Post-ssri Sexual Dysfunction Recognized As Medical Condition

randolf_faust

Experienced Member
My Regimen
Reaction score
306
maybe its interesting for some of you guys.

the numbers are horrendous if you ask me and thats without affecting dht in any way. i come more and more to the conclusion that long lasting side effects of finasterid are mostly caused by effect of finasterid on neurosteroids and neuroreceptors.

however compared to ssri finasterid looks really safe. crazy that so many people take ssri these days without thinking twice.

The announcement came earlier this week. On June 11, the European Medicines Agency formally declared that it was recognizing Post-SSRI Sexual Dysfunction (PSSD) as a medical condition that can outlast discontinuation of SSRI and SNRI antidepressants.

After lengthy and extensive review, the agency’s Pharmacovigilance Risk Assessment Committee determined that “sexual dysfunction, which is known to occur with treatment with SSRIs and SNRIs and usually resolves after treatment has stopped, can be long-lasting in some patients, even after treatment withdrawal.

The newly recognized condition is “characterized by the fact that patients continue to present sexual side effects after the discontinuation of the drugs,” the authors of a case study noted earlier this year, with symptoms “mainly consist[ing] of hypo-anesthesia [marked numbness] of the genital area, loss of libido, and erectile dysfunction.”

A 2018 literature review went further, describing the condition as “debilitating” and under-recognized, with “common PSSD symptoms” including “genital anesthesia,” as well as failure to become aroused or orgasm, “pleasure-less or weak orgasm, decreased sex drive, erectile dysfunction and premature ejaculation.”

Formal recognition of the condition is a victory for the many thousands of patients who since the late 1990s have participated in studies, following widely reported sexual side effects from patients worldwide. One study involving 1,022 outpatients determined in 2001, “The incidence of sexual dysfunction with SSRIs and venlafaxine (Effexor) is high, ranging from 58 percent to 73 percent, as compared with serotonin-2 (5-HT2) blockers.” Citalopram (Celexa) was found to have the highest incidence, at 72.7 percent, with paroxetine (Paxil) second at 70.7 percent, but fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox) all produced outcomes in the 58-62 percent range, much higher than official figures advised. At the time, the condition was known as “Antidepressant-induced sexual dysfunction.

The same study found that “men had a higher frequency of sexual dysfunction (62.4 percent) than women (56.9 percent),” following discontinuation, “although women had higher severity. About 40 percent of patients showed low tolerance of their sexual dysfunction.” Four-in-ten, that is, found that even after ending treatment their sexual side effects were broadly intolerable. One need only imagine the toll placed on relationships, individual well-being and sexual health, and, more broadly, on public health, given the numbers of people prescribed the medication worldwide.

We are not, in this case, starting with a blank slate. In 1997, a study of 344 patients concluded that sexual dysfunction was “positively correlated with dose” and that most patients “experienced substantial improvement in sexual function when the dose was diminished or the drug was withdrawn.” Complete disappearance of symptoms within six months was limited to just 5.8 percent of patients, however, and fully 81.4 percent “showed no improvement at all by the end of this period.”

Among the hypotheses behind the condition: “dopamine-serotonin interactions, serotonin neurotoxicity, and downregulation of 5-hydroxytryptamine receptor 1A.” The latter problem, discussed in my book Shyness: How Normal Behavior Became a Sickness, highlighted in 2007 that for many patients prescribed SSRIs for anxiety and depression, 5-HT1A (serotonin subtype) receptors “aren’t as malleable as other kinds.” Nor are they as resilient in returning even months later to pre-drug levels.

That even limited victory could be declared more than two decades after the first studies were published is down to the pressure of independent research groups such as RxISK, led by Dr. David Healy in the UK, which in May 2018 petitioned for adjusted warnings about post-SSRI sexual dysfunction and persistent genital arousal disorder (PGAD) at the moment of prescribing, to caution and better inform patients about the risk of adverse effects, including after treatment. Of the petition’s twenty-two endorsing signatories, the majority were “peer-reviewed authors of the medical literature on PSSD and PGAD.” In addition, the petition served as an up-to-date review of the medical literature on both disorders, itself published in the International Journal of Risk and Safety in Medicine.

