Wicca Wiki

"PSSD" stands for "Post-SRI Sexual Dysfunction" or "Post-SSRI Sexual Dysfunction".

This subject is relevant because people who are interested in magic and/or the occult are
statisticly much more vulnerable to getting PSSD in response to SRI drug consumption.
That is due to such people statisticly having higher HDAC2 in their neurons.
HDAC2 has broad-ranging effects, both positive and negative.
If you are interested in magic and/or the occult, and are also generally a "nerd", then your HDAC2 is high.

The following is the entire text of the september 30th 2022 version of pssd.html.
This information, in previous versions, was previously on 0catch.com, upload.run, and referata.com,
before the cyber-terrorist organization called the NSA used their DDoS'ing system called QUANTUM to
successively perma-DDoS all of those websites.

All About Post-SRI Sexual Dysfunction

Contrary to popular belief, serotonin is not a neurotransmitter of happiness or calmness.
In truth, it is the neurotransmitter of challenge and defeat, thus being similar to cortisol.
Serotonin is also involved in creating some social emotions, but only those of the submissive and dependent type.

If the dose-to-bodyweight ratio of an SRI (either an SNRI or SSRI) is sufficiently high,
then it causes a permanent, usually irreversible condition called 'PSSD'.
'PSSD' stands for 'post-SSRI sexual dysfunction' or 'post-SRI sexual dysfunction'.

Due to various research papers about PSSD that were published in 2006 through 2008,
all psychiatrists have been aware of PSSD since that time, though the vast majority of psychiatrists continue to
prescribe SRI drugs, which indicates a high prevalence of psychopathy among psychiatrists.
Although all psychiatrists have been aware of PSSD since that time,
many psychiatrists have been aware of that effect since a much earlier time- at least as early as the mid 1990s,
and thus at least 10 years before the condition was officially recognized in scientific papers.
In the early 1990s, there were three scientific studies that established the fact that the SNRI
clomipramine and the SSRI fluoxetine decrease physical sexual sensitivity in both males and females,
thus alerting the psychiatric community to the fact that SRIs in general decrease sexual sensitivity.
It was not long after that that some psychiatrists, especially those who worked in psychiatric institutions
(due to the large number of drugged people that they work with), recognized that such effects
are sometimes permanent.

origin of the term:
The term "post-SSRI sexual dysfunction" was coined at least as early as december of 2005,
when it was used by James Skinner on Wikipedia, but it was most likely coined earlier in 2005,
in the Yahoo group ssrisex, which James Skinner belonged to.
The term could have been coined by anyone in that goup, including, among other people,
James Skinner himself, and the creator of the group and original publicizer of the condition, Antonei Csoka.
That term was made official by the psychologist Audrey Bahrick, in a scientific paper that she wrote in september of 2006.
PSSD affects more than just a person's sexuality, but sexuality is what is most severely affected.
The term "post-SSRI sexual dysfunction" is the term that is usually used for the condition,
but it is partially a misnomer, because the condition is caused not only by SSRIs, but also by other SRIs,
mainly the SNRIs, so the term "post-SRI sexual dysfunction" is the accurate term, but it is rarely used.
There is also the fact that the symptoms of PSSD are broader than just sexual symptoms.
Because of that, the generic term "post-SSRI syndrome", abbreviated as PSS, was invented.
That term was invented much later than PSSD, but no later than 2017.
That term likewise falsely uses the word "SSRI" instead of "SRI", thus falsely indicating that only SSRIs,
as opposed to all SRIs, cause the condition.

