Processed foods: the scientific explanation of why we get hooked on them

The worse we eat, the more desire to continue. If you eat a hamburger, you associate it with fries and a soda.. If he goes out for a snack with some bravas or some tapas 'the body asks for' a beer. and so everything. A vicious circle of which our brain becomes a prey. And it is useless to list over and over again the virtues of a healthy diet, if the origin is in the complex mechanisms of neurobiology.

For this reason, scientists look for the keys in neurons. What mechanisms are those that promote some habits or others? An investigation published in PNAS is one of the last that tries to offer an answer. Its author, Michiru Hirasawa, from the Memorial University of Newfoundland (Canada), specializes in understanding the fundamental mechanisms underlying the regulation of body weight by the brain..

The abundance of tasty and high-fat diets in modern societies has contributed to the epidemic increase in obesity, according to the publication. This is believed to be due in part to HFD-induced inflammation in the hypothalamus, a brain region critical in energy balance..

However, it is not clear how inflammation, typically associated with the disease, can cause excessive weight gain.. Here, “we show that an inflammatory molecule prostaglandin E2 is induced in the hypothalamus by high-fat diets and directly activates a group of appetite-promoting neurons,” Hirasawa summarizes in the paper.. The work has analyzed this scheme in an animal model.

“Blocking this activation protects mice from obesity and fatty liver. This identifies a direct link between hypothalamic inflammation and weight gain, which may serve as a potential therapeutic target for obesity and metabolic syndrome.”.

From the point of view of neurobiology, an attempt is made to respond to the obesogenic adaptive pattern (PAO) where the functioning of the nervous system would be organized early by increasing intake as the main stress regulator.. In a work from the University of Chile, he proposes the pattern as an understanding model based on the lack of early integration between the various systems that regulate the HPA (hypothalamic-pituitary-adrenal) axis..

“It would be an early maladaptive response that preferentially links reward systems to modulation of the HPA axis in the absence of sufficient social regulation and that could explain early childhood obesity”. That is to say, associating a diet rich in fats, normally varied in ultra-processed foods, with a positive response to stress situations from childhood.

What is the impact of obesity in the world?

The data on obesity worldwide are alarming. The World Atlas of Obesity 2023, published by the World Obesity Federation, already predicts that the global economic impact will reach 4.32 billion dollars a year in 2035 if measures are not put in place.. This represents almost 3% of world GDP, figures similar to the impact of Covid-19 in 2020.

The majority of the world's population (51%, or more than four billion people) will be living with overweight or obesity by 2035 if current trends prevail: one in four (nearly two billion) will develop obesity. And the diseases that go hand in hand: type 2 diabetes, hypertension, stroke, cancer, depression, etc..

By 2035 the impact on the child population could be doubled compared to 2020. Rates are projected to grow more among girls than boys. In addition, the World Atlas of Obesity 2023 shows that the increase is faster among the child population compared to the adult population. Which means that they will live longer with associated diseases and the pathological risk will rise.

The objective pursued by Hirasawa's team is to combat obesity by determining the cellular-molecular mechanisms that underlie the central control of energy balance (food intake and energy expenditure), which will translate into new therapeutic targets for the obesity and eating disorders.

What is sought in the brain to curb obesity?

It is not the first study that looks for answers in the brain. Food intake is regulated by complex mechanisms involving circuits in the hypothalamus and rhombencephalon.. This has already been pointed out in several papers..

Given the relationship of obesity with other pathologies, an investigation published in Molecular Psychiatry from the Xidian University Neurological and Molecular Imaging Engineering Research Center and the Neuroimaging Laboratory of the National Institute on Alcohol Abuse and Alcoholism in Bethesda conducted a review on the neural changes that occur in obese people. Accumulating evidence from neuroimaging studies suggests that “obesity negatively affects brain function and structure, especially within the fronto-mesolimbic circuitry,” the authors conclude..

In this work it is pointed out that “obese people show abnormal neural responses to food cues, taste and smell, resting-state activity and functional connectivity, and cognitive tasks that include decision making, inhibitory control, learning/memory, and attention. Furthermore, obesity is associated with altered cortical morphometry, reduced gray-white matter volume, and poor white matter integrity.”.

What is known about how eating patterns are regulated?

Evidence showing that reward systems are also important in regulating eating behavior. In this context, the amygdala is considered a key extra-hypothalamic area that regulates feeding behavior in humans and rodents.. A review in Behavioral Brain Research focuses on the regulation of food intake by the amygdala and the mechanisms of insulin resistance in this area of the brain..

The authors from the University of Medicine of Campinas expose these complicated mechanisms (also in murine models) that a diet rich in fat and saturated fatty acids induce, such as inflammation, ER (endoplasmic reticulum) stress and the activation of serine kinases such as PKC (protein kinase C theta), JNK (c-Jun N-terminal kinase) and IKK (inhibitor of nuclear factor kappa). The data suggest that PKC and ER stress are the main mechanisms of insulin resistance in the amygdala of obese rats and play an important role in the regulation of feeding behavior.