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PTSD Symptoms Exacerbated by Sex

sex ptsd anxiety vagus vagal

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#1 JR7

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Posted 03 November 2016 - 11:20 PM


   Strange thread title, I know. After some fairly traumatic incidents in early 2014, I walked away with a diagnosis of PTSD that Im still dealing with. Most of the time, the symptoms are manageable. A trend Ive noticed though is the day after intercourse, my PTSD symptoms are magnified drastically. The 2 main sensations are nonstop nervousness in the stomach (as if I were giving a presentation before a large crowd) coupled with a deep depression feeling in the chest. As a whole, my body becomes very hyper vigilant. 

   The two areas I've been looking at as potential culprits are possible dopamine receptor down regulation from orgasm and vagus nerve "issues" (whatever that may be). Ive seen several psychiatrists and none has been able to figure out what is going on with my brain to cause these symptoms. The sensations are VERY intense and last for up to 2 weeks. Any ideas are welcomed!! 



#2 JR7

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Posted 04 November 2016 - 02:36 AM

Well, a quick Google search and this explains a bit: http://sites.tufts.e...-and-the-highs/


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#3 jaiho

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Posted 04 November 2016 - 02:57 AM

I've heard of this in some circles, people who crash into a depression after exercise, or sex/orgasm.

Some psychiatrists prescribe a low dose SSRI to counter it. 



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#4 gamesguru

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Posted 04 November 2016 - 10:36 AM

The stomach nervousness, chest tightness (dysautonomia) and hyper-vigilance make me think hyperactive norepinephrine/beta receptors are involved.  Since low dopamine is probably playing a role in your symptoms and ginseng increases both DA and NE, I can recommend that at 2400mg.  Allow 12 weeks for it to start working.  Something to help with the shame/anxiety too, maybe just read some good articles, get exposure or theanine, idk.  Forskolin boosts oxytocin and energy levels, but can be slightly anxiogenic.

 

It's usually the women experiencing the so-called postcoital dysphoria (PCD), in part because they are more likely to be victims of rape.  In most PCD is an unpredictable phenomenon, occurring only once or twice over a lifetime.  For others it's a daily reality.  Most probably, a combination of sexual abuse and maladapted parenting strategies are to blame for the chronic subject's pathological shame (in the acute subject, alcoholic regrets are the typical culprit).  It's worth noting PTSD can push you the other way, too, with clear trends towards hypersexuality and shamelessness (seen in cases of non-sexual abuse and in the related condition, borderline syndrome).

 

Although PTSD affects dopamine transport and reactivity, I find the likelier explanation to be non-pharmacologic.  Certainly, SSRIs involve frontal dopamine and norepinephrine, and this somehow treats PCD, but PCD is not to be confused with the shame of PTSD.  Like the girl's parents, your 2014 experiences are to blame.  The OP's abuse, if I may stab a guess, was sexual, and to this day, the shame connected with an encounter endures for weeks.  Allowing for the recency of the trauma and other uncontrollable life factors, the severity of your symptoms today is not so surprising.  Given time and a supportive environment, a 90% recovery is possible.

 

I am not one who believes sexual deprivation to ever be good.  Freud argued it was the main source of neurosis, an unresolved condition, the life force of frustrated chumps.  Regardless what Freud thinks, the fear of intimacy explains your change of heart, shame, and difficulty connecting; you just have to work within it.  Perhaps as sex becomes more regular (exposure), the body will re-acclimate itself and the negative effects will become less intense.


Edited by gamesguru, 04 November 2016 - 10:37 AM.

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#5 jack black

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Posted 04 November 2016 - 11:21 AM

I've heard of this in some circles, people who crash into a depression after exercise, or sex/orgasm.
Some psychiatrists prescribe a low dose SSRI to counter it.


exercise or sex always made me feel worse (afterwards of course) emotionally, but only rarely disabling. Not sure how to explain it at the level of neurotransmitters.

