red bull and potato chips are the only plausible alternative to Atkins all my honest pity is with you...

 

If you want to make me state the obvious. That was  a sarcastic exaggeration. My mother used to be addicted to foods that provided quick sugar spikes and now she has come past that addiction, which can be quite obviously attributed to a quasi Atkins diet. I agree long term ketogenic diets are hardly sustainable in the majority of the population, but short term they help severely health compromised individuals regain back their metabolic flexibility with regards to the ability to oxidate fat - something which is impossible when high levels of insulin due to excess carbohydrate consumption are present.

[robertredfern]

I trust the readers of this article understand this article is completely wrong and does not make any sense healthwise and nutritionwise. A really Healthy diet is: vegetables, nuts, seed, beans, dark skinned fruits, fish and grass fed meats. The last two are optional for good health and are an indulgence. The foods to avoid which is shown in hundreds of studies to be the prime causse of all diseases are: All Grains (inc. Whole grains, Cereals, Corn, Potatoes, High Sugar fruits, High Sugar Drinks, all processed foods and of course anything that you could not pick and eat raw when they are young.  

RobertRedfern reallyhealthyfoods website. 

Edited by robertredfern, 08 June 2014 - 10:31 PM.

[tunt01]

 

The Rice Diet, which consisted exclusively of white-rice, fruit, juice and table-sugar.

 

The Rice Diet was given to diabetics who were on the verge of death due to sever diabetic complications. These folks were going blind, losing their kidney-function, developing atherosclerosis and becoming obese. Once put on the Rice Diet, their diabetes was quickly reversed along with all of the other complications of diabetes. These results were published in the medical-literature and was (and still is) considered the "ultimate diet therapy" [2-4].

 

 

This was the part where I literally went, "What the fuck?"  

 

 

 

I have to agree with the underlying premise of a carb-centric diet, but not via syrup/white rice/whatever.  It should be complex carbs, limited protein/fat intake. 

Edited by prophets, 08 June 2014 - 10:49 PM.

[prolongevity]

In a type two diabetic, the consumption of rice and white flour products typically shoots glucose levels pretty high. And the more regularly these foods are consumed, the higher glucose levels will be, and that includes morning fasting glucose levels as well as glucose levels throughout the day. Doing what this article suggests will simply lead to more pancreatic beta cell burnout, more abdominal and visceral fat stores, and increased insulin resistance.

[robertredfern]

Correct and not to mention massive Glycation. Cultures that eat white rice have a population that mainly need spectacles and suffer many other sugar disease whereas cultures that do not eat grain and cereal foods never need spectacle and do not suffer (until they move to living in a sugar/carb consuming culture).

Stopping eating all sugar/carbs immediately stops epilepsy. 

PS When you get to my age, 68, a high protein (vegetable based) diet is essential for maintaining great health. Low protein leads to muscle loss and feebleness.

RobertRedfern ReallyHealthyFoods 

[StephCThomp]

Interesting. Confounding.  Worth exploring.  But note:

 

Nathan apparently ate huge amounts of fat and sugar before his diagnosis, including "a pint of ice cream" every day.  He must have been overweight.  He also had some kind of Lymphoma around the same time - just before or after, I'm not sure.

 

After his coronary diagnosis in 1956 he apparently "...had become a vegetarian. He also started running three to four miles daily... By January 1960...his coronary insufficiency had disappeared."  It seems that he was (or his doctors were, I'm not sure) also able to clear his Lymphoma.

 

So he changed to a predominantly whole-food plant-based diet, presumably ingesting more normal calories each day, and exercised vigorously.  Not surprising, then, that something changed for the better metabolically.  (The modern Pritikin diet does not advocate simple carbs at all, BTW, but whole foods.)

 

Nevertheless, he lived to only 69 years of age.  His heart and arteries were in fine condition, yet he came down with another type of Lymphoma.

 

Clearly arterial health and diabetes must not be simply a question of the relative proportions of macro nutrients.  Contradictory results is various feeding studies are clues in themselves - that we should be looking for the 'something elses' that are the common and causative factors among these superficially very different interventions.

 

Also we must be careful not to prevent one condition just to pay for it with a worse one.

Edited by Finley, 15 June 2014 - 04:28 AM.

