A mountain of evidence points to the conclusion that bearing excess body fat, particularly visceral fat, is harmful to long-term health. The more visceral fat and the longer you have it the worse off you are. That fat tissue causes chronic inflammation, alters metabolism in ways that harm organs and important biological systems, and raises the risk of suffering all of the common age-related diseases, including those that erode the mind. In general: visceral fat tissue damages you, and degenerative aging is at root an accumulation of damage.
So if you want to live a shorter life with larger medical expenses, more pain and suffering, and less of an ability to do the things you like to do, then by all means let your weight go. It's easy to get fat in a society this wealthy: we are swimming in a sea of low-cost calories and exceedingly attractive foodstuffs, having achieved a state of security from hunger that our ancestors of a few hundred years past could only have dreamed of.
We work to build the world we desire, and we are hardwired by our evolutionary past to greatly desire food without limit. It's still your choice to become fat and suffer the consequences. Easy and hardwired are no excuse, and do not remove your ability to exercise free will in the pursuit of your goals. Thin people in wealthy countries are not thin because they have magic genes, but because they choose to be thin, and put in the necessary exercise of will to stay that way.
Here are a couple more items to add to the mountain of research linking visceral fat with ill health and shorter lives. The first is of interest for the methodology the scientists are using in order to work around the primary challenge of any human epidemiological study, which is how to show cause and effect rather than just correlation:
These scientists studied whether a gene variant in the FTO gene, which regulates the appetite and thereby increases the individual's [body mass index, or BMI], is also linked to a series of cardiovascular diseases and metabolism. The risk variant is common in the population, and each copy of the risk variant increases BMI by an average of 0.3-0.4 units. Since an individual's genome is not affected by lifestyle and social factors, but rather is established at conception, when the embryo randomly receives half of each parent's genome, the method is thus called "Mendelian randomization". To achieve reliable results a large study material was needed, and nearly 200,000 individuals from Europe and Australia participated.
"Epidemiological studies look for associations in large populations, but it is usually difficult to reliably determine cause and effect - what we call causality. By using this new genetic method, Mendelian randomization, in our research, we can now confirm what many people have long believed, that increased BMI contributes to the development of heart failure."
The results show that an increase of one unit of BMI increases the risk of developing heart failure by an average of 20 per cent. Further, the study also confirms that obesity leads to higher insulin values, higher blood pressure, worse cholesterol values, increased inflammation markers, and increased risk of diabetes.
Moderate-intensity exercise reduces fat stored around the heart, in the liver and in the abdomen of people with type 2 diabetes mellitus, even in the absence of any changes in diet. "Based on previous studies, we noticed that different fat deposits in the body show a differential response to dietary or medical intervention. Metabolic and other effects of exercise are hard to investigate, because usually an exercise program is accompanied by changes in lifestyle and diet."
For the new study, [researchers] assessed the effects of exercise on organ-specific fat accumulation and cardiac function in type 2 diabetes patients, independent of any other lifestyle or dietary changes. The 12 patients, average age 46 years, underwent MRI examinations before and after six months of moderate-intensity exercise totaling between 3.5 and six hours per week and featuring two endurance and two resistance training sessions. The exercise cycle culminated with a 12-day trekking expedition.
MRI results showed that, although cardiac function was not affected, the exercise program led to a significant decrease in fat volume in the abdomen, liver and around the heart, all of which have been previously shown to be associated with increased cardiovascular risk.
It is in fact possible to diet your way out of type 2 diabetes via a sustained low calorie intake, even at fairly late stages in the progression of the condition. That may operate partially through the mechanism of reducing the amounts of visceral fat tissue present in the body. All in all type 2 diabetes really is a self-inflicted and self-maintained medical condition for most people these days, now that it isn't just a disease of the very old and frail. With sufficient application of effort any non-frail patient can make his or her condition largely go away at any point before its end stages.