It treats erectile dysfunction and has beneficial effects on prostate enlargement, cardiovascular problems and other diseases
Viagra has a bad press.
Many experts, when discussing erectile dysfunction (ED), will tell you that Viagra can eliminate it, but… there is always a “but.”
Maybe they’ll say something about addressing the psychological causes of ED. Other times is some drivel about “aging naturally.” Often, it’s the inevitable “but what about the women?” feminist swerve. A lot of ideology comes into play when discussing something that links men and sex so intimately.
Let me start by clarifying that Viagra is the commercial name for sildenafil, which is just the best known compound of a class of drugs called phosphodiesterase-5 (PDE5) inhibitors. I used Viagra in the title because of its name recognition, but this article is about all PDE5 inhibitors.
This article is a summary of the scientific information about PDE5 inhibitors written in accessible language. I want to address this controversial subject with scientific rigor, so I support what I say with references to scientific papers in peer-reviewed journals. I use links to Wikipedia to back well-established knowledge.
Disclaimer: I am not a medical doctor. This article is for information purposes and should not be considered medical advice. In the USA and many other countries, PDE5 inhibitors are prescription-only. Before taking them, you should always consult your doctor. Buy them from a reputable pharmacy.
How erections work
To penetrate the vagina and to be able to thrust during sex, the penis must be hard.
There are many ways to achieve an erection. Penises could have a bone inside—in fact, the penises of dogs, wolves, gorillas and chimps have it (it is called baculum). There could be a muscle inside the penis that contracts to achieve that hardness, as happens for nipple erection.
In humans, erections are achieved by pumping the penis full of blood. This happens even in animals with a baculum.
In the stem of the penis there are two large bodies, called the corpora cavernosa, that are filled with blood during an erection. The corpus spongiosum, which runs along the urethra and fills the glans, also fills with blood, but to a lesser extent.
The mechanism that keeps the blood in the penis is counter-intuitive, but key to understand how PDE5 inhibitors enhance erections.
Erections are initiated by erotic stimuli in the brain. This mental state of sexual arousal activates nerves in the parasympathetic branch of the autonomic nervous system. The autonomic nervous system controls the cardiovascular state of the body: how fast the hard beats and the contraction of the arteries that set blood pressure.
A particular set of parasympathetic nerves goes from the sacral spinal cord to the penis. There, they release the neurotransmitter acetylcholine, which acts on receptors on other neurons and endothelial cells to make them release nitric oxide (NO) (Goldstein et al., 2019). NO is a gas that acts as a neurotransmitter. It diffuses from the endothelial cells into the walls of the trabecular arteries inside the corpora cavernosa, penetrating the smooth muscle cells that control the dilation of these arteries.
Smooth muscle is quite different from the striated muscle that we use to move and exercise. Its contraction is involuntary. It is involved in the functioning of hollow organs like the arteries, stomach, intestines, bladder and uterus. The smooth muscle in the walls of the arteries determines blood pressure and the blood flow into particular parts of the body. Here, we are interested in blood flow into the penis.
The counterintuitive part is that relaxation of smooth muscle is what makes the penis hard, while relaxation of other muscles makes them flaccid. The more relaxed the smooth muscle, the wider the arteries. Wider arteries mean more blood flow into the corpora cavernosa. This causes erection by making the corpora cavernosa inflate like two elongated balloons. At the same time, the veins that drain blood from corpora cavernosa are compressed by its expansion, making sure that blood stays inside the penis.
How Viagra and other PDE5 inhibitors increase erections
In the smooth muscle cells, NO activates the enzyme guanylate cyclase, which produces the second messenger cyclic guanosine monophosphate (cGMP). cGMP activates protein kinase G, which opens calcium-dependent potassium channels in the membrane of the smooth muscle cells. The resulting increase in membrane potential (hyperpolarization) reduces their contraction.
In turn, cGMP is degraded by a series of enzymes called cyclic nucleotide phosphodiesterases (abbreviated here as PDE), of which there are 11 families (PDE-1 through PDE-11). PDE5 is particularly active in the trabecular arteries of the penis (Wang et al., 2023).
Since cGMP is necessary for smooth muscle relaxation, the pooling of blood in the corpora cavernosa and erection, the more active PDE5, the less of an erection. Viagra, Cialis and similar drugs inhibit PDE5, so they increase erections.