PSSD symptoms:
PSSD includes permanent physical and psychological sexual anhedonia (absence of pleasure),
such that a person can usually still get erections (including internal erections in the case of females),
and can still get ejaculatory muscle contractions and their female equivalent,
but the pleasure of those functions disappears,
and pleasurable lust is replaced by a mostly-empty sense of sexual tension.
Not only do the genitals lose pleasurable sensitivity, but so do the nipples in women.
(The loss of orgasmic pleasure is not to be confused with the condition called "anorgasmia".
Anorgasmia is the inability to get those muscle contractions regardless of the duration of stimulation,
and it is usually caused by excessive prolactin. Anorgasmia is counteracted via the drug cabergoline,
but cabergoline usually has no effect on PSSD.)
Ejaculation, and the equivalent female muscle contractions, are often premature.
Dilation of the smooth muscle layer of the urethra during ejaculation is lost.
That loss of urethra dilation corresponds to the loss of orgasmic pleasure in males,
suggesting that they are related.
Wake-up erections, which are commonly called "morning wood", become rare or non-existent.
Due to the lack of libido, it becomes usually or always impossible to get a full erection from erotic
psychological stimulation alone (mainly visual and/or audio stimuli, either real or imagined).
Although the penis can still become erect, the glans of the penis becomes non-erectile.
Erections become weaker, causing a reduction in erect penis size, which is sometimes called "shrinkage".
Full erections that occur not long after an ejaculation result in internal tissue tearing and associated
pain in the penis, which in turn results in internal scar tissue in the penis.
That internal tissue tearing is caused by differential erection, in which outer parts of the penis become erect,
but a lower inner part of the penis does not become erect due to the PSSD,
such that the erect outer parts pull upon the non-erect lower inner part, causing tearing between them.
The cremaster reflex in the crotch disappears.
Yawning becomes diminished in both strength and frequency.
Other permanent anhedonia effects include amorous anhedonia
(the elimination or great reduction in the ability to feel love, "butterflies", and related emotions),
social anhedonia, and general anhedonia.
As a result of the low dopamine, there is also reduced energy, AKA chronic fatigue,
and hyperthermic spikes after eating, and sometimes during sex or masturbation, and/or after the pseudo-orgasms.
The amorous instincts may remain intact, but lack the emotion to fill them in and make them worthwhile.
The pleasures of taste and smell are left intact though, because they rely upon different neural pathways.
Various recreational drugs, including caffeine, nicotine, alcohol, and opioids, often lose their pleasure-producing effect.
SRI drugs also cause two other bad effects which are typically not considered part of PSSD,
but which are major and are little-known-of.
One of those effects is that it causes or exacerbates autistic tendencies.
The other effect is that it decreases a person's sex hormones- testosterone and estradiol.
The lower testosterone in males causes a higher-pitched voice,
and the loss of the production and excretion of the powdery-smelling male armpit pheromone called androstenol.
The lower estradiol in females causes a lower-pitched voice,
and the loss of the production and excretion of the female armpit pheromone estratetraenol.
The sex-hormone-decreasing effect causes permanent bodily damage if it is given to adolescents,
because it stunts their sexually dimophic body development, resulting in a physique that is closer to gender-neutral.

PSSD symptom variants:
There are different variants of PSSD.
There is a heightened-anxiety variant of PSSD, an unchanged-anxiety variant of PSSD, and a lowered-anxiety variant of PSSD.
The heightened-anxiety variant of PSSD also typically includes a sleep disorder.
Half of people with PSSD have the lowered-anxiety variant, one-third have the unchanged-anxiety variant,
and the remaining one-sixth have the heightened-anxiety variant.
There is also a cognitively-impaired variant of PSSD, which includes symptoms such as "brain fog".
In a rare variant of PSSD, there is complete genital anesthesia,
which means that the genitals become completely numb.
There is also a moderate, incomplete form of PSSD, in which real orgasms are still present,
but it takes an exceptionally long duration of stimulation to get to them,
with people reporting stimulation duration requirements ranging from around 30 minutes in relatively moderate cases
to two hours in extreme cases.
There is also a distinction between tractable PSSD and intractable PSSD.
Tractable PSSD can be cured, or sustainably fully suppressed, by the use of certain supplements or pharmaceuticals,
whereas intractable PSSD cannot be.
Only around 5 to 10 percent of cases of PSSD are tractable PSSD.

comparison with MAO-A inhibitor symptoms:
Most MAO inhibitors that are available are non-selective MAO inhibitors,
which means that they are MAO-A inhibitors, and therefore increase serotonin.
MAO-A inhibitors, like SRIs, increase the activity of serotonin in the brain and spinal cord.
However, SRIs have a more potent effect in that regard, because they pack the synapses with serotonin.
MAO-A inhibitors consequently have anti-sexual effects, and there is some overlap between
the MAO-A inhibitor anti-sexual effects and the SRI anti-sexual effects.
Namely, MAO-A inhibitors cause decreased libido and decreased dopamine production for orgasms,
which causes delayed orgasms, thus mirroring the effect of the moderate form of PSSD.
However, those symptoms typically reverse with the cessation of the drug, in contrast to SRIs.
There is, however, a permanent effect of MAO-A inhibitors, called "tachyphylaxis", that occurs in some people.
"Tachyphylaxis" means that the drug rapidly stops working, and never works again thereafter.
The same phenomenon occurs with SRIs, but the term "tachyphylaxis" is, in practice,
typically used only when speaking of MAOIs.
That tachyphylaxis is associated with a permanent decrease in libido and pleasure in general,
but not nearly enough to rise to the level of being called "anhedonia".
MAO-A inhibitors thus do cause some permanent damage, but it is much more mild than what SRIs cause.

PSSD secondary effects:
There are various secondary effects that result from PSSD's various symptoms.
One very common effect is suicidality and suicide.
Another common secondary effect is excessive masturbation and/or often-illegal recreational-drug-seeking behavior,
as a consequence of the feeling of restlessness that results from the absence of pleasure.
Some people with PSSD become fixated on food, because it is the only substantial pleasure that they have left.
Around half of the people who are afflicted with PSSD can no longer hold down their job or formal education,
as a consequence of their loss of energy, loss of motivation, and loss of the pleasure that counterbalances their
work and staves-off depression.
Due to the loss of lust, physical sexual pleasure, and amorous emotions,
people who get PSSD who are not already in a long-term relationship typically remain single,
and, as an additional consequence, childless.

