Energy and Hormones P1

Bioenergetics is a branch of biochemistry that deals with how living systems manage and use energy. The term originated in 1956 from Nobel laureate Albert Szent-Györgyi. The field expanded with the development of Peter Mitchell’s chemiosmotic hypothesis in 1961, explaining how cells produce adenosine triphosphate (ATP) in the mitochondria. When we eat food, our cells produce energy in the form of ATP in the mitochondria through a set of redox reactions that contribute to reactive oxygen species (ROS) production. Once thought of as a simple by-product of metabolism, mitochondrial ROS are signaling molecules required for diverse cellular functions such as differentiation, proliferation, death, and adaptation to stress. What we feed our mitochondria determines what they tell our cells. What has become increasingly evident is that the mitochondria are not only the powerhouses of the cells, they regulate cellular functions and dictate cell fate.

There is no fast or slow in metabolic health. Our metabolisms are regulatory systems. The human body is miraculous in its ability to compensate, adapt, and address underlying problems. Overall, the body strives to maintain a balance, known as homeostasis. When someone complains of a ‘slow metabolism,’ what they suffer from is an intrinsic metabolic abnormality. This is not the slowing of an engine, it is the result of the wrong inputs.

Insulin’s metabolic control is mediated through reactive oxygen species generation. Reactive oxygen species (ROS) are natural byproducts of producing energy in an oxygen-rich environment. Insulin signaling is intrinsically related to the actions of ROS. Insulin signaling is ROS-dependent: Low concentrations activate insulin signaling (cellular hunger), while high concentrations inhibit insulin signaling (cellular satiety). Saturated fats generate ROS at physiologically appropriate levels leading to cellular satiety. Increasing the consumption of polyunsaturated fatty acids (PUFAs), results in decreased generation of ROS and fails to limit insulin signaling at physiological levels. The reason for this has to do with the chemical structure of saturated fatty acids versus PUFAs. The presence of the double bonds in PUFAs undergoing β-oxidation blunts ROS production.  Since the mitochondria integrate the total energy availability in a cell, a failure to generate appropriate levels of ROS can fail to develop resistance to insulin-facilitated nutrient ingress into cells. This disorder in fuel partitioning leads to reduced fat oxidation and trapped energy in adipose tissue, resulting in a compensatory rise in food consumption, a decrease in energy expenditure, or both. In simple terms, getting fat makes you hungry.

Increased and frequent consumption of refined carbohydrates facilitates frequent insulin secretion and insulin signaling activation at the cellular level. Adding high quantities of seed oils to the mix prolongs the insulin signal and allows more time to drive fat into fat tissue without cellular satiety (i.e., shutting down insulin signaling). Obesity results from dysfunction in limiting insulin signaling at cellular levels by an evolutionarily conserved core signaling system–ROS.