“Viagra for Women” – Thumbs Up or Thumbs Down?

Doc Gumshoe looks at flibanserin

[ed. note: Michael Jorrin, who I like to call Doc Gumshoe, writes mostly non-financial articles about health topics for our readers a couple times a month — he is not a doctor (he’s a longtime medical writer), he chooses his own topics, and his words and opinions are his own. Enjoy!]

It was only a couple of weeks ago that the news hit the headlines. An FDA advisory committee voted 18 to 6 to recommend approval of a drug that, it is hoped by some – certainly including the drug’s manufacturer – would enhance sexual desire in women and attain the same kind of market appeal that Viagra and the other drugs that treat erectile dysfunction have attained.

Usually when an FDA advisory committee votes a recommendation by such a decisive margin, the FDA heeds the advice. This time, most observers are not so sure the FDA will go along. According to the news releases, every single advisor who supported approval for the drug did so with important reservations.

I think FDA approval of this drug would do more harm than good, and I hope the FDA resists the pressure that is being placed on it and rejects the application.

The drug is flibanserin, which was initially developed by Boeringer Ingelheim, who dropped it after the FDA rejected it twice – first in 2010 and then again in 2013. A very small company, Sprout Pharmaceuticals, then acquired the rights to flibanserin. Since then, Sprout has mounted a campaign to persuade the FDA that flibanserin should be approved based more on the “fairness” issue than on efficacy and safety.

The “fairness” issue can be stated simply, although somewhat moronically in my view: There are a couple of dozen drugs approved by the FDA that improve sexual performance in men, but there are no FDA drugs that do the same for women. That constitutes gender discrimination. Therefore flibanserin must get FDA approval, regardless of its efficacy and safety data.

Sprout has organized and backed a pressure group called “Even the Score” whose mission has been to mount a campaign whose theme is that the lack of a drug that improves women’s sexual desire is a glaring example of the FDA’s gender bias. And, of course, the phrase “Viagra for women” is the slogan that sums it up.

It’s entirely usual for pharma outfits to do whatever they can to get the FDA to approve the drugs that they have spent billions to develop. They design clinical trials in such a way as to increase the chance that their candidate drug will be viewed as safe and effective, and they enlist the support of experts whom they think the FDA will pay attention to. But approving a drug on the proposition that if there’s Viagra for men, there ought to be Viagra for women? Let’s take a look at that.

“Viagra for women” is very great nonsense.

Really, we should know better. The phrase should have elicited jeers. Viagra, and the other drugs that treat erectile dysfunction, are not aphrodisiacs. They do not treat sub-optimal male libido. What they do is very basic: they inhibit an enzyme, one of the phosphodiesterases (PDE5), which breaks down a molecule called cyclic guanosine monophosphate or cGMP. In turn, cGMP relaxes smooth muscle which leads to increased blood flow, and prolongs the activity of an important mediator of vasodilation, which is nitric oxide (NO). The activity of cGMP permits blood flow to the penis, and thus, erections. PDE5 counteracts that activity, inhibiting erections. The Viagra-type drugs are PDE5 inhibitors, and they prevent that from happening, thus enabling erections. That’s the whole story.

Of course, the capacity to attain and sustain an erection sufficient for sexual intercourse in itself would likely add to male libido. But the underlying libido has got to be there first, or else the guys wouldn’t be taking the pills.

Are you getting our free Daily Update
"reveal" emails? If not,
just click here...


What is flibanserin … and more to the point, what does it do?

The supposed mechanism of action of flibanserin is based on the Kinsey theory that there are dual forces acting on sexual desire – not one single agent that increases or decreases in activity, but one agent or group of agents that increase libido, and another agent or group of agents that decrease libido. The agents that increase libido have been identified as dopamine and norepinephrine, and the one that decreases libido is serotonin.

This makes intuitive sense. All three of those neurotransmitters have a pretty big range of functions, but dopamine, for example, is linked to pleasure and reward. Norepinephrine is a neurotransmitter that helps get you going, when your body switches from sleep mode to waking mode – it speeds up your heart rate, among other actions. And serotonin does the opposite – it calms you down, helps you get to sleep, and helps you digest your food while you’re dozing.

Flibanserin activates the dopamine and norepinephrine receptors, which has the effect of increasing sexual desire or receptivity. And at the same time it dials down the serotonin receptors, inhibiting serotonin’s calming and sleep-inducing effects. This dual activity has the result – at least theoretically – of increasing sexual desire.

