By Ross Walker

Over the past few decades, there has been an explosion of obesity and type 2 diabetes in the Western world. Currently, around 8% of the Australian adult population are type 2 diabetic. 70% of Australian males are obese or overweight, along with 50% of females.

There’s no doubt that this epidemic of type 2 diabetes and obesity is clearly related, in many ways, to lifestyle issues. In particular, the excessive consumption of high density, poor nutrient food such as quick-fix, take away food, processed, packaged muck masquerading as food and bakery items, along with many people living sedentary lifestyles.

The insulin resistance gene

However, especially over the past decade, there’s increasing evidence that metabolic factors, genetics and the gut microbiome may also be contributing. As I’ve mentioned before, the human body was only physiologically designed to work well for 30-40 years wandering around a jungle with a spear. When we hit our use by date of around 40 years old, our metabolism starts to slow, and without a rearrangement of our energy equation, i.e. calories in versus calories burnt, it’s not difficult for the fat to start accumulating around the belly.

This is especially so for the 30% of Caucasians, the 50% of Asians and close to 100% of people with darker skin who carry the gene for insulin resistance. This gene is a survival advantage if you are hunter-gatherer, but a survival disadvantage if you live in modern society. The gene aids your survival in the hunter-gatherer environment by storing some fat temporarily around the belly until your next major feed following the kill of an animal, and also runs your blood sugar levels slightly higher to maintain normal brain function. Enter the world where we have 3 square meals a day (with snacking in between) along with increasing sedentary jobs and the vast array of mechanical forms of transport.

This insulin resistance gene is the major factor contributing to type 2 diabetes, hypertension, cholesterol abnormalities with increased cholesterol, increased triglycerides and low HDL, along with the ever-present and ever-increasing fat around the belly.

For males, this becomes an issue when the waist circumference is greater than the 95cm, and for females with a waist circumference greater than 80cm.

The research

Now, let's bring in the elegant work of Professor Clay Semenkovich from Washington University in St Louis. Professor Semenkovich has performed seminal work in mice around the enzyme system fatty acid synthase. This particular enzyme system is vitally important in the generation of fat in our body. The fat produced by this enzyme in the lining of the gut acts as a protective coating preventing bacteria and crossing the bowel wall. With the unhealthy, pro-inflammatory bacteria created by our modern diets, it’s likely that there’s also damage to the enzyme system and the vicious cycle created leads to more pro-inflammatory chemicals leeching into the bloodstream.

Interestingly, Professor Semenkovich’s group has also demonstrated that reducing fatty acid synthase, in particular inflammatory cells, paradoxically prevents the generation of obesity, type 2 diabetes and metabolic syndrome in the mice studied. The key here is to develop pharmaceutical drugs that will block fatty acids synthase within inflammatory cells, but not in the bowel wall.

The second interesting consideration here is looking at a toxic fats known as Ceramides. These ceramides prevent fat tissue from working normally. When we overeat, excess fat is either stored or burned as energy. But, in some people, excess fat is converted to ceramides which have three different and damaging actions to the body. Firstly, Ceramides can contribute to the death of pancreatic cells. Ceramides increase insulin resistance and decrease insulin gene expression. These are three major factors that can contribute to type 2 diabetes, regardless of bodyweight. This may also explain why some people still develop type 2 diabetes.

Finally, that spare tyre sitting around your belly is not just an ugly lump of lard but depending on your exposure to synthetic chemicals over the years, may also be a toxic reservoir. Many of the chemicals I have already mentioned, but also the well-known chemicals from plastics and the lining of aluminium cans such as BPA, can accumulate in fat. It’s been shown, for example, that obese people with the highest levels of BPA compared with those with the lowest levels have a 30 times higher rate of type 2 diabetes.

The bottom line

Clearly, our lifestyle is the strongest contributing factor to type 2 diabetes and obesity. However there are many more subtle factors that we're just beginning to understand that may explain why some people gain weight more easy easily, and also why some people who are overweight do not appear to have such severe metabolic problems such as type 2 diabetes.

This comes back to the age old saying, “it’s your genes that loads the gun but your environment that pulls the trigger". The key here is finding what particular environmental triggers we can actually affect.