“The general message from doctors,” Healy told the Daily Mail following the EMA decision, “has been that this happened to a minority of people … and that these sexual problems were very short-term. Another argument was that depressed people tend to lose their sex drive anyway—but in drug trial data I have had access to as an expert witness, even the healthy volunteers taking the medication reported problems with their sex drive, and that is without prompting.”

“In the early 2000s,” he continued, “there were a number of case reports from doctors who had experienced the problems themselves—and they still had sexual difficulties ten years after stopping their SSRIs. We know that blocking sodium currents (which all SSRIs do) can cause genital numbness. We don’t know why the effects become long-lasting in some. Sometimes people are told it’s their mood disorder coming back—but, if you recover from depression, your sex drive and ability to orgasm returns. Yet, after taking SSRIs, this doesn’t always occur.”

Bearing out that concern is the 1997 study, mentioned above, which in testing six months after discontinuation found that 81.4 percent of participants “showed no improvement at all by the end of this period.”

Despite such numbers, many of the same patients reported being “disbelieved” repeatedly by their doctors and other prescribers, receiving recommendations instead for higher dosage or a different SSRI. One woman posted to this blog, following recent news reports on generalized withdrawal from the antidepressants, “I am a 30-year-old woman with PSSD for over 4 years after citalopram suspension. There was nothing more traumatic in my life than losing the sexuality that had always grown with me. My body no longer reacts to any sexual stimulation, I can no longer feel excitement and pleasure.”

“I did not receive honest information on the harms or informed consent and could in no way supposedly ‘weigh up the benefits and risks ratio,’” posted another. “By the time I was supposed to be entering adult life at 21 years old I became impotent and it is like my genitals are not even there anymore. My body cannot even wake itself to be aroused since only my head is there … [The condition] is criminal not to be warned about... How could my government do this to me? I was a vulnerable defenseless child.”

“My original illness was nothing compared to all the new symptoms brought on by antidepressants and withdrawal,” wrote a third. “SSRI and SNRI medications have left me with feeling permanently chemically lobotomized and castrated.”

The announcement by the European Medicines Agency comes just two weeks after the Royal College of Psychiatrists advised that it would tighten its prescribing guidelines to recognize that antidepressant withdrawal can be “severe” and last for weeks, even months.

A response to the EMA ruling is also expected from the U.S. Food and Drug Administration, which was petitioned at the same time using the same data that encouraged the European-wide decision. The federal agency indicated thus far that “no decision had yet been made” and that its review was “still ongoing.”

Given the depth, range, and statistical power of the research, it would be remarkable if the agency reached a conclusion different from its European counterpart.

https://www.psychologytoday.com/nz/...xual-dysfunction-recognized-medical-condition
 
Last edited:

randolf_faust

Experienced Member
My Regimen
Reaction score
306
Very good news. Yes it's very remarkable that post SSRI and post Accutane victims suffer from the same sexual side effects as PFS victims.

The SSRI market is also a lot bigger than that of oral AA's I imagine.

i have the feeling there is little research on how finasterid interacts with neurosteroids

like we know 1mg finasteride lowers dht 70% but we don't know the exact percentage when it comes to neurosteroids
 

BadInvertor

Banned
My Regimen
Reaction score
108
Somebody posted on this forum a while ago a neurosteroids analysis after treatment with finasteride and all neurosteroids showed depletion but i can't seem to find it !

3. Potential adverse effects of 5α-R therapy on the CNS

The CNS has the capacity and the machinery to synthesize a host of neurosteroids [72]. Neurosteroids play a pivotal role in modulating neural activity through interaction with neurotransmitter receptors and neurotransmitter-gaited ion-channels [73]. These neurosteroids interact with a host of neurotransmitter receptors and modulate seizure susceptibility, anxiety, stress, and depression [74]. 5α-R reaction is the rate limiting step in the conversion of testosterone, progesterone, cortisol, corticosterone, and Doctor into their respective 5α-dihydro-deratitves, which serve as precursors for 3α-hydroxysteroid dehydrogenase which transfroms such precursors into their respective neurosteroids (androstanediol, allopregnanolone [AP], tetrahydrocortisol, tetrahdyrocorticosterone, and tetrahydrodeoxycorticosterone) (Fig. 1) [1,2]. All three isoforms of 5α-R are expressed in the various regions of brain and are thought to be critical for brain development since fetal brain express high concentrations of 5α-R [1,2].