I can think of no reason whatever that flibanserin should not work equally well in males as in females, if it works at all. Except that males are presumed not to need any libido-enhancers, since by nature men are lecherous beasts. However, pasting that “Viagra for women” slogan on flibanserin seems to Doc Gumshoe to be more than a bit sexist and condescending.

Next question: how well does it work?

The short answer is, it does work, but not all that well. And its use will be limited by side effects of considerable concern. The combination of limited efficacy and adverse effects is what led the FDA to reject flibanserin twice, as mentioned earlier. Sprout Pharma has not presented new data regarding flibanserin’s efficacy to the FDA – what they have done instead is mounted a campaign to convince the FDA that the drug should be approved despite its limited efficacy, on the ground that in the absence of anything else, it would be a service to women to have flibanserin available.

Flibanserin has not been extensively studied as far as I can tell. Only 14 clinical trials with the drug have been registered with NIH, and many don’t really address efficacy in the target population.

The best efficacy data flibanserin can come up with is from a trial enrolling 987 women, average age in the mid-30s. The trial ran 24 weeks during which women took flibanserin 100 mg per day, but the efficacy data was just from a 4-week span in that period. The outcome measure of greatest interest was what they called Satisfying Sexual Events (SSEs), and the 542 women taking flibanserin reported an increase of 2.5 SSEs during that period, while the 545 women taking placebo reported an increase of 1.5 SSEs. So the result of taking the drug for six months was an increase of one satisfying sexual event more than the placebo group experienced. Not nothing, but not much.

Other outcome measures mostly consisted of so-called “instruments,” including one called the Female Sexual Function Index Desire Domain Score. Here the women taking flibanserin reported an increase of 1.0 on that score, while the placebo group had an increase of 0.7.

And there were other instruments on which women taking flibanserin showed similarly small improvements in benefit compared with placebo. For example, there is a Female Sexual Distress Scale, and women on flibanserin showed a decrease of 1.0 points on that scale, while the placebo group had a decrease of 0.7 – a mirror image of the score on the desire domain. In each case, the improvement was 0.3 points on a scale of 1 to 5.

Another trial compared two flibanserin doses with placebo, and the outcome measures again showed some benefit. About 50% of women taking the 100 mg daily dose reported improvement in sexual desire, as did about 40% of women taking the 50 mg daily dose. But so did about 30% of women taking placebo. Moreover, one of the outcome measures was daily recording of sexual desire via an eDiary, and improvement in sexual desire recorded this way did not reach statistical significance.

What about the placebo effect?

You may have noticed that the placebo effect was pretty robust in both of these studies. In the first study I mentioned, women taking placebo reported an increase of 1.5 satisfying sexual events during a 4-week period. In the second study, 30% of women on the placebo reported an improvement in sexual desire. What gives? Is taking a totally inactive pill that just might be a libido enhancer every night at bed-time enough to boost sexual desire? Or might the fact that the women are enrolled in a clinical trial that focuses on sexual desire be a contributing factor? Taking the sugar pill at bedtime might just focus the mind on the objective of the study. The subjects want the drug to work – of course they do, who wouldn’t?

But it puts one in mind of the huge number of trials that have been done with drugs to treat depression. What plagues these studies, again and again, is the large response to the placebo. Depression studies frequently use instruments similar to the ones used in the flibanserin trials, and subjects in these trials taking only placebo frequently demonstrate improvement on those instruments that would be judged to be both statistically significant and clinically meaningful. Which is to say, the outcomes are not the result of chance – i.e., they are real – and they make a real difference to the subjects in the trial. One could almost say to a person with depression, “go ahead and enroll in any clinical trial you can find, because you’ll feel better whether you get the real drug or placebo.”

A big question, which applies not only to depression and so-called “hypoactive sexual desire disorder,” is why is the placebo effect so large? Are the subjects in these studies deceived by the sugar pill? Or is that that they are in fact in a therapeutic setting? They are getting treatment. Health professionals are discussing their condition with them, and they are taking tests – filling out questionnaires – focusing on what ails them and whether they’re feeling better, the same, or worse. In that kind of situation, many people feel a bit better – whether or not the drug they’re taking is having any effect.