PSSD and suicidality:
SRI drugs are said to cause a risk of suicidality and suicide, especially in adolescents and young adults.
But there is no such thing as stand-alone suicidality; suicidality is always caused by something else.
PSSD more often than not causes suicidality, and sometimes suicide, especially in young adults,
though suicide would in fact be a largely redundant act because the person is mostly dead already.
When SRI drugs have a warning about the risk of suicidality and suicide, what they are really talking about,
euphemisticly, is the cause thereof, which is PSSD. The most famous case of PSSD-induced suicide was that of
the lead Columbine Highschool shooter, Eric Harris, back in 1999, several years prior to PSSD having been made public.
Eric Harris, of course, took several other people along with himself as a consequence of other SRI-induced
neuropsychological alteration, and few people know that he had PSSD. Eric Harris's PSSD was caused by very high
doses of fluvoxamine (under the brand name luvox)- 100mg and 200mg.

In about two-thirds of cases, PSSD begins while a person is taking the SRI drug,
whereas in about one-third of cases, PSSD begins after a person stops taking the SRI drug.
In the latter case, serotonin receptors become down-regulated to adapt to the increased serotonin,
but do not up-regulate in response to the lower serotonin thereafter.
In cases in which PSSD begins while taking the drugs, the onset time varies.
In some cases, it is caused by a single dose of an SRI- usually a large dose in such cases.
In some other cases, the PSSD symptoms appear gradually over a span of months.
The most common onset time is around 1 month.
PSSD can be induced at any age- not only after one's sexuality has developed,
but also beforehand, during childhood.
An experiment on pregnant female rats has demonstrated that PSSD can even be induced in
the fetuses of females that are given SRIs.

neurology in the brain:
PSSD is caused by the over-stimulation, and resulting epigenetic desensitization, of three serotonin receptor types-
5-ht1a receptors, 5-ht2a receptors, and 5-ht2c receptors.
Presynaptic 5-ht1a receptors inhibit serotonin release from the dorsal raphe nuclei.
5-ht2a receptors in the ventral tegmental area (VTA) are necessary to stimulate the production and release of dopamine
(by inducing the production of dopamine-synthesizing enzymes) from the VTA neurons onto the rostrodorsal nucleus accumbens shell,
which is a major pleasure center.
5-ht2c receptors serve the function of storing up dopamine for large phasic releases,
by activating GABAergic interneurons that release GABA onto the presynaptic bulbs of the projecting axons
of VTA neurons that produce dopamine and release it onto the rostrodorsal nucleus accumbens shell.
5-ht2c receptors are present in the nucleus accumbens area, where they store up dopamine for both erections and orgasms,
and possibly also one or more other pleasures.
However, the loss of orgasmic pleasure is caused more by effects outside of the brain, in the spinal cord.
5-ht2c receptors also induce the production and release of oxytocin from oxytocin-producing neurons in the brain,
mainly in the hypothalamus, such that the desensitization of the 5-ht2c receptors causes a major impairment of
oxytocin function in the brain, and thus all of the emotions that are dependent upon oxytocin.
The cognitively-impaired variant of PSSD is caused by the epigenetic desensitization of
the 5-ht2a and/or 5-ht2c receptors in the frontal lobe, as contrasted with the 5-ht2a and 5-ht2c receptors in the mesolimbic system,
which are more prone to being epigeneticly desensitized.
Postsynaptic 5-ht1a receptors mediate both pro-anxiety and anti-anxiety effects,
and PSSD can cause those receptors to be either excessively stimulated in the long term,
or desensitized, such that the effect of PSSD upon anxiety is variable.
5-ht1a receptors are present on GABAergic interneurons in the medial prefrontal cortex,
and those GABAergic interneurons inhibit glutamate-mediated anxiety effects,
such that the activation of those 5-ht1a receptors increases anxiety.
5-ht1a receptors are also present on GABAergic interneurons that project onto oxytocin-producing neurons
that have downstream anti-anxiety effects,
such that the activation of those 5-ht1a receptors decreases anxiety.
The SRI-induced sex-hormone-decreasing effect is the result of
increased serotonin excretion from the disinhibited raphe nucleus axons,
falling upon postsynaptic inhibitory 5-ht1a receptors that are on
GnRH(gonadotropin-releasing hormone)-excreting neurons in the medial preoptic nucleus of the hypothalamus.
That GnRH is excreted onto the parts of the anterior pituitary gland that in turn release the
gonadotropins LH (luteinizing hormone) and FSH (follicle-stimulating hormone) into the bloodstream,
such that the increased serotonin excretion causes decreased gonadotropins.
The decreased gonadotropins in the bloodstream in turn cause
decreased sex hormone production from the testicles and ovaries.
The SRI-induced chronic fatigue is the result of the SRI-induced decreased dopamine secretion
from the ventral tegmental area onto the ventromedial part of the arcuate nucleus of the hypothalamus.
That part of the hypothalamus contains D1 dopamine receptors which induce the production of
growth-hormone-releasing hormone (GHRH), and release it onto the anterior pituitary gland,
which in turn secretes growth hormone into the blood stream,
and that growth hormone in turn induces the conversion of glucose into ATP in the muscle cells, which imparts energy.
The SRI-induced pro-autistic effect is the result of the fact that the highest density of serotonin axons,
from the raphe nuclei, are in the frontal lobe and hippocampus.
The high serotonin in those areas activates unidentified serotonin receptors which, when activated,
induce broad-ranging gene methylation, which shuts-down or impairs the genes.
That gene methylation in turn induces the production of the enzyme HDAC2 (histone deacetylase 2),
which tightens the chromosomes, which impairs or eliminates access to various other genes,
resulting in autistic symptoms. The high HDAC2 in the frontal lobe is much more responsible for the
autistic effects than is the high HDAC2 in the hippocampus.

