Obesity and Health Have a Complex Relationship According to Research

Research makes obesity issues more complex

The conversation around obesity is evolving to incorporate the more complex and multifaceted relationship between weight and health that is emerging from an ever increasing pool of research on the topic. No longer is obesity merely an issue of weight gain and weight loss. A person’s size is proving to be far more complicated than just lifestyle choices and less can be determined about a person’s health by simply labeling them obese.

That is not to say that lifestyle has no role in a person’s weight. Let it be acknowledged, immediately, that healthy eating and exercise are absolutely contributing factors to a person’s weight and health. However, most mainstream conversations begin and end on this point and give rise to the notion that those who are overweight have “done it to themselves,” are lazy, or have no willpower. Sweeping judgments about a person’s health often accompany these deeply convicted assumptions and a whole lot of people are forced to deal with a whole lot of stereotypes that are thrust upon them. Meanwhile, myriad other factors grind along behind the scenes, adding weight to frames already weighed down by misconceptions.

While some laymen will assume all knowledge has been gleaned regarding the topic of obesity, researchers see a completely different picture. One where restrictive diets and exercise alone are not yielding reliable results in weight management. Many are seeking to find out what the missing pieces are to this puzzle of obesity.

One source of insight into the complicated nature of obesity comes from a study published in the Cell Press Journal. In it, researchers claimed to have found a genetic mutation that leads to obesity in a small minority of the population. Known as the “hunger gene,” the Kinase suppressor of Ras 2 (KSR2) gene has been identified as problematic when mutations occur. Mutations in this gene can lead to increased hunger and decreased metabolism, meaning that energy is burned by the body at a slower rate. The biological repercussions of the abnormalities in this gene are thought to cause severe early-onset obesity.

What this means is that children who are severely obese may not be that way because of anything that they or their parents can control. The common assumptions about diet and exercise do not apply to these children and holding to these assumptions can lead to significant harm coming to the child. Harm that can come in the form of stigmas and shaming, or in the form of state interventions that remove the child from their parents, an extremely traumatic experience for young children to endure.

Other consequences of this abnormal gene include a predisposal towards significant insulin resistance. There are some researchers who theorize that insulin resistance could be a precursor for obesity, as the body inappropriately stores energy when cells become resistant to insulin, instead of burning it as insulin is intended to do. The discovery of a gene whose mutation creates all of the scenarios previously attributed to poor eating habits lends credibility to the notion that while food intake could exacerbate the problem, it is not the end of source or solution to the problem.

Further research adds another complex layer to obesity as the relationship between environmental factors and health yield insight into another potential factor to the increased rates of obesity in the last few decades.

A study published in the BMC Medicine journal found that exposure to DDT during certain developmental phases could increase the chances of the development of a disease. Researchers indicate that exposure during the phase where reproductive organs develop increase the risk of disease, not by mutation of genes, but by increasing the likelihood of certain types of gene expression later on. The increased rate of susceptibility is passed over generations in a process called transgenerational epigenetic inheritance.

DDT was most commonly used in the early through the mid 1900s. Its use was discontinued in the United States after concerns of environmental safety were successfully raised and supported. Three generations later, obesity rates have risen to the “epidemic” proportions of one-third of all Americans being classified as obese. This study into transgenerational epigenetic inheritance was able to recreate this same generational timeline in rats who had been exposed to DDT, showing increased vulnerability to disease and increased obesity rates three generations after exposure.

These findings are important because they demonstrate that genetics play a significant role in the development of obesity; a notion that is both common knowledge and generally overlooked in favor of the eat-less-exercise-more mentality. They add credibility to the decision by the American Medical Association to classify obesity as a disease rather than a simple consequence of lifestyle.

They also adds hope for those who have struggled to maintain their weight or who have suffered from diseases associated with weight gain. Knowing that a specific gene has malfunctioned and created a problem allows for medication to be developed that can control the protein the gene encodes. This can treat not only the minority of those with the mutated gene but can be used to treat others who deal with complications connected to that gene. For example, knowing that those with the KSR2 gene mutation tend to have severe insulin resistance, a precursor for type 2 diabetes, means that controlling for that effect with medical interventions could benefit all who have insulin resistance or type 2 diabetes.

Alternatively, knowing that DDT exposure increases obesity rates by making people more vulnerable to disease through genes expressing themselves more readily means that medical professionals can check for biomarkers and determine risks for disease much earlier, forming interventions before the disease presents itself.

Findings like this could have a tremendous impact not only on popular understanding of the complex relationship between obesity and health, but also on the types of interventions offered to those who struggle with the two issues. Addressing the problem of this chronic disease needs a more comprehensive approach than the dichotomized mindset of healthy or fat currently prescribed to the issue and research is increasingly helping to bring the much needed diversity in how obesity is addressed.

By Vanessa Blanchard

Cell Press Journal

BMC Medicine

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