Hormonal and Dietary Characteristics in Obese Human Subjects with and without Food Addiction

Abstract: The concept of food addiction (FA) is a potentially important contributing factor to the development of obesity in the general population; however, little is known about the hormonal and dietary differences between obesity with and without FA. Therefore, the aim of our study was to explore potential biomarkers, including various hormones and neuropeptides, which regulate appetite and metabolism, and dietary components that could potentially differentiate obesity with and without FA. Of the 737 adults recruited from the general Newfoundland population, 58 food-addicted and non-food-addicted overweight/obese individuals (FAO, NFO) matched for age, sex, BMI and physical activity were selected. A total of 34 neuropeptides, gut hormones, pituitary polypeptide hormones and adipokines were measured in fasting serum. We found that the FAO group had lower levels of TSH, TNF-α and amylin, but higher levels of prolactin, as compared to NFO group. The total calorie intake (per kg body weight), the dietary intake of fat (per g/kg body weight, per BMI and per percentage of trunk fat) and the percent calorie intake from fat and carbohydrates (g/kg) was higher in the FAO group compared to the NFO group. The FAO subjects consumed more sugar, minerals (including sodium, potassium, calcium and selenium), fat and its components (such as saturated, monounsaturated and trans fat), omega 3 and 6, vitamin D and gamma-tocopherol compared to the NFO group. To our knowledge, this is the first study indicating possible differences in hormonal levels and micro-nutrient intakes between obese individuals classified with and without food addiction. The findings provide insights into the mechanisms by which FA could contribute to obesity.

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Alex’s Notes: When discussing obesity, chronic overconsumption of calories plays a fundamental role in the etiology of the disease (yes, it is a disease now). This is fact, no matter what the anti-calorie gurus preach. However, this fails to address the “why” portion of the question. That is, we know “how” obesity happens (eating too much), but we don’t know why the persons have the eating patterns they do or why the amount of food intake is too much. These “why” answers is very much where obesity research is heading because clearly the message to eat less and move more does not work.

One reason for chronic compulsive overeating is food addiction. It has previously been demonstrated that the symptoms of food addiction are significantly associated with the severity of obesity, and that food addicts lose control over food consumption despite the negative consequences. On the other hand, the regulation of food intake is controlled by a very intricate and complex web of homeostatic and hedonic pathways. Thus, there is clearly a dysregulation of at least one of these pathways in persons with food addiction, and the current study aimed to explore potential biomarkers that may differentiate being obese with and without food addiction by comparing levels of 34 molecules listed below.


Gut Hormones

Pituitary Polypeptide Hormones


Neuropeptide Y (NPY)




Alpha-melanocyte-stimulating hormone (α-MSH)

Glucagon-like peptide-1 (GLP-1)

Adrenocorticotropic hormone (ACTH)




Brain-derived neurotrophic factor (BDNF)




Luteinizing hormone (LH)



Gastric Inhibitory Polypeptide (GIP)

Follicle-stimulating Hormone (FSH)

Plasminogen activator inhibitor-1 (PAL1)

Monocyte chemotactic protein-1 (MCP-1)


Growth Hormone (GH)



Pancreatic Polypeptide (PP)

Thyroid-stimulating Hormone (TSH)



Pancreatic Peptide YY (PYY)

Ciliary Neurotrophic factor (CNTF)


Orexin A


Agouti-related peptide (AGRP)

Connecting Peptide (C-peptide)


Substance P


The researchers screened 737 persons from the general Newfoundland and Labrador population for study inclusion and ultimately recruited 29 participants with BMIs >25 kg/m2 and met the criteria of food addiction by the Yale Food Addiction Scale (YFAS). The food addicted group (FAO) was then age-, sex-, and BMI-matched with 29 non-food-addicted control subjects (NFO) for comparison.

In addition to the 34 hormones and peptides listed above, the researchers also measured blood lipids, glucose, insulin, and body composition (DXA). Physical activity was assessed with a questionnaire about work, sport, and leisure activities, and food intake was assessed with a food frequency questionnaire (FFQ) for intake over the past 12 months.

Just a few differences

As per study design, the anthropometric and demographic variables were not different between the groups. The average age was 42 years; the average BMI was 32 kg/m2; the average body fat percentage was just over 42%; and 82% of the participants were women. There were also no differences in blood lipids, glucose, or insulin.

Only a handful of hormones and peptides differed significantly between the groups. By far the largest difference was in TSH, with the FAO group having levels that were 20% of the concentration seen in the NFO group. It is interesting to note that a previous study of alcohol dependence found a significant inverse correlation between TSH levels and the degree of alcohol craving, and that another study found a trend for TSH to inversely correlate with duration of opium consumption in addicts. The only other significantly different pituitary hormone in the current study was prolactin, which was about 20% higher in the FAO group. Converse to TSH, levels of prolactin have been shown to be significantly higher in opium addicts, and that increasing prolactin levels predict tolerance to heroin usage. Together, it does appear that lower circulating TSH and higher prolactin concentrations are associated with addiction, including food addiction.

For the Adipokines, only TNF-α was significantly different between groups, being about 7% lower in the FAO group. While this difference is small, it is noteworthy that TNF-α is a known anorexigenic cytokine that reduces food intake and has been investigated as a potential biomarker for the early stages of methamphetamine addiction. However, given that TNF-α is typically increased in obesity compared to healthy controls, there may be some form of signaling resistance or impaired action in the obese.  Regardless, this small reduction in the FAO group may help explain the food addiction.

The final significant hormonal finding was a 32% lower amylin concentration in the FAO group. It appears that amylin is affected by the macronutrient composition of meals, with a previous study showing significantly greater concentrations after consumption of a high-carbohydrate meal compared to a high-fat meal. As we’ll discuss in a moment, dietary fat intake was much greater in the FAO group which could partially explain the lower amylin levels. However, based on the controlled trial mentioned earlier, the lower amylin levels are likely secondary to food choice.

About that food

Ignoring the countless flaws present in a FFQ that requires estimation of food intake over the past year, the FAO group showed a significantly greater intake of calories per kilogram of bodyweight (24.4kcal/kg) compared to the NFO group (19.5kcal/kg). They also consumed significantly more fat expressed on an absolute intake in grams, expressed per unit of bodyweight and BMI, and expressed as a percentage of caloric intakes. Carbohydrate intake per kilogram of bodyweight was also greater. Protein intake was not significantly different between the groups and averaged about 1.0g/kg bodyweight or 19% of total energy intake.

Taken in conjunction with the finding that the obese addicts also consumed significantly more sugar and sodium, it would not be unreasonable to assume that the food addicted persons consume more hyper-palatable junk foods that are notorious for having high amounts of fat, sugar, and salt.

Bottom line

Obesity is a complex multifaceted disease. Hunger and satiety may play a central role in its etiology, as a dysregulation of hormonal secretions can lead to overeating and consequently, obesity. Food addiction may be one viable explanation, and it is interesting that there are similarities in the hormonal responses to food addiction and other forms of substance abuse. So far, these similarities appear to be low TSH, high prolactin, low or impaired TNF-α, and possibly lower amylin concentrations.

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