Our experience of health and disease will always be the result of an interplay between our genes and ‘environmental’ factors such as diet, exercise and exposure to potential toxins or health hazards. We hear a lot about the role of specific genes in specific conditions such as diabetes and heart disease. However, as Professor Steve Jones ” professor of genetics at University College London in the UK ” recently pointed out in a newspaper article, gene identification has not really got us very far in terms of understanding the mechanisms behind disease and how best to prevent and treat them.
Also, we know that there as been a relative explosion of certain chronic conditions, including obesity and type 2 diabetes, in just the last few decades. Assuming that our genetic make-up s a species has changed very little in this blinking of an eye, then really and truly, it is likely that it’s changes in environmental factors that has led to the steep rise in the rates of these health issues: Genes may load the gun, but it’s environment that is largely responsible for pulling the trigger.
Recently, I came across an article on the website Science Daily that was entitled ‘Factors other than genes could cause obesity, insulin study shows’. Fortunately, I don’t always let article titles that appear to be stating the obvious put me off actually reading them. This article is interesting in that it talks about a study which attempted to see what it is about fat cells that seems to lead to some storing more fat than others. The relevance of this is that obesity may be regarded as a condition of excessive fat storage. So, if we understand the mechanisms behind this, we might be in a better position to do something about it.
Now, a lot of people in the nutritional field believe that they know what causes people to be overweight: eating too much and/or not exercising enough. This view is based on the calorie principle that basically maintains that if we eat more calories than we burn we will gain weight, but we’ll lose weight if we consume fewer calories than is burned in the body.
While this makes sense, it is also somewhat simplistic. For example, if calorie consumption is reduced, energy expenditure tends to reduce too (reducing calories can put a dent in the metabolic rate). And exercising more can, ultimately, result in the body compensating with an increase in food intake (as a result of increased hunger). These mechanisms help explain why both calorie-reduced diets and aerobic exercise have been found to be generally useless for the purposes of weight loss.
The idea that obesity is a disorder of fatty accumulation (and not just down to the calorie principle) is explored in Gary Taubes’ book The Diet Delusion (titled Good Calories, Bad Calories in the USA). In this book, Taubes’ exposes the fallaciousness of the calorie principle, and instead goes after what might cause fatty accumulation in the body.
Now, fat is stored in fat cells as substances called triglycerides. Triglyceride is made from substances known as free fatty acids. It takes 3 fatty acids and one molecule of a substance known as glycerol to make triglyceride. The free fatty acids are absorbed from the bloodstream into the fat cells. They can flow out again too. What ‘fixes’ them in the fat cells is their conversion to triglycerides.
The conversion of free fatty acids to triglyceride is dependent on the supply of a substance called alpha glycerol phosphate. This is produced when glucose is metabolised in the cell. In other words, the more glucose that gets into the fat cells, the more fat will tend to get fixed there.
For most people glucose comes from sugars and starches (carbohydrates) in the diet. But to get into the cells it requires the action of the hormone insulin. So, dietary carbohydrate supplies the glucose necessary for the manufacture of triglycerides, and also stimulate the secretion of insulin which gets the sugar into the cells. Insulin also stimulates triglyceride formation through its action on other hormones (lipoprotein lipase, glycerol phosphate acyltransferase and hormone sensitive lipase).
In short, what this means is that carbohydrate and insulin will tend to cause the accumulation of fat in the cells.
What’s this got to do with the Science Daily article I mentioned earlier? Well, in this study researchers determined genetically identical fat cells were found to have widely differing propensity to accumulate fat. The difference was found to be related to the rate at which cells process insulin: the faster the processing, the more the cells tended to accumulate fat.
This finding is predictable from an understanding of the critical role that insulin plays in fatty accumulation. It should also serve to remind us that the form that calories (not just the number of calories) can affect our propensity to lose or gain weight. And finally, there is good evidence that fatty accumulation is stimulated by the consumption of carbohydrates, particularly those that tend to cause considerable and/or sustained rises in blood sugar. For many, weight loss will come about by simply lowering insulin levels in the body. And the obvious way to achieve this end is to eat less carb.