Causal Relationships between Diabetes and Heart Disease

The leading cause of death in the United States is heart disease, affecting one in four people (both men and women). Finding the cause, or following the causal links, may lead to strategies for prevention. One of the causal links appears to be Type II diabetes.

Before they show signs of Type II diabetes, however, many people develop what is called Metabolic Syndrome or Syndrome X. There is evidence that Metabolic Syndrome predisposes people to both Type II diabetes and heart disease. The problem with diagnosing Metabolic Syndrome is that it consists of more than one symptom or marker. One marker is obesity, especially if body fat accumulates at the waistline which signals that the body is having trouble with fat metabolism. Other symptoms are: high blood pressure and elevated blood glucose (blood sugar). Other symptoms include chronically high levels of inflammation and Vascular Dysfunction (abnormal blood vessel function), which are also early indicators of heart disease.

Type II diabetes is characterized by high blood glucose levels after a 12 hour fast. High fasting blood glucose levels results from two processes: the chronic over- consumption of carbohydrates than the body needs and can use quickly; and, the chronic over-production of insulin to counteract the excess blood glucose. If not immediately used by the body, insulin stores blood glucose in fat cells. With continued high carbohydrate consumption causing excess blood glucose and a constant high level of insulin to counteract that level of blood glucose, cell membranes, including those lining the walls of the arteries, become more and more resistant to the action of insulin. A process called Insulin Resistance.  (Buyken et al. Carbohydrate nutrition and inflammatory disease mortality in older adults. American. Journal of Clinical. Nutrition. 2010. 92(3): p. 634-43). Over time, insulin becomes less and less able to counteract the effects of elevated blood glucose

Insulin Resistance is a clear indicator of intolerance to excess carbohydrates in the diet. In effect, the body is reacting to carbohydrates as an allergen. The body sets up mechanisms to protect itself from allergens. If not removed, the body starts to show signs of inflammation.

Inflammation, especially a chronic low grade inflammation, is now being considered as a direct link to other chronic diseases such as obesity, heart disease and cancer.  A single high carbohydrate meal, in susceptible individuals, can trigger inflammation. Chronic consumption of a high carbohydrate diet can lead to a chronic state of inflammation. (Hu et al. Inflammatory markers and risk of developing Type II diabetes in women. Diabetes. 2004. 53(3)): p.693-700.

Eighteen million Americans are estimated to have Type II diabetes with another eight million totally unaware than they have it. Although there is a genetic component to the development of Type II diabetes, there is an even more compelling link between diet and the development of diabetes.

What the research has demonstrated is the physiological process after ingesting a high carbohydrate meal. The carbohydrate portion of the meal is absorbed into the blood stream as glucose. The pancreas must send out enough insulin to counteract this infusion of blood glucose and restore it to its normal level. The more carbohydrate eaten, the more insulin needed to counteract it. Over time, usually years, the pancreas can wear out and stop producing enough insulin to counteract glucose. Additionally, the cells which had been open to receiving the blood glucose and store it as fat (insulin is the fat storage hormone) start to balk at the constant bombardment and begin refusing to open up (Insulin Resistance).  If dietary carbohydrate remains uncontrolled, type II diabetes usually results.

While excess insulin is floating around the blood stream, trying to control the blood glucose, it is scraping against artery walls as well as the walls of the heart. As this is going on, an inflammatory process begins to appear. Over time, plaques begin to form to protect these sensitive membranes, and over time they begin to solidify and harden.  A high carbohydrate diet, therefore, lends itself to chronic inflammation and Vascular Dysfunction which then leads to heart disease.

A provocative study published in the Journal of the Medical Association (JAMA) in 2007, compared a group of overweight women who were over forty years of age. The women were separated into four groups: a low carbohydrate (Atkins type) diet, a low fat (Dean Ornish diet), Kelly Brownell’s LEARN program diet (basically the FDA’s Food Pyramid diet); and, the Zone diet by Barry Sears (which is also called the 40-30-30 diet as the three major food groups must be eaten at the correct percentage, carbohydrate having 40 percent of the daily intake and fat and protein each having 30 percent of the  calorie intake per meal). The women were monitored constantly for 12 months in relation to their diet, calories consumed, weight and blood work. The startling findings for the researchers were that the women in the Atkins (low carbohydrate) group performed better than the other 3 groups ( low fat/high carbohydrate) on all parameters!  In other words, overweight women who were on a low carbohydrate diet for over twelve months reversed all the symptoms of Metabolic Syndrome whereas the women on low fat diets did not. This study has been essentially ignored by the medical community. (Gardner et al. Comparison of the Atkins, Zone, Ornish and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A to Z weight loss study. JAMA. 2007. 297(9) p. 969-77)

More recent studies have confirmed the findings of the Gardner study. A low carbohydrate diet out-performs a low-fat diet every time in relation to glucose control and blood lipid measures. (Dashti et al., Ketogenic diet modifies the risk factors of heart disease in obese patients. Nutrition. 2003. 19(10). P. 901-3;) Scientists agree it is the small dense fat molecules (lipoproteins) that lead to heart disease while the large fluffy molecules appear to be relatively harmless. (Lamarche et al. The small dense LDL phenotype and the risk of coronary heart disease: epidemiology, pathophysiology and therapeutic aspects. Diabetes.Metabolism. 1999. 23(3). P. 199-211.) Subjects eating a low fat diet have far greater amounts of small dense lipoproteins while those on the low carbohydrate diet have very low amounts of these lipoproteins and far more large fluffy lipoproteins. (Forsythe et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids. 2008. 43 (1): p. 65-77)

The link between diabetes and heart disease can be traced physiologically starting with the chronic, excess consumption of carbohydrates. The process begins in the mouth and ends in the heart. The tragedy for victims of heart disease is that much of it could have been prevented by eating fewer carbohydrates. The science is clear. The pathways are documented.  (Howard et al. Low fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled dietary modification trial. JAMA. 2006. 295(6). P. 655-66.)

The process described above is being shown in book after book, blog after blog, research after research. But the USDA still recommends a high carbohydrate diet as being the most healthy for Americans.

The myths surrounding diet and disease have created such a smoke screen, that the medical community has been slow to see the connection between high carbohydrate diets, onset of Type II Diabetes and eventual heart disease.  The polemic as to what causes heart disease, a high fat diet or a high carbohydrate diet, is as heated as any argument on politics or religion. Trying to get past the emotional attachment to any one hypothesis is difficult. This paper has attempted to do so by providing some of the science underlying the link between diabetes and heart disease.