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Monday, 26 May 2014

Diabetes as an Iatrogenic Disease - the Indian Experience

Diabetes and dairy fat in India.

     The epidemics of diabetes, cardiovascular disease and related conditions in India have been called iatrogenic (Raheja B.S. 1994), a product of diets high in linoleic acid as a result of “chasing the phantom of cholesterol” (Raheja et al. 1993). The traditional Indian diet (39% fat) supplied 20.3%E as saturated fats, mainly from ghee, with 5% from linoleic acid. Concerns that this diet is atherogenic have resulted in replacement of ghee with high-linoleate oils; the modern urban diet being 31.9% fat, with 5.6%E as saturated fat, and 16.9% linoleic acid (Raheja, B.S. et al. 1993).
   
     In children and young individuals, a high intake of n-6 PUFA is correlated with fasting hyperinsulinaemia, and dietary supplementation with n-3 PUFA leads to an improved lipid profile but not insulin sensitivity. In adults, high-carbohydrate meal consumption was reported to cause hyperinsulinaemia, postprandial hyperglycaemia and hypertriacylglycerolaemia. (Misra, A. 2009).



The association of ghee consumption in the Indian diet with a lower rate of diabetes is consistent with the correlation between serum markers of dairy fat consumption and reduced diabetes risk (Mozaffarian et al. 2010, 2013). The NZ Ministry of Health currently recommends a wide range of linoleic acid and alpha-linolenic acid in the diet; the lower recommended intake of LA being 4%, the upper being 10%, and the lower recommended intake of ALA being 0.4%, the upper 1% (the omega 6-3 ratio at median intakes thus being 10:1). Saturated fat intake below 10%E is recommended. (Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. 2012 MOH).

     The message from the Indian researchers into the causes of their diabetes epidemic is that higher consumption of dairy fat protected marginal dietary omega-3 intake from abrogation by excessive intakes of omega-6 fatty acids. Replacing highly saturated dairy fats with diets higher in linoleic acid and refined carbohydrate, which is the same effect that the campaign against saturated fat has had among more disadvantaged New Zealanders, has increased the rate of diabetes, which is consistent with the New Zealand experience, suggesting that the increased incidence of diabetes in New Zealand has been in large part an iatrogenic phenomenon.

     "T
he present epidemic of DM and ACVD in Asian indians and possibly in other communities is iatrogenic resulting from what may be called modern malnutrition due to increased intake of total and n-6 fats and decreased intake of n-3 fat and antioxidants. Such a diet induces oxidative stress and activates the immune system. Imbalance between n-6 and n-3 fats result in inappropriate immune response. It also leads to increased and unbalanced biosynthesis of metabolites of n-6 fats. These are immune suppressive, proinflammatory and thrombogenic. They also contribute to insulin resistance and dyslipidemias. This makes DM and atherosclerosis as malnutrition related oxidative immune inflammatory disorders. Various risk factors are also the result of the same inappropriate response. Our intervention studies give considerable support to this hypothesis. It is suggested that simple correction of diet defects can reverse the disease process and thereby offer a simple, practical therapeutic option not only for the primary prevention of each of these disorders or their complications but also for the so called risk factors for these diseases. It is suggested that the real remedy for DM, ACVD and all the risk factors lies not in drugs or surgery but in the kitchen."
- B. S. Raheja

Misra, A. et al. (2009). South Asian diets and insulin resistance. Br J Nutr. 2009 Feb;101(4):465-73. doi: 10.1017/S0007114508073649

Mozaffarian, D. et al. (2010). Trans-Palmitoleic Acid, Metabolic Risk Factors, and New-Onset Diabetes in US Adults. Ann Intern Med. Dec 21, 2010; 153(12): 790–799. doi:  10.1059/0003-4819-153-12-201012210-00005

Mozaffarian D. et al. (2013). Trans-Palmitoleic acid, other dairy fat biomarkers, and incident diabetes: the Multi-Ethnic Study of Atherosclerosis (MESA). Am J Clin Nutr. 2013 Apr;97(4):854-61. doi: 10.3945/ajcn.112.045468.

Raheja B.S. (1994). Diabetes and atherosclerosis as immune-inflammatory disorders: options for reversal of disease processes. J Assoc Physicians India. 1994 May;42(5):385-90, 395-6. PMID:7829439

Raheja, B.S. et al. (1993). Significance of the N-6/N-3 Ratio for Insulin Action in Diabetes. Annals of the New York Academy of Sciences, 683: 258–271. doi: 10.1111/j.1749-6632.1993.tb35715.x

Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. (2012) New Zealand Ministry of Health.
http://www.health.govt.nz/system/files/documents/publications/food-and-nutrition-guidelines-for-healthy-children-and-young-people-p4.pdf

5 comments:

Tucker Goodrich said...

Great post. Are you familiar with Malhotra's 1967 paper, "Epidemiology of Iscaemic Heart Disease in India with Special Reference to Causation"?

"...Our data, however, do not support this association of high fat intake with the liability to develop ischemic heart disease, because while in the north the consumption of fats, most of which are animal fats, is 19 times more than in the south (Indian Council of Medical Research, 1964), the disease is 7 times less in the north than in the south. Moreover, while the milk fats eaten in the north have a preponderance of
saturated fatty acids, the seed oils used in the south are mainly composed of unsaturated fatty acids (Indian Council of Medical Research, 1963). This inverse association is noteworthy, especially because others have also observed this association of high intake of animal fats and freedom from cardiovascular disease (Shaffer et al., 1964; Shaper, Jones, and Kyobe, 1961; Mann, Shaffer, and Rich, 1965)."

Simplie Amazing said...

"Such a diet induces oxidative stress and activates the immune system."

I would say that the elevated OS actually overwhelms the immune system first, leaving TLR 2,4 signaling impotent to maintain N-O levels. (pun intended)...the absence of N-O then allows increased ROS/atherosclerosis.

George Henderson said...

Here's the Malhotra paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487855/pdf/brheartj00329-0083.pdf
thanks for that tip.

Raheja's diabetes mechanism, via prostaglandins that direct insulin response, with excess of n-6 products suppressing phase 1 insulin response and promoting phase 2 (the delayed insulin response characteristic of DM2), shows that immunity is governing metabolism in this regard.
It also explains the amylase gene adaptation to carbohydrate; salivary amylase level determines first phase insulin response to starch. Perhaps through prostaglandins released through the sublingual immune pathways, whatever they are.
Omega 3s are part of the endothelial NO system (critical for liver health too - NO is antifibrotic), superoxide from OS /reductive stress output quenches NO to ONOO.

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