I have no simple answer for you, unfortunately.
You can lower your risk of type 2 diabetes significantly by avoiding overweight and obesity, by exercising regularly, and by choosing the right parents. These provide clues as to the causes of diabetes. The Mediterranean diet also prevents diabetes.
UpToDate.com offers a deceptively simple answer:
Type 2 diabetes mellitus is caused by a combination of varying degrees of insulin resistance and relative insulin deficiency. [Insulin is the pancreas hormone that lowers blood sugar.] Its occurrence most likely represents a complex interaction among many genes and environmental factors, which are different among different populations and individuals.
So, what causes the insulin resistance and relative insulin deficiency?
Understanding the pathogenesis [cause] of type 2 diabetes is complicated by several factors. Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes. Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state.
The UpToDate article then drones on for a several thousand words discussing mouse studies, various genes, free fatty acids, adiponectin, leptin, amylin, insulin secretion, insulin resistance, impaired insulin processing, insulin action, body fat distribution, inflammation, various inflammatory markers, low birth weight, high birth rate, prematurity, etc. More excerpts:
Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors, have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications.
Insulin resistance may, at least in part, be related to substances secreted by adipocytes [fat cells] (“adipokines” including leptin adiponectin, tumor necrosis factor alpha, and resistin).
Type 2 diabetes most likely represents a complex interaction among many genes and environmental factors.
That’s the simplest answer I can give now.
Reference: “The Pathogensis of Type 2 Diabetes Mellitus” by David K McCulloch, MD, and R Paul Robertson, MD, at UpToDate.com, updated June 2012, and accessed November 19, 2012.
10 responses to “What Causes Type 2 Diabetes?”
Yes, I believe you have 50 % of issue but object to this circling of the wagons on the genes adn lower pancreas output. Factors to be sure but overlooking the effects and actions of thje liver and balance of the system involving the rest of the complex chemical plant involved in digestion.
The present fanaticism to stare at the front part of the cycle involving the front part of cycle – input, digestion and insulin while critical for type 1 diagnosis completely ovelooks the back half of the cycle involving the absorption, consumption, storage and burn of glucose and offering no real solution to type 2 diabetes and involved hormones from thyroid, liver, intesttines, skeletal muscles and fat cells.
Please take off the black eye shades and start using science properly to analyze the full cycle and lets get this mess under control. In addition, lets get some 23rd century tools to watch the human body 24/7 and its chemical plant and properly tune it to get it back into the correct quadrent for healthier operation.
Jim, the authors of the UpToDate.com review article are typically medical school professors who are paid (I assume) to do a thorough review. With my limited time and resources, it’s hard for me to out-do them.
Well, the big problem is the word “cause.” “Cause” has a lot of baggage and is in a sense a very comprehensive and final word, like proof, and truth. Cause therefore represents an ideal, not a reality.
So, getting past that issue is a big step. We could then more reasonably ask: what are the factors that are associated with the onset of Diabetes?
Obesity is one, but that raises its own issues of “cause…” The idea is to keep it simple, so obesity has to be included, but what do we associate with obesity: Excess consumption of PUFA, wheat, and table sugar and fructose. How much is excess? Anything that tends to cause obesity and diabetes.
And we could say that fat people do not exercise and so they are fat, but from what I have seen and read, fat people don’t engage in strenuous exercise precisely because they are fat. It doesn’t feel good and they don’t want to do it. Exercise will make people feel better, and it’s part of the solution, but life isn’t that simple. So simple “movement” (like walking) has to be part of avoiding obesity and diabetes.
So what do people need to eat to avoid diabetes? More saturated fat and green vegetables, and various colored vegetables, while avoiding PUFA and wheat and the too-sweet sugars. That should result in weight loss too.
Is that so difficult?
“Is that so difficult?” Apparently it is, for many folks.
I agree that avoiding over-consumption of refined grains, concentrated sweets, and PUFA helps with obesity prevention. A recent epidemiologic study linked high fructose corn syrup with type 2 diabetes, but I don’t know if they factored out (controlled for) obesity.
More recent is the “acellular carbohydrate theory of obesity”: http://paleodiabetic.com/2012/11/28/could-acellular-carbohydrates-be-the-cause-of-obesity/
You really want saturated fat plus seafood omega 3; the omega 3 decreases gluconeogenesis.
You can have insulin sensitivity too:
“In type 2 diabetes, hepatic insulin resistance is associated with increased glucose production (HGP) and ApoB-containing lipoprotein secretion. The former is arguably the cause of deteriorating glucose control experienced by most diabetic patients over time, regardless of therapy (Monnier et al., 2003). The latter underpins the predisposition to atherosclerosis, which ultimately will be responsible for nearly one in two deaths among diabetics (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).
But the two abnormalities can hardly be subsumed under the common rubric of insulin resistance. For while it’s increasingly clear—and strongly supported by the papers by Kubota et al. and Dong et al. in this issue (Kubota et al., 2008; Dong et al., 2008)—that an impairment of insulin receptor signaling to Foxo1 can explain insulin’s inability to restrain HGP, one would predict that, if the liver were wholly insulin resistant, triglyceride (TG) synthesis and assembly into ApoB-containing lipoproteins would also be impaired. But the opposite is true in the diabetic liver.
In recent years, the idea that the diabetic liver may harbor a noxious brew of insulin resistance and excessive insulin sensitivity has gained a second wind. The concept is neither new nor limited to the liver. Several manifestations of insulin resistance—e.g., polycystic ovarian disease and acanthosis nigricans—reflect excessive rather than reduced insulin signaling. But whereas in those tissues insulin can act through IGF-1 receptors—if blood insulin levels are high enough—hepatocytes lack IGF-1 receptors, and thus the explanation for the metabolic admixture of sensitivity and resistance to insulin in liver must reside within the different branches of insulin receptor signaling.”
George, thanks for that erudite comment.
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