Genetic and Epigenetic factors in energy balance and body weight.
An individual’s predisposition to a healthy energy balance and body weight is determined by a variety of influences, both genetic and epigenetic. In addition to the instructions laid down in an individual’s genetic blueprint, environmental influences (epigenetics) during both critical developmental periods, and further on into adult life, are instrumental in determining the outcome of those instructions.
Natural selection is the process whereby organisms better adapted to their environment tend to survive and produce more offspring. And energy availability is the most important environmental factor for sustainable reproduction . This is a fundamental part of the puzzle when considering why our bodies lay down fat stores when energy (food) input is high.
This is where epigenetics steps in.
Never before have we as a species had access to such an unfailing abundance of food. Unfortunately our evolutionary blueprint has yet to catch up with this knowledge, so continues to store for leaner times ahead, a time that simply never arrives. Adding to this genetic predisposition, it would appear that obese mothers tend to have significantly more children than their lean counterparts; obesity is therefore likely to increase from generation to generation for purely genetic reasons . And apparently ‘the exquisite system for regulation of energy balance is established just once in each individual’s life’ .
So whilst genetics can certainly lay down the blueprint for obesity it is our epigenetic influences that are the greatest determiner of outcome. In the context of energy balance we have to look at the simple fact that in our society we see an alarming increase in daily energy intake, alongside this phenomenon we also see that energy expenditure has been dramatically decreasing, predominantly due to advances in technology and the ever increasing nature of sedentary work practices. However the popularly touted ‘energy in’ versus ‘energy out’ theory is only part of the puzzle.
For the purposes of this article I will look at what I consider to be two of the most influential factors predisposing individuals to problems with energy balance and body weight; they are Leptin and Hedonic Hunger.
Leptin is our master hormone and is amongst other things, responsible for telling our brain we have had enough energy in take, stop eating! Unfortunately leptin is susceptible to negative epigenetic influences which lead to leptin resistance. These influences are varied; however they include poor food choices, electron availability in our environment, triglyceride levels and even energy expenditure. To put simply what Leptin resistance is, it is when the body is producing leptin but the brain can’t see it, therefore the brain thinks you are starving. As a result your body will increase energy storage (store fat), and conserve energy use (feel lethargic). The obvious consequences are imbalanced energy and body weight.
Hedonic Hunger is a term used to describe cravings associated with food addiction. It is now recognised that highly palatable foods activate the mesocorticolimbic reward circuits of the brain by the release of dopamine, as well as other neurotransmitters and hormones like the endogenous opiates.  In simpler terms ‘as food became more processed and altered by the manufacturing industry, they began to take on more and more properties of addictive drugs, largely because of the ingredients that were added to enhance the taste of food .
Even with this brief look at energy balance and the effect on body weight we can see that both genetic and epigenetic influences make up a very complex and possibly overwhelming picture considering the obesity epidemic we, as a developed country, are facing. However I would argue that knowledge is power, and being empowered to change the epigenetic influences that we now know are so causative in this picture, we are equipped to make important changes to benefit the lives of many.
References http://www.hindawi.com/journals/isrn/2013/435027/  http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=241085  http://www.ncbi.nlm.nih.gov/pubmed/24850387  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714382/  http://www.ncbi.nlm.nih.gov/pubmed/21999688