What do you know about eating disorders and the 5ht2c gene? And what info can you find on the efficacy of asenapine and binge eating or bulimia? It's a new antipsychotic, or sort of new.
In terms of serotonergic genes, most of the focus has been on the 5HTTLPR transporter gene and the 5-HT2A receptor genes, for both AN and BN. The findings are generally mixed. You’ll find a few studies in support of an association of one allele and then a roughly equal amount of studies that do not find a significant association.
According to Trace et al. (2013), “Additional 5-HT transporter genes, including 5-HT2C, 5-HT1B, 5-HT1D, and 5-HT3B, have shown significant associations with AN.” (They don’t mention it for BN).
There are the studies I found on 5-HT2C:
https://www.ncbi.nlm.nih.gov/pubmed/17055531
We detected significant evidence of association between the -995A/-759T/-697C/Cys23 haplotype of the 5HT2C gene and different anxious and depressive subscales of the SCL90-R instrument, that included Somatization (p = 0.029), Obsessive-Compulsiveness (p = 0.021), Depression (p = 0.032), Anxiety (p = 0.004), Hostility (p = 0.028), Phobic Anxiety (p = 0.029) and Paranoid Ideation (p = 0.008), in BN patients. We also observed a strong association between the 5HTTLPR polymorphism of the SLC6A4 gene and Anxiety in the same group of BN patients (p = 0.004).
Oddly, Trace et al. cited 3 papers by Ribases et al. but did not cite this one. I’d be very sceptical of these findings. They report associations, but the p values are not particularly convincing to me and I don’t know if they properly controlled for multiple testing (I didn’t bother downloading the paper). And it is only 82 patients...
https://www.ncbi.nlm.nih.gov/pubmed/11232918
These guys looked at AN; 45 sister-pairs where one had AN and the other didn’t:
The sisters with anorexia nervosa differed from their healthy sisters in terms of personal vulnerability traits and exposure to high parental expectations and sexual abuse. Factors within the dieting risk domain did not differ. However, there was evidence of poor feeding in childhood. No difference in the distribution of genotypes or alleles of the DRD4, COMT, the 5HT2A and 5HT2C receptor genes was detected. These results are preliminary because our calculations indicate that there is insufficient power to detect the expected effect on risk with this sample size.
In other words, I wouldn’t hold my breath.
https://www.ncbi.nlm.nih.gov/pubmed/16343451
This might be interesting, but it is in rats:
These results are consistent with the hypothesis that medial PBN neurons mediate anorexia through 5HT2C receptors.
https://www.ncbi.nlm.nih.gov/pubmed/16433010 (and https://www.ncbi.nlm.nih.gov/pubmed/22249823)
Serotonin (5-HT)2C receptors play an important role in the modulation of monoaminergic transmission, mood, motor behaviour, appetite and endocrine secretion, and alterations in their functional status have been detected in anxiodepressive states. Further, 5-HT2C sites are involved in the actions of several classes of antidepressant. At the onset of treatment, indirect activation of 5-HT2C receptors participates in the anxiogenic effects of selective 5-HT reuptake inhibitors (SSRIs) as well as their inhibition of sleep, sexual behaviour and appetite. Conversely, progressive down-regulation of 5-HT2C receptors parallels the gradual onset of clinical efficacy of SSRIs. Other antidepressants, such as nefazodone or mirtazapine, act as direct antagonists of 5-HT2C receptors. These observations underpin interest in 5-HT2C receptor blockade as a strategy for treating depressive and anxious states.
I am always hesitant to comment on psychiatric drugs because I just always think about the file drawer effect, particularly when it comes to drugs that companies want to market. I didn’t find anything on it for binge eating or bulimia on PubMed.