3.16

Genes, and mitochondria expression at the cellular level influence our mental health, as well as our body composition, drive to eat, and even our eating behaviors. Current research suggests that almost all mental and metabolic health disorders can be traced to mitochondrial dysfunction of some kind [106]. Cells that are overly excited due to chronic stress or anxiety, may cause over activity in cells. In the body this may lead to atrial fibrillation which increases the risk for a subsequent heart attack. In the brain, this excitability may produce transient ischemic attacks that often precede a strokes. We also see this excitability in the manic phases of bipolar disorder, PTSD, panic disorder, and other conditions marked by mania. Cells can also be sluggish and underactive as seen with metabolic disorders and depression. Or in some cases, cells may be dying faster than they’re supposed to, resulting in shrinking of or brain.

So far all the gene mutations that lead to metabolic disorders have their normal function in the hypothalamus, the area of the brain (Brian) we know controls our appetite and energy expenditure [50]. With respect to mental health, there is no one gene or cellular dysfunction that activates a particular psychiatric disorder or any other complex psychological trait. In fact, many genes and cells interact to influence the human brain. Normal and disordered psychological characteristics are polygenic, meaning that they are each shaped by a large number of genes [52]. While rare mutations in certain genes may have a disproportionate impact, for the most part, each of the many relevant genetic differences plays a very small role in increasing or decreasing risk of a particular condition or influencing a given trait [52].

Polygenic risk scores (PRS) are predictors of the genetic susceptibility to diseases [49]. On their own, PRS will never be able to establish or definitively predict a diagnosis of common complex conditions (eg, mental health disorders), because genetic factors only contribute part of the risk and PRS will only ever capture part of the genetic contribution [53]. Consider the individual who has inherited a predisposition for alcohol dependence (alcoholism) from one or both parents, or grandparents. If that person doesn’t drink, it’s highly unlikely they’ll trigger the genetic ON switch for this disease. That said, they still may have a higher likelihood for developing other types of addictive disorders or behaviors. We can help ourselves and future generations if we talk about our genetic inheritance with providers [52, 53].