A “theory neutral” analysis of the 23andMe data of chromosomes 1-22 has been completed .
That is, no particular marker was intentionally searched for with bias, but a very “by the book” associative analysis of a subset of quality-controlled genotyped and imputed SNPs from chromosomes 1-22 was performed to see if any broke past the established ‘standard’ GWAS significance threshold of p<5x10^-8.
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Unfortunately, and quite expectedly, no single SNP was observed beyond this significance threshold.
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There didn’t appear to be any greater correlation between either case group or control group and over-represented SNPs in any trait/disease featured on ImputeMe.
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Nothing in the top results of the gene or pathway analyses this round sticks out as indicative of epigenetic mechanisms, known diseases, common symptoms in PFS/PAS/PSSD, steroid metabolism, AR signalling, known diseases, immunity, autoimmunity, gluten intolerance, etc…
Basically, a proverbial “needle in the haystack” wasn’t discovered in these results.
However; there were multiple SNPs in a small region of chromosome 4 in the imputed data (only 1 of these was present in the genotyped 23andMe data) that were near the significance threshold at Nx10^-7. I am going to approach an acquaintance with GWAS experience to ask if this may be suggestive of anything. It appears to be an intergenic region of little known consequence.
Links to the summary results and gene and pathway analyses will be posted soon. Be patient.
If it is advisable, some more imputed genomes could be easily added to the analysis since the process is practically automated after all this hard work. A strictly post-finasteride patient analysis could also be easily performed soon. Chromosome X analysis may or may not be worth the time and effort but I will briefly look into it.