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Re: PSSD Genome Project [Megathread]

Unread postPosted: Tue Oct 02, 2018 10:02 pm
by Ghost
This may be of interest for a sample set:

NESDA sample
NESDA is a longitudinal, naturalistic cohort study examining the course and consequences of depressive and anxiety disorders. The collection and genotyping of the NESDA sample has been described elsewhere.17 In brief, 2981 participants were recruited through mental health care organizations (n=807), the community setting (n=564) and primary care (n=1610). They were assessed using the Composite Interview Diagnostic Instrument to diagnose depressive and anxiety disorders according to the Diagnostic and Statistical Manual of Mental Disorders—Fourth Edition. The interview also provided information on age of onset, number of major depressive disorder episodes and specific symptoms of depression. At baseline, detailed assessment was made of psychopathology using different inventories and scales. Many other data were collected including sociodemographic data and health indicators.

https://www.nature.com/articles/tpj201216
(Read about the significance of this gene in my loggings)

Re: PSSD Genome Project [Megathread]

Unread postPosted: Mon Oct 22, 2018 6:25 am
by anacleta

Re: PSSD Genome Project [Megathread]

Unread postPosted: Thu Oct 25, 2018 6:12 pm
by TalkingAntColony
Here is the list of genes shown by that recent study to be epigenetically regulated by citalopram. It could be insightful to see if any of these genes overlap with PSSD genome abnormalities.

https://docs.google.com/spreadsheets/d/ ... sp=sharing

Re: PSSD Genome Project [Megathread]

Unread postPosted: Sat Oct 27, 2018 1:45 pm
by anacleta

Re: PSSD Genome Project [Megathread]

Unread postPosted: Wed Jan 16, 2019 2:38 am
by Adweit saha
I was suffering from pssd for 2 years from fluoxetine which I used for only 1 year.I had completely lost my hope that time.My anxiety was peak nd I returned to fluvoxamine.I used it for 2 months..nd then stopped it.pssd was still there.Someone suggest me to try Shilajit a Ayurveda herb..nd I tried it
Nd my life completely changed..I found pssd improved by 70 percent in 2 weeks.Ithink all this happened due to half life.Fluoxetine has the highest half life of all drugs.It takes more time to go out of your system..Nd then also some short of withdrawal symptoms you will find.When I tried fluvoxamine ..it changed the brain chemistry it changed the impact which was made by fluoxetine ..after stopping fluvoxamine which has a very short half life period..it goes away fromy system..Nd the other part is done by shilajit

Re: PSSD Genome Project [Megathread]

Unread postPosted: Wed Jan 16, 2019 3:16 am
by John321
Adweit saha wrote:I was suffering from pssd for 2 years from fluoxetine which I used for only 1 year.I had completely lost my hope that time.My anxiety was peak nd I returned to fluvoxamine.I used it for 2 months..nd then stopped it.pssd was still there.Someone suggest me to try Shilajit a Ayurveda herb..nd I tried it
Nd my life completely changed..I found pssd improved by 70 percent in 2 weeks.Ithink all this happened due to half life.Fluoxetine has the highest half life of all drugs.It takes more time to go out of your system..Nd then also some short of withdrawal symptoms you will find.When I tried fluvoxamine ..it changed the brain chemistry it changed the impact which was made by fluoxetine ..after stopping fluvoxamine which has a very short half life period..it goes away fromy system..Nd the other part is done by shilajit


So are you taking shilajit on a regular basis or you stopped after taking it for a while?

Re: PSSD Genome Project [Megathread]

Unread postPosted: Fri Feb 08, 2019 9:57 am
by theloneranger86
hey Ghost do you see any changes to the Interleukin 1 Beta on your data ?

Heres some research based on that gene . Is there a way to TAG Ghost on some of these posts we want him to see ?



Interleukin-1β causes fluoxetine resistance in an animal model of epilepsy-associated depression.

