Diabetes: Causes

Is diabetes caused by poor diet or lack of exercise or both?

Yes and no. Diet, as the research has consistently shown, is the main contributing factor to the prevention, progression, and reversal of type II diabetes. According to the Center for Disease Control and prevention (2017c), individuals at high risk for developing diabetes can delay or prevent the onset of the disease by losing weight, exercising (approximately 30 minutes a day, 5 days a week) and eating a healthier diet.

Eating You Alive – Ray Cronise “Diet or Exercise?”

Multiple studies have shown that providing lifestyle advice to individuals, such as eating a healthier diet, consisting of lower fat foods, less oil, less meat, less dairy, high fiber, more fruits, more vegetables and daily physical activity along with losing weight reduces the risk of developing type II diabetes (Pan, 1997; Tuomilehto, 2001; Diabetes Prevention Program, 2002; Salas-Salvadó, 2011). Sugar sweetened beverages also play a significant role in the development of type II diabetes. According to Schulze et al., (2004) “Besides their potential contribution to weight gain, sugar-sweetened soft drinks might also increase risk of type 2 diabetes because of their high amount of rapidly absorbable carbohydrates” (p. 933).  

Simple sugars, or simple carbohydrates, such as table sugar also play a role in the development of type II diabetes. The Center for Science in the Public Interest developed the video below explaining the risk associated with consuming sugar sweetened beverages.

While exercise is essential for optimal health general day to day activities that keep individuals up and moving around may be beneficial to reducing the risk of diabetes. According to Hu, Li, Colditz, Willett & Manson (2003), “Standing or walking around at home was associated with a modestly lower risk of diabetes” (p. 1788). Therefore light to moderate, non-strenuous, walking is encouraged. Always seek medical advice before starting any exercise program. 


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A clue to the cause of type II diabetes?

Insulin resistance plays a key role in the development of type II diabetes according to the Center for Disease Control and prevention ([CDC], 2016). However, the CDC (2016) states “it isn’t clear exactly what causes insulin resistance.” In regards to the cause of type II diabetes Insulin resistance plays a key role in the development of the disease however, the “exact mechanism” is unknown (para. 8). While all the contributing factors, or causes, of type II diabetes may take years to fully understand, because there are a variety of contributing factors to the disease, it seems that researchers consistently reach the same conclusion. According to John McDougall, MD (2012), a board certified internist, physician, and low fat plant-based advocate promoting a starch based diet, “fat paralyzes insulin, making diabetes worse” (para. 42). Dr. McDougall has written many books on the topic of diabetes and has been reversing type II diabetes in his patients since the 1970’s. He treats the cause of the disease, which he attributes to the rich western diet high in animal products and fat. In his view, animal products and fat are the main contributor to the development of diabetes and many other chronic western diseases. While moderate weight loss and exercise is important The American Diabetes Association (2008) also recognizes that “…dietary strategies including reduced calories and reduced intake of dietary fat, can reduce the risk for developing diabetes and are therefore recommended” (p. S63). Research has shown that increased levels of dietary fat lead to a condition called insulin resistance. According to Taylor (2012) the cause of insulin resistance seems to be the presence of excess fat stored within muscle cells as well as intra organ fat stores, which eventually culminates into diabetes (Taylor, 2012, p. 267).

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What causes insulin resistance?

The cause of insulin resistance seems to be the presence of excess fat stored within muscle cells as well as intra organ fat stores, which eventually culminates into diabetes (Taylor, 2012). According to Lichenstein and Schwab (2000), “saturated fat, relative to monounsaturated and polyunsaturated fat, appears to be more deleterious with respect to fat-induced insulin sensitivity” (p.227). Estadella et al. (2013) recognize that the types of fat that leads to insulin resistance is saturated fat and trans fats, which are found in meat and dairy products as well as oils (p.1). Their research lead them to the conclusion that daily dietary choices, the consumption of meat and dairy as well as tropical oils, which are the only source of high levels of saturated and trans fat in the diet that could lead to the development of type II diabetes. Therefore, dietary pattern may be the number one predictor of developing insulin resistance.

Insulin resistance means the muscle tissue has become resistant to insulin. Meaning Insulin is not readily absorb by the muscle cells.

Dr. Michael Greger of Nutritionfacts.org explains insulin resistance in this video.

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Is insulin resistance responsible for Type II Diabetes?

A consensus statement written by the American Diabetes Association ([ADA], 2000) stated that in regards to diabetes “the evolution from normal to impaired glucose tolerance is associated with a worsening of insulin resistance” (p. 384) and “it is well recognized that resistance to insulin-stimulated glucose uptake is a characteristic finding in patients with type 2 diabetes and impaired glucose tolerance” (p. 384). The ADA (2002) also noted that the “the failure of the Beta-cell to continue to hypersecrete insulin underlies the transition from insulin resistance (with compensatory hyperinsulinemia and normoglycemia) to clinical diabetes (with overt fasting hyperglycemia and increased hepatic glucose production)” (p.384).

