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 20th 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.