Commentary on Type 2 Diabetes

Also see:
The Randle Cycle
Master List – Ray Peat, PhD Interviews
Ray Peat, PhD on Low Blood Sugar & Stress Reaction
Aldosterone, Sodium Deficiency, and Insulin Resistance
Sugar (Sucrose) Restrains the Stress Response
Thumbs Up: Fructose
Ray Peat, PhD Quotes on Therapeutic Effects of Niacinamide
Diabetes: Conversion of Alpha-cells into Beta-cells
Errors in Nutrition: Essential Fatty Acids
Women, Estrogen, and Circulating DHA
Insulin Inhibits Lipolysis
PUFA Breakdown Products Depress Mitochondrial Respiration
PUFA Decrease Cellular Energy Production
TNF-alpha, Obesity, Endotoxin, Insulin Resistance, and Diabetes
Fish Oil Toxicity
Free Fatty Acids Suppress Cellular Respiration
Soybean oil causes more obesity than coconut oil and fructose
The common oil that science now shows is worse than sugar

Quotes by Ray Peat, PhD:
“The picture that I think explains many of the features of diabetes is that an energy deficit produces an alarm state, causing increased production of adrenalin and cortisol.”

“It’s the prolonged shock-like state that contributes to the degenerative diseases, which typically begin with a sort of diabetes, an inability to use glucose for energy because of the accumulation of too much of the wrong kind of fat.”

“Inflammation, interfering with cellular energy production, is probably the essential feature of the things called diabetes.”

“Although diabetes is described as an inability to use glucose, diabetics usually have increased lactate in their blood, indicating that glucose is being used wastefully, at the same time that some energy is produced from fat. Mitochondria damaged by chronic exposure to PUFA have a low rate of oxygen use and energy production.”

“Sugar, by reducing the level of free fatty acids in the body, actually tends to protect against these toxic effects of the PUFA. Diabetes, like cancer, has been known for a long time to be promoted by unsaturated oils in the diet, rather than by sugar. The seed oil industry has been more effective than the sugar industry in lobbying and advertising, and the effects can be seen in the assumptions that shape medical and biological research.”

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Diabetes mellitus results in excessive urination and sugar spilling into the urine and was thought to be a “sugar disease.” Some individuals diagnosed with type 2 diabetes are diagnosed not based on the aforementioned but because they have high blood sugar and then are given insulin (because of an assumed “insulin deficiency”) without the consideration of the multitude of other factors that can cause blood sugar to rise. When non-diabetics are given insulin, they can develop the same complication as diabetics making the insulin strategy counterproductive. Patients aren’t made aware of this potential danger.

Contrary to what is popularly believed, sugar doesn’t cause type 2 diabetes. Bernardo Houssay’s work (which won him the Nobel Prize in Medicine in 1947) on diabetes proved polyunsaturated fats’ causative role in diabetic conditions. In his experiment, saturated fat in the form of coconut oil was found very protective; protein and sugar proved protective against diabetes but to a lesser extent.

To correct any disease, a strategy needs to be designed to limit exposure to disruptive substances and increase exposure to the protective ones. Polyunsaturated fatty acids (PUFA) are a central figure in age-related degeneration in humans and universally toxic to the human body and poison energy production in a variety of ways. PUFA block the oxidation of glucose by cells (Randle Cycle or Randle Effect) and are responsible for oxidative stress. High amounts of PUFA in the blood raise the blood sugar as a result of their blocking of glucose oxidation. Excess cortisol has the same effect. The glucose that does happen to be oxidized produces lactic acid, further burdening the energy reserves of the body as the lactic acid will have to be converted back to glucose by the liver using stored glycogen in the process. Diabetics tend to have high lactic acid levels.

Sucrose and ripe fruits keep PUFA in storage, lower cortisol, and support thyroid function as serve as protective foods for the diabetic. Ripe fruits also tend to be less glycemic than complex carbohydrates like pastas, cereals, and breads (which are promoted as part of a diabetic diet) and also contain potassium which has insulin-like function. These sugars have also shown beneficial in repairing β-cell function of the pancreas which secrete insulin.

Avoiding dietary PUFA and reducing situations and substances that liberate these fats (lipolysis) into the bloodstream (stress, adrenaline, hypothyroidism, estrogen, cortisol, trauma, etc) would limit exposure to disruptive substances. Consumption of foods lacking the polyunsaturated fats reduces the likelihood of increased oxidative stress, protects the thyroid and the energy producing systems, decreases estrogen’s effects, and improves glucose utilization. A diet rich in saturated fats, like coconut oil, offset the detrimental effects of PUFA.