It has recently been shown that patients who had been treated with finasteride have reduced or undetectable levels of neuroactive steroids in their cerebro-spinal fluid and plasma, and exhibited higher levels of precursor steroids [75]. This observation strongly suggests that 5α-RIs have a deleterious effect on the biosynthesis and function of neurosteroids in the central nervous system. Finasteride treatment resulted in decreased levels of 5α-DHT and 3α, 5α-tetrahydroprogesterone (AP) and increased levels of testosterone supporting the hypothesis that deleterious effects of finasteride may be persistent or irreversible. This may explain some of the noted symptoms such as anxiety, depression and suicide in patients who have been treated with finasteride [76].

Go to:
NEUROPROTECTIVE EFFECTS OF NEUROSTEROIDS
Neuroactive steroids elicit important neuroprotective effects during trauma and injury to the central nervous system [75]. AP is shown to be beneficial in the treatment of traumatic brain injury, attenuating edema, trauma, stress, inflammation, apoptosis, and reducing oxidative stress [76,77,78]. AP is not only a protective agent in ischemia, but also in maintaining blood brain barrier integrity, and in memory and learning [78,79,80,81]. Studies on CNS injury in which asphyxiation was induced in fetal sheep to stimulate neurological stressors, in the presence or absence of finasteride, showed an increase in apoptotic cell death in the cerebellum and hippocampus in the animals treated with finasteride (Fig. 5) [82]. Furthermore, treatment with an AP analogue, alfaxalone, prevented cell death as assessed by the increase in activity of caspace-3 and expression of ki-67 protein. This observation suggests that AP exerts a neuroprotective role in the brain, which is inhibited by finasteride.

FIG. 5
Effects of finasteride on the number of activated capsase-3 positive cells present in the cerebellar molecular and granular layers. Photomicrographs showing activated caspase-3 immunoreactivity in the granular layer of the cerebellum of a fetus at 24 hours after infusion with vehicle (control, A), finasteride (B), finasteride+alfaxalone (C), and alfaxalone (D). All fetuses were 131±3 days of gestation at the time of autopsy and tissue collection. (A-D: Scale bar, 10 µm). Color was visualized using streptavidin horseradish peroxidase conjugated to diaminobenzidine. Adopted from Yawno T, et al. Neuroscience 2009;163:838-47, with permission of Elsevier Inc. [82].

The neuroprotective effect of AP was further illustrated during injury to the rat hippocampus slices induced by tributyltin treatment, which resulted in significant cell death. Administration of progesterone (P) with finasteride showed similar cell death to that induced by tributyltin treatment, in the various regions of the hippocampus. In contrast, P treatment without finasteride provided a protective effect. This is attributed to the conversion of P to 5α-DHP by 5α-Rs and to AP by 3α-HSD. To confirm that this is due to the neuroprotective effect of AP, the latter was administered with or without finasteride. While the tributyltin induced cell death was significant, administration of AP with and without finasteride produced a markedly protective effect as assessed by the reduced cell death [83]. These findings suggest that 5α-Rs play a pivotal role in neuroprotection.

Neurosteroid synthesis in the hippocampus is suggested to be critical for neuroplasticity in the brain [84]. Inhibition of 5α-R by finasteride is thought to contribute to reduced neuroplasticity due to structural changes resulting from inhibition of neurogenesis in the hippocampus. Finasteride treatment in mice showed decreased cell proliferation in the hippocampus, suggesting that inhibitors of 5α-R blocks neurogenesis [84].

As reported by Mellon [85] in an adult animal model of Niemann-Pick disease type C the biosynthesis of AP is significantly reduced, and this was supported by significant reduction in the activity of 5α-R and 3α-HSD in the brain of these animals [85]. The activity of 5α-R was markedly reduced with the progression of the disease. This reduced 5α-R activity may contribute to the observed accumulation of cholesterol in neurons and gangliosides, cerebro, perkinje cell degeneration, dysmyelination and neurodegeneration [85]. Thus, loss of 5α-R and 3α-HSD activity is attributed to loss of neurons expressing these enzymes. Treatment with AP early at postanatal day 7 was found most effective in preventing neurodegeneration and correlates with reduced tremor, ataxia, and increased lifespan. In the animal model, these findings indicate that the loss of neurosteroid biosynthesis may be responsible for the disease state and its progression. Therefore inhibition of 5α-R by finasteride and dutasteride in the course of treatment of nonlife threatening conditions, such as male pattern baldness (alopecia) or BPH may have detrimental effects on the CNS.