neurology in the spinal cord:
In addition to those PSSD effects upon the brain, there are clearly also PSSD effects upon the spinal cord and/or peripheral nerves,
which cause the symptoms of the non-erectile glans, the loss of the cremaster reflex, the loss of wake-up erections,
premature ejaculation, genital anesthesia, loss of urethra dilation, and probably the orgasmic anhedonia.
The loss of ejaculatory pleasure coincides with the loss of urethra dilation, which indicates a relation between those two symptoms.
The cause of those peripheral neural problems has not been studied much,
but they can be caused by the same epigenetic desensitization of one or more of
the same three serotonin receptors (5-ht1a, 5-ht2a, and 5-ht2c), just as it is in the brain.
One researcher has theorized that the problem is in the lumbar area of the spinal cord.
The 5-ht2a and 5-ht2c receptors are known to play a prominent role in the lumbosacral region of the spinal cord,
and the 5-ht1a receptors are known to play a role in the lumbar region of the spinal cord, all of which supports that theory.
Dysfunctional 5-ht2c receptors in the lumbosacral spinal cord have been shown to cause muscle spasms in the legs,
so they could just as easily cause premature ejaculation.
Yet 5-ht2c is an excitatory receptor, which means that its desensitization, like in the brain,
could only cause excitatory effects if it is expressed on GABAergic interneurons,
such that its desensitization would render the inhibitory GABAergic neurons inactive.
There are in fact GABAergic interneurons in the lumbosacral spinal cord, and not only that,
but their non-function causes excessive contraction of the bladder muscle,
which means that their non-function could just as easily cause premature contraction of the orgasm muscles.
The moderate variant of PSSD, in which real orgasms are still present but are highly delayed,
is caused by the epigenetic desensitization of the dopamine-producing 5-ht2a receptors in the brain,
without the epigenetic desensitization of the 5-ht2c receptors in the lumbosacral spinal cord.
Apparently the 5-ht2c receptors in the brain are responsible for storing-up dopamine for both erections and orgasms,
whereas the 5-ht2c receptors in the lumbosacral spinal cord are necessary for releasing the stored-up dopamine for orgasms.

The vulnerability to PSSD varies between people.
One of the major factors in determining a person's vulnerability to PSSD is
their level of baseline serotonin in the brain and spinal cord.
The higher that baseline level of serotonin, the lower the dose of SRI that is required in order to inflict PSSD.
The majority of people's brains and spinal cords have some ability to heal themselves from SRI-induced sexual dysfunction,
and to prevent the more severe symptoms from occurring.
The main factor in determining how well a person can heal from those effects is a person's level of the protein HDAC2
in their neurons. The higher the HDAC2, the more impaired the neuron's ability to heal themselves,
because HDAC2 tightens the chromosomes, and consequently makes the neural healing genes inaccessible.
If HDAC2 is sufficiently high, then a person is on the autism spectrum, and the higher the level of HDAC2
beyond that threshold, the lower the person is on that spectrum.
In a poll conducted upon PSSD victims, 2 out of 5 of them reported being on the autism spectrum,
and some of them mentioned having asperger's syndrome in particular.
But HDAC2 has other effects at lower levels, such that there are non-autistic people with
relatively high HDAC2 who have various distinctive traits.
At the upper end of the autism spectrum is asperger's syndrome, but right above it,
at the low end of the non-autistic spectrum, is "high sensitivity personality", aka HSP.
People with HSP are highly vulnerable to PSSD just like aspergics are.
Other traits that result from high HDAC2, and may or may not co-occur with HSP,
include being a "nerd", being an introvert, and having social anxiety and/or other anxiety problems.
In a poll conducted upon PSSD victims, 4 out of 5 of them reported being an introvert or loner prior to getting PSSD.

