Summary: Elevated opioid neurotransmission in the brain may underlie appetite loss and emotional symptoms in anorexia nervosa. Compared to healthy controls, patients with anorexia had increased opioidergic tone, which regulates appetite, pleasure, and mood.
Despite severe malnutrition, glucose uptake in the brains of anorexia patients remained comparable to controls, suggesting the brain prioritizes maintaining function. These findings may explain the interplay between appetite regulation, anxiety, and depression in anorexia and provide new directions for treatment development.
Key Facts:
- Elevated Opioidergic Tone: Anorexia patients showed increased brain opioid activity compared to controls.
- Energy Use Preserved: Brain glucose uptake remained steady despite severe malnutrition.
- Mood Regulation Link: Changes in opioid activity may contribute to anxiety and depression in anorexia.
Source: University of Turku
A study conducted at Turku PET Centre in Finland showed that changes in the functioning of opioid neurotransmitters in the brain may underlie anorexia.
Anorexia nervosa is a serious psychiatric disorder characterised by restricted eating, fear of gaining weight, and body image disturbances, which may lead to severe malnutrition, depression and anxiety.
A new study from Turku PET Centre shows how changes in neurotransmitter function in the brain may underlie anorexia.
“Opioid neurotransmission regulates appetite and pleasure in the brain. In patients with anorexia nervosa, the brain’s opioidergic tone was elevated in comparison with healthy control subjects.
“Previously we have shown that in obese patients the activity of the tone of this system is lowered. It is likely that the actions of these molecules regulate both the loss and increase in appetite,” says Professor Pirjo Nuutila from the University of Turku, Finland.
In addition, the researchers measured the brain’s glucose uptake. The brain accounts for about 20% of the body’s total energy consumption, so the researchers were interested in how a reduction in the energy intake affects the brain’s energy balance in anorexia.
“The brains of patients with anorexia nervosa used a similar amount of glucose as the brains of the healthy control subjects.
“Although being underweight burdens physiology in many ways, the brain tries to protect itself and maintain its ability to function for as long as possible,” says Professor Lauri Nummenmaa from Turku PET Centre and continues:
“The brain regulates appetite and feeding, and changes in brain function are associated with both obesity and low body weight.
“Since changes in opioid activity in the brain are also connected to anxiety and depression, our findings may explain the emotional symptoms and mood changes associated with anorexia nervosa.”
The study was carried out in collaboration with the Turku University Hospital and Pusan National University in South Korea.
The brains of patients with anorexia nervosa and the healthy control subjects were imaged using positron emission tomography at Turku PET Centre.
About this neuroscience and eating disorders research news
Author: Tuomas Koivula
Source: University of Turku
Contact: Tuomas Koivula – University of Turku
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“Anorexia nervosa is associated with higher brain mu-opioid receptor availability” by Lauri Nummenmaa et al. Molecular Psychiatry
Abstract
Anorexia nervosa is associated with higher brain mu-opioid receptor availability
Anorexia nervosa (AN) is a severe psychiatric disorder, characterized by restricted eating, fear to gain weight, and a distorted body image.
Mu-opioid receptor (MOR) functions as a part of complex opioid system and supports both homeostatic and hedonic control of eating behavior.
Thirteen patients with AN and thirteen healthy controls (HC) were included in this study. We measured (1) MOR availability with [11C]carfentanil positron emission tomography (PET), (2) brain glucose uptake (BGU) with 2-deoxy-2[18F]fluoro-D-glucose ([18F]FDG) PET during hyperinsulinemic-euglycemic clamp and (3) blood-oxygen-level-dependent signal with functional magnetic resonance imaging.
All subjects underwent a screening visit consisting of physical examination, anthropometric measurements, fasting blood samples, an oral glucose tolerance test, psychiatric assessment, and an inquiry regarding medical history.
Body fat mass (%) was measured and M value was calculated. MOR availability from caudate and putamen was higher in patients with AN and those from nucleus accumbens (NAcc) and thalamus showed the higher trend in patients with AN.
There was no area where MOR availability was lower in patients with AN. BGU was not different between AN and HC. MOR availability and BGU were negatively correlated in caudate, NAcc and thalamus and showed the trend of negative association in putamen.
In conclusion, AN is associated with higher MOR availability in the brain regions implicated in reward processing, while BGU remains unaltered.
Therefore, the endogenous opioid system might be one of the key components underlying AN. This better understanding of AN could support the development of new treatments for AN.