It has been reported that AP levels were significantly decreased in postmortem human brains of Alzheimer disease (AD) patients [86]. An inverse correlation was noted between AP levels and the degree of neurological degeneration in pathological section of AD patient [86]. One of the interesting findings was that pregnenolone levels were greater in the temporal cortex of AD patients suggesting that this may be a compensating mechanism for reduced 5α-R activity. We speculate that 5α-RIs may contribute to reduced levels of neurosteroids in the CNS and this may enhance the progression of neurodegenerative disease, such as AD.

Conversion of polyprenol into dolichol is critical for N-glycosylation of membrane proteins [3]. 5α-R type 3 was shown to be critical for catalyzing this reaction [3]. A mutation in this enzyme lead to mental retardation and opthamologic and cerebral defects [3]. Intraoperative Floppy Iris Syndrome (IFIS) is also a complication experienced during cataract extraction. The syndrome is defined by floppy, or flaccid iris. Studies have indicated a correlation between finasteride and the occurrence of cataracts and IFIS indicating inhibition of glycosylation may contribute to this pathology [87].

Go to:
EPILEPSY/CONVULSION
P is an effective anticonvulsing agent in humans [88]. The anticonvulsive properties of P diminished when animals were treated with finasteride. In a mouse model of pentylenetetrazol-induced seizures, there was an approximately 50% decrease in the protective effect of P in mice when treated with finasteride [89]. Higher dosages of finasteride produced more persistent symptoms of pentylenetetrazol-induced seizures [89]. However, when AP was administered together with finasteride, the pentylenetetrazol seizure activity was reversed. This finding indicates that the antiseizure properties of P are attributed to its metabolite AP emphasizing the critical role of 5α-Rs [89,90,91].

Go to:
DEPRESSION
Anxiety is often found as a comorbidity of depression. The administration of AP produces antidepressant and anxiolytic effects [92,93]. Coadministration of finasteride and P blocked P's anxiolytic effect [94]. This finding suggests that a metabolite of progesterone is responsible for the anxiety reducing effect of P. An inverse relationship between levels of AP and depression has been demonstrated in male patients with depression [95]. Preclinical studies have suggested that reduction in AP levels by 5α-RIs may contribute to depressive symptoms [96]. Increased depressive symptoms are thought to be linked to finasteride treatment [97]. A statistically significant correlation was observed between use of finasteride and depressive symptoms [98]. Persistent side effects have been noted even after discontinuation of finasteride treatment [76] from 3 months to 11 years, suggesting that the adverse effects of finasteride may be permanent

Source : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/
 
Last edited:

BadInvertor

Banned
My Regimen
Reaction score
108
Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients.
Melcangi RC1, Santi D2, Spezzano R3, Grimoldi M4, Tabacchi T5, Fusco ML4, Diviccaro S3, Giatti S3, Carrà G5, Caruso D3, Simoni M2, Cavaletti G4.
Author information
1
Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy. Electronic address: roberto.melcangi@unimi.it.
2
Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy.
3
Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
4
Experimental Neurology Unit and Milan Center for Neuroscience, School of Medicine and Surgery, University of Milano Bicocca, Monza, Italy.
5
Department of Medicine and Surgery, University of Milano Bicocca, Monza, Italy.
Abstract
Recent reports show that, in patients treated with finasteride for male pattern hair loss, persistent side effects including sexual side effects, depression, anxiety and cognitive complaints may occur. We here explored the psychiatric and andrological features of patients affected by post-finasteride syndrome (PFS) and verified whether the cerebrospinal fluid (CSF) and plasma levels of neuroactive steroids (i.e., important regulators of nervous function) are modified. We found that eight out of sixteen PFS male patients considered suffered from a DSM-IV major depressive disorder (MDD). In addition, all PFS patients showed erectile dysfunction (ED); in particular, ten patients showed a severe and six a mild-moderate ED. We also reported abnormal somatosensory evoked potentials of the pudendal nerve in PFS patients with severe ED, the first objective evidence of a neuropathy involving peripheral neurogenic control of erection. Testicular volume by ultrasonography was normal in PFS patients. Data obtained on neuroactive steroid levels also indicate interesting features. Indeed, decreased levels of pregnenolone, progesterone and its metabolite (i.e., dihydroprogesterone), dihydrotestosterone and 17beta-estradiol and increased levels of dehydroepiandrosterone, testosterone and 5alpha-androstane-3alpha,17beta-diol were observed in CSF of PFS patients. Neuroactive steroid levels were also altered in plasma of PFS patients, however these changes did not reflect exactly what occurs in CSF. Finally, finasteride did not only affect, as expected, the levels of 5alpha-reduced metabolites of progesterone and testosterone, but also the further metabolites and precursors suggesting that this drug has broad consequence on neuroactive steroid levels of PFS patients.

