Did you know DNA affects your adioponectin levels and your type 2 diabetes risk?
From Friend to Foe: Why our evolutionary need to store fat is now an obstacle in the fight against diabetes
Humans have evolved to store fat. Yet this very same capability is now at the root of the obesity health crisis, and the array of other associated health problems, such as heart disease and type 2 diabetes. Our capacity to store fats probably hasn’t changed in hundreds of years. What has changed, is our relationship with fats. Unlike our ancestors, we don’t expend energy looking for food. Often we can even obtain food from the comfort of our homes.
Our body’s ability to store ‘extra’ energy for times of need has become obsolete, almost to the point of being unsafe. However, rather than trying to confront millions of years of evolution overnight, one of the better ways to tackle this problem might be by way of our genes. As we uncover genetic changes that account for body fat storage differences, like in the ADIPOQ gene, we just might be able to challenge evolution one cookie at a time.
Without the ability to store fat, humans as a species would never have survived this long. The main function of adipose (fat) tissue is energy storage, as well as to cushion and insulate our bodies. But that’s not all – fat cells actually are the source of hormones called adipokines that control everything from blood pressure, fat and sugar breakdown to inflammation. This explains why obesity is often a precursor for cardiovascular disease and type 2 diabetes.
Adiponectin (encoded by the ADIPOQ gene) is the most abundant adipokine released from fat cells. It’s also quite unique from the rest of the adipokines, because adiponectin enhances fat breakdown and lowers blood sugar levels. There are three different sizes of adiponectin in our blood, designated low, middle and high, with the high weight adiponectin being the most active.
One would assume an obese person with more fat tissue would produce more adipokines than a person of average weight. Paradoxically this is not the case at all with adiponectin. The levels of this hormone are actually inversely correlated with body mass index, and lower adiponectin levels are linked to both type 2 diabetes and cardiovascular disease. Here’s where genetics comes in handy for figuring out how we might be able to ‘trick’ our bodies into storing less fat and to minimize our risk of metabolic disorders like type 2 diabetes.
There are differing versions of the ADIPOQ gene that occur due to small changes in the genetic (DNA) code. Some of these changes are associated with higher adiponectin levels, offering protection from obesity and weight regain following a diet. Other ADIPOQ changes lower adiponectin levels, increasing the likelihood of elevated body mass indices. Lower adiponectin levels also enhance our predisposition to diseases such as type 2 diabetes and metabolic syndrome. However diet, exercise and weight loss can all increase adiponectin levels, essentially mitigating our propensity to gain weight.
Letting go of excess stored fat is not a simple problem, because our bodies have evolved to actually protect fat stores for times of need. ADIPOQ illustrates why the best way to get a grip on our body weight and the risk of diabetes might be through genetics. Understanding why our bodies resist weight-loss allows us to tailor our strategies accordingly. The journey is bound to be unique to each of us, just like our DNA.