Over the last 50 years, there has been an unprecedented boom in science, technology and medicine. Yet, despite our ever-increasing knowledge of how the body works, diseases such as obesity, type 2 diabetes, coronary heart disease, hypertension, and cancer have reached epidemic proportions especially over the last 2 decades. Many “experts” have attributed this increase to the growing population of baby boomers who have been kept alive longer because of our enhanced medical skills. However, the growth rate of obesity, diabetes and cardiovascular disease far exceeds the growth rate of aging. The only conclusion is that we are not bringing what we learn about health and disease to clinical and practical application.

However, this concept is even more complicated than is implied by articles that attempt to simplify this concept. Scientists such as myself have known for many years that fat and fat cells (adipocytes) can act as potent regulators of metabolism and, therefore, health and disease. In fact, the many forms of fats (saturated, unsaturated, long-chain, short-chain) can differentially regulate genes responsible for fat and energy metabolism. The type of fat presented to your genes is a result of how fats are metabolized by the cell.

This, in turn, is greatly influenced by the “dietary context” in which the fat is seen. This idea of “dietary context” refers to the nutrient breakdown of an individual’s diet; that is, how much carbohydrate, fat, and protein a person is eating and the various forms that make up each of the nutrient groups. For example, how many calories are derived from fat, carbohydrates and protein can greatly influence the way your body handles fat. If you are a good fat burner by optimizing your ability to use fat as the major source of energy than you can tolerate a wider, more diverse, intake of the types of fat in food.

The cascade of metabolic events that follows can impact many different processes including the manufacturing of lipoprotein particles (LDL, VLDL, HDL) and triglycerides. And, although some articles discuss that saturated fats appear to positively impact HDL levels, this may not always be a good thing.

For example, we now know that HDL particles in the wrong environment can be quite detrimental to your health, a fact that is not (yet) widely distributed. For example, in a highly oxidative, inflammatory environment, such as occurs in someone with diabetes, the beneficial effects of HDL particles can be dramatically compromised by oxidation.

To conclude, dietary intake can greatly affect the biochemistry and biology of fat. In the past, we have attempted to simplify this idea by making blanket statements about the different types of fat and how it affects your health. Our bodies are far too sophisticated for these types of generalizations. However, the hope is to change the way people think about fat and its impact on health and disease.

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