A major reason that some people in these clinical trials feel worse is that drugs have side effects. This is certainly true of antidepressants – in fact, one of the common side effects of the class of antidepressants called selective serotonin reuptake inhibitors is reduced sexual desire. So maybe the recommendation to a person with depression might be, enroll in any clinical trial you can find, but try to finagle your way into the placebo group, because that way you’ll get the benefit of being in a therapeutic setting without risking the side effects of the antidepressants.

What about side effects with flibanserin?

The same thing could be said of the flibanserin trials. At least, some women in the placebo group definitely benefitted. But what about the side effects in the women who got the active drug? Well, it turns out that flibanserin’s side effects are not inconsequential. They include nausea, fatigue, somnolence, dizziness, and sedation. In the clinical trial I cited above, 9.7% of the women taking flibanserin discontinued the drug due to the side effects.

Of considerable concern is that the adverse effects of flibanserin are magnified when the drug is taken with alcohol. That essentially nixes the possibility of a romantic dinner with a couple of glasses of wine. And because flibanserin is taken daily, that more or less rules out alcohol – not just no wine on the evenings when a romantic encounter might ensue, but no wine (or any booze) ever. Some of the FDA advisors even raised the issue of an alcohol contraindication in the label for flibanserin.

And alcohol isn’t the only thing that has to be avoided. Another is fluconazole, a drug that is very commonly used to treat yeast infections, which, of course, are by no means rare in sexually active women. A clinical trial in which some women were taking fluconazole concomitantly with flibanserin was terminated because the incidence of those adverse events was mounting.

The likely reason for this is that both flibanserin and fluconazole are excreted through the action of the liver, and employ the same route of excretion. This is a familiar issue for folks who develop drugs. When a person takes a drug (or, indeed, ingests just about anything), it has to be excreted somehow. It doesn’t – or it shouldn’t! – just continue to accumulate. Some drugs are excreted in the urine, some in the feces. Drugs that are excreted in the feces pass through the liver, where they are metabolized by the action of hepatic cytochromes. Certain substances affect the action of these pathways, in some cases speeding them up, and in other cases slowing them down. Fluconazole (and a number of other drugs) slow down the activity of one of those pathways in the liver (specifically, in the P450 system, the cytochrome labeled CYP3A4), which means that anything else employing the same pathway has to wait in line. The elimination of flibanserin is delayed when other drugs are clogging up that exit lane, so the concentration of flibanserin increases, and along with the concentration, the side effects increase in severity.

And it’s not just drugs that affect those hepatic pathways – some things that we routinely eat or drink have the same action, for example, grapefruit juice. Might grapefruit juice have to be contraindicated with flibanserin?

Those side effects – nausea, fatigue, somnolence, dizziness, and sedation – might not sound all that severe. But bear in mind that they increase the risk of falls, of auto accidents, of sustaining injuries while carrying out fairly routine tasks. And because flibanserin is taken daily, the risk of these side effects continues for as long as women want to boost their libidos.

Another issue: what is the condition that flibanserin is supposed to “treat?”

It’s called “hypoactive sexual desire disorder,” (HSDD). My Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition), commonly known as the DSM 4, has a longish paragraph describing this condition, from which I will quote only the following snippet: “Because of a lack of normative age- or gender-related data on frequency or degree of sexual desire, the diagnosis must rely on clinical judgment based on the individual’s characteristics, the interpersonal determinants, the life context, and the cultural setting. The clinician may need to assess both partners when discrepancies in sexual desire prompt the call for professional attention. Apparent ‘low-desire: in one partner may instead reflect on an excessive need for sexual expression by the other partner. Alternatively, both partners may have levels of desire within the normal range but at different ends of the continuum.”

That’s in the DSM-4. The fifth edition of the DSM, published in 2013, has dropped HSDD as a disorder, and replaced it with a new construct, which is termed “sexual interest/arousal disorder.” The criteria are much stricter, and are likely to result in a much lower prevalence than did the looser criteria for HSDD. Here’s a brief summary:

The disorder is defined by a complete lack of or significant reduction in sexual interest or sexual arousal. Symptoms include:

  • Absence of interest in sexual activity
  • Absence of fantasizing or even thinking sexual or erotic thoughts
  • The female is disinclined to initiate sexual encounters with her partner and exhibits no sense of pleasure during sexual acts
  • Symptoms must have persisted for a minimum of six months and result in distress on the part of the patient
  • There is no evidence of a physical, biological or substance induced cause of the condition
  • The problem may be lifelong or only acquired
  • The problem may be situational – occurring only in some instances and not others; or generalized – with no apparent limitations.