Source : https://www.ncbi.nlm.nih.gov/pubmed/28408350
 

randolf_faust

Experienced Member
My Regimen
Reaction score
306
@BadInvertor too bad - maybe someone else can remember it.

however reading this just proves my point:

It has recently been shown that patients who had been treated with finasteride have reduced or undetectable levels of neuroactive steroids in their cerebro-spinal fluid and plasma, and exhibited higher levels of precursor steroids [75]. This observation strongly suggests that 5α-RIs have a deleterious effect on the biosynthesis and function of neurosteroids in the central nervous system. Finasteride treatment resulted in decreased levels of 5α-DHT and 3α, 5α-tetrahydroprogesterone (AP) and increased levels of testosterone supporting the hypothesis that deleterious effects of finasteride may be persistent or irreversible. This may explain some of the noted symptoms such as anxiety, depression and suicide in patients who have been treated with finasteride [76].


people should less be worried about reduced dht and more worried about what the f*** is going on in their brain when they take finasteride. as we can ssri is enough to give you permanent ed and that without interfering in any way with dht
 
Last edited:

BadInvertor

Banned
My Regimen
Reaction score
108
@BadInvertor too bad - maybe someone else can remember it.

however reading this just proves my point:

It has recently been shown that patients who had been treated with finasteride have reduced or undetectable levels of neuroactive steroids in their cerebro-spinal fluid and plasma, and exhibited higher levels of precursor steroids [75]. This observation strongly suggests that 5α-RIs have a deleterious effect on the biosynthesis and function of neurosteroids in the central nervous system. Finasteride treatment resulted in decreased levels of 5α-DHT and 3α, 5α-tetrahydroprogesterone (AP) and increased levels of testosterone supporting the hypothesis that deleterious effects of finasteride may be persistent or irreversible. This may explain some of the noted symptoms such as anxiety, depression and suicide in patients who have been treated with finasteride [76].


people should less be worried about reduced dht and more worried about what the f*** is going on in their brain. as we can ssri is enough to give you permanent ed and that without interfering in any way with dht

Found it :
 

Attachments

  • 2i2afzs.png
    2i2afzs.png
    71.1 KB · Views: 167

BadInvertor

Banned
My Regimen
Reaction score
108
They were right in the scientific literature i think, it's not DHT that causes all of this sides, it's the enzyme that it's blocked and that has different functions in the body and the brain itself.. That's why recently they found out that actually DHT causes acne much more than testosterone does like they previously thought... It was clear at least from what i learned in school and from other doctors that those enzymes have a deep role that it's not that well understood and how could all the people that take this kind of medicine know if the scientists that are studying them don't actually know exactly...

People are dumb in most cases and really think that the human body is a toy that you can play with it and it's hormones ingesting pills and maneuvering it's course the way you like it with this pills and without any actual notion of how the human body actually works or without thinking of how you will have to suffer in the future because of this... Thank "God", my parents and the school that gave me a proper education and my instincts that don't let me follow the herd of stupid ship at any costs, regardless of how desperate i would have been because of my hair loss !