true mental health drugs:
Although SRIs are prescribed for depression, anxiety, and obsessive-compulsive disorder,
the truth is that low serotonin does not cause any of those conditions, nor does it cause any other bad condition.
Depression is a sensation that is caused by NMDA glutamate receptors that contain the 2B subunit,
and those receptors can be blocked by taking a high dose of an over-the-counter soluble form of magnesium.
Most forms of magnesium other than magnesium oxide and magnesium hydroxide are soluble.
General anxiety disorder is caused by excessive activity of the neurotransmitters glutamate and epinephrine in the amygdala,
and can therefore be counteracted by taking a benzodiazepine and/or propranolol.
Obsessive-compulsive disorder (OCD) is caused by excessive activity of
the neurotransmitters glutamate and histamine in the caudate nucleus,
which is a part of the brain that regulates attention by regulating the communication between the thalamus and the cortex.
OCD can be counteracted by taking the glutamate release inhibitor riluzole,
or one of the H2 histamine receptor antagonists- cimetidine, ranitidine, or famotidine,
though taking too much of an H2 antagonist is dangerous because it can make a person careless.
H2 antagonists are typically sold over-the-counter as antacid drugs.
Also, the brain's level of histamine, and thus obsessive-compulsiveness,
is reduced by ejaculations and the corresponding uterine contractions,
because initiating those functions consumes histamine in the brain.

citalopram and escitalopram:
There are two particular SRI drugs, one of which is called citalopram, and the other is called escitalopram.
Citalopram is also known by its original and most common brand name, "celexa", and
escitalopram is also known by its original and most common brand name, "lexapro".
Citalopram consists of two enantiomers in equal proportion, one of which is active, and the other is inactive.
Escitalopram is the purified active enantiomer of citalopram, and is thus twice as potent as citalopram per unit of weight.
Both citalopram and escitalopram were created jointly by the New-York-City-based company Forest Laboratories, and the
Copenhagen-based company Lundbeck, and those are the only two drugs that were created jointly by those companies.
Citalopram was FDA-approved in 1998, and escitalopram was FDA-approved in 2002, which was later than most of the
other SRI drugs, which were FDA-approved in the late 1980s through the mid 1990s.
Citalopram and escitalopram, unlike other SRI drugs, act upon the serotonin transporter (SERT) in an allosteric way,
rather than by blocking it. That allosteric mechanism makes citalopram and escitalopram much more potent SRIs,
and thus much more effective at causing PSSD, and causing more severe PSSD, than other SRIs.
Together, citalopram and escitalopram are the cause of about half of all PSSD cases.
Escitalopram's powerful PSSD-causing effect has been demonstrated in an experiment with rats in 2009.
Consequently, escitalopram is the SRI of choice for psychiatrists who strongly want to give their subject PSSD.
There are some exceptionally psychopathic psychiatrists who actually target people who already got PSSD from
some other SRI drug, by trying to convince them to take escitalopram, and thus make their PSSD more severe,
typically for the purpose of trying to drive their mark to suicide. In addition to the psychiatrists,
the drug company itself- Forest Laboratories, has tried extensively to inflict PSSD upon (and thus internally murder)
people at as early an age as possible, by illegally promoting the government-unapproved use of citalopram and
escitalopram in children.

SSRIs versus SNRIs:
SNRIs are typically classified into two types, which are the tricyclic SNRIs and the non-tricyclic SNRIs.
The tricyclic SNRIs were invented at an earlier time than were the non-tricyclic SNRIs.
All of the tricyclic SNRIs except for clomipramine have a much weaker SRI effect than do the SSRIs,
and therefore do not normally cause PSSD.
In contrast, clomipramine and all of the non-tricyclic SNRIs have as strong an SRI effect as do the SSRIs,
and therefore cause PSSD. Those drugs may be called "the strong-SRI SNRIs".
Not only do the strong-SRI SNRIs cause PSSD, but they cause PSSD with a higher frequency per capita,
and higher average severity, than do the non-allosteric SSRIs.
Strong-SRI SNRIs are less-commonly prescribed than SSRIs though,
and therefore cause a much smaller portion of the PSSD cases than do the SSRIs.
The most common strong-SRI SNRI to cause PSSD is venlafaxine.
The reason that strong-SRI SNRIs cause a higher frequency and average severity of PSSD than do
non-allosteric SSRIs is because the norepinephrine transporter causes serotonin reuptake to a small extent,
which means that a strong-SRI SNRI inhibits serotonin reuptake even more effectively than the
non-allosteric SSRIs do, and therefore keeps a high concentration of serotonin in the synapses for a longer time,
and therefore causes more damage.

