Insulin Resistance: The Slippery Slope to Type II Diabetes

QUINOA IS ANCIENT GRAIN THAT IS LOW ON THE GLYCEMIC INDEX AND HAS A LOW GLYCEMIC LOAD

Insulin is the hormone that regulates cellular nourishment by aiding in the absorption and metabolism of nutrients from the blood.  Insulin resistance can be defined as the body’s inability to use insulin to metabolize glucose. It used to be considered an aging issue and a result of hormonal changes, but in the last decade or so insulin resistance has been discovered not only in young adults, but also in teenagers and children.

Insulin resistance is a silent bodily process that gets progressively worse over time. Anyone whose diet is high in sugar and refined carbohydrates will eventually face insulin resistance. Fortunately, the problem, if realized in a timely manner, can be controlled and even reversed without the use of pharmaceuticals.

The process begins with the body’s detection of higher blood sugar levels. In response, beta cells in the pancreas step up the secretion of insulin to deal with the blood sugar spike, facilitating glucose transport through cell membranes and lowering blood sugar. But when blood sugar levels are chronically elevated, the pancreas becomes stressed and progressively more dysfunctional, unable to produce enough insulin to deal with the spikes.

One symptom of insulin resistance is high glucose levels even after fasting (no food for 24 hours). In Canada, normal fasting glucose levels are <6.1 mmol/L, and optimal levels are <5.6 mmol/L. Higher levels warn that the development of diabetes is impending.

Insulin resistance is the key contributing factor to Metabolic Syndrome, which includes the following:

• Cardiovascular risk factors such as hypertension, the development of abdominal obesity and high cholesterol, and hardening of the arteries;

• Abnormalities in elevated blood triglycerides, elevated LDL (low-density lipoprotein), and reduced HDL (high-density lipoprotein);

• Development of advanced glycation end products (AGEs), i.e. the cross-linking of proteins and glucose caused by chronically elevated levels of glucose and insulin in the blood causing hyperglycemia and hyperinsulinemia.

Any combination of these symptoms is classified as metabolic syndrome. The consequences include nephropathy, neuropathy, cataracts, and atherosclerosis caused by the proliferation of foam cells in the arterial walls.

INSULIN RESISTANCE AND OBESITY

Insulin resistance and metabolic syndrome also play an important role in the obesity epidemic because excess body fat impairs insulin sensitivity.  Cells require glucose for energy production, but glucose that is not absorbed by cells is eventually converted into body fat, usually around the waist.  In this case, it is the liver that becomes resistant to insulin’s suppression of hepatic glucose production. As JD McGarry stated in his 2001 Banting lecture, “…the hyperinsulinemia turns the liver into a ‘fat-producing factory’ with all of its negative downstream effects.”   These cycles accelerate, and eventually pancreatic insulin production collapses and fat is no longer oxidized.

Because obesity has also been related to hormonal abnormalities (elevated cortisol and estrogens and waning androgens, the latter two acting to regulate fat when operating at proper levels), these issues may impede the body’s ability to metabolize glucose. These clinical markers for insulin resistance, leading to metabolic syndrome and obesity, are the precursors for Type II diabetes.

The key factor that links obesity and diabetes is inflammation. Fat cells secrete inflammatory proteins that interfere with insulin receptors, exacerbating insulin resistance. This results in hyperglycemia and pancreatic beta-cell dysfunction, especially when repeatedly exposed to oxidative stress.

KEY LIFESTYLE CHANGES TO IMPROVE INSULIN SENSITIVITY

Diabetes is modifiable, and even reversible, with the implementation of holistic lifestyle modifications, such as changes in diet, exercise, stress reduction, and the use of nutraceuticals. These modifications have a remarkable impact on prevention and treatment. Controlling insulin resistance – not the resulting high sugar levels – is the key to success.

– Anti-Inflammatory Diet

You are what you eat – that is a self-evident truth.  Foods that are highly acidic (high protein foods such as beef, pork, poultry, fish, seafood, and other meat) have a higher correlation with the production of AGEs than unrefined, alkaline foods such as fresh fruits, vegetables, whole grains, raw nuts, and other unprocessed foods. Meat, as well as refined, high sugar foods, are usually cooked or processed at high temperatures and therefore produce glycotoxins.  Here is an example:

Although broiling is believed to be a “healthier” cooking method than frying, it doesn’t make much difference whether you broil or fry a chicken breast; you will end up with about the same amount of glycotoxins: 58 kU/g and 61 kU/g, respectively. … In comparison, fresh fruits and vegetables barely make the charts for dietary glycotoxins (apples 0.13 kU/g, bananas 0.01 kU/g, and carrots 0.1 kU/g).