In other words, as the muscle cells gradually lose their ability to effectively absorb glucose from the bloodstream the beta producing cells of the pancreas slow the production of insulin while the liver produces more sugar. Over the course of years this culminates in the development of type II diabetes.

According to Hannon, Rao, and Arslanian (2002), “insulin resistance which develops as a result of both genetic and environmental factors, is strongly associated with obesity. Moreover, insulin resistance is now widely believed to be the first step in the development of T2DM, cardiovascular disease and other conditions” (pp. 473-474).

According to Scrauwen-Hinderling, Hesselink, Schrauwen, & Kooi (2006) “physically inactive humans consuming a high-energy, high-fat diet, a positive energy and fat balance may occur chronically, resulting in fat accumulation in adipose tissue and probably also in skeletal muscle” (p. 362). According to Kraegen and Cooney (2008) the “acute exposure to fatty acids causes insulin resistance in muscle, and excess dietary lipid and obesity are strongly associated with muscle insulin resistance” (abstract, para. 1). Thus meaning, the ingestion of fat impairs the muscle cells ability to effectively uptake insulin. Which leads to excess sugar in the blood stream. Individuals who are overweight or obese (having excess adipose tissue, or fat) tend to be at increased risk for developing diabetes. Researchers concluded “whether the initial events leading to muscle insulin resistance are direct effects of fatty acids in muscle or are secondary to lipid accumulation in adipose tissue or liver remains to be clarified” (Kraegen and Cooney, 2008, abstract, para. 3).

According to Scrauwen-Hinderling, et al., (2006), “fat can be stored not only in adipose tissue but in other tissues such as skeletal muscle” (P. 357). Fat droplets contained within the muscle cells, intramyocellular lipids (IMCL), are “valuable energy stores during prolonged exercise, which, however, in the absence of regular physical activity and with overconsumption of fat, can have detrimental effects on muscular insulin sensitivity” (Schrauwen-Hinderling et al., p. 357). This excess consumption of fat leads to an accumulation of fat droplets in all skeletal muscle within the body and has been given the name intramyocellular lipids.

Intra = Inside, myo = muscle, cellular = cell, lipids = fat. Intramyocellular lipid (IMCL) means fat within the muscle cell

According to Scrauwen-Hinderling et al. (2006) excess fat or the:

elevation of plasma fatty acid levels or dietary fat content also increases IMCL content, suggesting that skeletal muscle also stores fat simply if the availability of fatty acids is high under these conditions, the uptake into skeletal muscle may have negative consequences on insulin sensitivity (p. 357).

Rachek, (2013), recognizes that “Lipotoxicity, characterized by the accumulation of ectopic lipids in skeletal muscle, is a major factor in the etiologies of insulin resistance and type 2 diabetes” (p. 269).

Lipo = Fat, Toxicity = toxic, excess fat is toxic; Ectopic = in an abnormal place; Etiologies = the cause of a disease. The cause of disease is fat where it doesn’t belong, which increases the risk of insulin resistance and can eventually lead to the development of type 2 diabetes.

Rachek, (2013) continues that “the development of skeletal muscle insulin resistance can be independent of a family history of type 2 diabetes” (p. 269). This means family history/genetics may not be a determining factor in the development of insulin resistance in some individuals. Unger, Clark, Scherer, and Orci, (2010) further clarified this statement “although genes determine susceptibility to environmental factors, the epidemic is clearly due to increased consumption of calorie-dense, highly lipogenic foods, coupled with a marked decrease in physical exertion resulting from modern technologies” (Para. 1).

*Lipo = fat, genic = creation of. Researchers believe that our sedentary lifestyles along with the excess consumption of high fats foods results in the progression of type II diabetes.

Dr. Neal Barnard – “Genes are not dictators”

In this Video Clip by Dr. Neal Barnard he explains how fats play a large role in the development of insulin resistance which over time results in the development of type II diabetes.

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How does insulin resistance lead to the development of type II diabetes?

Taylor (2013) recognizes that “people who are relatively insulin resistant in muscle-and who therefore have a raised plasma insulin level-are especially likely to accumulate fat in the liver” and as fat builds up in our organs their ability to function properly diminishes (p. 269). In the case of the liver, “Nonalcoholic fatty liver disease is the buildup of fat in the liver that is NOT caused by drinking too much alcohol” and risk factors include insulin resistance (Medline Plus, 2016). Based upon this information if Nonalcoholic fatty liver disease is not caused by drinking alcohol it must be caused by something in our diets and Almeda-Valdes, Cuevas-Ramos, and Aquilar-Salinas, (2009) state lipotoxicity increases the risk of both nonalcoholic fatty liver disease and metabolic syndrome.

Lipotoxicity: Lipo = Fat, Toxicity = Toxic; toxic fat within the body.  

According to Estedalla et al. (2013) the:

Composition of the diet exerts an important role in the development of non-alcoholic fatty liver disease and its treatment and that it is essential to consider excessive saturated fatty acid intake as a critical risk factor for development of non-alcoholic fatty liver disease (p. 6).   