Erectile dysfunction (ED)
“Erectile dysfunction (ED) is defined as the consistent inability to attain and maintain an erection sufficient to perform satisfactory sexual intercourse.” (Wang et al., 2023)
In the United States, ED affects between 14.6% and 33.7% of men, according to two surveys done in 2011 (Goldstein et al., 2019). ED increases with age: it is present in 64% of men over 40 and in 70% of men over 70 (Wang et al., 2023).
Contrary to what you hear from anti-porn and anti-masturbation ideologues, viewing porn or masturbating does not cause ED. This was demonstrated in a study with a sample size of 3,586 men (Rowland et al., 2022). Quoting from the abstract of that paper:
Results indicated that frequency of pornography use was unrelated to either erectile functioning or erectile dysfunction (ED) severity […]. Masturbation frequency was also only weakly and inconsistently related to erectile functioning or ED severity. […] Frequency of pornography use did not predict either sexual or relationship satisfaction. (Rowland et al., 2022).
The same paper shows that ED is caused by:
age,
anxiety or depression,
low sexual interest,
low relationship satisfaction,
chronic medical conditions.
These chronic medical conditions include cardiovascular disease and the impairment of erections caused by nerve damage during prostate surgery.
ED is usually diagnosed using the International Index of Erectile Function questionnaire (IIEF) (Goldstein et al., 2019; Stridh et al., 2020).
The lurid history of treating ED with PDE5 inhibitors
The development of PDE5 inhibitors to treat ED is full of lurid tales and chance discoveries.
On April 18, 1983, in front of a large audience at the meeting of the American Urological Association in Las Vegas, doctor Giles Brindley wiped out his penis and proceeded to inject phenoxybenzamine into his corpus cavernosum (Goldstein et al., 2019). His penis became instantly erect.
His bold demonstration was meant to convey an important point: that ED could be treated with drugs. Until then, ED was considered having psychological causes and was treated with psychotherapy, much to the despair of the male patients and their sexual partners. If they complained too much, they were considered being one of the few men with “organically caused ED” and treated with penile implants: surgically implanted prostheses that made their penises permanently hard (Wang et al., 2023).
Today we know that 80% of ED is due to non-psychological causes (Stridh et al., 2020). Psychological counseling to treat ED was a failure. Something to keep in mind when you hear criticisms of PDE5 inhibitors because they supposedly hide some obscure mental causes of ED.
Dr. Giles’ shocking public experiment set off a search for pharmacological agents to treat ED. Phenoxybenzamine, the drug he self-injected, is a blocker of α-adrenergic receptors used to treat high blood pressure. Other compounds that showed efficacy were smooth muscle relaxants like phentolamine, thymoxamine, imipramine, verapamil, papaverine, and naftidrofuryl (Goldstein et al., 2019).
Scientists were on the right track. They knew that, to induce lasting erections, they needed to relax the smooth muscle in the walls of the arteries that supplied blood to the penis. What eluded them was the compound that directly caused smooth muscle relaxation.
That compound was found in 1991-1992 by three groups of researchers. It turned out to be a gas, nitric oxide (NO). In 1998, Dr. Ignarro, Dr. Furchgott and Dr. Murad received the Nobel Prize in Medicine and Physiology for this discovery. It was important not only for ED but also to develop medicines to treat hypertension and cardiovascular diseases.
The next step was to find the enzyme where NO acted. It turned out to be PDE, and PDE5 was found to be the main PDE in the penis. There was a search for ways to increase NO production, instead of decreasing its degradation, but this turned out to be a dead-end street.
The discovery of Viagra to treat ED was due to sheer luck. In 1986, the pharmaceutical giant Pfizer was looking for drugs to treat angina—chest pain caused by lack of blood supply to the heart. They focused on PDE inhibitors as a way to relax the smooth muscle in the carotid artery. One of the compounds tested was coded UK-92,480 and was later named sildenafil.
There is an urban legend about the Pfizer sildenafil clinical trial:
“Anecdotes from early clinical trials describe study participants being unwilling to return unused pills because of the positive erectile effects of the study drug.” (Stridh et al., 2020)
In any case, scientists at Pfizer noted that powerful erections were a side effect of sildenafil. In contrast, its effects on chest pain were a disappointment. Less than a week before sildenafil was going to be taken out of the research studies, Pfizer scientists Peter Ellis and Nick Terrett proposed a mechanism by which it could increase erections (Goldstein et al., 2019).
