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~ Reliable information on improving sexual health. Herbs, drugs, and more. This site offers research-based solutions for managing ED. You can contact us at: menznews@yahoo.com.

Menznews – News for Sexual Health

Category Archives: Research/Experimental

Taurine Supplementation Improves Erectile Function in Rats

17 Thursday Nov 2016

Interesting study, in part because taurine is something that is easy to get.

I’m not recommending it yet, but here is a study to chew over. What do you think?

J Sex Med. 2016 May;13(5):778-85. doi: 10.1016/j.jsxm.2016.02.164. Epub 2016 Mar 24.

Taurine Supplementation Improves Erectile Function in Rats with Streptozotocin-induced Type 1 Diabetes via Amelioration of Penile Fibrosis and Endothelial Dysfunction.

Abstract

INTRODUCTION: For patients with diabetes, erectile dysfunction (ED) is common and greatly affects quality of life. However, these patients often exhibit a poor response to first-line oral phosphodiesterase type 5 inhibitors.

AIM: To investigate whether taurine, a sulfur-containing amino acid, affects diabetic ED (DED).

METHODS: Type 1 diabetes mellitus was induced in male rats by using streptozotocin. After 12 weeks, an apomorphine test was conducted to confirm DED. Only rats with DED were administered taurine or vehicle for 4 weeks. Age-matched nondiabetic rats were administered saline intraperitoneally for 4 weeks.

MAIN OUTCOME MEASURES: Erectile function was evaluated by electrical stimulation of the cavernous nerve. Histologic and molecular alterations of the corpus cavernosum also were analyzed.

RESULTS: Erectile function was significantly reduced in the diabetic rats compared with in the nondiabetic rats, and was improved in the diabetic rats treated with taurine. The corpus cavernosum of the rats with DED exhibited severe fibrosis and decreased smooth muscle content. Deposition of extracellular matrix proteins was increased in the diabetic rats, while expression of endothelial nitric oxide synthase/cyclic guanosine monophosphate/nitric oxide pathway-related proteins was reduced. Taurine supplementation ameliorated erectile response as well as histologic and molecular alterations.

CONCLUSION: Taurine supplementation improves erectile function in rats with DED probably by potential antifibrotic activity. This finding provides evidence for a potential new therapy for DED.

Here is the study link: Study link

Research Update: What’s New in Erectile Dysfunction Research

16 Wednesday Nov 2016

Some updates on ED research from March, 2016:

Nothing terrible new here, but a good summary:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4979545/

 

CPAP and ED

11 Friday Nov 2016

There is a lot of medical literature that suggests a link between sleep apnea – a condition where people stop breathing at night – and ED. I was reading an article today (LINK HERE) that shows treatment of sleep apnea with CPAP (continuous positive airway pressure) helps men with erectile dysfunction (ED) after 1 month. They also reported that men with less oxygen during sleep had more ED.

Bottom line: If you have sleep apnea, get a CPAP mask. If you have a mask, use it every night!

Research on the Possible Benefits of Taurine for ED

18 Tuesday Oct 2016

Fundam Clin Pharmacol. 2014 Aug;28(4):394-404. doi: 10.1111/fcp.12041. Epub 2013 Jul 12.

Chronic treatment with taurine ameliorates diabetes-induced dysfunction of nitric oxide-mediated neurogenic and endothelium-dependent corpus cavernosum relaxation in rats.

Dalaklioglu S1, Kuscu N, Celik-Ozenci C, Bayram Z, Nacitarhan C, Ozdem SS.

Author information

Abstract

This study was aimed to examine the effect of chronic taurine treatment on corpus cavernosum dysfunction in diabetic rats and to investigate possible underlying mechanisms. Thirty male rats were randomized to three groups of 10 each, including control, diabetic, and taurine-treated diabetic. Diabetes was induced in rats by streptozotocin (STZ, single intraperitoneal dose of 50 mg/kg body weight). Taurine was administered orally for 12 weeks (1% w/v in drinking water) from the day on which STZ was injected. At the end of the 12th week, strips of corpus cavernosum were suspended in an organ bath system for functional studies. Nitric oxide (NO)-mediated endothelium-dependent and neurogenic corpus cavernosum relaxation were evaluated by acetylcholine (ACh, 0.1-100 μm) and electrical field stimulation (EFS, 30 V, 5 ms, 2-32 Hz), respectively. The expressions of endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) (Ser-1177), neuronal nitric oxide synthase (nNOS), NADPH oxidase subunit gp91(phox) , Rho A, and Rho kinase in corpus cavernosum were semi-quantitatively assessed by immunohistochemistry. Induction of diabetes resulted in significant inhibition of NO-mediated endothelium-dependent and neurogenic corpus cavernosum relaxation. Furthermore, eNOS, p-eNOS, and nNOS expressions decreased significantly in diabetic rats compared to controls, while gp91(phox) , RhoA and Rho kinase expressions increased significantly. The diminished relaxation response to ACh and EFS as well as diabetes-related changes in expressions of these proteins in corpus cavernosum of diabetic rats was significantly improved by taurine. Taurine treatment improves NO-mediated relaxations of corpus cavernosum in diabetic rats probably by inhibiting NADPH oxidase/Rho kinase pathways.

Something You Can Do Yourself: Reservatrol + Viagra

28 Wednesday Sep 2016

Life Sci. 2015 May 23. pii: S0024-3205(15)00273-8. doi: 10.1016/j.lfs.2015.04.020. [Epub ahead of print]

Resveratrol and sildenafil synergistically improve diabetes-associated erectile dysfunction in streptozotocin-induced diabetic rats.

Bai Y1, An R2.