As for the PTSD, propranolol is great. I witnessed a very traumatic crime this year and took propranolol shortly after and I have only vague recollection without emotions, like I saw a movie. I wish I knew that when I had a major car crash with injuries when young.
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#6 gamesguru

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Posted 04 November 2016 - 01:56 PM

I've heard of this in some circles, people who crash into a depression after exercise, or sex/orgasm.
Some psychiatrists prescribe a low dose SSRI to counter it.

exercise or sex always made me feel worse

... I have only vague recollection

 

You could replace propanolol with cannabis and achieve similar vague recollection?

 

Btw, some people have "exercised-induced" food allergy that certain foods within a few hours, exercise makes them sweat, itch, and finally progress onto hives or swelling.  Similar to exercised-induced asthma.  But I don't think that's what's going on here.  What's going on with exercise-induced depression is perhaps an profoundly exaggerated release of endoopioids and endocannabinoids, which induces transmitter depletion and receptor downregulation, leading into depressive and anxious symptoms.  And this phenomenon, of exercise-induced depression, is unlikely to explain the OP's postcoital dysphoria unless they're going at it like athletes do at the oympics

 

To get a better idea for which NTs are important here, the OP could compare exercise, masturbation and sex, and compare the negatives.  Since 5-HT1A is involved in both PSSD and PTSD, it makes sense to look there, e.g. Ginkgo biloba (5-ht1a antagonist).  Throw ginseng, shilajit or maca into the mix (for dopamine) you could have an effective cure to a complicated situation


Edited by gamesguru, 04 November 2016 - 02:07 PM.


#7 JR7

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Posted 04 November 2016 - 09:52 PM

The stomach nervousness, chest tightness (dysautonomia) and hyper-vigilance make me think hyperactive norepinephrine/beta receptors are involved.  Since low dopamine is probably playing a role in your symptoms and ginseng increases both DA and NE, I can recommend that at 2400mg.  Allow 12 weeks for it to start working.  Something to help with the shame/anxiety too, maybe just read some good articles, get exposure or theanine, idk.  Forskolin boosts oxytocin and energy levels, but can be slightly anxiogenic.

 

It's usually the women experiencing the so-called postcoital dysphoria (PCD), in part because they are more likely to be victims of rape.  In most PCD is an unpredictable phenomenon, occurring only once or twice over a lifetime.  For others it's a daily reality.  Most probably, a combination of sexual abuse and maladapted parenting strategies are to blame for the chronic subject's pathological shame (in the acute subject, alcoholic regrets are the typical culprit).  It's worth noting PTSD can push you the other way, too, with clear trends towards hypersexuality and shamelessness (seen in cases of non-sexual abuse and in the related condition, borderline syndrome).

 

Although PTSD affects dopamine transport and reactivity, I find the likelier explanation to be non-pharmacologic.  Certainly, SSRIs involve frontal dopamine and norepinephrine, and this somehow treats PCD, but PCD is not to be confused with the shame of PTSD.  Like the girl's parents, your 2014 experiences are to blame.  The OP's abuse, if I may stab a guess, was sexual, and to this day, the shame connected with an encounter endures for weeks.  Allowing for the recency of the trauma and other uncontrollable life factors, the severity of your symptoms today is not so surprising.  Given time and a supportive environment, a 90% recovery is possible.

 

I am not one who believes sexual deprivation to ever be good.  Freud argued it was the main source of neurosis, an unresolved condition, the life force of frustrated chumps.  Regardless what Freud thinks, the fear of intimacy explains your change of heart, shame, and difficulty connecting; you just have to work within it.  Perhaps as sex becomes more regular (exposure), the body will re-acclimate itself and the negative effects will become less intense.