Depression represents a common comorbidity of epilepsy and is frequently resistant to selective serotonin reuptake inhibitors (SSRI). We tested the hypothesis that the SSRI resistance in epilepsy associated depression may be a result of a pathologically enhanced interleukin-1β (IL1-β) signaling, and consequently that the blockade of IL1-β may restore the effectiveness of SSRI. Epilepsy and concurrent depression-like impairments were induced in Wistar rats by pilocarpine status epilepticus (SE). The effects of the 2-week long treatment with fluoxetine, interleukin-1 receptor antagonist (IL-1ra), and their combination were examined using behavioral, biochemical, neuroendocrine, and autoradiographic assays. In post-SE rats, depression-like impairments included behavioral deficits indicative of hopelessness and anhedonia; the hyperactivity of the hypothalamo-pituitary-adrenocortical axis; the diminished serotonin output from raphe nucleus; and the upregulation of presynaptic serotonin 1-A (5-HT1A) receptors. Fluoxetine monotherapy exerted no antidepressant effects, whereas the treatment with IL-1ra led to the complete reversal of anhedonia and to a partial improvement of all other depressive impairments. Combined administration of fluoxetine and IL-1ra completely abolished all hallmarks of epilepsy-associated depressive abnormalities, with the exception of the hyperactivity of the hypothalamo-pituitary-adrenocortical axis, the latter remaining only partially improved. We propose that in certain forms of depression, including but not limited to depression associated with epilepsy, the resistance to SSRI may be driven by the pathologically enhanced interleukin-1β signaling and by the subsequent upregulation of presynaptic 5-HT1A receptors. In such forms of depression, the use of interleukin-1β blockers in conjunction with SSRI may represent an effective therapeutic approach.

Re: PSSD Genome Project [Megathread]

Unread postPosted: Fri Feb 08, 2019 11:29 am
by Ghost
I've published the results from this summer on my site: https://pssdlab.wordpress.com/logging/

There are only three SNPs that I go into depth on. I cut out a lot of them that didn't meet strict protocol. These three deserve further analysis by the community.

Since I started working on this report, I have received many new genomes. These will be added to the database and I will start the process of analyzing again from the beginning.

Re: PSSD Genome Project [Megathread]

Unread postPosted: Fri Feb 22, 2019 8:56 pm
by RainebowGirl
Is it too late to join this effort?

Re: PSSD Genome Project [Megathread]

Unread postPosted: Sat Mar 16, 2019 3:26 pm
by anacleta
Serotonin 2A −1438 G/A and G-Protein Beta3 Subunit C825T Polymorphisms in Patients with Depression and SSRI-Associated Sexual Side-Effects
https://www.nature.com/articles/1301090
"persons with a GG genotype of the 5HT2A −1438 single nucleotide polymorphisms (SNP) were significantly more likely to be categorized as having sexual dysfunction than persons with a GA or AA genotype (OR=3.6; 95% CI 1.03, 12.6; p=0.046). Furthermore, the 5HT2A −1438 GG genotype was a significant predictor of lower arousal scores (p=0.022) after accounting for other measures. There was no significant relationship between any outcome measure and GNB3 genotype."

Effects of SNS activation on SSRI-induced sexual side effects differ by SSRI.
https://www.ncbi.nlm.nih.gov/pubmed/19466669
"each SSRI has a unique portfolio of secondary binding properties to other neurotransmitters such as norepinephrine (NE). As 5HT(IA) receptors mediate NE neurotransmission, SSRIs that are highly selective for 5HT(IA) are more likely to reduce NE efficiency; however, in SSRIs that are less selective for 5HT(IA), this could be counteracted by secondary binding to NE. Norepinephrine is the major neurotransmitter of the sympathetic nervous system (SNS), which has been shown to mediate genital arousal in women; thus, it is possible that increasing SNS activity in women taking SSRIs that are highly selective for 5HT(IA) may counteract sexual side effects in those women. To test this hypothesis, we conducted a reanalysis of Meston (2004)'s 8-week, double-blind, cross-over, placebo-controlled study of the effects of ephedrine (50 mg taken 1 h prior to sexual activity) on self-reported sexual functioning of women taking paroxetine (N = 5), sertraline (N = 7), or fluoxetine (N = 7). As predicted, women taking SSRIs, which are highly selective for 5HT(IA) (sertraline, paroxetine), showed improvement in sexual arousal and orgasm. By contrast, women taking SSRIs, which are less selective for 5HT(IA) relative to NE (fluoxetine), showed no change or decrease in sexual functioning. "

A Genome-Wide Association Study of Female Sexual Dysfunction
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035041
"associations with the phenotypic dimension of arousal (rs13202860, P = 1.2×10−7; rs1876525, P = 1.2×10−7; and rs13209281 P = 8.3×10−7) on chromosome 6, around 500kb upstream of the locus HTR1E (5-hydroxytryptamine receptor 1E) locus, related to the serotonin brain pathways. We could not replicate previously reported candidate SNPs associated with FSD in the DRD4, 5HT2A and IL-1B loci."