EU Obesity Research Explores Food-Gut-Brain Mechanisms Gabriela C. Wagner, Sue P. Bird, and Julian G. Mercer | March 2013, Volume 67, No.3

EC-funded Full4Health project brings together 19 academic and industry collaborators to develop dietary strategies and a food solution across various life stages to the obesity epidemic.

Food-Gut-Brain Mechanisms

There has been a huge increase in the amount and variety of inexpensive food available to the average consumer in developed countries over the past 70 years. On the face of it, this appears to be good news and indeed was a situation that could only have been dreamed of in Europe after years of rationing during and after World War II. However, there have been some unintended consequences of this food boom, and the food and drink industry may now be perceived as a victim of its own success.

The underlying problem is that the drive to produce ever cheaper food that is palatable and enjoyable to eat has resulted in an increase in the variety of foods containing relatively high levels of fat and sugar. Combined with our increasingly sedentary lifestyles, this food bonanza has proved to be the perfect recipe for the increase in overweight and obese populations that we see across most developed and developing countries.

Accumulation of excess body fat is associated with metabolic diseases such as type 2 diabetes and cardiovascular disease that have a major impact on longevity and quality of life. A different but related problem is the increasingly aging population. Elderly people often suffer from a loss of appetite
(relative anorexia), which can lead to gradual weight loss, loss of muscle mass leading to reduced mobility, and a dramatic decrease in quality of life. Cachexia or wasting syndrome is defined as a loss of weight and muscle mass accompanied by fatigue, weakness, and loss of appetite in people who are not actively trying to lose weight. This inappetence is a clinical issue in patients recovering from major traumas or chemotherapy.

Food and dietary components interact with the gastrointestinal tract, which in turn signals hunger and satiety to the brain through as yet not well understood mechanisms.Hunger and Satiety
The increase in overweight and obese populations, and the problem of age-related and clinical anorexia are opposite ends of the same spectrum—namely, how our physiological systems interact with the food we eat in our current environment, how our appetite is controlled, and how these systems become sufficiently dysregulated to allow conditions of chronic energy imbalance to develop. The hunger and satiety systems are highly complex and multi-faceted, involving integration of  signals of peripheral origin (from abdominal organs and fat tissue) by the brain. As a first step, and as part of “mealprocessing”, there is the release of hormones from the gut in response to the consumption of food. Such short-term dynamic signals are complemented by more chronic signals arising from accumulated fat stores which signal to the brain how much energy is already stored and the flux of energy into and out of these reserves. Beyond the mere regulation of energy requirements (energy balance), there is also a higher level of control driven mostly by our pleasure and reward eating behavior. All these signals, alongside a range of other environmental and social information, are processed in the brain, leading to a stimulation or reduction in food consumption, and to feelings of hunger or satiation (feeling full).

A protein-enriched diet allows eating to appetite at a lower caloric intake. This leads to weight
A protein-enriched diet allows eating to appetite at a lower caloric intake. This leads to weight loss without hunger pangs.

The control of hunger and appetite, and the likelihood of developing chronic non-communicable diseases such as obesity or diabetes, can be established at the very beginning of our lives, before we are even born. Women often look at pregnancy as a time for guiltfree “eating for two” but nutritional experience during this critical developmental phase may have long-term consequences for the developing fetus reaching far into adulthood.

Epidemiological evidence confirms that susceptibility to obesity and other chronic diseases can be related back to the mother’s level of nutrition during pregnancy. A particularly compelling body of information has been collated relating to the so-called “famine winter” in the Netherlands during World War II (Roseboom et al., 2006; Bouret, 2010), during which levels of caloric intake were markedly reduced due to acute food shortages over a period of months. Exposure to this caloric restriction in utero had a marked effect on rates of obesity, diabetes, and other health problems, depending on the timing of the pregnancy relative to the period of extreme rationing. Similarly, but at the opposite end of the nutritional spectrum, children born to obese and/or diabetic mothers in the current obesogenic environment, and who consequently experience hypernutrition or overnutrition in early life, have a greater risk of developing obesity and diabetes in later life. The true magnitude of these current-day nutritional programming effects is hard to quantify precisely, but they seem likely to be a contributory factor in the alarming trends in childhood obesity, with recent statistics estimating that 20% of children are overweight or obese in Europe, according to the European Association for the Study of Obesity (EASO).

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