Even the Score, the organization that was created by Sprout Pharmaceuticals to pressure the FDA, has claimed that up to 43% of women experience sexual dysfunction. This has been characterized as misleading in the extreme by a number of recognized experts in the field of female sexuality. Cynthia Graham, the editor in chief of the Journal of Sex Research, who was one of the working group that developed the new DSM-5 category, has bluntly called the claim “propaganda.”

The flibanserin FDA application is based on treating the former disorder, HSDD, not the more recently-defined disorder – naturally, since the drug was developed before the publication of DSM-5. But the HSDD description in DSM-4 makes it clear that in some cases a “patient” might be identified with HSDD simply because the partner wants sex more than the patient. It’s no doubt easier to stick the woman with the “low libido” label than to call the man a sex fiend.

Looking at the DSM-5 criteria for this disorder, Doc Gumshoe wonders why a woman who has no interest in sexual activity and does not have erotic thoughts and takes no pleasure in sexual acts would even remotely consider taking a daily pill with significant side effects to address her “disorder.” That is, unless she was under considerable pressure from her partner.

Remember HRT?

Hormone replacement therapy (HRT) is still around, but it’s not the colossal money-maker it was back in the half-century span when products such as Premarin and Prempro were the biggest-selling pharmaceuticals in the USA. For most of that period, HRT was promoted as a product that would enhance women’s sexuality and keep them young and desirable well into old age. Increasingly, this was viewed as a practice that was pushed on women by a male medical establishment with the objective of reducing women to sex objects. The HRT movement got a big boost in 1991 with the publication of the Nurses’ Study, which found that women taking HRT had significantly lower rates of cardiovascular disease (CVD). This was seen as making excellent sense, because up to menopause, women have lower cardiovascular risks than men, but when their production of estrogen tapers off, the CVD rates go right back up, and HRT replaces the missing estrogen, keeping the CVD rates lower.

This view was squashed in 2001 with the publication of the Women’s Health Initiative (WHI), which reported increases in heart attacks and breast cancer in women taking HRT. As a result, more than 60% of women quit taking HRT, and many fewer women started using this therapy as they entered menopause.

However, the WHI had serious flaws:

  • Even though at the time the study got under way, most women who took HRT did so to deal with the symptoms of menopause, the great majority of the women enrolled in the trial were well past the menopausal years. Only 3.5% of the women in the trial were between the ages of 50 and 54, whereas nearly 20% were over the age of 70.
  • The increases in absolute risk with the study drug were miniscule – fewer than 10 cases in 10,000 patient-years each for MI, stroke, and breast cancer. These were somewhat offset by a decrease in colorectal cancer and hip fractures. And there was no increase in overall mortality in women taking the study drug.

These findings – increases in absolute risk of less that 0.1% – were disseminated to the media as alarmingly large increases in relative risk. For example, the MI rate for women taking HRT was 37 per 10,000 patient-years, compared with 30 for those taking placebo – an absolute difference of 7 per 10,000 patient years. This was announced as a 23% increase in relative risk (7 on a base of 30) rather than as an increase in the absolute risk. For other outcomes in which the total numbers of women affected were smaller, the announced relative risk increases were even larger.

However, recent studies based on the original WHI data support the use of HRT during the menopausal years, and even concede that during those years, HRT confers some CVD risk reduction.

The motivation for the WHI study seems to have been to discredit the marketing of HRT as the fountain of youth, and to counter the male-dominated perception of women as sex objects. No disagreement with that objective here. Where I do fault the WHI is that women who could safely have taken HRT to mitigate the symptoms of menopause were dissuaded from doing so because of misrepresentation of risk factors.

(Doc Gumshoe did a blog on the subject back in April of 2014, “HRT: From Panacea to Anathema – And Back,” which you can find here.)

What does that have to do with “Viagra for Women?”

Just this: if HRT was pilloried as a strategy to reduce women to the lowly status of sex objects, isn’t flibanserin much the same? If the “patient population” for which this drug is appropriate has no sexual desire and takes no pleasure from sexual activity, it seems evident that they will be taking this drug only to accommodate their partners. Thus, how does flibanserin not reduce women to that same lowly status as sex objects?