I had a doctor at school who wanted to give me a couple of ssri's because i had a minor depressive state because of an event that occurred in my life but i refused because i have a different perspective about pills and would never take any except if my life would depend on it.. After i started documenting myself on them and reading the studies and how many people they actually kill every year around the world i was so proud of myself that i actually got out of my depressive state without any help or medicine... Besides the fact that recent studies show and admit that the medical science behind mental illnesses is not well understood and scientists admitted that actually this pills can make things worse for 90% of the cases in which they are prescribed and even to those who respond "good" at the start of the treatment, but in long term they are more than fucked ! Now they are studying Ketamine and Methamphetamine in patients with depression and some already started in prescribing this and seeing a lot better results than with the ssri's... And even if Ketamine is considered the most anti-depressant drug that ever existed, they are not well understood either, it creates dependency and will take a lot of time until they will start to understand it and replace those ssri's with something better, especially at the alarming rates on which doctors prescribe them and people take them like sugar pills !

Recent studies showed after brain scan that similar depressive symptoms have different patterns in which they affect the brain and this could revolutionize the way that medicine could be prescribed from now on, to every individual itself in function of how the brain is affected by the symptoms he has or by the illness he has.. That's why they don't let psychiatrists to do brain scans, it's not done for a reason, who would take this sh*t pills if people would really know the truth.

The most important lesson from 83,000 brain scans | Daniel Amen | TEDxOrangeCoast
https://www.youtube.com/watch?v=esPRsT-lmw8
 
Last edited:

randolf_faust

Experienced Member
My Regimen
Reaction score
306
They were right in the scientific literature i think, it's not DHT that causes all of this sides, it's the enzyme that it's blocked and that has different functions in the body and the brain itself.. That's why recently they found out that actually DHT causes acne much more than testosterone does like they previously thought... It was clear at least from what i learned in school and from other doctors that those enzymes have a deep role that it's not that well understood but how could all the people that take it know if the scientists that are studying them don't actually know exactly...

People are dumb in most cases and really think that the human body is a toy that you can play with it and it's hormones ingesting pills and maneuvering it's course the way you like it with pills and without any actual notion of how the human body actually works... Thank "God", parents and the school that gave me a proper education and my instincts that don't want to follow the herd of stupid ship at any costs, regardless of how desperate i would have been because of my hair loss !

I had a doctor at school who wanted to give me a couple of ssri's because i had a minor depressive state because of an event that occurred in my life but i refused because i have a different perspective about pills and would never take any except if my life would depend on it.. After i started documenting myself on them and reading the studies and how many people they actually kill every year around the world i was so proud of myself that i actually got out of my depressive state without any help or medicine... Besides the fact that recent studies show and admit that the medical science behind mental illnesses is not well understood and scientists admitted that actually this pills can make things worse for 90% of the cases in which they are prescribed and even to those who respond "good" at the start of the treatment, but in long term they are more than fucked !

Recent studies showed after brain scan that similar depressive symptoms have different patterns in which they affect the brain and this could revolutionize the way that medicine could be prescribed from now on, to every individual itself in function of how the brain is affected by the symptoms he has or by the illness he has.. That's why they don't let psychiatrists to do brain scans, it's not done for a reason, who would take this sh*t pills if people would really know the truth.

The most important lesson from 83,000 brain scans | Daniel Amen | TEDxOrangeCoast
https://www.youtube.com/watch?v=esPRsT-lmw8

we can fly to the moon but we still dont understand the human body in even the slightest. especially the brain. or the gut. or the immune system. not even f*****g hairloss. everything is quite superficial.
 

BadInvertor

Banned
My Regimen
Reaction score
108
we can fly to the moon but we still dont understand the human body in even the slightest. especially the brain. or the gut. or the immune system. everything is quite superficial.

Exactly and only the open minded and smartest ones know that, the rest are just sheep and victims of the ones who actually know this things and don't share them with the public.. If the truth about a lot of things would have been known by the general public, a lot of industries would collapse or at least they would have much less buyers and clients than they actually have now because of the misinformation and lack of information !
Watch that video, it will make you understand more than you think !
 

BadInvertor

Banned
My Regimen
Reaction score
108
they should scan the brain of people before and after finasterid use lol

They should do a lot of things that they don't do, in many departments and especially in the medical field, but unfortunately it's not in their general interest and i don't think it will be in the future as well but this is another story !
 
Top