Not to mention good old fashioned observation. In societies obsessed with body image and self-indulgence, it is becoming increasingly difficult to reconcile beauty and gluttony. Before giving into an ungainly, young death, let’s first explore the mechanisms underlying obesity, which is the only way to understand what can be done.
Firstly, where does excess weight come from? Glucose is the primary source of energy for the body and is also important for synthesising other molecules. The excess after the body’s needs have been met is stored as glycogen and as triglycerides in the all too familiar adipose tissue, fat. The amount of glucose required and stored is determined by metabolism, the chemical reactions occurring within cells in the body, sustaining life. People with an efficient metabolism are more effective at storing excess glucose, while others are less efficient and have difficulty putting on weight, losing a lot of energy as heat. The idea of these people having a ‘fast’ metabolism is a misconception. Obesity is a problem of energy intake. Although energy output (only voluntarily controlled by exercise) is an important factor, energy input is the primary determinant of body mass. Energy intake is regulated by appetite, which is in turn governed by hunger and satiety, behavioural mechanisms easily misconstrued as more subjective feelings. The brain is of course the ultimate controller.
The control of appetite is an entanglement of neurons, signals and pathways. A collection of neurons in the hypothalamus called the arcuate nucleus responds to signals concerning appetite, whilst satiety is controlled by the nucleus tractus solitarius (NTS) in the brain stem. These neurons respond to chemical signals from various parts of the body, resulting in a signalling cascade that ultimately creates the feelings of hunger and fullness dictating food intake. The short-term control of meal size and frequency is determined by blood glucose levels and hormones produced by the gastrointestinal tract. Physiological ingenuity becomes apparent in these pathways. For example, a hormone called cholecystokinin is released by the small intestine during the course of a meal. It not only facilitates the digestion of nutrients, but secretion correlates with the amount of nutrients present and directs the NTS accordingly. This is why we stop eating before ingested food is actually digested.
The hormone ghrelin, produced by the stomach to stimulate appetite before meals, demonstrates how the interplay of other factors with feeding behaviour can arise. Ghrelin also stimulates the release of brain peptides called orexins, which play a role in sleep. Researchers have found that less than 7-9 hours of sleep can greatly increase the risk of obesity. The maintenance of a relatively stable weight during adulthood is also influenced by hormones, namely leptin, which is produced by fat cells (adipocytes). As fat stores increase, as does leptin secretion, acting on the arcuate nucleus to decrease food intake. Inherited genetic mutations in the leptin-signalling pathway could contribute to obesity. Appetite is not a straightforward, established mechanism, and there are many influences on that final decision: to eat or not to eat.
The intermingling of metabolic pathways can have sinister consequences by linking obesity to deadly diseases. Diabetes, heart disease and arthritis are among the known side effects of excess body fat. Connections are not all fully understood, but one link between diabetes and obesity goes as follows. Adipocytes produce proteins that decrease insulin sensitivity of cells. More adipocytes, lower sensitivity: hello type 2 diabetes. It cannot be emphasised enough that the cross-linked nature of these pathways means there may yet be repercussions to emerge.
How can this knowledge be used to tackle the growing epidemic? Drugs that mimic the actions of the body’s own hormones are one possibility. For example, a drug used in the treatment of type 2 diabetes is chemically similar to a gastrointestinal hormone. It increases insulin secretion, decreases levels of glucagon and increases satiety, ultimately helping maintain healthy glucose levels and assisting in weight loss. A hormone used to treat motor neurone disease caused unexpected, significant weight loss by activating leptin-like pathways. The manipulation of neurons themselves is currently under investigation as a means of direct control over feeding behaviour. Ultimately, combating obesity comes down to drastic lifestyle changes. Controlled energy input, assisted by increased energy output. Train your mind or trick your body.