Liver cells require glucose to convert T4 to T3 so diabetics become hypothyroid by default. The lack of cellular energy in diabetics causes cells to take up excess calcium leading to calcification of soft tissues and a variety of complications. The calcification of mithochondrion as well as the poisoning of energy production by PUFA are major factors in many diseases, including type 2 diabetes. Correcting the resulting energy deficit associated with diabetes and other diseases appears beneficial. Broda Barnes, MD, PhD gave his diabetic patients with a low basal temperature natural dessicated thryoid and none of them developed the expected complications of diabetes.

Women are more likely than men to develop diabetes because estrogen increases free unsaturated fatty acids in the blood blocking glucose utilization, creating insulin resistance and over stimulation of the pancreas. Substances that oppose the actions of estrogen (i.e. progesterone, vitamin E) would prove beneficial for the type 2 diabetic as it would discourage the chronic release of fatty acids, counteract the excitatory effects of estrogen, prevent the stress reaction, decrease oxidative stress, and improve β-cell function.

Adrenaline tends to be high in the hypothyroid encouraging lipolysis. As a result of this process, a high concentration of liberated PUFA have the unfortunate tendency to oxidize creating dangerous free radicals while at the same time increasing production of inflammatory prostaglandins. Diabetic conditions have a strong link to increased oxidative stress leading to deterioration of the insulin producing β-cells.

Anti-inflammatory substances found in gelatin have been shown to inhibit lipolysis allowing for the correction of diabetic conditions. Gelatin has been used therapeutically for well over 100 years in a variety of inflammatory diseases. A gelatin rich diet would also restrict the consumption of trytophan and, therefore, the production of cortisol, serotonin, prolactin, aldosterone, estrogen, TNF, IL-6, and other inflammatory substances.

FPS coaches at 12 to 16 week nutrition course based solely on the methodology of Ray Peat, PhD. Please click here for more information.

Resources:
“Gelatin, stress, longevity” by Ray Peat

“Diabetes, scleroderma, oils and hormones” by Ray Peat

“Glycemia, starch, and sugar in context” by Ray Peat

Science. 1947 May 23;105(2734):548-9.
Experimental Diabetes and Diet.
Houssay BA, Martínez C.
“In rats fed other high fat diets (olive oil, butter) the actions of alloxan were not modified, but there was a slight diminution when high oleomargarine or corn oil diets were fed. However, complete protection was observed when a high coconut oil diet was administered.”
“Mortality was zero on the high coconut oil diet, 100% on the high lard diet. It was 90% on the low protein diet, and 33% on the high protein diet. With a combination of coconut oil and lard, 20%.” –Ray Peat, PhD

Diabetes. 2002 Jun;51(6):1825-33.
The composition of dietary fat directly influences glucose-stimulated insulin secretion in rats.
Dobbins RL1, Szczepaniak LS, Myhill J, Tamura Y, Uchino H, Giacca A, McGarry JD.
“These data indicate that prolonged exposure to saturated fat enhances glucose-stimulated insulin secretion (but this does not entirely compensate for insulin resistance), whereas unsaturated fat, given in the diet or by infusion, impairs GSIS. Inferences regarding the impact of fatty acids on GSIS that are based on models using unsaturated fat may not reflect the effects of saturated fat.”

Diabetes. 1989 Oct;38(10):1314-9.
Effects of fish oil supplementation on glucose and lipid metabolism in NIDDM.
Borkman M1, Chisholm DJ, Furler SM, Storlien LH, Kraegen EW, Simons LA, Chesterman CN.
“In summary, dietary fish oil supplementation adversely affected glycemic control in NIDDM subjects without producing significant beneficial effects on plasma lipids. The effect of safflower oil supplementation was not significantly different from fish oil, suggesting that the negative effects on glucose metabolism may be related to the extra energy or fat intake.”

Diabetes Care. 1996 Nov;19(11):1249-56.
Metabolic effects of dietary sucrose and fructose in type II diabetic subjects.
Malerbi DA1, Paiva ES, Duarte AL, Wajchenberg BL.
“Our data suggest that in the short and middle terms, high fructose and sucrose diets do not adversely affect glycemia, lipemia, or insulin and C-peptide secretion in well-controlled type II diabetic subjects.”

Diabetes Care. 1993 Sep;16(9):1301-5.
Metabolic effects of dietary sucrose in type II diabetic subjects.
Bantle JP1, Swanson JE, Thomas W, Laine DC.
“A high sucrose diet did not adversely affect glycemia or lipemia in type II diabetic subjects.”

Am J Med. 1984 Dec;77(6):1015-22.
Graded sucrose/carbohydrate diets in overtly hypertriglyceridemic diabetic patients.
Jellish WS, Emanuele MA, Abraira C.
“This study suggests that isocaloric sucrose and carbohydrate restriction below usual daily levels (120 g per day) offers no consistent benefit in glycemia or lipid control in overt type II diabetes.”