First and foremost, thank you very much for your well thought out response. The hyperactive norepinephrine/beta receptors are definitely an area I will look into. Something is definitely off in my system as I had NEVER experienced symptoms prior to the aforementioned event. To offer a bit more detail, the PTSD eliciting event was not sexual in nature. I had a near death experience from a pulmonary embolism that scared me to a degree Ive never experienced before (Im now 39). So with that said, I find it odd that the chemical release that takes place during sex could have such a proofed negative affect for weeks.


 

I've heard of this in some circles, people who crash into a depression after exercise, or sex/orgasm.
Some psychiatrists prescribe a low dose SSRI to counter it.


exercise or sex always made me feel worse (afterwards of course) emotionally, but only rarely disabling. Not sure how to explain it at the level of neurotransmitters.

As for the PTSD, propranolol is great. I witnessed a very traumatic crime this year and took propranolol shortly after and I have only vague recollection without emotions, like I saw a movie. I wish I knew that when I had a major car crash with injuries when young.

 

Thank you for your input. Ive thought about propranolol but Im cautious as my resting heart rate is so low now, usually in the upper 40s. 



#8 gamesguru

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Posted 05 November 2016 - 11:44 PM

I found some association between cardiac events and high serotonin, that SSRIs to lower serotonin might help?  Also, dopamine (serotonin and norepinephrine) are released during hypoxia, accounting for neuron death and psychiatric events in the case of post-cardiac depression and anxiety.  The heart, breathing and metabolic functions grind to a halt.. the body runs low on oxygen, and this has all sorts of consequences from the bones to the brain.  Something similar might apply to embolisms.  But this generally clears up in a few months, and yours was in 2014?  It's possible your nucleus accumbens (the reward center of the brain) was hard hit by this lack of oxygen, and to this day remains hypersensitive to intercourse (with dramatic after-effects).  It's also possible you've developed chronic postcoital dysphoria, and this development has no connection to your embolism.

Metab Brain Dis. 1989 Jun;4(2):143-53.

Dopamine and serotonin in rat striatum during in vivo hypoxic-hypoxia.

Broderick PA1, Gibson GE.

Abstract

Dopamine and serotonin were determined in extracellular fluid of rat striatum by semiderivative in vivo voltammetry during normoxia and a single or repeated exposure to 15% O2 (i.e., mild hypoxia) or 12.5% O2 (i.e., moderate hypoxia). A single exposure to 15% oxygen increased extracellular dopamine 76%. With reintroduction of air to the animals, dopamine values returned to baseline. During a second episode of 15% oxygen, dopamine increased 63% and remained elevated even during a final exposure to air. On the other hand, serotonin was unaffected by 15% oxygen. Moderate hypoxia (12.5% oxygen) increased dopamine (79%) and serotonin (26%) and both remained elevated even after the initial reintroduction of air. These studies demonstrate that in vivo hypoxia increases rat striatal extracellular dopamine and, to a lesser extent, extracellular serotonin. Furthermore, after repeated, mild hypoxic episodes or moderate hypoxia, the increases in rat striatal extracellular dopamine and serotonin continue even during normoxia. These studies further support a role for dopamine and serotonin in hypoxic-induced changes in brain function. The hypoxic-induced elevation of these two neurotransmitters during normoxia may be important in the production of hypoxic/ischemic-induced cell damage.

 

Cardiol Rev. 2001 Jan-Feb;9(1):45-51.

Depression after myocardial infarction.

Ziegelstein RC1.