[misterE]

I think many members here (Eruditus, robertredfern, prolongevity and perhaps prophets, in particular) misunderstand the OP. Eating carbohydrates lowers blood-sugar by lowering glucocorticoids. The mainstream view that eating carbohydrates (even refined carbohydrates like white-flour, white-rice and table-sugar) isn't what causes sustained elevated blood-sugar, only acute elevations which the body is able to handle properly as long as you are insulin-sensitive ... it is the unsuppressed gluconeogenesis that is occurring due to a lack of insulin that causes sustained elevated blood-sugar. The only way to lower gluconeogenesis is by eating carbohydrates.

 

 

 

Edited by misterE, 15 June 2014 - 04:35 PM.

[Eruditus]

Why would the body waste more protein on gluconeogenesis then it needs glucose? If anything some additional protein in the diet will by this conversion help maintain stable glucose levels reducing the need for constant carb refeeds.

 

I think I now understand more what you may be referring to. If it is in anyway related to the transient increased blood sugar levels seen in some intial ketogenic dieters then I am very sorry to burst your bubble but this is a non pathological form of insulin resistance which is not expressed in the central nervous system. This allows muscle to forego all glucose uptake and limits glucose supplies to those neurons that lack the mitochondria for beta oxidation of fats. The reason this approach works for pre diabetics and people with higher volumes abdominal/visceral fats has little to do with this non pathological form of insulin resistance but rather the uncoupling of the mitochondria and during the keto-adaptive phase allows the body to relearn long term benefits of fat beta oxidation, thereby also drastically reducing glucose requirements by providing this alternate much more stable source of calories. 

 

If you were not specifically referring to ketogenic adaptive process then again I have to disagree with you based on the fact that someone who is fat adapted which is sign of a healthy metabolic flexibility and high insulin sensitivity can get by on only 100 - 150 gram of carbs without experiencing any symptoms of low blood sugar.

 

Even better is someone who is fat adapted and engages in intermittent fasting as these individuals will have greater glycogen stores and become more efficient at glycogen sparing. These are all protective benefits and I don't understand why you are arguing that acute elevations in glucose are not relevant because the way I and most people see it is that acute elevations in glucose cause acute elevations in insulin cause decreased insulin receptor sensitivity causes increased insulin production causes pancreases to give up and you have yourself a very basic diabetic causative model. 

 

Oh and fyi ketoacidosis does not equal ketosis, because I've seen you refer to the high ketone levels in diabetics and this is not a valid link whatsoever

Edited by Eruditus, 15 June 2014 - 05:51 PM.

[misterE]

Eruditus--

 

On low-carb diets (or ketogenic-diets) the body becomes insulin-resistant due to an elevation of glucocorticoids. These glucocorticoids induce proteolysis and lipolysis to liberate amino-acids and glycerol to convert into glucose for the brain, while the rest of the organs utilize free-fatty-acids as fuel, this is why people with insulin-resistance have an accumulation of fat in their muscles and organs along with elevated gluconeogenesis and blood levels of amino-acids and glycerol. Diabetics have a hard time replenishing their glycogen stores because all of their blood-sugar is being used by the brain, not the muscles and liver.

 

Acute glucose elevations and acute insulin-spikes are a healthy and natural part of human-physiology. Insulin is required for many different and important metabolic functions and depriving your body of "insulin-spikes" will cause serious metabolic harm. Eating carbohydrates and spiking your glucose and insulin doesn't make the pancreas "give up" as you put it, nor does it cause insulin-resistance... those are all myths. The real cause of pancreatic beta-cell dysfunction and insulin-resistance is an accumulation of FFAs, caused by excessive amounts of glucocorticoids. This is all well published in the literature. Low-carbohydrate and ketogenic-diets mimic the hormonal environment of a type-1 diabetic.  

Edited by misterE, 16 June 2014 - 03:33 AM.

[Eruditus]

A to Z diet study and this 

Edited by Eruditus, 16 June 2014 - 04:27 PM.

[LawrenceHarasim]

I am sure not many people on our forum want to make waves but I will have to agree to dissagree with the OP...IMHO Low carbs are the way to health..for diabetics and more normal folks ....but I will also say every persons biology can be different ...for me Low carb is the winner

[misterE]

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

[misterE]

 I will have to agree to dissagree with the OP...

 

What aspect do you disagree on?
 

[maxwatt]

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 

Why then are most type 2 diaetics overweight?

 

Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 

A better understanding of genetics might clarify the diet wars.

[misterE]

 

 

 

Why then are most type 2 diaetics overweight?