In addition, animal proteins like milk casein, animal fats, and heat-treated vegetable oils reduce the sensitivity of insulin.

On the other hand, whole unrefined grains and fresh fruits and vegetables have all been shown in various studies to lower blood sugar and improve insulin sensitivity. For example, quinoa is a grain that contains all nine essential amino acids, making it a complete protein. It is low on the glycemic index and has a low glycemic load, helping to reduce insulin levels by increasing insulin sensitivity. It also contains fibre, magnesium, and Vitamin E, which all enhance insulin sensitivity.

High glycemic foods such as white rice, white flour-based foods, and processed foods, are quickly converted into blood sugar, causing insulin spikes.  Low glycemic carbohydrates such as broccoli, cabbage, and green beans are slowly converted into blood sugar, causing a gradual rise in insulin levels which is much healthier.

Eating a diet rich in fibre improves insulin sensitivity and reduces circulating insulin levels. Fibre slows gastric emptying and the passage of food through the gut, slows the breakdown of high-glycemic starchy foods, and delays glucose uptake into the blood.

Healthy fats, such as cold-pressed flaxseed oil and extra virgin olive oil, have anti-inflammatory and antioxidant properties shown to protect against insulin resistance.  The omega-3s in flaxseed oil also contribute to the flexibility of cell membranes. This is important for diabetics because flexible cell membranes are much better able to respond to insulin and to absorb glucose than the stiff membranes that result when the diet is high in saturated and/or hydrogenated (trans-) fats.

– Exercise Reduces Diabetes Risk

 Exercise reduces the effect of insulin resistance.  Conditioned muscles are more responsive to insulin and blood sugar than non-conditioned muscles, possibly due to an increase in the number of insulin receptors on the muscle cell. Depending on his or her level of fitness, a person could start by walking around the block three times a day, and increase the distance from there. It should be understood, however, that the more vigorous the exercise, the more excess glucose is removed from the blood. Also remember that adrenaline/epinephrine suppresses the release of insulin. So a moderate walking pace is recommended for improving blood sugar balance.

In addition to exercise, stress reduction is crucial. Yoga, meditation, or simply sitting quietly and listening to your breath can have a calming effect.

– Nutraceuticals to Improve Blood Sugar Balance

It is also beneficial to add nutraceuticals to the equation in order to protect organs and proteins from damage caused by high blood sugar. Here is a simple, but by no means comprehensive, protocol.

ALPHA LIPOIC ACID (PREFERABLY AS R-ALPHA LIPOID ACID)

 • Influences glucose uptake and brings down blood glucose by increasing its transport into skeletal muscle

• Helps keep the body’s cells sensitive to insulin’s signals

• Lowers triglycerides

• May serve as a first line of defence against impaired energy utilization in diabetes and the associated nerve damage

• Proven effective in reducing symptoms of diabetic neuropathy (pain, burning, numbness) without significant adverse reactions

• Increases nerve conduction velocity in diabetic neuropathy sufferers, which is crucial to improved nerve signalling;  this diminishes fat oxidation in nerve cell membranes and leads to improvements in the local blood supply around nerves, a result of improved mitochondrial functioning

BENFOTIAMINE (LIPID AND WATER-SOLUBLE FORM OF VITAMIN B1)

 • Helps reverse early kidney disease in diabetics

• Its higher bioavailability strongly increases glycation-fighting thiamine levels in the blood and tissues in normal people and in sufferers of either type 1 or 2 diabetes

• Powerfully reduces AGE production and damage to vascular endothelial cells under high-glucose conditions

• Blocks three distinct pathways of sugar-induced tissue damage to protect against retinal damage in diabetes

• Works synergistically with alpha lipoic acid

• Helps relieve the pain of diabetic neuropathy

• Prevents glycotoxin-induced inflammation, endothelial dysfunction in the vascular system, and oxidative stress

