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Does Food Addiction Really Exist?

Obesity has become one of the biggest health care burdens since the second World War ended. It is a major contributing factor to several chronic conditions. Given the social and economic burden associated with the “obesity epidemic” there has been considerable global interest across many disciplines including medicine, nutrition, neuroscience, psychology, sociology, and public health in order to reverse this trend.

Virtually all investigators have asked the question of what has changed in this relatively short period of time? A common theory is an increase in sedentary lifestyles. Some contend that this alone explains the epidemic, arguing that energy expenditure, rather than food consumption, has significantly decreased in modern society compared to our hunter-gatherer ancestors. Multiple studies support this concept of a direct correlation between physical inactivity, television watching hours, and obesity.

A second theory is the availability and consumption of highly palatable foods, which has surged in the past few decades. Nestle reported the appearance of 11,000 new food products added to the supermarket shelves every year in 1998, introducing countless new and attractive flavor combinations for food consumers.

 Investigations into the link between the “food environment” and obesity have led to the conclusion that ubiquitous access to relatively inexpensive and convenient “snack” foods have changed normal eating behavior, including less time spent preparing meals at home. Industrialization of the food supply has decreased the cost of energy dense foods by adding refined sugars, grains, and/or fats to their products. Consumption of these processed foods has increased in children and toddlers.

While behavioral and lifestyle interventions remain the mainstream “treatment” approach for obesity, dietary adherence remains an obstacle. Recent research suggests that highly processed foods are addictive and the hedonic mechanisms (pleasure-seeking pathways) may play a critical role in the pathogenesis of obesity.

It has also been suggested that the focus on calorie counting is misguided, and that future strategies should emphasize dietary quality and individual factors such as hormonal regulation of metabolism, and the gut microbiome.

The food addiction  framework for understanding obesity is the notion that highly processed “hyperpalatable” foods have hijacked the reward centers in the brain thus impairing the decision-making process, similar to drugs of abuse. The major assumption is that biochemistry drives behavior.

 The sugar addiction theory bridges current gaps between food science and neuroscience, and between nutrition and psychology. There is a subtlety to food addiction where a significant majority of the people who meet criteria may not be aware of it, likely because it is not widely accepted as a social norm.

Eating behavior is an example of a phenomenon that results from synergistic interactions among biological (hunger) and social (eating cues) levels.

Food addiction is not limited to obesity, as this construct has been extended to non-obese populations which makes causal inference difficult to assess. Much of the appetite-related research does not include the term “food addiction” likely due to the cultural stigmas associated with addiction.

There is strong evidence of the existence of sugar addiction, both at preclinical and clinical level. From an evolutionary perspective, we must consider addiction as a normal trait that permitted humans to survive primitive conditions when food was scarce. As we evolved culturally, the neural circuits involved in addictive behaviors became dysfunctional and instead of helping us survive they are in fact compromising our health.

Written by nutritionist Riin Reimer

 

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234835/

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