Analysis: research shows how the gut talks to the brain controls what, how much and when we decide to eat
Bodyweight is a pervasive preoccupation of the modern day psyche, especially excess bodyweight or obesity. Despite strong evidence to the contrary, current dogma contends that any individual can reduce their bodyweight by deciding to eat less and by moving more.
Individuals that are unable to reduce their bodyweight are often reproached for having insufficient willpower. This perspective fails individuals and society by underplaying many factors intrinsic to the individual or symptomatic of the "obesogenic" pressures of our modern sedentary consumer society.
One element that remains almost completely obscured to public consciousness is the degree to which food intake and energy expenditure are subject to control mechanisms that lie beyond or behind the conscious decision making higher functions of the brain. Decades of research have led us to discover that there is extensive hardwiring and blood-borne mediator-based message exchange occurring between the gut and more primitive parts of the brain before, during and after eating.
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These pathways acts as the fundamental regulators of food intake and help balance bodyweight around a favourable set-point when operating optimally. A key message for scientists to communicate is that when message relay is corrupted along this axis, appropriate control of appetite and food intake can be lost in such a fundamental way as to render it virtually resistant to the application of willpower.
If we accept that hunger and appetite are intrinsically normal responses of the body, designed to activate an "energy-in" pattern of behaviour (eating, basically), what then establishes what quantity of energy will be taken in? And how frequently the pattern will be invoked?
Lets do some physiology 101 to get closer to the answer. Healthy people typically start the day with breakfast. When the food consumed enters the gut, hormonal and neural signals are transmitted from the lining of the gut as a response to its arrival and stimulate activity of other organs such as the liver and pancreas, recruiting them to assist with the digestion and absorption of nutrient.
Signals from the gut are modulated by the multitude of bacteria, known as microbiota, that live in the gut with net positive or negative consequences dependent upon composition. Many of the signals from the bowel are also received by unconscious parts of the brain such as the brain stem, hypothalamus and basal nuclei that collectively provide autonomous control of bodily function.
The way the gut talks to the brain controls what, how much and when we decide to eat
When signals from the gut to the brain reach a certain threshold during eating, we experience the feeling of satiety and a stop signal is activated which changes desire on our part from "wanting to eat" to "wanting to stop eating". These gut-derived signals progressively wane in intensity, resulting in a renewed feeling of "wanting to eat", with the usual outcome being a further intake of food at lunch. Thus, the way the gut talks to the brain controls what, how much and when we decide to eat.
The collective evidence obtained from the work of my group and many others internationally demonstrates that there is disruption to the flow of conversation between the gut and the brain following food intake in patients with clinical obesity. This points to an intrinsic defect in the signalling system controlling food intake in such individuals.
One way to correct this is for the brain to ask the gut to shout a little louder - that is, to generate higher levels of signal following food intake. Fortunately, bariatric surgery has offered a means of achieving this signal amplification, based on reconfiguration of the gut and attendant changes in the progress of ingested food through it.
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For example, food passes much more rapidly into the more distal regions of the gut in patients after gastric bypass surgery. Prompt contact of food with the gut wall in these regions causes an exaggerated neural and hormonal relay of messages to the brain signalling satiety. This means that the "wanting to eat" programme is interrupted earlier and consequently less food is consumed. Gastric bypass surgery typically allows patients to feel less hungry and more satisfied resulting in 20 to 30 percent bodyweight loss. The message amplification from the gut to the brain is universally accepted as one of the key drivers of its effects.
Science and surgery have allowed a breakthrough in our understanding of obesity as having a fundamental basis in communication difficulties between the gut and the brain. Surgery and new drugs that mimic some of the effects of surgery can help to compensate for deficits therein. The next time you eat and experience the onset of satiety, remember that this is the product of finely balanced message transfer and receipt from the gut to the brain. It should be conceptually easy to appreciate that this signal can become broken in people who have the disease of obesity and thus overeating and weight gain would be the logical consequence.
Professor Carel le Roux is Head of Pathology and Chair of Experimental Pathology at UCD. He has received the President of Ireland Young Researcher Award from Science Foundation Ireland, a Clinician Scientist Award from the National Institute for Health Research in the UK and a Wellcome Trust Clinical Research Fellowship amongst others. He was awarded an Irish Research Council Consolidator Laureate Award in 2018.
The views expressed here are those of the author and do not represent or reflect the views of RTÉ