CHROMIUM PICOLINATE

 • Helps support optimal insulin action, normalizing blood sugar levels and reducing total cholesterol

• Helps keep the body’s cells sensitive to insulin’s signals  by enhancing insulin-dependent transport of glucose into the cell, likely by facilitating the binding of insulin to the receptor site

• Need increases with intensive exercise

• Improves metabolism of carbs, proteins, and lipids

• Used in combination with vitamins C and E to lessen oxidative stress and reduce insulin resistance

COENZYME Q10 (PREFERABLY UBIQUINOL)

 • Improves the four pillars of metabolic syndrome: hypertension, blood lipoproteins, insulin resistance, and obesity

(Diabetics and others are often prescribed statin-type lipid-lowering medications to control their cholesterol levels. These drugs deplete CoQ10 and can cause muscle pain that may be related to this depletion. CoQ10 overcomes this problem, improving endothelial function in diabetic patients on statins.)

CURCUMIN (DERIVED FROM TURMERIC)

 • Imposes an anti-inflammatory blockade, enhancing glucose control and insulin sensitivity

• Enhances liver, kidney, and endothelial function

• Increases sugar uptake from the blood, decreases new glucose formation, and increases insulin’s effectiveness

• Blocks the formation of AGEs, including the suppression of some of the AGE-induced diabetic retinopathy, by lowering the levels of growth factors that promote capillary proliferation

• Reduces the production of inflammatory cytokines in fat tissue, lowering the burden of inflammation and insulin resistance produced by obesity

• Can mitigate diabetic neuropathy caused by high sugar levels in nerve and brain tissue

FLAXSEED OIL – OMEGA 3 EFAs

 • Lowers triglyceride levels and cholesterol circulating in the bloodstream

• Improves glycemic control  and the function of beta cells

• Reduces the risk of heart attack and stroke in patients with atherosclerosis or diabetic heart disease

• Reduces inflammation throughout the body

• Maintains the fluidity of cell membranes, allowing them to better respond to insulin and absorb glucose

• Decreases platelet aggregation, preventing excessive blood clotting

• Reduces the risk of obesity and improves the body’s ability to respond to insulin by stimulating the secretion of leptin, a hormone that helps regulate food intake, body weight, and metabolism, and is expressed primarily through adipocytes (fat cells)

• Improves insulin sensitivity, and lowers triglycerides and  inflammation.

MAGNESIUM

 • Works synergistically with fibre  to prevent diabetes

• Helps control and balance  insulin and blood sugar by improving insulin sensitivity

• Protects against metabolic syndrome, a precursor to diabetes

• Deficiency is common among diabetics, which is believed to disrupt insulin secretion and the hormone’s capacity to transport glucose

• Lowers fasting glucose levels and raises beneficial HDL in type 2 diabetics

VITAMIN C

 • Used in combination with chromium and vitamin E, it lessens oxidative stress and reduces insulin resistance

• Lowers blood glucose, inhibits glycation, prevents the accumulation of sorbitol (which causes cataracts), and synergizes and replenishes other antioxidants

• Reduces the level of C-reactive protein, helping to quench the inflammatory response in diabetics and lowering cardiovascular risk

• Is usually deficient in diabetics, so supplementation is crucial

VITAMIN D

 • Reduces susceptibility to type 2 diabetes by slowing the loss of insulin sensitivity

• Helps to control and balance insulin and blood sugar

• Helps in preventing the development and progression of diabetic heart disease

• Has been associated with insulin secretion by the beta cells of the pancreas, as well as insulin activity, once released into the bloodstream

VITAMIN E (AS MIXED TOCOPHEROLS AND MIXED TOCOTRIENOLS)

 • Enhances sensitivity to insulin and reduces oxidative stress when used in combination with chromium and vitamin C

• Helps improve vascular function and increases magnesium levels inside the cells of type 2 diabetic patients

• Minimizes diabetic complications, especially from kidney damage

• Prevents omega-3s from becoming oxidized

• Is synergistic with curcumin

CONCLUSION

Insulin resistance is a warning sign of future problems, but in order to reverse it all contributing causes must be dealt with simultaneously.  This means that the initial cause(s) of insulin resistance must be addressed – diet must be optimized. This includes the avoidance of:

1. “white” foods

2. soft drinks and sweetened beverages

3. anything containing high-fructose corn syrup

4. high-fat, grilled meats and caramelized sugars

5. hydrogenated and partially hydrogenated oils (ie. margarine, corn oil, sunflower oil, soy oil, etc.)

