With the focus being on diabetes in November, the time is ripe for readers to take note of an interesting publication on 'Body Fat and Insulin Resistance' by Ali and Crowther which has recently been published in the SA Medical Journal.
These authors give an insightful summary of what we know at present of the interrelationship between abdominal fat, insulin resistance and the development of conditions such as type 2 diabetes.
If you ingest more energy from food than you expend (for basic metabolic processes and exercise), then the excess energy will be stored in the so-called fat depots of the body.
New research indicates that adipocytes or fat cells don't just store fat inactively, but are actually metabolically active tissues and produce a number of hormones and other compounds that can affect human metabolism.
According to Ali & Crowther (2005), many factors such as gender, age and ethnicity determine where fat will be stored in the body. So-called 'android' obesity develops when most of the stored fat occurs in the upper body.
Android fat distribution is found mainly in men. On the other hand, body fat that is distributed in the lower part of the body (thighs, buttocks) as occurs more usually in women, is called 'gynoid' obesity.
The authors also point out that women of all ages, even before birth, have more fat stores than men. Unfair, but a reality laid down by genetic codes so that the female body has greater reserves for 'emergency' situations like pregnancy and lactation.
As individuals get older, more fat tends to be deposited in the abdomen.
Abdominal fat and insulin resistance
Studies have shown that insulin resistance is closely linked to abdominal fat distribution. In turn, insulin resistance makes people more vulnerable to developing diseases such as type 2 diabetes, high blood pressure, heart disease, breast cancer, and stroke.
When an individual suffers from insulin resistance, the insulin he/she produces is unable to control glucose production in the liver and to remove glucose from target tissues. Insulin resistance is also associated with derangements of other insulin functions, which relate to insulin's effect on protein and fat metabolism.
Body cells in an insulin-resistant person require more and more insulin as these cells become more resistant. The pancreas reacts to these increased demands by producing more and more insulin until it literally 'burns out'.
When a person is no longer able to produce sufficient insulin because the beta-cells of the pancreas have been exhausted due to the demands of insulin resistant cells, type 2 diabetes develops.
Persons with abdominal obesity often suffer from the metabolic syndrome. This is a collective name for a number of metabolic derangements that can occur in a patient at the same time, namely insulin resistance, raised blood lipid levels, raised fasting blood glucose levels and high blood pressure.
Researchers have identified considerable differences in the occurrence of abdominal fat, insulin resistance and metabolic syndrome in different ethnic groups.
In South Africa, studies found that Indian subjects had higher waist-to-hip-ratios (WHRS) (a measure of abdominal fat) than black subjects. White subjects tend to have larger abdominal fat depots than black South Africans, which could be one factor why black people have a lower incidence of insulin resistance, type 2 diabetes and metabolic syndrome.
This protective effect could, however, be lost as our black population becomes increasingly urbanised and changes to a diet rich in fat and highly processed carbohydrates. It has been said that we are sitting on a 'time bomb' of type 2 diabetes and cardiovascular disease in South Africa, which will explode in the near future because of the change in eating habits and reduced physical activity caused by urbanisation of the black population.
There is evidence that up to 50% of the differences in abdominal fat deposition are genetically determined.
On the one hand, the genetic predisposition to develop abdominal fat when linked to the genetic tendency to develop type 2 diabetes makes this problem even more complex. But on the other hand, Ali and Crowther (2005), feel that this suggests "that the development of therapies targeting visceral fat accumulation may not be out of reach".
Ali and Crowther (2005) point out that we still don't know exactly why some people have a greater tendency to deposit fat in the abdomen and develop insulin resistance. But researchers are busy studying many aspects of this problem and its consequences, so in the not too distant future novel treatments of type 2 diabetes may become available and thus improve the outcome of this condition.
At present, treatment consists of eating a low-fat diet with a low glycaemic index (GI) and glycaemic load (GL), taking antidiabetic medications such as Glucophage, and doing as much regular exercise as possible.
Always consult a clinical dietician if you suffer from insulin resistance, metabolic syndrome or type 2 diabetes, because the correct diet plays such a vital role in treatment of these conditions.
Readers often ask me if these are a cure for insulin resistance. Research has shown that losing weight, eating low GI diets and doing exercise can reduce insulin resistance to such an extent that patients no longer need to use medications.
We don't as yet have a total cure because people with insulin resistance need to stick to the low GI diet and exercise for the rest of their lives, but this condition is at least controllable and the future seems bright for new solutions. – (Dr Ingrid van Heerden, DietDoc, November 2005)
(Reference: Ali, AT, Crowther, NJ (2005). Body fat distribution and insulin resistance. SA Medical Journal, Vol 95, No 11, 878-880.