A large series of clinical trials on the effect of sildenafil on ED ensued. They showed that it was effective when taken orally and increased erection within one hour. It was more effective than a placebo when given instead of sildenafil, or when sildenafil was switched to placebo without the knowledge of the patient.
Importantly, sildenafil did not produce erections on its own, only when coupled with sexual stimuli. It acts on the penis, not on the brain to increase sexual desire.
Sildenafil was given the commercial name of Viagra. It was approved by the FDA for the treatment of ED on March 27, 1998 (Goldstein et al., 2019). Soon afterwards, on September 14, 1998, it was approved by the European Medicines Agency (EMA). Since November 2017, Viagra is available without prescription in pharmacies in the UK.
At present, four PDE5 inhibitors have been approved by the FDA: sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra) and avanafil (Stendra or Spedra) (Wang et al., 2023).
Beneficial cardiovascular effects of PDE5 inhibitors
The failure of Viagra to treat chest pain was because PDE5 is absent from the heart.
However, all the arteries in the body have a layer of smooth muscle. When it contracts, it makes the arteries thinner, which increases blood pressure. The sympathetic and parasympathetic branches of the autonomous nervous system control the dilation of arteries in different parts of the body. For example, if you swim in cold water, the arteries that supply blood to your skin contract to avoid losing too much heat.
Arterial smooth muscle has PDE5, which means that NO controls arterial dilation. It also means that PDE5 inhibitors dilate the arteries and therefore reduce blood pressure. So, even though the initial studies of sildenafil on heart pain didn’t show an effect, PDE5 inhibitors may affect the heart indirectly by dilating the arteries of the body.
The bad news is that men with low blood pressure may have to avoid taking PDE5 inhibitors for ED. The good news is that men with high blood pressure—which are most aging men—may derive additional benefits from taking PDE5 inhibitors.
Numerous studies support the idea that PDE5 inhibitors have beneficial cardiovascular effects. Here I discuss just a few of them.
Tadalafil decreased blood pressure in men with ED, who generally had higher blood pressure than men without ED (Özdabakoğlu et al., 2017). Tadalafil produced this effect by decreasing aortic stiffness and increasing the elasticity of arteries, both large and small.
Apart from increasing the diameter of the arteries, PDE5 inhibitors may improve cardiovascular function by increasing the health of the endothelium of blood vessels, by directly protecting the cells of the heart, by having an anti-inflammatory effect, or by reducing the aggregation of platelets to form blood clots (Kloner et al., 2024).
A meta-analysis of animal studies (Ölmestig et al., 2017), which included 32 papers and 3,646 animals, showed that PDE5 inhibitors protected against the brain damage produced by stroke. PDE5 inhibitors decreased neuronal death, oxidative stress and neuroinflammation, and increased cerebral blood flow and the formation of new blood vessels in the damaged area of the brain. Treatment with PDE5 inhibitors was effective when given up to 24 hours after a stroke.
A recent study (Kloner et al., 2024) looked at health insurance claims database for men taking tadalafil for ED (8,156 men) and not taking it (21,012 men). Then it examined the occurrence of major cardiovascular events in both groups. It found that the men that had been taking tadalafil had 19% lower cardiovascular events than those who didn’t. In particular, they had less coronary revascularization (p=0.006), less angina or chest pain (p=0.003) and reduced cardiovascular-related mortality (p=0.032). There were significant reductions of stroke, heart failure and myocardial infarction in men who had taken the larger doses of tadalafil. Death by any cause was 44% lower in men that had taken tadalafil (p<0.001).
One paper (Cai et al., 2019) advocates giving PDE5 inhibitors to men with high blood pressure since they will take them to improve their sex lives, while compliance with regular blood pressure medication is low.
What does all this mean for you? Well, first of all, if you have problems getting erections, it may be a sign that you are at risk of cardiovascular disease. How high is your blood pressure? If it’s in the normal range, you are probably fine. However, if you have high blood pressure and ED, you may want to take a daily dose of 5 mg Cialis or another PDE5 inhibitor. Cialis is preferable to Viagra because it will stay in your body for a whole day—its half-life is 17.5 hours—while Viagra is short-lived (Kloner et al., 2024). PDE5 inhibitors will lower your blood pressure, protect your arteries and your heart, and reduce brain damage if you had a stroke. Talk to your doctor!