6. dairy products

Exercise and weight loss are integral to the process – there is no magic bullet.  The grassroots approach, using fundamental tools such as diet, exercise, stress relief, and nutraceuticals, will prevent the progression of insulin resistance to metabolic syndrome and full-blown diabetes.

References

http://www.diabetes-blood-sugar-solutions.com/guidelinesbloodsugarlevels.html

http://www.jonbarron.org/diabetes-program/01-29-2007.php

McGarry JD.:  Banting lecture 2001: dysregulation of fatty acid metabolism in the etiology of type 2 diabetes. Diabetes. 2002 Jan ;51(1):7-18.

http://www.lef.org/magazine/mag2008/apr2008_Guard-Your-Proteins-Against-Premature-Aging_01.htm

Barnard ND, et al.: The effects of a low-fat, plant-based dietary intervention on body weight, metabolism, and insulin sensitivity. Am J Med. 2005 Sep;118(9):991-7

Riccardi G, Rivellese A. Dietary treatment of the metabolic syndrome–the optimal diet. Br J Nutr. 2000 Mar;83 Suppl 1:S143-8

Chandalia M, Garg A, Lutjohann D, von Bergmann K, Grundy SM, Brinkley LJ. Beneficial effects of high dietary fiber intake in patients with type 2 diabetes mellitus. N Engl J Med. 2000 May;342(19):1392-8.

While omega 3s are more readily available from fish and fish oils, my preference is for vegetarian sources.   The reason for this is that while animal sources contain both DHA and EPA, vegetarian sources also contain alpha-linolenic acid, a complex form of omega 3.  Once it is broken down, the body then has access to ALA as well as DHA and EPA.  EPA is important because of its anti-inflammatory activity, and enhancement of the immune system.  The only time that a problem can occur in the conversion of ALA to DHA and EPA is if there is an issue with the overconsumption of omega 6s, thus inhibiting the enzyme (delta-6-desaturase) from doing its work.  A way around this is to supplement with GLA (evening primrose oil, for example) which is a metabolite of the delta-6-desaturase enzyme.

Hu FB, Manson JE, Stampfer MJ, et al. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. N Engl J Med. 2001 Sep;345(11):790-7

Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb;346(6):393-403.

Shay KP, et al.: Alpha-lipoic acid as a dietary supplement: molecular mechanisms and therapeutic potential. Biochim Biophys Acta. 2009 Oct;1790(10):1149-60. Epub 2009 Aug 4

Butler, J.A., et al.:  Lipoic acid improves hypertriglyceridemia by stimulating triacylglycerol clearance and downregulating liver triacylglycerol secretion.  Arch Biochem Biophy, February 2009

Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung. 1995 Aug;45(8):872-4.

Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week multicentre randomized controlled trial (ALADIN Study). Diabetologia. 1995 Dec;38(12):1425-33.

Sachse G, Willms B. Efficacy of thioctic acid in the therapy of peripheral diabetic neuropathy. Horm Metab Res Suppl. 1980;9:105-7.

Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week multicentre randomized controlled trial (ALADIN Study). Diabetologia. 1995 Dec;38(12):1425-33.

Tankova T, Koev D, Dakovska L. Alpha-lipoic acid in the treatment of autonomic diabetic neuropathy (controlled, randomized, open-label study). Rom J Intern Med. 2004;42(2):457-64.

Tankova T, Koev D, Dakovska L. Alpha-lipoic acid in the treatment of autonomic diabetic neuropathy (controlled, randomized, open-label study). Rom J Intern Med. 2004;42(2):457-64.

Androne L, Gavan NA, Veresiu IA, Orasan R. In vivo effect of lipoic acid on lipid peroxidation in patients with diabetic neuropathy. In Vivo. 2000 Mar-Apr;14(2):327-30.

Haak E, Usadel KH, Kusterer K, et al. Effects of alpha-lipoic acid on microcirculation in patients with peripheral diabetic neuropathy. Exp Clin Endocrinol Diabetes. 2000;108(3):168-74.