Abstract

Depression is an independent risk factor for increased postmyocardial infarction morbidity and mortality, even after controlling for the extent of coronary artery disease, infarct size, and the severity of left ventricular dysfunction. This risk factor takes on added significance when one considers that almost half of patients recovering from a myocardial infarction have major or minor depression and that major depression alone occurs in about one in five of these individuals. Despite the well-documented risk of depression, questions remain about the mechanism of the relationship between mood disturbance and adverse outcome. The link may be explained by an association with lower levels of social support, poor adherence to recommended medical therapy and lifestyle changes intended to reduce the risk of subsequent cardiac events, disturbances in autonomic tone, enhanced platelet activation and aggregation, and systemic immune activation. Unfortunately, questions about the pathophysiologic mechanism of depression in this setting are paralleled by uncertainties about the optimal treatment of depression for patients recovering from a myocardial infarction and by a lack of knowledge about whether treating depression lowers the associated increased mortality risk. Ongoing research studies will help to determine the benefits of psychosocial interventions and of antidepressant therapy for patients soon after myocardial infarction. Although the identification of depression as a risk factor may by itself be a reason to incorporate a comprehensive psychological evaluation into the routine care of patients with myocardial infarction, this practice should certainly become standard if studies show that treating depression reduces the increased mortality risk of these patients.


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#9 Mind_Paralysis

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Posted 06 November 2016 - 02:00 AM

 

I found some association between cardiac events and high serotonin, that SSRIs to lower serotonin might help?  Also, dopamine (serotonin and norepinephrine) are released during hypoxia, accounting for neuron death and psychiatric events in the case of post-cardiac depression and anxiety.  The heart, breathing and metabolic functions grind to a halt.. the body runs low on oxygen, and this has all sorts of consequences from the bones to the brain.  Something similar might apply to embolisms.  But this generally clears up in a few months, and yours was in 2014?  It's possible your nucleus accumbens (the reward center of the brain) was hard hit by this lack of oxygen, and to this day remains hypersensitive to intercourse (with dramatic after-effects).  It's also possible you've developed chronic postcoital dysphoria, and this development has no connection to your embolism.

Metab Brain Dis. 1989 Jun;4(2):143-53.

Dopamine and serotonin in rat striatum during in vivo hypoxic-hypoxia.

Broderick PA1, Gibson GE.

Abstract

Dopamine and serotonin were determined in extracellular fluid of rat striatum by semiderivative in vivo voltammetry during normoxia and a single or repeated exposure to 15% O2 (i.e., mild hypoxia) or 12.5% O2 (i.e., moderate hypoxia). A single exposure to 15% oxygen increased extracellular dopamine 76%. With reintroduction of air to the animals, dopamine values returned to baseline. During a second episode of 15% oxygen, dopamine increased 63% and remained elevated even during a final exposure to air. On the other hand, serotonin was unaffected by 15% oxygen. Moderate hypoxia (12.5% oxygen) increased dopamine (79%) and serotonin (26%) and both remained elevated even after the initial reintroduction of air. These studies demonstrate that in vivo hypoxia increases rat striatal extracellular dopamine and, to a lesser extent, extracellular serotonin. Furthermore, after repeated, mild hypoxic episodes or moderate hypoxia, the increases in rat striatal extracellular dopamine and serotonin continue even during normoxia. These studies further support a role for dopamine and serotonin in hypoxic-induced changes in brain function. The hypoxic-induced elevation of these two neurotransmitters during normoxia may be important in the production of hypoxic/ischemic-induced cell damage.

 

Cardiol Rev. 2001 Jan-Feb;9(1):45-51.

Depression after myocardial infarction.

Ziegelstein RC1.

Abstract

Depression is an independent risk factor for increased postmyocardial infarction morbidity and mortality, even after controlling for the extent of coronary artery disease, infarct size, and the severity of left ventricular dysfunction. This risk factor takes on added significance when one considers that almost half of patients recovering from a myocardial infarction have major or minor depression and that major depression alone occurs in about one in five of these individuals. Despite the well-documented risk of depression, questions remain about the mechanism of the relationship between mood disturbance and adverse outcome. The link may be explained by an association with lower levels of social support, poor adherence to recommended medical therapy and lifestyle changes intended to reduce the risk of subsequent cardiac events, disturbances in autonomic tone, enhanced platelet activation and aggregation, and systemic immune activation. Unfortunately, questions about the pathophysiologic mechanism of depression in this setting are paralleled by uncertainties about the optimal treatment of depression for patients recovering from a myocardial infarction and by a lack of knowledge about whether treating depression lowers the associated increased mortality risk. Ongoing research studies will help to determine the benefits of psychosocial interventions and of antidepressant therapy for patients soon after myocardial infarction. Although the identification of depression as a risk factor may by itself be a reason to incorporate a comprehensive psychological evaluation into the routine care of patients with myocardial infarction, this practice should certainly become standard if studies show that treating depression reduces the increased mortality risk of these patients.

