What causes obesity is an important question in our current culture. But do we really know the real solution?
Epigenetic research papers on obesity are now showing a direct link between epigenetic mechanism’s and obesity. So, the two are quickly becoming inseparable in discussions.
For decades, we have seen a relatively high rate of heritability of obesity, yet the search for a common genetic variants has never been found. So, since genetics has been unable to explain the heritability of obesity, epigenetic research has been pursued, to understand other forms of variation, and has shown a clear relationship and increased susceptibility to obesity, through different epigenetic mechanism.
What causes obesity? In particular, epigenetic marks, known as imprinting, which are tissue specific and include DNA methylation and histone modifications that can be inherited by the two previous generations. As usual, this epigenetic mechanism affects the gene expression without making any changes the DNA sequence. And, while they have been shown to increase the susceptibility of obesity in children, other epigenetic consequences, such as environmental exposures during critical developmental periods, have also been shown to change the epigenetic profile.
Now, although, this article will provide evidence that obesity can be inherited, from both parents, through different epigenetic mechanisms, it is very important for the reader to understand that epigenetic changes can be reversed through proper nutrition and other lifestyle changes.  
Obesity in the United States is a Concern
A statistic from the most recent National Center for Health Statistics (a division of the Centers for Disease Control and Prevention) report indicated that 69.2 percent of Americans are considered “overweight” or “obese” and that the adult obesity rate remains greater than 33.8 percent overall. The obesity issue is not something that is projected to impact the U.S. in five or 10 years, it’s already here.
For decades, scientists have pursued the science of genetic determinism to establish causation of obesity in families, and they believed that it was somehow encoded into a person’s DNA. More recent studies have instead realized that the epigenetic profile of family members provides a more fruitful a path to establish causation.
What Causes Obesity? Epigenetic Markers Are Linked to Obesity
In a study published online on Dec 3rd 2015 in journal Cell Metabolism, Barres and colleagues to studied the epigenetic profile of and analyzed sperm from 10 men who were obese and 13 men with a normal weight. The investigators found that the two groups showed different DNA methylation patterns in their sperm — including in gene regions linked to appetite control.
Beyond nutritional factors, what causes obesity requires a more holistic approach, exploring what other type of life experiences are responsible for activating and deactivating these genes, such as appetite control, is now an important question for future epigenetic research. For example, a recent meta-analysis study conducted by researchers at Karolinska Institutet that included over 112,000 participants, found the risk of obesity to be much higher for those who experienced abuse in their childhood.  So, one could suggest, what causes obesity goes beyond nutrition, and includes negative thoughts and emotions acquired through challenging life experiences.
A series of epigenetic research studies conducted at Texas suggested that while we inherit a random mix of genes from our ancestors, people may also receive “a biological imprint of their [parent’s] behavior and lifestyle” through DNA Methylation; an epigenetic mechanism that we have often discussed. So, while we have inherited same sets of genes from our ancestors, differences in methylation patterns could have a significant effect in the genetic expression of our genes, resulting in different amounts of functional proteins and hence different extent of functions.  
Lifestyles Matter For Both Parents
In another study conducted by Soubry, in April 2015 in which three different genes were studied, included human imprinted genes involved in early growth regulation, such as MEST, PEG3, pleiomorphic adenoma gene-like 1 (PLAGL1), epsilon sarcoglycan and paternally expressed gene 10 (SGCE/PEG10), neuronatin (NNAT) and maternally expressed gene 3 (MEG3). The three different genes were chosen to be representing the three different kinds of tissues, maternal, paternal and zygote. The study aimed to estimate the roles each tissues plays in obesity. In the end, it was concluded, that a fathers obesity, acquired through his life experiences, also contributed to the genetic expression of obesity in the child.
In general, the literature supports the idea that maternal lifestyle is very important for optimal development of the fetus.  While few epidemiologic studies have investigated the potential influence of paternal lifestyle or body composition on the next generation, the studies conducted show important results.
For one, Figueroa-Colon et al.  showed that the paternal body fat may be a predictor for percentage of body fat in the offspring. Other long-term cohort studies show that overeating before puberty may increase the risk of death from cardiovascular disease or diabetes in the grandchildren and this transgenerational association was only detected through the male line.  Further, studies on animal models further suggested that other imbalanced diets, such as a low protein diet in male mice, resulted in changes in hepatic expression of genes involved in lipid and cholesterol biosynthesis.  Similarly, paternal food deprivation in mice affected metabolism-related factors in the offspring, represented by low levels of serum glucose. 
Future Epigenetic Research Could Explore How Lifestyle Changes Can Reverse Unfavorable Genetic Expression
In is becoming evident that there exists an important transgenerational epigenetic effects from nutrition, lifestyles and life experiences. And, while the studies mentioned above provide a critical path to better understanding causation, there is still a lot of information that we do not know.
For one, these new understandings should inspire research scientist to explore how unfavorable genetic expression, that cause obesity, can, in theory and practice, be reversed through life experiences, without the need for pharmaceutical interventions.
So, it will be up to future educational programs to build a system that better understands each individual’s epigenetic profile and life events to offer specialized lifestyle programs that enhance ones favourable genetic expression and reverse unfavorable methylations.