Diabete Metab. 1995 Apr;21(2):79-88.
[Role of free fatty acids in the insulin resistance of non-insulin-dependent diabetes].
[Article in French]
Girard J1.
“Studies performed in the rat suggest that impaired glucose-induced insulin secretion could also be related to chronic exposure of pancreatic beta cells to elevated plasma free fatty acid levels. The role of the glucose-fatty acid cycle in normal subject must be clarified, and its contribution to decreased glucose-induced insulin secretion in NIDDM requires further investigation.”

J Clin Endocrinol Metab. 1991 Jan;72(1):96-107.
The role of free fatty acid metabolism in the pathogenesis of insulin resistance in obesity and noninsulin-dependent diabetes mellitus.
Groop LC1, Saloranta C, Shank M, Bonadonna RC, Ferrannini E, DeFronzo RA.
“The hypothesis is advanced that in uncomplicated obesity, increased availability and oxidation of FFA leads, by the FFA/glucose cycle, to the impairment in glucose utilization.”

Clin Immunol Immunopathol. 1995 Apr;75(1):51-6.
Augmented production of tumor necrosis factor-alpha in obese mice.
Yamakawa T1, Tanaka S, Yamakawa Y, Kiuchi Y, Isoda F, Kawamoto S, Okuda K, Sekihara H.
“Taken together, it is postulated that TNF-alpha produced by monocytes/macrophages may also play an important role in the genesis of insulin resistance in obesity.”

Arterioscler Thromb Vasc Biol. 2004 May;24(5):816-23. Epub 2004 Feb 19.
Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited.Ceriello A1, Motz E.
“In conclusion, a puzzle of many pieces of evidence suggests that free radical overgeneration may be considered the key in the generation of insulin resistance, diabetes, and cardiovascular disease.”

Diabetes Care. 1996 Mar;19(3):257-67.
Oxidative stress and diabetic vascular complications.
Giugliano D1, Ceriello A, Paolisso G.
“Evidence has accumulated indicating that the generation of reactive oxygen species (oxidative stress) may play an important role in the etiology of diabetic complications. This hypothesis is supported by evidence that many biochemical pathways strictly associated with hyperglycemia (glucose autoxidation, polyol pathway, prostanoid synthesis, protein glycation) can increase the production of free radicals.” “A rational extension of this proposed role for oxidative stress is the suggestion that the different susceptibility of diabetic patients to microvascular and macrovascular complications may be a function of the endogenous antioxidant status.”

Circulation. 2002 Oct 15;106(16):2067-72.
Inflammatory cytokine concentrations are acutely increased by hyperglycemia in humans: role of oxidative stress.
Esposito K1, Nappo F, Marfella R, Giugliano G, Giugliano F, Ciotola M, Quagliaro L, Ceriello A, Giugliano D.
“Hyperglycemia acutely increases circulating cytokine concentrations by an oxidative mechanism, and this effect is more pronounced in subjects with IGT. This suggests a causal role for hyperglycemia in the immune activation of diabetes.”

Diabetes. 2003 Jan;52(1):1-8.
Are oxidative stress-activated signaling pathways mediators of insulin resistance and beta-cell dysfunction?
Evans JL1, Goldfine ID, Maddux BA, Grodsky GM.
“In addition, there is evidence that in type 2 diabetes, the activation of these same pathways by elevations in glucose and free fatty acid (FFA) levels leads to both insulin resistance and impaired insulin secretion. Therefore, we propose here that the hyperglycemia-induced, and possibly FFA-induced, activation of stress pathways plays a key role in the development of not only the late complications in type 1 and type 2 diabetes, but also the insulin resistance and impaired insulin secretion seen in type 2 diabetes.”

Metabolism. 2000 Feb;49(2 Suppl 1):27-9.
Oxidative stress and glycemic regulation.
Ceriello A
“Several studies show that an acute increase in the blood glucose level may impair the physiological homeostasis of many systems in living organisms. The mechanisms through which acute hyperglycemia exerts these effects may be identified in the production of free radicals. It has been suggested that insulin resistance may be accompanied by intracellular production of free radicals. In adipocytes cultured in vitro, insulin increases the production of hydrogen peroxide, which has been shown to mimic the action of insulin. These data allow us to hypothesize that a vicious circle between hyperinsulinemia and free radicals could be operating: insulin resistance might cause elevated plasma free radical concentrations, which, in turn, might be responsible for a deterioration of insulin action, with hyperglycemia being a contributory factor. Data supporting this hypothesis are available. Vitamin E improves insulin action in healthy, elderly, and non-insulin-dependent diabetic subjects. Similar results can be obtained by vitamin C administration.”

