Genome wide analysis is a brute force technique, that relies on associating known variations in the genome and caseness. It requires very large numbers, as the large number of tests imply that without a very high level of significance any association is likely to be spurious. Instead of accepting 1:100 chance of error, the standard significance level is on in a hundred thousand, or one in ten million.
A recent paper in molecular psychiatry meta analyzed a GWAS from multiple databases. As you can see, there is are associations.
The authors note (CC is case control, FS is Factor Score)
In the CC model, we identified a novel genome-wide association within an uncharacterized non-coding RNA locus LOC152225 on chromosome 3q12.3. We found no extant reports for this locus in PubMed or the NHGRI Catalogue of Published GWAS. In the FS model, we detected genome-wide significant associations at SNPs in three genes within a large LD block on chromosome 2p21, each of which has reported expression in brain: (1) SLC3A1 encoding the large subunit of a heterodimeric dibasic/neutral amino acid transporter (solute carrier family 3 (amino acid transporter heavy chain), member 1); (2) PREPL encoding a putative prolyl endopeptidase belonging to the prolyl oligopeptidase family; and (3) CAMKMT encoding a calmodulin-lysine N-methyltransferase. This region is well-known for two contiguous gene-deletion syndromes, the hypotonia–cystinuria syndrome and the more severe 2p21 deletion syndrome.31 Deletion of SLC3A1 results in the autosomal-recessive form of cystinuria,32 while PREPL deletion causes hypotonia at birth, failure to thrive and growth hormone deficiency.33 The evolutionarily conserved class I protein methyltransferase encoded by CAMKMT acts in the formation of trimethyllysine in calmodulin, which is involved in calcium-dependent signaling.34 Interestingly, GWAS of SCZ and BIP have highlighted other genes encoding proteins involved in calcium-dependent signaling.35 Although the most significant SNP, rs1067327, is located in an intron of CAMKMT, in silico analyses suggest rs698775 is the most likely functional candidate with a cis regulatory effect possibly specific to PREPL.
This is not a full answer. There is no consideration of the interaction of gene and enviroment, and the mechanisms of calcium regulation and pathophysiology are unclear, let alone the relationship of pathophysiology with specific anxiety disorders — if they are indeed independent. This type of research emphasises the commonalities between each of the current syndroms in DSM or ICD.
But papers like this indicate where to look, and what parts of neural biochemistry need to be investigated further.
[…] also happens with the disadvantaged. We may be assorting people by dysfunction. And, given that there are genetic underpinnings of most anxiety disorders, this could be increase the burden on society, and the unhappiness of the […]