I recently attended the International Society for Psychiatry Research’s first annual conference. This conference was PACKED with the latest in connections between nutrition, mood & metabolic pathways.
A theme that came up over and over again? Our nutrient status is closely interwoven with neurotransmitter (brain chemical) regulation and signaling.
A number of nutrients are ‘cofactors’ in the creation of neurotransmitters (or ‘brain chemicals’). A cofactor is a substance (other than the substrate) whose presence is essential for the activity of an enzyme (source)-meaning that, without sufficient amounts of certain nutrients, we simply cannot regulate neurotransmitters appropriately.
There are well over 100 different neurotransmitters in the brain alone, including one called dopamine. When thinking about ‘altered neurochemical function’, it’s pretty important to think about whether or not we have enough nutrients-in the right form-on board to help keep our neurotransmitter levels in check!
As an example, let’s just take a peek at a couple of nutrients, related genetics, levels of Dopamine, and their emerging relationship to the ‘reward center’ in binge eating disorder:
Key diagnostic features of Binge Eating Disorder (BED), the most common eating disorder in the United States, are:
- Recurrent and persistent episodes of binge eating. Binge eating episodes are associated with three (or more) of the following:
- Eating much more rapidly than normal
- Eating until feeling uncomfortably full
- Eating large amounts of food when not feeling physically hungry
- Eating alone because of being embarrassed by how much one is eating
- Feeling disgusted with oneself, depressed, or very guilty after overeating
2. Marked distress regarding binge eating
3. Absence of regular compensatory behaviors
(If you think that you might be struggling with BED, reach out for support: https://www.nationaleatingdisorders.org/help-support/contact-helpline)
How could nutrition relate? Both Folate and B12 are cofactors for catechol-0-Methyl transferase, which regulate the breakdown noradrenaline and dopamine in the synaptic cleft. What’s dopamine? It’s the main modulator of the brain ‘reward’ system-with a significant role in food intake. In one study, Wang et al (2011) showed that dopamine release in the caudate was correlated with the severity of binge eating in individuals with and without BED (source). Wiss & Brewerton (2017) review the biological vulnerabilities involved in food addiction, including impaired dopamine signaling (source).
Recent research has even begun to link certain genetic profiles linked to dopamine metabolism to binge eating, In the words of Hersrud & Stoltenberg (2009):
“Previous studies of the interaction between COMT and DAT1 genes reported these genotypes to be associated with altered reward sensitivity and cognitive function. This supports our findings in that persons with food and weight problems have deficits in cognition and reward processing compared to normal controls as cited above. This and the work of others (e.g. Bilder et al., 2004) suggests that Val158Met and DAT1 VNTR interact to produce two alternative phenotypes susceptible to disordered eating—one characterized by an understimulated reward system and cognitive rigidity (Met/10; too little COMT activity and too much DAT activity) and the other characterized by an overactive reward system and impulsive distractibility (Val/9; too much COMT activity and too little DAT activity).” (link)
Although, of course, eating behaviors are complex and influenced by a number of environmental, social, and personal factors…the concept that biology shapes our behavior or tendencies should not be ignored. Addressing concerns related to food-related rewards, pleasure, and motivation should take into account biological drive…with beneficial modulation from nutrient support where possible.
When it comes to dopamine, a couple of other interesting things to note from ISNPR: not having enough Omega-3 during brain development can lead to a decrease in ventral stratal D2 like receptors. Interestingly, low levels of DHA (a type of Omega-3) was the only type of fatty acid consistently correlated to adult ADHD (where dopamine is a target of drug therapy) in a recent meta-analysis (source). Check with your medical provider before considering any type of supplementation regimen.
Are you curious about Cravings?