sometimes-effective treatments and cures:
PSSD has been cured in some cases, and has been significantly counteracted in a larger number of cases,
by the use of various drugs and supplements. Those drugs and supplements include estradiol, the anti-depressant
dopamine reuptake inhibitor bupropion (aka wellbutrin), the 5-ht1a partial agonist buspirone AKA buspar
(which is used against anxiety), the 5-ht2a/2c antagonist and 5-ht1a agonist nefazodone (which is used against depression),
the 5-ht2a/2c antagonist cyproheptadine (which is used against allergies because of its H1-antagonist effect),
the D3 receptor agonists pramipexole and ropinirole (which are used against parkinson's disease and restless leg syndrome),
the GABA precurser GHB (which activates the same dopamine-storing GABA receptors that the 5-ht2c receptors do),
boron, yohimbine, chasteberry extract (aka vitex), quercetin at at least 1 gram per day, saint john's wort,
high-dose inositol (at 10-to-18 grams per day), licorice root taken consistently at at least a half-gram per day for 3 months,
black cohosh root, MSM, maca, nettle root at at least 1 gram per day, saffron at at least 200mg per day,
the H1 antagonist loratadine at at least 10mg per day, cannabigerol (CBG), and lithium.
Saint john's wort, however, raises serotonin to some extent, and can therefore exacerbate PSSD in the most serotonin-sensitive
people, possibly after causing a short-term benefit.
Lithium can have a broad range of effects on PSSD, either greatly reducing it or greatly worsenning it,
depending upon the person and the dosage.
Ginseng should not be consumed by people with PSSD, because a substance within it acts as a weak SNRI.
Rhodiola should not be consumed by people with PSSD, because its active ingredient acts as a non-selective MAO inhibitor,
such that it raises serotonin.
Yohimbine is also available in ground whole yohimbe root,
but yohimbe root should not be eaten, because it also contains toxic chemicals that
irritate the stomach and cause nausea and vomiting.
Choline reduces the propensity for erectile dysfunction in particular, but doesn't have any other PSSD-related benefits.
Niacin mainly reduces the propensity for erectile dysfunction in particular, and has little benefit for other PSSD symptoms.
The typical anti-erectile-dysfunction drugs, such as sildenifil, are effective against the erectile dysfunction symptom that is common
in PSSD, but have little benefit for the other symptoms.
Of all of those substances, buspirone has the highest rate of efficacy, but its effect is usually only temporary and short-lasting-
lasting for only about two hours, due to the short half-life of the chemical.
A few people have reported that consuming an SRI drug at a low dose has cured their PSSD,
but in those cases, it has always been fluoxetine in particular that has done so.
That is because fluoxetine, unlike the other SRI dugs, is a 5-HT2C antagonist,
and therefore can re-sensitize the 5-HT2C receptor when used at a low dose,
whereas at a higher dose, its SRI effect overpowers its 5-HT2C antagonist effect.
Estradiol works by binding to neuron nuclear receptors which induce the production of 5-ht2c receptors.
Estradiol is more effective at restoring the 5-ht2c receptors in the brain (which erectile pleasure and orgasmic pleasure are
both dependent upon), than it is at restoring the 5-ht2c receptors in the lumbosacral spinal cord (which orgasmic pleasure is
also dependent upon).
Boron works by inhibiting a liver enzyme, called sex hormone binding globulin (SHBG),
which breaks down the sex hormones, including estradiol.
Black cohosh root and licorice root work by containing chemicals- including glycyrrhizin in the case of licorice root,
which imitate estrogens by weakly binding to the estrogen receptors.
Chasteberry extract works by somehow raising estradiol and progesterone.
Inositol works by facilitating the intracellular messaging systems of the 5-ht2a and 5-ht2c receptors.
Getting a prolonged dangerous microbial lung infection is more effective against PSSD than any of the aforementioned
over-the-counter drugs, because the infection activates cytokines which induce the synthesis of estradiol and estrogen receptors.
5-ht2a/2c antagonists, including nefazodone and cyproheptadine, work by resensitizing those receptors that they block.
Lithium acts upon the 5-ht1a receptor, and upon the intracellular proteins that receptors activate.
Lithium works best when combined with testosterone, because the lithium's pre-synaptic 5-ht1a-sensitizing effect
decreases the serotonin that falls upon the 5-ht2a receptors and desensitizes them,
whereas the testosterone induces production of those same 5-ht2a receptors.
Cannabigerol works by blocking the 5-ht1a receptor, which allows it to re-sensitize.
The 5-ht1a partial agonist buspirone works by blocking the over-stimulation of the presynaptic 5-ht1a receptors,
thus allowing them to re-sensitize, while stimulating the receptors enough to activate them,
thus decreasing serotonin release from the raphe nuclei, and in turn allowing the mesolimbic 5-ht2a and 5-ht2c receptors to re-sensitize.
Nefazodone works by re-sensitizing the mesolimbic 5-ht2a and 5-ht2c receptors by blocking them,
and by decreasing serotonin release onto the mesolimbic system by activating the presynaptic 5-ht1a receptors.
D3 receptor agonists work via a double inhibition mechanism, such that they inhibit the firing of neurons that inhibit sexual neurons.
In theory, the HDAC2 inhibitor drugs valproic acid and romidepsin, and especially the latter,
can counteract PSSD by increasing the accessibility of a person's own demethylating genes.
The prescription drugs have a much higher rate of efficacy than the over-the-counter substances.
In addition to those aforementioned drugs and supplements, PSSD can be counteracted to a small extent by exercise,
because exercise increases both dopamine and oxytocin in the brain.

