(stroke, heart failure), and various metabolic diseases. One of the methods of mitigating these effects is reduction of adipose tissue; this can be done by 2 methods—decreasing energy expenditure (physical exercise) or dietary modification. Research regarding the epigenetic effect of physical exercise on obesity is still in slightly uncharted. Much of the data that is collected simply compares epigenetic changes in patients that have been diagnosed as obese and patients that haven’t. However, this cannot discount the role of physical exercise and epigenetics as many of the epigenetic differences are correlated with BMI and waist circumference, both of which can be controlled via physical exercise. With that mentioned, since the research is new, there’s a plethora of information, much of which is unreviewed. Overall, the evidence for the effect of obesity on epigenetics lies in a specific set of genes that controls waist circumference(WC) and body mass index(BMI)--the evidence is not more concrete than this. In a study that combined methylation data from 10,000 blood samples, 187 CpG sites were shown to be associated with BMI. What they found was highly interesting: deviations in DNA methylation in blood are usually assumed to be the result of obesity, and on some occasions, the cause. Using quantitative genetic analysis techniques, the researchers attempted to find either a causative or consequential relationship between the implicated genes and the obesity. They found that most of the interactions between the genes of interest and obesity were consequential—demonstrating that any alteration in gene activity is most likely the result of obesity, not a factor that caused it. This study was verified by testing within adipose tissue. CD38 (cluster of differentiation 38) is a glycoprotein with enzymatic activity found on the surface of specific immune cells. The ectoenzyme has been shown to be important in nicotinic acid adenine dinucleotide phosphate (NAADP) synthesis. NAADP is an intracellular second messenger implicated in Ca2+ release. When knocked-out in mice, the result was an increased metabolic rate and obesity resistance (induced by a high-fat diet). This tells us that CD38 is an important factor in the epigenetic change in regards to obesity. As found in an additional study, MSI2, a gene encoding the Musashi RNA-binding protein 2 was found to be associated with eating behavior. The same study found that LARS2 (mitochondrial gene) was implicated with BMI and waist circumference. In both cases, the researchers noted that for a +1 unit