Diabetes. 2003 Sep;52(9):2338-45.
Intramuscular heat shock protein 72 and heme oxygenase-1 mRNA are reduced in patients with type 2 diabetes: evidence that insulin resistance is associated with a disturbed antioxidant defense mechanism.
Bruce CR1, Carey AL, Hawley JA, Febbraio MA.
“These data demonstrate that genes involved in providing cellular protection against oxidative stress are defective in patients with type 2 diabetes and correlate with insulin-stimulated glucose disposal and markers of muscle oxidative capacity. The data provide new evidence that the pathogenesis of type 2 diabetes involves perturbations to the antioxidant defense mechanism within skeletal muscle.”

Diabetes. 2003 Mar;52(3):581-7.
Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection.
Robertson RP1, Harmon J, Tran PO, Tanaka Y, Takahashi H.
“Clinically, consideration of antioxidants as adjunct therapy in type 2 diabetes is warranted because of the many reports of elevated markers of oxidative stress in patients with this disease, which is characterized by imperfect management of glycemia, consequent chronic hyperglycemia, and relentless deterioration of β-cell function.”

Biochem Biophys Res Commun. 2003 Jan 3;300(1):216-22.
Mitochondrial reactive oxygen species reduce insulin secretion by pancreatic beta-cells.
Sakai K1, Matsumoto K, Nishikawa T, Suefuji M, Nakamaru K, Hirashima Y, Kawashima J, Shirotani T, Ichinose K, Brownlee M, Araki E.
“Pancreatic beta-cells exposed to hyperglycemia produce reactive oxygen species (ROS). Because beta-cells are sensitive to oxidative stress, excessive ROS may cause dysfunction of beta-cells.” “Our data suggested that high glucose induced mitochondrial ROS, which suppressed first-phase of GIIS, at least in part, through the suppression of GAPDH activity. We propose that mitochondrial overwork is a potential mechanism causing impaired first-phase of GIIS in the early stages of diabetes mellitus.”

Diabetes Care. 1992 Jan;15(1):1-7.
Glutathione infusion potentiates glucose-induced insulin secretion in aged patients with impaired glucose tolerance.
Paolisso G1, Giugliano D, Pizza G, Gambardella A, Tesauro P, Varricchio M, D’Onofrio F.
“Glutathione infusion enhances insulin secretion in elderly people with impaired glucose tolerance.”

Diabetes. 2001 Apr;50(4):803-9.
Uncoupling protein 2: a possible link between fatty acid excess and impaired glucose-induced insulin secretion?
Lameloise N1, Muzzin P, Prentki M, Assimacopoulos-Jeannet F.
“The data are compatible with a role of UCP2 and partial mitochondrial uncoupling in the decreased secretory response to glucose observed after chronic exposure of the β-cell to elevated fatty acids, and suggest that the expression and/or activity of the protein may modulate insulin secretion in response to glucose.”

J Clin Endocrinol Metab. 1996 Dec;81(12):4244-8.
Does free fatty acid infusion impair insulin action also through an increase in oxidative stress?Paolisso G1, Gambardella A, Tagliamonte MR, Saccomanno F, Salvatore T, Gualdiero P, D’Onofrio MV, Howard BV.
“This four-part study aims at investigating the association between FFA and oxidative stress in healthy volunteers.” “In conclusion, fasting plasma FFA seems to enhances oxidative stress, which might contribute to the disruptive effects of plasma FFA on insulin-mediated glucose uptake.”

Metabolism. 2002 Oct;51(10):1340-7.
Chronic exposure to free fatty acids or high glucose induces apoptosis in rat pancreatic islets: possible role of oxidative stress.
Piro S1, Anello M, Di Pietro C, Lizzio MN, Patanè G, Rabuazzo AM, Vigneri R, Purrello M, Purrello F.
“These data indicate that chronic exposure to elevated FFA or glucose levels increases apoptosis in rat pancreatic islets and these cytotoxic effects could be mediated by oxidative stress. This may contribute to the beta-cell failure that occurs in most in type 2 diabetic patients few years after clinical diabetes onset.”

N Engl J Med. 2001 May 3;344(18):1343-50.
Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.
Tuomilehto J1, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M; Finnish Diabetes Prevention Study Group.
“The reduction in the incidence of diabetes was directly associated with changes in lifestyle.”
“Type 2 diabetes can be prevented by changes in the lifestyles of high-risk subjects.”

Am J Med. 1984 Jun;76(6):1041-8.
Evidence for hyperestrogenemia as the link between diabetes mellitus and myocardial infarction.
Phillips GB.
“A higher mean serum estradiol level (p less than 0.001) and estradiol-to-testosterone ratio (p less than 0.005) were observed in the patients with diabetes, whereas the mean serum testosterone level was not significantly different.”