 

 

 

It's not being overweight that causes diabetes per say, but rather dysfunctional adipocytes. Dysfunctional adipocytes are undergoing lipolysis and spewing out FFAs and inflammatory cytokines that induce insulin-resistance. Diabetics, although overweight or obese, are actually undergoing lipolysis and burning fat as their main source of fuel. Type-2 diabetes is the body's way of trying to lose weight. It's an adaptation to constant overnutrition and the subsequent weight-gain.
 

Edited by misterE, 18 June 2014 - 03:41 AM.

[maxwatt]

please reread my question in context

Edited by maxwatt, 18 June 2014 - 04:02 AM.

[misterE]

Insulin-sensitive people, when constantly overfed, gain weight until the adipocytes become overloaded. Once overloaded, the body becomes insulin-resistant (insulin being a storage hormone) to prevent anymore storage of energy, because the system is already saturated with energy. Without proper insulin-signaling, the body is forced into burning its stored energy. Starvation and low-carb diets also prevent the storage of energy and forces the body to burn its stored energy. So both starvation and overnutrition will decrease insulin-signaling.

Edited by misterE, 18 June 2014 - 04:09 AM.

[Chupo]

 

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 

Why then are most type 2 diaetics overweight?

 

Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 

A better understanding of genetics might clarify the diet wars.

 

 

I am an Apo E2 carrier.  My Triglycerides were 447 on SAD.  They were 239 on a starch-based, no overt fat diet.  They are in the 60's on a high fat low carb diet.  Conversion of VLDL to LDL is slow in E2 carriers. Eating fat and increasing chylomicron production will stimulate ASP (acylation stimulating protein), which will take fat out of the blood. 

[JohnD60]

 

On low-carb diets (or ketogenic-diets) the body becomes insulin-resistant due to an elevation of glucocorticoids.

Only an ideologue would make this association

[maxwatt]

 

 

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 

Why then are most type 2 diaetics overweight?

 

Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 

A better understanding of genetics might clarify the diet wars.

 

 

I am an Apo E2 carrier.  My Triglycerides were 447 on SAD.  They were 239 on a starch-based, no overt fat diet.  They are in the 60's on a high fat low carb diet.  Conversion of VLDL to LDL is slow in E2 carriers. Eating fat and increasing chylomicron production will stimulate ASP (acylation stimulating protein), which will take fat out of the blood. 

 

 

Wow.  The opposite of 23andme's advice, APOe2 gain weight if more than 30% of calories from fat. 

 

[Chupo]

 

 

 

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 

Why then are most type 2 diaetics overweight?

 

Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 

A better understanding of genetics might clarify the diet wars.

 

 

I am an Apo E2 carrier.  My Triglycerides were 447 on SAD.  They were 239 on a starch-based, no overt fat diet.  They are in the 60's on a high fat low carb diet.  Conversion of VLDL to LDL is slow in E2 carriers. Eating fat and increasing chylomicron production will stimulate ASP (acylation stimulating protein), which will take fat out of the blood. 

 

 

Wow.  The opposite of 23andme's advice, APOe2 gain weight if more than 30% of calories from fat. 

 

recommended

 

Where do they say that? All I can see on my 23andme report pertaining to ApoE is about Alzheimer's.   Most everything I've read  recommends the most fat intake for E2, the least for E4 with E3 middle of the road.  The recommendations are so ridiculously close though, that I don't think it'd make much difference.  It's usually something like 25% fat for E4, 30% for E3 and 35% for E2.  

 

[JR7]

 

 

 

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 
Why then are most type 2 diaetics overweight?
 
Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 
A better understanding of genetics might clarify the diet wars.
 

 
I am an Apo E2 carrier.  My Triglycerides were 447 on SAD.  They were 239 on a starch-based, no overt fat diet.  They are in the 60's on a high fat low carb diet.  Conversion of VLDL to LDL is slow in E2 carriers. Eating fat and increasing chylomicron production will stimulate ASP (acylation stimulating protein), which will take fat out of the blood. 
 

 
Wow.  The opposite of 23andme's advice, APOe2 gain weight if more than 30% of calories from fat. 

 
recommended

 
Where do they say that? All I can see on my 23andme report pertaining to ApoE is about Alzheimer's.   Most everything I've read  recommends the most fat intake for E2, the least for E4 with E3 middle of the road.  The recommendations are so ridiculously close though, that I don't think it'd make much difference.  It's usually something like 25% fat for E4, 30% for E3 and 35% for E2.  

 

Sorry if this is off topic. Is 23andme still worth doing? They're advertising as an ancestry tool now.

[Chupo]

 

Sorry if this is off topic. Is 23andme still worth doing? They're advertising as an ancestry tool now.

