Why Is Meat a Risk Factor for Diabetes?

We’ve known that being overweight and obese are important risk factors for type 2 diabetes, but until recently, not much attention has been paid to the role of specific foods.

A 2013 meta-analysis of all the cohorts looking at meat and diabetes found significantly higher risk associated with total meat consumption, and especially processed meat—particularly poultry. But why?

There’s a whole list of potential culprits in meat. Maybe it’s the saturated fat and animal fat. Maybe it’s the trans-fats that are naturally found in meat. Maybe it’s the cholesterol, or the animal protein. The heme iron in meat can lead to free radicals, and this iron-induced oxidative stress may lead to chronic inflammation, and type 2 diabetes. Advanced glycation end products (AGEs) are another problem. They promote oxidative stress and inflammation, and food analyses show that the highest levels of these so-called glycotoxins are found in meat—particularly roasted, fried, or broiled meat, though any foods from animal sources can be potent sources of these pro-oxidant chemicals. In this study, they fed diabetics foods packed with glycotoxins, like chicken, fish, and eggs, and their inflammatory markers shot up—such as tumor necrosis factor, C-reactive protein, and vascular adhesion molecules. Thus, in diabetes, dietary AGEs promote inflammatory mediators, leading to tissue injury. The good news, though, is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating these foods, or sticking with just steaming and boiling meat, may greatly reduce the already heavy burden of these toxins in the diabetic patient. These glycotoxins may be the missing link between the increased consumption of animal fat and meats, and the development of type 2 diabetes in the first place.

Since the 2013 meta-analysis was published, this study came out, in which about 17,000 people were followed for about a dozen years. They found an 8% increase in risk for every 50 grams of daily meat consumption. So, that’s just like a quarter of a chicken breast’s worth of meat for the entire day may significantly increase the risk of diabetes. Yes, it could be the glycotoxins in meat, or the saturated fat, or the trans-fat in meat, or the heme iron, which could actually promote the formation of carcinogens called nitrosamines (though they could also just be produced in the cooking process itself). But this is new. There appears to be a clear excess of diabetes in those who handle meat for a living. Maybe there’s some kind of diabetes-causing zoonotic infectious agents, like viruses present in fresh cuts of meat, including poultry.

Overstimulation of the aging enzyme TOR pathway by excess food consumption may be a crucial factor underlying the diabetes epidemic—but not just any food. Animal proteins may not only stimulate IGF-1, but provide high amounts of leucine, which stimulates TOR activation, and appears to burn out the insulin-producing beta cells in the pancreas and contribute to type 2 diabetes. So, it’s not just the high fat and added sugars; critical attention has to be paid to the daily intake of animal protein.

In general, lower leucine levels are really reached only by the restriction of animal protein. As I noted before, to reach the leucine intake provided by dairy or meat, we’d have to eat nine pounds of cabbage or 100 apples. These calculations exemplify the extreme differences in leucine amounts provided by a more standard diet in comparison to a more plant-based diet.

I’ve previously reviewed the role endocrine-disrupting industrial pollutants in the food supply may play, in a three-part video series. Clearly, the standard American diet and lifestyle contribute to the epidemic of diabetes and obesity, but these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and therefore may be an underappreciated cause of obesity and diabetes. Consider what’s happening to our infants: obesity in a six-month old is not related to diet or lack of exercise. They’re now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (obesity generating). The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live, and the choices we make every day in the food we eat. As this 2014 review of the evidence on pollutants and diabetes noted, yes, we can be exposed through some toxic spill, but most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of persistent pollutant intake is through dietary intake of animal fat.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

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• R Zoncu, A Efeyan, DM Sabatin. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol. 2011 Jan;12(1):21-35
• EJ Feskens, D Sluik, GJ van Woudenbergh. Meat consumption, diabetes, and its complications. Curr Diab Rep. 2013 Apr;13(2):298-306
• MA Hyman MA. Environmental toxins, obesity, and diabetes: an emerging risk factor. Altern Ther Health Med. 2010 Mar-Apr;16(2):56-8
• M Peppa, T Goldberg, W Cai, E Rayfield, H Vlassara. Glycotoxins: a missing link in the "relationship of dietary fat and meat intake in relation to risk of type 2 diabetes in men". Diabetes Care. 2002 Oct;25(10):1898-9
• BC Melnik. Leucine signaling in the pathogenesis of type 2 diabetes and obesity. World J Diabetes. 2012 Mar 15;3(3):38-53
• T Koschinsky, CJ He, T Mitsuhash, R Bucala, C Liu, C Buenting, K Heitmann, H Vlassara. Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6474-9
• DJ Magliano, VH Loh, JL Harding, J Botton, JE Shaw. Persistent organic pollutants and diabetes: a review of the epidemiological evidence. Diabetes Metab. 2014 Feb;40(1):1-14

Images thanks to Radu Razvan via 123rf.

• advanced glycation end-products (AGEs)
• animal fat
• animal products
• antioxidants
• boiling
• C-reactive protein
• carcinogens
• chicken
• children
• cholesterol
• cooking methods
• diabetes
• eggs
• exercise
• fat
• fish
• glycotoxins
• heavy metals
• heme iron
• IGF-1
• industrial pollutants
• infants
• inflammation
• insulin
• meat
• nitrosamines
• obesity
• obesogens
• oxidative stress
• phytonutrients
• poultry
• pregnancy
• processed meat
• saturated fat
• trans fats
• turkey
• weight loss
• zoonotic disease