Prostate enlargement
A common problem in aging men is the enlargement of the prostate. Since the urethra traverses the prostate, it gets compressed with this enlargement, impeding urine flow. Urinating becomes difficult, with discontinuous flow, incomplete voiding of the bladder and, sometimes, pain during urination. Older men often have to get up several times at night to urinate (nocturia).
Tadalafil (Cialis) has been approved by the FDA for the treatment of prostate enlargement (benign prostate hyperplasia, BPH) and lower urinary tract symptoms (LUTS) (Cantrell et al., 2013).
Tadalafil is preferred over the other PDE5 inhibitors because it last longer in the body. However, similar effects on prostate enlargement were produced by other PDE5 inhibitors, like Viagra (Ko et al., 2017).
If you are a man over 50, you have to get up often at night to pee, and your urine stream is not what it used to be, PDE5 inhibitors may offer an additional advantage to you. Not only they will give you better erections and lower your cardiovascular risk, they may make peeing easier and reduce those nightly trips to the bathroom.
More things to mention to your doctor.
Other beneficial effects of PDE5 inhibitors
Pulmonary artery hypertension is a deadly disease consisting of an increase in blood pressure in the arteries of the lungs. It causes death in 2-3 years by triggering heart failure. It affects more women than men. After it was proposed that it could be treated with PDE5 inhibitors (Singh, 2010), the FDA approved tadalafil to treat it.
Premature ejaculation: Tadalafil reduced premature ejaculation. Its effect improved when given in combination with the serotonin reuptake inhibitor fluoxetine (Mattos et al., 2008).
Kidney protection: Experiments in salt-sensitive rats show that tadalafil protects the kidneys against damage produced by a high-salt diet, an effect independent of its lowering blood pressure (Tomita et al., 2020).
Alzheimer’s disease: Icariin, a plant aphrodisiac that acts by inhibiting PDE5, improved learning and memory in transgenic mice that model Alzheimer’s disease (Jin et al., 2014).
Adverse effects of PDE5 inhibitors
Everything in life comes at a price, so there are drawbacks to taking PDE5 inhibitors.
PDE5 inhibitors have interactions with α-adrenergic antagonists, nitrates and cytochrome P450 inhibitors (Cantrell et al., 2013). They should not be taken with these medications, or taken under close medical supervision.
Moderate side-effects of PDE5 inhibitors include back pain, dyspepsia, headache and dizziness.
More serious side effects may include ischemic optic nerve neuropathy (Pomeranz, 2017), in which the optic nerve is damaged for lack of adequate blood flow. However, it is still controversial that PDE5 inhibitors do this. A survey of 615,838 men treated with PDE5 inhibitors for ED and 175,725 men treated for prostate enlargement showed no association of PDE5 inhibitors and any ocular event, including ischemic optic neuropathy, serous retinal detachment and retinal vascular occlusion (Belladelli et al., 2023).
Another possible side effect is sudden hearing loss, for which there is an incidence of 4.35-5.58 /10,000 person-years for users of PDE5 inhibitors compared with 2.38 /10,000 person-years for non-users (Liu et al., 2018). This is just a moderate increase.
Recreational use
What happens when men without ED take PDE5 inhibitors?
Well, what happens is that these men have erections that are harder and last longer than usual. Which, for most men, means a more enjoyable sexual experience because a harder penis produces more pleasure. A strong erection causes the pleasure nerves in the penis to become more sensitive to mechanical stimulation.
Many women derive more pleasure from having sex with a man with a harder penis. However, there are also women who experience more pain during penetration if the penis is harder. The same goes for male gay couples, although there seems to be a general enthusiasm for strong erections among them. Therefore, whether to use PDE5 inhibitors to have a stronger erection during sex is a personal decision to be negotiated between the persons having sex.
One aspect that I have not seen discussed is that PDE5 inhibitors improve the enjoyment of men during masturbation.
One study (Korkes et al., 2008) surveyed 167 young (average 21 years, range 17-31) male medical students. Although they all said that they had perfect erections, 9% of them had used PDE5 inhibitors. Of this group, 13% turned out to have ED. Interestingly, their erection problems often occurred when using condoms, so the PDE5 inhibitors served to encourage condom use.