Rabbani, N., et al.:  High-dose thiamine therapy for patients with type 2 diabetes and microalbuminuria:  a randomized, double blind placebo-controlled pilot study.  Diabetologia. 2008, December 5

Volvert ML, Seyen S, Piette M, et al. Benfotiamine, a synthetic S-acyl thiamine derivative, has different mechanisms of action and a different pharmacological profile than lipid-soluble thiamine disulfide derivatives. BMC Pharmacol. 2008;8:10.

Du X, Edelstein D, Brownlee M. Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetologia. 2008 Oct;51(10):1930-2.

Stirban A, Negrean M, Stratmann B, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetes. Diabetes Care. 2006 Sep;29(9):2064-71.

Pomero F, Molinar Min A, La Selva M, Allione A, Molinatti GM, Porta M. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol. 2001;38(3):135-8.

Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.

Du X, Edelstein D, Brownlee M. Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetologia. 2008 Oct;51(10):1930-2.

Haupt E, Ledermann H, et al. Benfotiamine in the treatment of diabetic polyneuropathy: a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther. 2005 Feb;43(2):71-7.

Lau FC, et al.: Nutrigenomic basis of beneficial effects of chromium(III) on obesity and diabetes. Mol Cell Biochem. 2008 Oct;317(1-2):1-10. Epub 2008 Jul 18. Review.

Broadhurst CL, Domenico P. Clinical studies on chromium picolinate supplementation in diabetes mellitus—a review. Diabetes Technol Ther. Dec 2006 Dec;8(6):677-87.

McCarty MF. Toward a wholly nutritional therapy for type 2 diabetes. Med Hypotheses. 2000 Mar;54(3):483-7.

Albarracin CA, et al.: Chromium picolinate and biotin combination improves glucose metabolism in treated, uncontrolled overweight to obese patients with type 2 diabetes. Diabetes Metab Res Rev. 2008 Jan-Feb;24(1):41-51

Balk EM, Tatsioni A, Lichtenstein AH, Lau J, Pittas AG. Effect of chromium supplementation on glucose metabolism and lipids: a systematic review of randomized controlled trials. Diabetes Care. 2007 Aug;30(8):2154-63.

Lai, MH.  Antioxidant effects and insulin resistance improvement of chromium combined with vitamin C and E supplementation for type 2 diaabetes mellitus.  J Clin Biochem Nutr. 2008 November; 43(3):  199 – 8

Feher J, Papale A, Mannino G, Gualdi L, Balacco Gabrieli C. Mitotropic compounds for the treatment of age-related macular degeneration. The metabolic approach and a pilot study. Ophthalmologica. 2003 Sep-Oct;217(5):351-7.

Marcoff L, Thompson PD. The role of coenzyme Q10 in statin-associated myopathy: a systematic review. J Am Coll Cardiol. 2007 Jun 12;49(23):2231-7.

Hamilton SJ, Chew GT, Watts GF. Coenzyme Q10 improves endothelial dysfunction in statin-treated type 2 diabetic patients. Diabetes Care. 2009 May;32(5):810-2.

Goepp, J.:  Combating the “diabesity” epidemic.  Life Extension Magazine, p. 40, August 2010

Jain, S.K., et al:  Effect of curcumon on protein glycosylation, lipid peroxidation, and oxygen radical generation in human red blood cells exposed to high glucose levels.  Free Radic Biol Med. 2006 Ju 1; 41(1):  92 – 6

Kowluru, R.A., et al.:  Effects of curcumin on retinal oxidative stress and inflammation in diabetes.  Nutr Metab (Lond). 2007; 4:8

Woo, H.M., et al.:  Active spice-derived components can inhibit inflammatory responses of adipose tissue in obesity by suppressing inflammatory actions of macrophages and release of monocyte chemoattractant protein-1 from adipocytes.  Life Sci. 2007 Feb 13; 80(10): 926 – 31

Gonzales, A.M., Orlando, R.A.:  Curcumin and resveratrol inhibit nuclear factor-kappaB-mediated cytokine expression in adipocytes.  Nutr Metab (Lond). 2008;5:17

Flachs P, et al.: Cellular and molecular effects of n-3 polyunsaturated fatty acids on adipose tissue biology and metabolism. Clin Sci (Lond). 2009 Jan;116(1):1-16. Review

Popp-Snijders C, Schouten JA, Heine RJ, et al. Dietary supplementation of omega-3 polyunsaturated fatty acids improves insulin sensitivity in non-insulin-dependent diabetes. Diabetes Res 1987 Mar;4(3):141-7 1987. PMID:8990.

Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, Jebb SA. Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Int J Obes (Lond).  2006 October  30(10):1535-44.

Schulze MB, Schulz M, Heidemann C, Schienkiewitz A, Hoffmann K, Boeing H. Fiber and magnesium intake and incidence of type 2 diabetes: a prospective study and meta-analysis. Arch Intern Med. 2007 May 14;167(9):956-65.

Chaudhary DP, et al.: Implications of Magnesium Deficiency in Type 2 Diabetes: A Review. Biol Trace Elem Res. 2009 Jul 24.

Masood N, et al.: Serum zinc and magnesium in type-2 diabetic patients. J Coll Physicians Surg Pak. 2009 Aug;19(8):483-6

Rodriguez-Moran, M., et al.:  Oral magnesium supplementation improves insulina sensitivity and metabolic control in type 2 diabetic subjects:  a randomized double-blind controlled trial.  Diabetes Care. 2003 Apr; 26(4):  1147 – 52

Liu S, Sonh Y, Ford ES, Manson JE, Buring JE, Ridker PM. Dietary calcium, vitamin D, and the prevalence of metabolic syndrome in middle-aged and older US women. Diabetes Care. 2005 Dec;28(12):2926-32.

Song, Y., et al.:  Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes;  a meta análisis of randomized double-blind controlled trials.  Diabet Med.  2006 Oct; 23(10): 1050 – 6

Lai, MH.  Antioxidant effects and insulin resistance improvement of chromium combined with vitamin C and E supplementation for type 2 diaabetes mellitus.  J Clin Biochem Nutr. 2008 November; 43(3):  199 – 8

Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ. Baseline serum 25-hydroxy vitamin D is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000. Diabetes. 2008 Oct;57(10):2619-25.

Liu S, Sonh Y, Ford ES, Manson JE, Buring JE, Ridker PM. Dietary calcium, vitamin D, and the prevalence of metabolic syndrome in middle-aged and older US women. Diabetes Care. 2005 Dec;28(12):2926-32.

Alvarez JA and Ashraf A. Role of Vitamin D in Insulin Secretion and Insulin Sensitivity for Glucose Homeostasis. International Journal of Endocrinology, vol. 2010, Article ID 351385, 18 pages. 2010

Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ. Baseline serum 25-hydroxy vitamin D is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000. Diabetes. 2008 Oct;57(10):2619-25.

Oh J, et al. 1,25 (OH) vitamin D inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus. Circulation  2009 August

Lai, MH.  Antioxidant effects and insulin resistance improvement of chromium combined with vitamin C and E supplementation for type 2 diaabetes mellitus.  J Clin Biochem Nutr. 2008 November; 43(3):  199 – 8

Wu, J.H., et al:  Effects of alpha-tocopherol and mixed tocopherol supplementation on markers of oxidative stress and inflammation in type 2 diabetes.  Clin Chem. 2007 Mar; 53(3):  511 – 9

Devaraj, S., et al.:  Gamma-tocopherol supplementation alone and in combination with alpha-tocopherol alters biomarkers of oxidative stress and inflammation in subjects with metabolic syndrome.  Free Radic Biol Med.  2008 Mar 15; 44(6): 1203 – 8

Rizzo, M.R., et al.:  Evidence for anti-inflammatory effects of combined administration of vitamina E and C in older persons with impaired casting glucose:  impacto n insulina action.  J Am Coll Nutr.  2008 Aug; 27(4):  505 – 11

Paolisso, G., et al.:  Chronic vitamin E administration improves brachial reactivity and increases intracellular magnesium concentration in type II diabetic patients.  J. Clin Endocrinol Metab.  2000 Jan; 85(1) 109 – 15

Kuhad A, Chopra K. Attenuation of diabetic nephropathy by tocotrienol: involvement of NFkB signaling pathway. Life Sci.   2009 February  84(9-10):296-301.

Ludwig, David S., et al.:  Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. The Lancet, Volume 357, Issue 9255, Pages 505 – 508, 17 February 2001

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