 

 

Sure.  You can still run your DNA through Promethease, which gives you much more information.
 

[maxwatt]

 

 

 

 

Sure, low-carb diets will make you lose weight... but so will uncontrolled diabetes.

 

Why then are most type 2 diaetics overweight?

 

Perhaps the OP's diet is correct for those carry the APOE2 genotype, who cannot handle too much dietary fat, nor an overabundance of protein in the diet. 

A better understanding of genetics might clarify the diet wars.

 

 

I am an Apo E2 carrier.  My Triglycerides were 447 on SAD.  They were 239 on a starch-based, no overt fat diet.  They are in the 60's on a high fat low carb diet.  Conversion of VLDL to LDL is slow in E2 carriers. Eating fat and increasing chylomicron production will stimulate ASP (acylation stimulating protein), which will take fat out of the blood. 

 

 

Wow.  The opposite of 23andme's advice, APOe2 gain weight if more than 30% of calories from fat. 

 

recommended

 

Where do they say that? All I can see on my 23andme report pertaining to ApoE is about Alzheimer's.   Most everything I've read  recommends the most fat intake for E2, the least for E4 with E3 middle of the road.  The recommendations are so ridiculously close though, that I don't think it'd make much difference.  It's usually something like 25% fat for E4, 30% for E3 and 35% for E2.  

 

 

 

It's kind of buried in one of their reports, somewhat an indirect reference . But consider this result albeit in mice:

 

Diabetes. 2013 Feb;62(2):382-91. doi: 10.2337/db12-0390. Epub 2012 Sep 6.

Apolipoprotein E2 accentuates postprandial inflammation and diet-induced obesity to promote hyperinsulinemia in mice.

Kuhel DG¹, Konaniah ES, Basford JE, McVey C, Goodin CT, Chatterjee TK, Weintraub NL, Hui DY.

Author information

Abstract

Genetic studies have revealed the association between the ε2 allele of the apolipoprotein E (apoE) gene and greater risk of metabolic diseases. This study compared C57BL/6 mice in which the endogenous mouse gene has been replaced by the human APOE2 or APOE3 gene (APOE2 and APOE3 mice) to identify the mechanism underlying the relationship between ε2 and obesity and diabetes. In comparison with APOE3 mice, the APOE2 mice had elevated fasting plasma lipid and insulin levels and displayed prolonged postprandial hyperlipidemia accompanied by increased granulocyte number and inflammation 2 h after being fed a lipid-rich meal. In comparison with APOE3 mice, the APOE2 mice also showed increased adiposity when maintained on a Western-type, high-fat, high-cholesterol diet. Adipose tissue dysfunction with increased macrophage infiltration, abundant crown-like structures, and inflammation were also observed in adipose tissues of APOE2 mice. The severe adipocyte dysfunction and tissue inflammation corresponded with the robust hyperinsulinemia observed in APOE2 mice after being fed the Western-type diet. Taken together, these data showed that impaired plasma clearance of apoE2-containing, triglyceride-rich lipoproteins promotes lipid redistribution to neutrophils and adipocytes to accentuate inflammation and adiposity, thereby accelerating the development of hyperinsulinemia that will ultimately lead to advanced metabolic diseases.

PMID:   22961083

Too much fat leads to metabolic disease, hyperlipedemia and inflamation.  I suspect the 35% fat many sources give for APoe2 is too high, based on incomplete data.  Both sugars and fats are problematic for this genotype.  When I try Atkins style high fat diets, my blood lipids and triglycerides shoot way up.  Sigh,  I love the smell o bacon.
 

[Chupo]

Mice have a different LDL receptor than humans so human apoe does not act the same in them.  I trust my own n=1 over any mouse study anyway. Keeping my carbs low and fats high has finally allowed me to express some longevity genes I have that reduce CETP and raise HDL.  On low fat, my high triglycerides were working against it by increasing CETP activity and lowering my HDL.  Now, my HDL is higher than my LDL and TG is low.

Edited by Chupo, 27 July 2014 - 10:28 AM.

[Chupo]

Maxwatt.

 

I've been thinking about your trigs going up on Atkins. I doubt it's due to your apoe2 status alone. The only other e2 carriers I know of who low carb (ItsTheWooo and HeartHawk) both have low trigs.   I think you may have a problem with something else like lipoprotein lipase.  E2 homozygotes who also have a defect in another gene that effects lipolysis can develop type III hyperlipidemia. 

[StevesPetRat]

I have a giant tub of dextrose; I guess I should just wear that thing like a feed bag?