Another study (Harte and Meston, 2011) surveyed 1,944 male undergraduates in the USA. Of them, 4% reported recreational use of PDE5 inhibitors. The authors found that recreational use increased with age and in gay/bisexual men. It also correlated with drug and alcohol use, risky sexual behaviors and number of sex partners. This is hardly surprising because the same disregard for societal norms that leads to the use of PDE5 inhibitors without prescription also leads to drug use, promiscuity and risky sexual behaviors.
The fact that recreational use of PDE5 inhibitors correlates with difficulties with erection indicates that such use may indicate a borderline ED and not just the desire for better sex.
The good news is that PDE5 inhibitors facilitate condom use. Many of us had the experience of losing an erection when putting on a condom, which makes it more difficult and risks not doing it right. Besides, our sexual partner may lose interest in sex in the process of regaining the erection and getting that condom finally on. Obviously, this discourages condom use. Using a PDE5 inhibitor may help keeping that penis hard during that gap in arousal.
Is the effect of PDE5 inhibitors on ED a placebo effect?
One frequent dismissive comment about Viagra is that its effect on ED is due to the placebo effect. In fact, placebo effects are common in many diseases, including chronic pain, anxiety, depression, asthma and Parkinson’s disease (Stridh et al., 2020). However, many of the clinical trials on PDE5 inhibitors showed that their effect on ED was statistically larger than that of placebo.
A meta-analysis of PDE5 inhibitors in ED clinical trials (Stridh et al., 2020) showed that they do have a substantial placebo effect. In common words, this means that if you get a man to take a pill thinking that it’s Viagra, he will experience a stronger erection if he takes it before sex. Results showed that placebo produced a “small to moderate improvement of erectile function” in men with ED, while PDE5 inhibitors produced “a large response” and there was “a large difference in favor of the active drug” (p<0.001).
Therefore, there is a placebo effect, but the effect of PDE5 inhibitors is larger than placebo.
What do the naysayers say?
The scientific research I summarized above shows that PDE5 inhibitors are an efficacious treatment of ED. Their side effects are rare and they have positive effects beyond increasing erections, mainly in reducing high blood pressure and prostate enlargement.
Then why do they have such a bad reputation?
Who is, indeed, afraid of the big bad Viagra?
Actually, my PubMed search found just a handful of articles critical of the use of PDE5 inhibitors to treat ED, other than the ones dealing with the side effects discussed above. I saved three of them into my database (Potts et al., 2003; Potts et al., 2004; Barnett et al., 2012). I could not download the full article of Barnett et el. (2012), which seems to be a review of the points made by the other two articles.
I found these two articles (Potts et al., 2003; Potts et al., 2004) appalling in their lack of scientific rigor and their peddling of ideology as science. Instead of an unbiased testing of hypotheses, the openly try to prove a series of feminist ideas, which the authors explain at length in the introduction.
Here are some of the statements made in the introduction:
“In western medical discourse, the ‘healthy’ and ‘functioning’ male body must be capable of producing ‘normal’ erections which deliver sexual satisfaction (via penetrative sex) to both the man and his (female) sexual partner; loss of ‘erectile function’ becomes synonymous with loss of manhood or masculinity.” (Potts et al., 2004).
It seems that erections and sexual satisfaction are suspect to the authors.
“Critics have long argued against the deterministic and reductionist view of bodies, ‘health’ and ‘illness’ espoused by medicine.” (Potts et al., 2004).
In other words, PDE5 inhibitors are bad because western medicine is bad. The genuine suffering experienced by patients and the loved ones who must care for them is disregarded in the name of an ideological celebration of ‘difference’ instead of disease.
“Nicolson has identified three prevalent discourses operating in medical and sexological constructions of ‘normal’ sex: a reproductive model of sexuality (that is, the privileging of biological, procreative aspects of sex), a coital imperative (the notion that penile–vaginal sex is the most ‘natural’ and ‘usual’ form of sexual activity), and an orgasmic imperative (the idea that orgasm—particularly male orgasm—is the goal towards which all sexual activity is directed, and the measure of ‘successful’ sex).” (Potts et al., 2004).
This points out that the real reason some feminists dislike PDE5 inhibitors: reproduction is bad, penetration is bad, and male orgasms are bad. Hence, PDE5 inhibitors are triply bad because they aid in all these things. In reality, PDE5 inhibitors only make more sexual choices available. If people want to have non-penetrative sex or sex without orgasms, the existence of PDE5 inhibitors does not prevent them from doing so.
