Epigenetics and Obesity

In a previous blog, I talked about the science of epigenetics and how it is possibly the most important medical breakthrough in years – providing powerful new information on how to lose weight and prevent chronic illness. 

The same epigenetic mechanisms that put us at greater risk for cancer and heart disease appear to increase the risk of weight gain and obesity. Researchers have been scouring the human genome to find the genetic connection to obesity. To date, there have been more than forty genetic variants associated with obesity. However, this explains only a small piece of the obesity epidemic, because over the time that there has been an explosion of worldwide obesity, there has been negligible change in the actual genetic sequence of the population. A larger factor might be the epigenetic marks influenced by diet and environmental toxicants, especially the endocrine-disrupting chemicals. 


Can obesity be inherited?

Heritability of obesity is found in 40 to 70 percent of individuals. This was determined through twin studies that measured body mass index, waist/hip ratios, and other obesity markers. In a 2011 study, Zhang and colleagues found that obese women tend to have obese children, with this outcome possibly modified by maternal weight loss during pregnancy. It is thought that epigenetic mechanisms in early development, heritable from the mother, determine much of the risk for obesity.


How the maternal diet affects obesity

One epigenetic aspect found in obesity is the lack of methylating dietary factors in the maternal diet, leading to lifelong obesity in the offspring. This is a similar finding to the increased risks of cancer in the offspring of mothers with low folate in their diet. In 2007, Sinclair and colleagues reported on the effects of restricting folate and B12 in the diet of pregnant sheep. They found that the offspring of these sheep were heavier and fatter as adults as a result of epigenetic changes in methylation status from the maternal low-folate diet. The effects of exposure in utero to lack of methylating factors lasted throughout the life of the offspring. It is possible that one cause of the obesity epidemic is epigenetic programming as a fetus or early in life. To reduce this risk, it is prudent for prospective parents to consume folate-rich foods such as green leafy vegetables, eggs (a source of choline and methionine), tofu, and organic meats to possibly normalize epigenetic mechanisms and reduce the heritable patterns of obesity. As with cancer and other epigenetic-related diseases, histone modifications are also linked with obesity. 

“You are what you eat”

The silencing of the genes that control hormones like leptin (a hormone produced by fat cells that suppresses appetite by communicating energy reserve information to the central nervous system and other organs) is one of many potential links between epigenetics and obesity. It is felt that both maternal undernutrition (the children of the Dutch women who suffered a famine in 1944 had impaired glucose tolerance and insulin secretion in adulthood) and overnutrition, so common in the Western diet today, induce epigenetic changes leading to obesity in the offspring as adults. Ong and Muhlhausler (2011) have shown that perinatal exposure to high-fat and high-sugar diets resulted in permanent changes in the central reward system of the offspring, leading to increased preference for fat and overconsumption of calories, resulting in obesity. They studied rats and found that, after exposure to what they called a junk-food diet during pregnancy, the offspring ate excessive junk food throughout their lives. 


Connections between POPs and obesity

Another aspect of the obesity epidemic is our exposure to obesogens, the same persistent organic pollutant chemicals that are putting us at greater risk for cancer and other maladies. BPA and other chemicals (persistent organic pollutants, or “POPs”) found in fat cells can greatly impact the risk of diabetes and obesity. In fact, when comparing groups of obese patients, those with higher levels of POPs were more likely to develop diabetes even if they were less obese. Lang and colleagues (2008) found that higher BPA concentrations measured in urine were associated with both diabetes and cardiovascular disease. 

Phthalates, another common plasticizer, have been linked to an increased incidence of abdominal obesity and diabetes, possibly through deregulation of metabolic pathways. A study of U.S. males (Stahlhut et al. 2007) showed that urine concentrations of four phthalate metabolites correlated with waist size and insulin resistance, a forerunner of diabetes. Other toxins linked to an increased risk of obesity and diabetes include PCBs and arsenic. It appears that the epigenetic mechanism of the POPs on weight gain is the same as it is for other conditions such as cancer: excess methylation of genes, leading to abnormal gene expression. The difference with obesity compared to cancer is the genes affected: those related to diabetes, abnormal metabolism, and obesity; or those involved with abnormal cell proliferation. 

Next steps: How to protect yourself (and your offspring) from obesity

Only a small part of the puzzle connecting epigenetics and obesity has been solved, but it is clear that following the prescription to use bioactive foods, methyl donors, and a wide variety of plant-based nutrients would assist in protecting yourself and your offspring from the epidemic of obesity. Emphasizing green tea, broccoli, fermented soy, turmeric, and garlic, along with the information presented in The Adaptation Diet (see recipes in the appendixes), will further empower weight loss while reducing the risk for chronic disease. In addition, curcumin from turmeric has been shown to actually reduce the production of fat cells by inhibiting transformation of pre-adipocytes to adipocytes. The epigenetic model implies that the early years of life have greater plasticity to reverse abnormal epigenetic marks, leading to a reduction of obesity and chronic disease through dietary and environmental methods. The message is to make dietary changes as early as possible, ideally in pregnancy, to reduce the risk of obesity in a child. 

If you’d like to learn more about epigenetics and controlling obesity (or The Adaptation Diet in general), please call us and set up an appointment. Whether you’re interested in living a healthier lifestyle or you’re trying to overcome a chronic condition, we can help you get to your goals.