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Obesity represents a major public health problem, not only because of the number of people affected, but also because of the severe medical complications and the healthcare costs it causes. Obesity is considered when a person has a body mass index (BMI) equal to or greater than 30 kg / m². A BMI equal to or greater than 40 kg / m² is considered extreme obesity. Overweight is defined between 25 and 29.9 kg / m².
According to the World Health Organization, the global prevalence of obesity has doubled from the 1980s to the present. In countries like Spain, 39.4% of the adult population is overweight and 22.9% is obese. If this trend continues to increase, it is estimated that in 2030 the number of overweight people will increase by 16% more, which would mean an added cost of 3.1 billion euros per year, only in medical costs.
What is food addiction?
Food addiction is a theoretical proposition with important experimental and clinical support. It considers that some individuals may suffer a similar response to drug use when they eat foods high in fat or refined carbohydrates such as sugar (Figure 1).
A recent systematic review analyzed 52 studies on obesity and addiction to food published between 1999 and 2017, both clinical and carried out in experimental animals. Their results revealed that the criteria that were present in both disorders were:
Preoccupation with food.
Overeating despite the health risks.
Losing control over your intake.
Discomfort when doing a weight loss regimen.
Deterioration of social life due to being overweight.
Chronicity of the disorder.
Tendency to relapse.
This theory remains controversial, especially since research to identify the addictive agent in food (for example, added sugar) is in its early stages.
However, there is growing support that food addiction could be related to a phenotype present in a subgroup of people with obesity. When the Yale scale for food addiction has been used, the presence of this disorder has been found in patients who binge on food, in those who suffer frequent cycles of weight loss and gain due to diets, and in people with obesity.
Among people with obesity, the prevalence of addiction ranges between 15 and 25% and is considered the causal factor for the development of overweight. In a recent work carried out in the general North American population, it has been confirmed that, of the 986 representative individuals of that country, 15% met the criteria of addiction and was associated with the presence of obesity, young age, women with a high body mass index and lower income.
Food addiction model
As can be seen in Figure 1, food, and more clearly food rich in carbohydrates or palatable fats (such as those that appear on the left side of the figure), interact with the body through three systems.
On the one hand, ingestion causes the release of hormones produced in different organs, such as the stomach or pancreas, or adipose tissue. These mediators interact with the hypothalamus to modulate the feeling of hunger or satiety.
On the other hand, they also stimulate the hedonic system involved in brain reward, through dopamine, as occurs with substances such as alcohol or cocaine.
The history of prior learning that each subject has carried out with the intake of different foods, in different circumstances and emotional states, facilitates learning by conditioning. In this way, the subject wants to eat said foods again when these contexts are repeated.
Interaction with these systems sets in motion the same three stages that occur in drug addiction. Initially, the person associates certain foods with a pleasant sensation induced by dopamine in the reward circuit.
Subsequently, the subject perceives that he misses the intake of these foods, and over time experiences the desire or craving for them. In this way, and more frequently, when you go through negative emotional states (boredom, anger or anxiety) or are exposed to those foods, you feel a significant craving. This causes the compulsion to ingest them.
Brain imaging studies indicate that the altered circuits in people with obesity are the same as those found in people with addiction to drugs of abuse and show an imbalance between those that motivate the behaviors (due to their involvement in reward and conditioning) and those that control and inhibit feeding responses.
The model in Figure 2 shows these 4 circuits: (i) reward-salience; (ii) motivation-drive; (iii) learning-memory; and (iv) inhibitory control circuit.
In vulnerable individuals, the consumption of palatable foods, in large quantities, can upset the normal balance between these circuits. This results in a higher hedonic value of the food and a weakening of the inhibitory control. Prolonged exposure to high-calorie diets can also directly alter conditioned learning and, therefore, readjust reward thresholds in these people. Changes in the descending cortical networks that regulate overbearing responses lead to impulsivity and binge eating.
How important is this in the treatment of obesity?
The lack of knowledge that at least a subgroup of people with obesity may have a food addiction has serious implications for the planning of the treatment program.
In the first place, in them the adequate follow-up of the dietary treatment is not a problem of will. The difficulties of these people to resist the motivational value of food constitute a barrier that professionals must know to avoid the unjust blame and the consequent stigma of people with obesity. Many of them express it with phrases such as: “Not to enjoy, but to avoid feeling bad.”
A widespread idea is that everyone should lose weight if they eat fewer calories than they expend. This linear approach does not hold for people with obesity and food addiction, where chronic stress is the norm.
Under these conditions, the activation of the hypothalamic-pituitary-adrenal axis causes an elevation of cortisol and glucocorticoids, which favors the production of visceral adipose tissue and food intake. In addition, the production of leptin decreases and the production of ghrelin increases, increasing the sensations of hunger.
Likewise, there is an increase in insulin and neuropeptide Y, which increases the intake of foods, especially those with high sugar and fat content. The overingest of sugars, in these circumstances, can interrupt satiety signals, modifying the homeostatic physiological mechanisms that regulate energy intake and lead individuals to increase it (hedonic eating).
If the effect of “yo-yo” diets (weight loss and rapid recovery) is very frequent, it is even more so in people with food addiction, and in fact these ups and downs tend to aggravate it.
In the cases of people who undergo bariatric surgery, treatment teams should adapt the subsequent treatment program and carry out psychotherapeutic interventions aimed at addiction, as well as take into account the tendency of these people to develop others, such as example to alcohol.
Another element to take into account is the high prevalence of depressive and anxiety disorders among obese subjects. The belief that these people are usually happy is another mistake, and underdiagnosis of these disorders is the norm.
Finally, another relevant issue is the exclusion or not of foods with high addictive capacity (chocolate, hamburgers, industrial pastries). In many diets it is allowed that people can eat, at least one day a week, the foods they want. However, in people with food addiction, exquisite care must be taken with this type of recommendation.
As in other addictive behaviors (alcohol, gambling), advertising encourages the consumption of this type of food (junk). In this sense, the Administration should include warnings on the labeling or inform about the health risks of certain foods.
This article was originally published on The Conversation. Read the original.
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