Best way to see your neurotransmitter levels is via OAT test, its measuring the urine metabolites of those substances.
What you describe doesnt look like its caused by genetic reasons (in your case if severely depressed - suicidal thoughts), based on their status you've posted above. To see the metabolism better you should test everything from everywhere. At least hair test + full metal panels of iron, copper, zinc, etc., the more the better. Maybe your MAO status holds some answers for you.
Measuring neurotransmitters is something that his hardly done within Psychiatry/psychology for a reason, it is simply not reliable or representing a good picture of the situation.
Thats why antidepressants are basically a trial and error strategy
Although the androgen receptor (AR) has been detected by ligand-binding assays, there is little known about the expression and regulation of the AR gene in human breast-cancer cells. AR mRNA, measured by Northern analysis in 18 cell lines, was found to be expressed predominantly in oestrogen- and progesterone-receptor-positive (ER+, PR+) lines as a single species of approximately 10.5 kb but was also comparatively abundant in I ER- and PR-negative cell line, MDA-MB-453. Dexamethasone (Dex), Organon 2058 (Org 2058), dihydrotestosterone (DHT), and all-trans-retinoic acid (RA) down-regulated AR mRNA levels in T-47D (ER+, PR+) cells 6 hr after treatment, whereas oestradiol (E2) had no effect. In MDA-MB-453 (ER-, PR-) cells, regulation of AR mRNA by RA differed from the other cell lines: RA increased the level of AR mRNA. DHT-binding assays indicated a corresponding increase in AR protein. Transfection of the androgen-responsive mouse mammary tumour virus long-terminal repeat (MMTV LTR) linked to a chloramphenicol acetyltransferase (CAT) reporter gene was used to examine the effect of altered AR levels on androgen action. The increased level of AR following RA pre-treatment in MDA-MB-453 cells resulted in enhanced induction of CAT activity by DHT and, conversely, a decrease in the level of AR following RA pretreatment in T-47D cells resulted in reduced induction of CAT activity by DHT. These data demonstrate that AR is expressed predominantly in ER+ and PR+ cell lines and its expression is regulated by ligands also known to regulate ER or PR, including progestins and retinoids. Androgen responsiveness measured by a transfected reporter gene was altered according to the extent of up- or down-regulation of AR expression, demonstrating that responsiveness is dependent on receptor concentration.
Retonic acid (like fin) seemed to increase androgen receptors at first, but then after treatment the increase in CAT activity from dht actually caused a down regulation of gene expression. this must be the reason dht makes us feel like shit. chloramphenicol acetyltransferase (CAT) seems to be the reason dht doesnt work for us anymore and makes us feel like shit. PFS could be a matter of purely androgen insensitivity along with PAS, but maybe PAS is a much worse condition. this is definitely some epi-genetics shit going on here.
is there anything we can do to manipulate this CAT that the study speaks on?
Can you look at ammonia in blood? Also comprehensive parasitology I’ve never had done but it makes most sense. A medical doctor who beat pfs “JN” recommends this as well. I’m not sure of lab but I’d just check that they are doing an in depth check on pathogens in your blood or stool.
gut bacteria is all about PH. Fin binds NADPH and kills glutathione. Glutathione transferase goes down. It cant metabolize fin out. glutathione transferase is activated by tyrosine, and serine.and cysteine. So those are heavily used. And your thyroid and digestion go down.
Read the fist post. Fin can still be in you.