Obesity’s Hidden Culprits

ISABELLE RIDDLE – On lazy afternoons, my roommates and I indulge ourselves in marathon watch-parties of My 600-Pound Life on TLC. Recently, this pastime led to a heated debate among us: 

Which is the responsible party when it comes to why some people are obese and others are not–is it an individual’s willpower, her genetics, her socio-economic status, her parents or even ancestors…? 

As future scientists, my roommates and I began an investigation, but quickly realized that we would have to cut through a lot of fat (product endorsements, baseless claims, body-shaming blogs, etc.) to get to the real scientific, peer-reviewed meat of this issue. Below is a lean-and-mean rundown of what we found:

There are a few cases in which obesity can be tied rather exclusively to one’s genetics. Monogenic obesity is caused by rare, spontaneous mutations in genes primarily found in the leptin-melanocortin pathway, which is responsible for energy homeostasis, appetite control, and food intake. Such mutations are involved in 2-3% of obese children and adults (1). Further, genetic syndromes caused by chromosomal abnormalities, such as Prader–Willi, disrupt satiety control regions in the brain and hormone levels throughout the body. Therefore, obesity is a hallmark of these genetic diseases (2).  

What about all the other cases, though–those which researchers refer to as “common obesity?” These cases are far more convoluted, involving the mysterious interaction of a sundry of distinct factors.

First: genetics. Evidence from animal models and association studies of large human populations suggests that variation in one’s susceptibility to obesity has a definite yet unclear polygenic component. For example, the estimated mean correlation of body mass index between identical twins is more than double that of fraternal twins and 12x that of adoptive relatives (3). However, it should be noted that lifestyle choices cannot be fully extricated from these results. 

In 2007, a genome-wide association study was able to locate the first obesity-related gene variants in a gene on chromosome 16, now known as the FTO gene (4). This variant is fairly common, and carriers have a 20-30% higher risk of obesity than the unaffected (5). At this time,  further genome-wide association studies have discovered approximately 30 candidate genes (on 12 different chromosomes) that are associated with body mass index (6). 

Although informative, genome-wide association studies like this do not provide a definitive causal link to a disease. Rather, they catch tiny alterations within standard, functioning genes. These variations, for reasons not understood, are found in higher proportions among obese individuals. One thing is certain, though: genetic mutations and polymorphisms of any type take multiple generations to spread within a population. Therefore, these obesity-related gene variants were just as common 40-50 years ago, before the rapid and global spread of obesity, so they cannot be the singular culprits for today’s obesity crisis.

Epigenetics, or modifications to gene expression levels rather than to the genetic code itself, also plays a role in the development of obesity. To simplify greatly, it appears that if our parents or grandparents went through famine, genes affecting energy storage and metabolism were turned up or down and passed on to us without being recalibrated, making obesity more likely. For more information on this fascinating and complex phenomena, look into the Dutch Hunger Study. 

Second: environment. We all know of that prescribed list of environmental obesity triggers like the back of our chubby hands: over-availability of high-calorie, processed foods, reliance on fast food, sedentary jobs and lifestyles, TV and phone time replacing active leisure activities, stress, lack of sleep, erratic snacking, etc. This list is so prolific because it is so true, and, although challenging, lifestyle changes to combat these systemic issues must be implemented if one is to have a chance in the fight against common obesity. That being said, there are some more esoteric environmental causes of obesity that the scientific community has recently pinpointed. 

For example, environmental forces are now believed to play a role in body development even before birth. A meta-analysis of studies tracking obesity levels of infants all the way into young adulthood found that maternal smoking during pregnancy, especially after the first trimester, correlates with a 50% higher risk of obesity in the child years later, despite the fact that smoking tends to slow fetal growth in utero (7). Excessive weight gain of the woman carrying a child also increases the risk (by up to four times that of non-excessive weight gaining mothers) that such child will develop and maintain an obese frame in their lifetime (8). This finding is alarming as more women today present with inordinate gestational gains. Further, the problem is exacerbated if a mother is overweight or obese before becoming pregnant. 

Forces acting shortly after birth also appear to correlate with obesity later in life. Breastfeeding was associated with a 13-22% reduced risk of obesity later in life when compared to bottle-fed children (9,10). Additionally, a meta-analysis of more than a dozen studies showed that each additional month that infants are breastfed correlates with a 4% lower risk of obesity later in life (11). These results cannot simply be taken at face value, for it is not clear that breastfeeding itself actually prevents obesity, as both breastfeeding and obesity may be influenced by similar socioeconomic and cultural factors. 

Some very new and exciting research suggests that alterations in the makeup and dynamics of the human gastrointestinal microbiome could play a major role in the development of obesity. Gut microbiota have been shown (in animal studies, at least) to influence energy utilization from one’s diet as well as alter the function of one’s energy expenditure and storage regulatory genes (12). Excitingly, the composition of the gut microbiome is not fixed, opening the door for new weight loss and obesity prevention treatments in the near future. 

To conclude, if you ever find yourself watching My 600-Pound Life in the future, you really cannot (and should never!) judge the individuals appearing on the show and in your day-to-day life for their appearance. Obesity is a complicated human circumstance caused by a web of multifaceted individual and societal triggers. It is best practice to focus on the health and wellbeing of yourself and your family. For starters, maybe don’t watch reality TV for hours on end like I do! 

Photography Source: http://theconversation.com/why-we-keep-playing-the-generation-blame-game-and-why-we-need-to-stop-82219