 

 

Interesting...

 

But if it's not connected to the Embolism, then what IS it connected to??

 

And regarding something I see you marked up there - "systemic immune activation" - could immuno-modulation then present a novel avenue of treatment? Some form of zink-compound, perhaps?

 

Zink-citrate maybe...

 

This isn't exactly the best of sources, but this men's health -article mentions the immunological aspect of it - you ARE mixing bodily fluids with an alien body - your partner - and it actually suggests... well... ALLERGY to sexual fluids! 0_o

 

http://blog.srhmatte...or-your-health/

 

It also mentions that taking anti-inflammatories before and after sex can help some people with the disease.

 

When taken into account that neuro-inflammation plays a big role in depression... I can see how there is some... logic to this.

 

OP:

 

Have you ever considered taking Ibuprofen and Cetirizine prior to sexy-time? And perhaps after as well.

 

Sounds dumb, but apparently there's something to it. I'll try and find some real, GOOD references on this.

 

Meanwhile, what do the rest of you say, about my little idea?



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#10 gamesguru

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Posted 06 November 2016 - 07:10 AM

Yes, but the fact that serotonin and dopamine increase dramatically after an embolism (leading to a long-term desensitization), paired off with the fact that fluoxetine (a 5-HT2C antagonist & dopamine releasing agent) tends to be particularly effective against post-cardiac depression.. and, you begin to build a strong case for the embolism, even if it's been since 2014 (you see, because without assistance, dopamine is the one neurotransmitter that can take forever to normalize).

 

The immune system may play a role, including inflammation at the oragenelle level (mitochondrial & endoplasmic).  In particular, production of cytokines and interferons is increased during and after a cardiac event (or any stressful event).  But the idea about mixing fluids leading to inflammation and depression, it's a bit of a stretch.  further, Zyrtec is unlikely to do much for cytokines, it doesn't do much for my eczema.

 

I would say herbal SSRIs, though weak, are more likely to help than ibuprofin (st johns, saffron, bacopa).  SSRIs are the only thing in the literature studied to treat PCD/PCT.  There are also choices for the reduction of cytokines, like zinc, ginger and dark choc or blueberries.  I also wonder what the effect of combining sex with marijuana, alcohol or lsd would be on the OP.  Anything that releases dopamine has the potential to enhance sex.  Maybe not the most responsible choice.. so do forskolin (oxytocin), bacopa (serotonin), ginseng (dopamine) and call it a day?



#11 psychejunkie

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Posted 06 November 2016 - 08:08 AM

Do you've ever experienced other difficulties specially before or during intercourse?

like Premature Ejaculation, Hypersexuality or Sleepiness?


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#12 jack black

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Posted 07 November 2016 - 01:33 PM

It's probably too late now, but brain damage due to hypoxia is mediated by NMDA, and studies show benefits of ventilation with xenon (NMDA antagonist).
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#13 JR7

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Posted 09 November 2016 - 12:22 AM

Hmmmm, I was initially thinking these symptoms were more PTSD related and wondering why sex exacerbated the symptoms. It seems some believe there may be a medical underlying cause we well. 



#14 JR7

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Posted 09 November 2016 - 12:24 AM

Do you've ever experienced other difficulties specially before or during intercourse?

like Premature Ejaculation, Hypersexuality or Sleepiness?

Prior to all of these, I would hyper sexuality prior to sex followed by moderate depression immediately after sex (for a span of a few hours). It's seems now as though the post sex symptoms are magnified a hundred times. Also, my overall libido has been little to none since the PTSD events. This is why I suspected dopamine was at play. 