Let me once again point to the essential differences between the erectile dysfunction drugs and flibanserin. The ED drugs are taken by men who want to get and keep an erection, and they are taken in preparation for sexual activity, not chronically. In contrast, flibanserin must be taken daily, and the evidence seems to be that the libido-enhancing effects don’t materialize until the drug has been taken for a considerable period – sometimes months.

And here’s another factor of concern: serious discussions of ED and the PDE5 inhibitors that treat ED invariably point out that ED can be a symptom of severe and potentially life-threatening diseases, such as diabetes and heart disease, and that a responsible physician should not prescribe a Viagra-type drug to any man without first making certain that the ED symptoms were not due to such a disease. However, despite all such warnings and recommendations, the ED drugs are widely and easily available with no such restrictions – and sometimes without a prescription at all.

Inevitably, if flibanserin gets the FDA nod, the same situation will prevail. The warnings and special considerations that the FDA advisors thought would be necessary to include in the label for flibanserin will be ignored. It will likely be available (on the internet) without prescription, and millions of women will buy it – some because they really would like to increase their libido and sexual pleasure, and also some because they want to accede to the wishes of their partners. Does that “even the score?” I think not.

This is not to say that efforts to come up with a way to boost libido and sexual satisfaction in women (and also in men!) who feel a need for medical assistance in this domain of life. The issue puts me in mind, once again, of the highly vexed issue of treating depression. In a nutshell, depression is not simply a question of brain chemistry. The most successful treatment for depression combines actual therapy with the little pills, because there are invariably contributing factors that need to be addressed. The same thing is almost certainly true of sexual dysphoria. A little pill might help, but there’s more to it.

* * * * * *

We’ve been seeing a lot of stuff lately about increasing our life expectancy. Doc Gumshoe is definitely interested. A lot of it is malarkey, but some of the malarkey is based on legitimate science. I will do some sleuthing and present my conclusions in an upcoming blog. In the meantime, I have put my cane away in a closet and am getting around with very little trouble. Many thanks for all the comments! Best, Michael Jorrin, (aka Doc Gumshoe)!


25
Share your thoughts...

avatar
17 Comment threads
8 Thread replies
0 Followers
 
Most reacted comment
Hottest comment thread
20 Comment authors
Michael Jorrin, greenfire67Tony @ Stock Market ValuationTed Goodmanmary Recent comment authors

This site uses Akismet to reduce spam. Learn how your comment data is processed.

lucid8
Member
👍0
lucid8

I have no medical background whatsoever, but I also strongly disagree with the acceptance of flibanserin. imo, at first mention, it just sounds like another way for people to get high. While there probably are women out there who genuinely want to increase libido, whether it be a personal decision or otherwise, these matters are highly psychological. If they want a magic pill to solve all of their problems, this won’t give it to them, however it may give them the side effects. For the people who already have libido but still want an increase, i.e. get high, this could… Read more »

Add a Topic
4853
Add a Topic
5790
Add a Topic
4853
Tony @ Stock Market Valuation
Guest

I agree with you. I don’t think viagra for men is the same as “viagra for women”. Women don’t really have any performance issues, so I don’t see how this solves a real need.

Ed Morgan
Guest
Ed Morgan

Off topic, but I am receiving sales pitches for tDCS, tACS and tRNS stimulators that purport to enhance brain functionality when engaging in activities such as intense gaming, cramming for exams or even doing math proofs. Is there any medical evidence that these devices help?

bluesharpbob
Member
👍120

Interesting article about the tangled web of lobbying concerning the approval of this drug-
http://www.nytimes.com/2015/06/14/us/aid-to-women-or-bottom-line-advocates-split-on-libido-pill.html

Jack W
Guest
Jack W

If you want to increase a women’s libido, tell them they’re pretty and perform random loving acts of kindness. It works on all of them………….

mary
Member
👍789
mary

You are very right…I still remember my husband sitting on the sofa watching tv and saying he felt sorry for me because I always had so much work to do (job, children, house, ect). If he had gotten up and helped, I wouldn’t have been too tired for sex.
A helping hand, loving words, and the feeling that we were a team would have made all the difference in the world.

Carbon Bigfoot
Guest
Carbon Bigfoot

As a man of experience—- flowers and champagne always works for me.

fabian
Guest
fabian

I was going to say the same.

William
Guest
William

The author points out that “a little pill might help, but there’s more to it.”
Men have spent thousands of years trying to figure out ways to increase female cooperation, which methods might be summarized: “Candy is dandy, but liquor is quicker.”

jav13037
Member
👍37
jav13037

liquor or lick her?