The video below explains Taylors research along with his results showing that a calorie restricted diet can reverse type II diabetes. A caloric restriction diet is not recommended but a whole foods plat-based diet is. Following a whole foods plant based diet consisting of 10 to 15% of calories from fat also has been shown to produce the same results.

One show …fatty liver & Diabetes Reversal

The consumption of excess fat within the diet, for a few days or years, leads to fat storage either subcutaneously, viscerally or in the liver. As fat continues to build in muscle cells and organs glucose can no longer effectively enter due to insulin resistance. Excess carbohydrate in the presence of fat is therefore turned into fat by a process of de novo lipogenesis (Taylor, 2013 p. 268-269).

De novo lipogenesis: De novo = to begin new, lipo = fat, genesis = creation. De novo lipogenesis means the creation of new fat.

This means glucose is only turned into fat by our body, in the presence of excess fat within the diet and on the body. The ingestion of excess fat causes de novo lipogenesis from glucose but according to Taylor (2013) “this process only happens in the liver in humans, and triglycerides synthesized in situ is particularly likely to be stored in hepatocytes rather than exported for storage subcutaneously” (p. 268). This means that as glucose reaches the liver in the presence of excess fat the sugar is stored as fat in the liver. Taylor’s (2013) research also indicates that as fat continues to store within the liver “this will cause relative resistance to insulin suppression of hepatic glucose production” which eventually results in a cycle of hyperinsulinaemia (P. 269).


According to Taylor (2012):

A vicious cycle of hyperinsulinaemia and increased liver fat will become established. Fatty liver leads to increased export of VLDL triacylglycerol, which will increase fat delivery to the islets, with excess fatty acid availability impairing the acute insulin secretion in response to ingested food. Eventually the fatty acid and glucose inhibitory effects on the islets will reach a trigger level, precipitating clinical diabetes (p. 269).

Taylor (2012) concluded that:

These self-reinforcing cycles between liver and pancreas eventually cause metabolic inhibition of insulin secretion after meals and onset of hyperglycemia. It is now clear that type 2 diabetes is a reversible condition of intra-organ fat excess to which some people are more susceptible than others (p. 267).

A representative model of “The twin cycles of type 2 diabetes Mellitus”

Image and text below retrieved 9/14/2016 from Taylor, R. 2013: http://onlinelibrary.wiley.com/doi/10.1111/dme.12039/epdf

This bicycle is controlled by handlebars representing chronic, excess (XS) calorie intake in the presence of muscle insulin resistance. Raised plasma insulin levels will expedite chronic excess calorie storage from carbohydrate via de novo lipogenesis, and hence promote liver fat storage. This will cause the liver to become relatively resistant to insulin and a small increase in plasma glucose will occur. In turn, insulin secretion will increase to control plasma glucose down. The further increased insulin levels will bring about a self-reinforcing cycle. Excess fat will result in increased export of VLDL (very low density lipoprotein) triglyceride from the liver, uptake by islets and inhibition of meal insulin secretion. At a personal threshold, the pancreas fat becomes too great a load and plasma glucose levels will then rise relatively rapidly. As the body becomes more insulin resistant it suppresses HGP, hepatic glucose production and leading to the development of fatty liver disease.

What causes diabetes?

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What foods are associated with increases in insulin resistance?

The foods associated with increased insulin resistance include those foods which contain large amounts of saturated fat. Those foods are meat (red meat, fish, pork, eggs, and poultry) and dairy, as well as oils including palm oil, palm kernel oil, coconut and coconut oil.

As Estadella et al. (2013) and Food and Drug Administration (2016) recognize that saturated fat and trans fats are found in all meat and dairy products as well as oils, including tropical oils. This includes all types of meat as well as eggs. Dairy products consist of milk, yogurt, cheese, cottage cheese, cream cheese, sour cream, and butter. While these are not exhaustive lists, these foods contain both saturated fats and trans fats which have not only been associated with the progression of diabetes but also heart disease, dyslipidemia, and obesity (Estadella et al., 2013, p. 1).

Dr Michael Greger, MD discusses diabetes and the dangers of low carb

Low carbohydrate, high protein, high fat diets have been popularized in many books and go by names like Atkins, Paleo, Grain Brain, and Wheat Belly. These diets are easy to follow and are very convenient for most people. These can also be considered fast food diets or window diets, where you pull up to a fast food window, order a burger, throw away the bun and you have a meal. Simple, easy! However, researchers have found that the short term benefits experienced by those following low carbohydrate diets may have long term health implications such as an increased risk of all cause mortality.

Recently, two published studies have shown the negative effects of low carbohydrate, or high animal protein diets. According to Lagiou et al., (2012), low carbohydrate or high protein diets have “… the potential for considerable adverse effects on cardiovascular health of these diets when they are used on a regular basis…” (P. 6). Another similar study published by Fung et al., (2010) concluded that “consumption of a vegetable-based low-carbohydrate diet were associated with a lower risk of all –cause and CVD (cardiovascular disease) mortality whereas a high scores for the animal-based low-carbohydrate diet were associated with a higher risk of overall mortality” (p. 8).

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