Similarly to SRI drugs, the 5-alpha reductase inhibitor drugs, and the retinoid drug isotretinoin, can likewise cause
permanent sexual dysfunction, though it is statistically less common than PSSD. Isotretinoin is typically known by
its brand name accutane, and is used against acne. 5-alpha reductase inhibitors include, but are not limited to,
finasteride and dutasteride, and they are used to reduce dihydrotestosterone, and thereby counteract an enlarged prostate
and hair loss. Finasteride is typically known by its brand name propecia. Those two drug-induced conditions are called
"post finasteride syndrome" (PFS) and "post-retinoid sexual dysfunction" (PRSD).
Also, D2 antagonist drugs, which are typically used on people with schizophrenia, can likewise cause persistent sexual
dysfunction, though unlike in the cases of PSSD, PFS, and PRSD, it typically goes away over time.
The recreational drug MDMA, aka ecstasy, can also cause the same symptoms as PSSD,
because it can desensitize serotonin receptors like SSRIs can, but it is more rare in the case of MDMA use,
because the effects of MDMA are acute rather than chronic.

parallels with "1984":
There are striking parallels between PSSD, and who is afflicted with it, and how it is caused,
with George Orwell's famous book "1984". The book 1984 is divided into 3 parts.
Each of those parts is divided into numbered sections. Part 3 is divided into 6 sections.
In the third and final part of the book, the protagonist Winston Smith is imprisoned in "the ministry of love",
wherein the inner party member "O'Brien" tells Winston the doctrine and goals of "the party", while torturing him.
In part 3, division 3, O'Brien tells Winston: "The sex instinct will be eradicated. ... We shall abolish the orgasm.
Our neurologists are at work upon it now.". The elimination of orgasmic pleasure, and of the sex drive,
are two of the core defining characteristics of PSSD, and those symptoms are caused via a neurological method-
neuroactive drugs. In part 3, division 2, O'Brien tells Winston: "And even if we chose to let you live out the
natural term of your life, still you would never escape from us. What happens to you here is forever.
Understand that in advance. We shall crush you down to the point from which there is no coming back.
Things will happen to you from which you could not recover, if you lived a thousand years.
Never again will you be capable of ordinary human feeling. Everything will be dead inside you.
Never again will you be capable of love, or friendship, or joy of living, or laughter, or curiosity, or courage,
or integrity. You will be hollow.". The "forever" and "a thousand years" statements correspond to the
permanence of PSSD. One of the symptoms of PSSD is a greatly reduced or eliminated ability to
feel love. General anhedonia and inner deadness are symptoms of PSSD. The loss of courage is caused
by the common heightened-anxiety variant of PSSD. The loss of curiosity is a symptom that occurs in the
uncommon cognitively-impaired variant of PSSD. In part 3, division 3, near the previously-mentioned quote
in that section, O'Brien tells Winston: "always there will be the intoxication of power ... Always, at every moment,
there will be the thrill of victory, the sensation of trampling upon an enemy who is helpless.".
There is no such emotion as "power", but there is the emotion of dominance.
Correspondingly, PSSD-inducing behavior is caused by the sensations of dominance and schadenfreud.
Note that this neuropsychological damage is done to Winston when he is in "the ministry of love".
George Orwell's inspiration for the ministry of love came from the Soviet Union's use of psychiatric prisons
upon political opponents, which began in 1948, right when Orwell was writing 1984.
Correspondingly, PSSD is sometimes caused by the forcible SRI drugging of psychiatric prisoners.
The doses of SRIs at psychiatric prisons are usually much higher than the doses that are given to
unimprisoned users, such that the frequency of affliction is much higher in psychiatric prisons.
But overall, the majority of PSSD-afflicted people are not afflicted as a result of psychiatric imprisonment,
simply because psychiatric imprisonment is relatively rare. And 1984 is not unique in using such
imprisonment upon political opponents. In the United States, there is a common de-facto practice of
using psychiatric imprisonment upon minors who support youth liberation and youth equality.
So apparently, 1984's fictional "party" ideology corresponds to the adult-supremacist ideology in real life.
It is unknown exactly how many of those youth-liberation-supporting minors were deliberately afflicted
with PSSD.

PSSD versus natural asexuality:
Some high-functioning autistic people, and people with the so-called "schizoid personality disorder",
and rare cases of people with both conditions, are asexual,
which means that they do not have any desire to have sex with anyone else.
Such people are usually "autochorisexual", which means that their only sexual desire is to
masturbate while looking at porn or thinking about sexy things.
PSSD usually destroys a person's sex drive, thus turning them asexual.
In a portion of cases, people are given PSSD before they even enter adolescence,
such that their sexuality never develops properly in the first place.
Such people are almost always unaware of the existence of PSSD,
and so they typically falsely assume that they are naturally asexual.
Such people may therefore be called "SRI pseudo-asexuals" or "SRI artificial asexuals".
One can tell the difference between a natural asexual and an SRI artificial asexual
because the former are fully capable of physical sexual pleasure,
whereas the latter have very little capacity for physical sexual pleasure.