JB
Guest
JB

Doc,
Why not have a legal drug that releases the dopamine?
I have read that ecstasy was once legally prescribed to couples who were having intimacy problems. I have never tried the drug, not because it’s illegal but because there are no controls in place for safety. I’m assuming it released dopamine? Same with cocaine?
Is releasing a little dopamine so bad for us once in a while? Why not a legal solution?
Thanks for any response.

fabian
Guest
fabian

To answer your question, another question; where is the money?

Gary Fox
Guest
Gary Fox

What’s the formulation (powder in a capsule)? Compressed tablet (grind-able?) Might the primary market turn out to be men to put in their wives’ (or girlfriends’) drinks?

stephencmyers
Member
👍191
stephencmyers

Funny –

Think you need a prescription. Also, possible side effects – dizziness, nausea, fainting and sleepiness. Maker of the drug says it won’t work like a date rape drug – may make women sleepy – not shagging the wall or incapacitated.

Also, some people say the company got this through by slick marketing – that a glass of wine or two may be better.

So, unless you want to go to jail…. I would stick with flowers, chocolate, champagne, dinners (and truth).

Michael Jorrin,
Guest
Michael Jorrin (aka Doc Gumshoe)

I seriously doubt that it will be the kind of drug that guys put in their girlfriend’s drinks, because the drug needs to be taken for several weeks before the effects (if any!) emerge. But that doesn’t mean some guys won’t try…

LostOkie
Member
👍302
LostOkie

Viagra for women. Definitely THUMBS UP! I think we should start putting it in the water! hehehehe. kidding folks! Just kidding! Ok I’m gonna go back and read the article now.

Add a Topic
540
Leo Sullivan
Guest
Leo Sullivan

JACK W has it right!.

Oak
Guest

I agree. Totally

fabian
Guest
fabian

I can’t wait to read your article about the “live forever young” genetic telomerase therapies.
I think it’s utter snake oil. I’m losing my hair for 26 years like millions of men and there are billions of dollars to be made out of it and nobody can. And now they pretend that they found a way for us to live until 150 whilst tap dancing with these nice Irish girls?

Add a Topic
359
jav13037
Member
👍37
jav13037

This looks like prescription Spanish Fly.
What would be the expected reaction from insurance companies? Would the insurance companies be shamed into covering the drug to avoid gender bias allegations?
Thank you for a thorough, informative article.

Add a Topic
882
Add a Topic
882
Martin
Guest
Martin

What are the meds available or natural remedies for a man on ssri’s with no libido?

Michael Jorrin,
Guest
Michael Jorrin (aka Doc Gumshoe)

… except that Spanish Fly is NOT, repeat NOT, an aphrodisiac. It;s a powerful irritant that, when excreted in the urine, causes severe itching and inflammation in the genital area, NOT sexual arousal. It also has serious side effects, including kidney toxicity. it’s called Spanish Fly because it’s made from a kind of beetle – the entire beetle is dried and ground up to make this so-called drug.

Add a Topic
5554
Ted Goodman
Guest

Great report; I love your logical approach and completely agree with your conclusions!
I was wondering if you have seen the latest teaser from David Lashmet for his Stansberry Venture? He’s touting a company that:
1. Is foreign
2. Has a viral oncology “vaccine” in Phase III trials
3. That has been financed by one of the large Pharma co’s to the tune of “$100’s of millions”‘
He doesn’t leave many additional clues, probably due to the fact that for one of his more recent recommendations for a biotech that has an antibiotic in phase III trials could be too easily identified.

Any toughts?

Thanks,
Ted

Add a Topic
4482
greenfire67
Irregular
👍83

DG
What is your opinion on Palatin Tech (PTN) here;

http://www.palatin.com/products/bremelanotide.asp

Michael Jorrin,
Guest
Michael Jorrin (aka Doc Gumshoe)

Many neurotransmitters could conceivably have a positive effect on sexual arousal, including the one Palatin’s investigational drug targets. But also, as I suggested in my piece, simply participating in a clinical study that has sexual events as an endpoint would be likely to boost libido – a kind of placebo response. I’m in wait and see mode. As for the “viral oncology vaccine” mentioned, quite a number of viruses could be active this way. Some viruses mobilize T-cells to attack specific cancer cells. The overall field of manipulating viruses is promising. Amgen, for one, was involved in a program to… Read more »

Add a Topic
3397