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#15 JR7

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Posted 09 November 2016 - 12:26 AM

 

I found some association between cardiac events and high serotonin, that SSRIs to lower serotonin might help?  Also, dopamine (serotonin and norepinephrine) are released during hypoxia, accounting for neuron death and psychiatric events in the case of post-cardiac depression and anxiety.  The heart, breathing and metabolic functions grind to a halt.. the body runs low on oxygen, and this has all sorts of consequences from the bones to the brain.  Something similar might apply to embolisms.  But this generally clears up in a few months, and yours was in 2014?  It's possible your nucleus accumbens (the reward center of the brain) was hard hit by this lack of oxygen, and to this day remains hypersensitive to intercourse (with dramatic after-effects).  It's also possible you've developed chronic postcoital dysphoria, and this development has no connection to your embolism.

Metab Brain Dis. 1989 Jun;4(2):143-53.

Dopamine and serotonin in rat striatum during in vivo hypoxic-hypoxia.

Broderick PA1, Gibson GE.

Abstract

Dopamine and serotonin were determined in extracellular fluid of rat striatum by semiderivative in vivo voltammetry during normoxia and a single or repeated exposure to 15% O2 (i.e., mild hypoxia) or 12.5% O2 (i.e., moderate hypoxia). A single exposure to 15% oxygen increased extracellular dopamine 76%. With reintroduction of air to the animals, dopamine values returned to baseline. During a second episode of 15% oxygen, dopamine increased 63% and remained elevated even during a final exposure to air. On the other hand, serotonin was unaffected by 15% oxygen. Moderate hypoxia (12.5% oxygen) increased dopamine (79%) and serotonin (26%) and both remained elevated even after the initial reintroduction of air. These studies demonstrate that in vivo hypoxia increases rat striatal extracellular dopamine and, to a lesser extent, extracellular serotonin. Furthermore, after repeated, mild hypoxic episodes or moderate hypoxia, the increases in rat striatal extracellular dopamine and serotonin continue even during normoxia. These studies further support a role for dopamine and serotonin in hypoxic-induced changes in brain function. The hypoxic-induced elevation of these two neurotransmitters during normoxia may be important in the production of hypoxic/ischemic-induced cell damage.

 

Cardiol Rev. 2001 Jan-Feb;9(1):45-51.

Depression after myocardial infarction.

Ziegelstein RC1.

Abstract

Depression is an independent risk factor for increased postmyocardial infarction morbidity and mortality, even after controlling for the extent of coronary artery disease, infarct size, and the severity of left ventricular dysfunction. This risk factor takes on added significance when one considers that almost half of patients recovering from a myocardial infarction have major or minor depression and that major depression alone occurs in about one in five of these individuals. Despite the well-documented risk of depression, questions remain about the mechanism of the relationship between mood disturbance and adverse outcome. The link may be explained by an association with lower levels of social support, poor adherence to recommended medical therapy and lifestyle changes intended to reduce the risk of subsequent cardiac events, disturbances in autonomic tone, enhanced platelet activation and aggregation, and systemic immune activation. Unfortunately, questions about the pathophysiologic mechanism of depression in this setting are paralleled by uncertainties about the optimal treatment of depression for patients recovering from a myocardial infarction and by a lack of knowledge about whether treating depression lowers the associated increased mortality risk. Ongoing research studies will help to determine the benefits of psychosocial interventions and of antidepressant therapy for patients soon after myocardial infarction. Although the identification of depression as a risk factor may by itself be a reason to incorporate a comprehensive psychological evaluation into the routine care of patients with myocardial infarction, this practice should certainly become standard if studies show that treating depression reduces the increased mortality risk of these patients.

 

 

"Chronic postcoital dysphoria"   Hmmm, very interesting suggestion. I always had minor signs of this before the stressful events. 







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