"Formerly 98":
Although a highly informative article for post-SSRI sexual dysfunction existed on Wikipedia beginning in december of 2005,
the article was deleted in january of 2014, after having existed for eight years.
That deletion was due to the extensive efforts of one man, who went under the Wikipedia username "Formerly 98",
and who formerly editted under his bare IP address, which was .
He editted under his bare IP address from october 19th 2013 to january 10th 2014,
and then editted as Formerly_98 from january 10th 2014 to May 28th 2015.
It was shortly after he started editting as Formerly_98, on january 19th 2014,
that he formerly proposed deleting the article, and by january 27th 2014, he succeeded.
In his copious arguments for deletion, Formerly_98 used numerous lies, which deceived the people who voted.
The voters overwhelmingly voted to merge the article into the SSRI article,
but a high-ranking wikipedian named Sandstein decided instead to simply make a redirect,
without any merging efforts.
In 2015, Formerly_98 had his username changed to the long random-alphanumeric username
User:Renamed user 51g7z61hz5af2azs6k6, so as to make it difficult to find him and his edit history,
because that username is virtually impossible to remember.
But you can see Formerly_98's edit history at the following URL:
en.wikipedia.org/wiki/Special:Contributions/User:Renamed user 51g7z61hz5af2azs6k6 .
An examination of the edit history of Formerly_98 and demonstrate that he is
clearly systematicly working on behalf of one of more pharmaceutical companies.
He is clearly not working for any single pharmaceutical company,
but is working for a broad range of pharmaceutical companies.
He has suppressed not only information about PSSD, but also PFS,
and other negative effects of various drugs, and benefits of cannabis
(which is seen as a competitor to the pharmaceutical industry),
and information about the corrupt relations between the pharmaceutical industry and the FDA,
and, in his very first edit, he has expressed frustration that more people are getting their news from
independent sources, rather than from the major television news networks (CBS, NBC, ABC),
which are constrained by their single biggest sponsor- the pharmaceutical industry.
He has done all of that because he is the head of the Honolulu branch of a company called United Pharma,
which is headquartered in Yemen, and which buys both patented and unpatented pharmaceuticals in bulk,
and distributes them at a marked-up price.
It is thus in the interest of United Pharma to increase the sales of all pharmaceuticals.
An examination of the writings of Formerly_98/ reveals that he severity of his psychopathy:
He exhibits willful dominance-induced delusionality, such that he willfully delusionally perceives
that any truth that defies the dominance of the pharmaceutical companies is false and bullshit.
It is possible that his name is James West, because he created another account,
which he then renamed to James_West_2015, but that is more likely than not a pseudonym.
Formerly_98 has since created new sockpuppet accounts, and monitored Wikipedia's SSRI article,
and has repeatedly used those sockpuppets to remove PSSD-related information from the article.

Asexuals have their own internet communities.
There is a prominent person in the asexual community (who is most likely not asexual himself),
who goes under the wiki username Chaoticcylinder, and under the sockpuppet username Osteophage.
Chaoticcylinder is hell-bent on suppressing knowledge of PSSD in the asexual community,
thus keeping SRI-induced pseudo-asexuals unaware of their condition.
Chaoticcylinder registered his sockpuppet account Osteophage immediately after such
information appeared on an asexual-oriented wiki, so as to use that sockpuppet to
delete the information, without the deletion being traced to himself.
Thus, Chaoticcylinder desires to suppress knowledge of PSSD, but he doesn't want other people
to know that he desires to suppress knowledge of PSSD.
The question though is: "what is his motive for doing so?".
Chaoticcylinder exhibits severely psychopathic truth-twisting behavior in his rhetoric,
which indicates that his motive for suppressing knowledge of PSSD is schadenfreud.

chronic interference by the NSA:
The U.S. NSA (National Security[-violating] Agency) has exhibited an odd obsession with PSSD,
trying to suppress knowledge of it by repeatedly DDoS'ing websites that are informative about it.
They first did so by sending a national security letter to shut down the "school survival forum"
right after PSSD was first mentioned therein.
On January 30th, 2020, they perma-DDoS'd pssdforum.com- the main forum of collaborative
information exchange about PSSD.
At the end of May of 2020, the NSA perma-DDoS'd the webspace website 0catch.com ,
which hosted a webspace that was full of information about PSSD.
In mid-October of 2020, the NSA launched a simultaneous long-term DDoS attack upon
upload.run and the webmail website secmail, right after those two sites were used to propagate information about PSSD.
All of that begs the question: Why is the NSA so obsessed with suppressing knowledge of PSSD?
The reason is that people with particular psychological traits are more vulnerable to PSSD,
and one of those traits is the far-sighted opposition to privacy violation by government agencies, such as the NSA.
Therefore the NSA hates such people, and does not want them to have pleasure in life, nor to eugenicly reproduce.
One might wonder: How can such a specific trait be genetic and/or epigenetic,
and how can it be related to increased vulnerability to PSSD?
The answer is that it is the result of the general trait of far-sighted perception,
which is caused in large part by the neurotransmitter acetylcholine.
High acetylcholine is caused in large part by high baseline serotonin acting upon 5-ht4 receptors,
high baseline serotonin being a major risk factor for PSSD.
Being on the autism spectrum (which is a major risk factor for PSSD) typically disables one or more
oxytocin functions which work in opposition to acetylcholine, such that acetylcholine function is enhanced.