The actual studies consisted of a series of interviews with men who use Viagra to treat ED and their female partners. The sample size is very small: 33 men (average age 60, age range 33-72) and 27 women. The first paper (Potts et al., 2003) interviewed the same 27 women. The authors warn that the studies a purely qualitative and, indeed, there is not the slightest attempt at quantification. This becomes a problem because, after stating that some men expressed views contrary to those of the authors, only supportive statements are given thereafter. The questions asked are not given, raising the suspicion that the authors just had a conversation with the subjects, leading them to their pre-established conclusions.
To summarize, this paper criticizes ED medication because:
“Erectile changes [are] a natural part of ageing.” And so is death.
Having an erection reaffirms a man’s self-esteem and masculinity. And this is bad, somehow.
Viagra is a “quick fix” that reinforces “the prevalent division in western culture of human subjectivity into mind (psychological) and body (physical) components.”
For some men, Viagra didn’t work or “produce desensitized or ‘numb’ erections.” No recognition is given to the numerous clinical trials proving the efficacy of PDE5 inhibitors. There is no evidence that PDE5 inhibitors desensitize the penis.
The effectiveness of Viagra declined over time. The technical name for this is tolerance. I could not find any evidence that there is tolerance for the effect of PDE5 inhibitors.
Conversely, some men said that they required lower doses of Viagra over time or experienced a permanent improvement in their erections after taking it. So, go figure!
Viagra produce “psychological addiction” because some couples needed it to have sex.
Viagra had detrimental effects on women, who felt pressured to have sex or preferred to have sex without penetration.
Viagra did not fix broken relationships, as advertised in some promotional material by Pfizer.
Viagra may encourage men to commit infidelity because of their “newfound sense of youth and virility.”
Viagra is “a tool that allows men to continue to function as machines in their presumably intimate relationships.”
Viagra promotes a sex life that centers intercourse and the erect penis.
The earlier paper (Potts et al., 2003) centers on the claim that Viagra is bad for the female partners of the men that take it. In particular, it argues that the decision to take Viagra should be taken by both members of a couple, and not the man alone. Contrast this with the feminist idea that taking birth control or having an abortion are decisions that women should be able to take by themselves. While Viagra does impact a couple’s sex life, a man could take it to improve his masturbation.
PDE5 inhibitors improve women’s sexual experience
In contrast to what the ideologues say, two papers reported that women enjoy sex more when their male partners take Viagra.
One double-blind, placebo-controlled study (Heiman et al., 2007) recruited 180 heterosexual couples in which the woman reported unsatisfactory sex at least half of the time. Women whose partners took Viagra, compared with women whose partners took placebo, reported a clear increase in satisfaction during sex (p<0.0001). Improvement in the sexual satisfaction of the man correlated with the improvement experienced by the woman. It’s a win-win situation!
The second study was done in France in 2006 (Chevret-Measson et al., 2009) and included 67 heterosexual couples. Sexual life satisfaction improved in 79% of the women (p<0.0001) compared with their previous experience—there was no placebo group in this study. The improvement in the women’s sex life correlated with the improvement in the men’s erections.
How I did the research for this article
This article references 24 scientific papers, all of them in peer-reviewed journals. I disregarded articles in magazines or in humanities journals publishing opinions and not actual evidence.
Science advances by reaching a consensus. Therefore, giving reliable scientific information requires summarizing a lot of information contained in many papers.
That is why this article has so many scientific references. I gathered them as follows.
I did a search in PubMed with “phosphodiesterase-5 inhibitors” [Title/Abstract], which retrieved 962 papers. Combining that search criterion with “erectile dysfunction” [Title/Abstract] selected 264 papers among them. I screened all those papers one by one, judging from the title and the journal if they were related to the topic I am discussing. This resulted in 68 papers, which I exported to a group in my EndNote database. Then I browsed their abstract and gave them one to five stars according to their quality and relevance. I downloaded the full version PDF of the papers that contained interesting information not given in the abstract.
For the background, I relied on my knowledge of physiology and biochemistry. I have a Ph.D. in biochemistry and 40 of research experience in molecular biology, physiology, neuroscience and drug development.
References
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