Abstract

AIMS:

Despite effective control of blood glucose levels in diabetic patients, complaints of diabetes-associated erectile dysfunction (ED) persist. Resveratrol has been indicated to possess anti-diabetic effects and therapeutic potential for ED. This study was conducted to observe the effect of resveratrol alone or in combination with sildenafil on ED in streptozotocin (STZ)-induced diabetic rats.

MAIN METHOD:

Among 58 adult male STZ-induced (60 mg/kg) diabetic Sprague-Dawley rats, 48 STZ-induced diabetic rats were randomized equally to four groups: untreated diabetic rats, resveratrol (25 mg/kg), sildenafil (5 mg/kg) or resveratrol (25mg/kg) plus sildenafil (5 mg/kg) through oral gavage for 8weeks. Additionally, 12 age-matched rats were chosen as controls. Intracavernous pressure (ICP) and mean arterial blood pressure (MAP) were used to measure erectile function. The cavernous level of cyclic guanosine monophosphate (cGMP), protein and mRNA of endothelial NO synthase (eNOS), neuronal NOS (nNOS), and phosphodiesterase-5 (PDE5) was measured.

KEY FINDINGS:

Treatment with either resveratrol or sildenafil improved ICP/MAP compared to the untreated diabetic rats (P<0.05). Treatment with resveratrol increased nNOS and eNOS expression, inhibited PDE5 expression, and increased the cavernous cGMP level compared to the untreated diabetic rats. Resveratrol significantly decreased superoxide anion and ROS production. Two-way ANOVA indicated that resveratrol in combination with sildenafil therapy had a significant synergistic effect in improving ICP/MAP and cavernous cGMP levels.

SIGNIFICANCE:

Resveratrol improves diabetes-associated ED in rats. Combination therapies with resveratrol and sildenafil have a synergistic effect in improving ED. The mechanisms might be attributed to its anti-oxidative properties and NO-cGMP signaling pathway upregulation.

Hydrogen Sulfide and ED

12 Monday Sep 2016

By now, I’m sure you know that nitric oxide is an important gas for achieving a normal erection. But new research is finding that other gases may also play an equally important role in sexual health.

Just published – a new study that suggests that hydrogen sulfide is another gas — along with nitric oxide — that plays a role in helping erections. That’s the good news. The bad news is that hydrogen sulfide is a poison gas (used by the British in WWI) that causes the smell of rotten eggs and flatulence. OK, so it’s not perfect. But new research suggests it plays an important role in many body processes.
As I’ve noted many times, there is still a lot we don’t know about the body, and many unknowns concerning erections. If we could only spend more money on medical research, then we would all live longer, happier lives. But the average person and the people who decide where our resources go seem oblivious to this fact. So, we have to deal with the world as it is. In this case, it means you searching the Internet for information on how to improve your sexual health. In my case, it means searching the medical literature for clues that can improve sexual health.

Anyway, back to hydrogen sulfite and information you can use. It is worth noting that hydrogen sulfite is produced by the breakdown of allicin, which is found in garlic. This fact supports the use of garlic for cardiovascular and sexual health. Whether there are other sources of hydrogen sulfite is something I am investigating — but for now, this is an easy way to support your general and sexual health – eat garlic or take allicin pills. By the way, allicin is produced when garlic is chopped or crushed, so just eating raw garlic isn’t the same as eating crushed garlic or allicin.

Horny Goat Weed Lowers Viagra Levels (That’s Bad)

14 Sunday Aug 2016

Many people add herbs like Horny Goat Weed (HGW) to Viagra or other ED drugs to improve the effect of these drugs. Is that a good idea? New research suggest that you shouldn’t do that.

In the past, I thought why not? I advocated using the traditional Chinese herb Epimedium (Horny Goat Weed) + Viagra (or similar drugs Cialis or Levitra). However, here is a study from China which says that combining HGW + Viagra (sildenafil) LOWERS levels of Viagra (which is a bad thing, because you get less active drug).

Here’s the information:

Abstract

Epimedium sagittatum (Sieb. et Zucc.) Maxim is one of the herbs used to treat erectile dysfunction in Traditional Chinese Medicine. Sildenafil is a phosphodiesterase 5 inhibitor used to treat erectile dysfunction in Western Medicine. This study evaluates the herbal-drug interaction of Epimedium sagittatum extract on the pharmacokinetics of sildenafil in rats by ultra-performance liquid chromatography. The rat plasma was sampled from each anesthetized rat after pretreatment with 3-daysEpimedium sagittatum extract (1/2 g/kg/day) and intravenous injection with sildenafil (10/30 mg/kg). The pharmacokinetic data demonstrate that the area under the concentration-time curve (AUC) of sildenafil (10 mg/kg) was significantly decreased in groups that received a high dose of Epimedium sagittatum extract. In conclusion, the study demonstrates that there was significant herb-drug interaction of Epimedium sagittatum extract on the pharmacokinetics of sildenafil at low and high daily doses, suggesting co-administration use of Epimedium sagittatum extract and sildenafil in clinical practice should be prevented due to possible herb-drug interactions.

Here is a link to the article, which includes a full-text PDF for free:

http://www.mdpi.com/1420-3049/18/6/7323

I am not familiar with the journal (Molecules) and can’t vouch for the research but I think it’s worth considering.

Nicorandil

13 Saturday Aug 2016

I am always looking for a new way to improve erections…consider the drug nicorandil. It seems to help blood vessels dilate – similar to Viagra. Someone actually applied for a patent in 2001 to use nicorandil for ED. The key is the most basic component of erection – the relaxation of the small muscles in blood vessels, which occurs with potassium and calcium ions adjust their levels. This is the atomic level of change! It doesn’t get more basic than this!

Anyway, if you can find a way to boost potassium levels, that helps blood vessels relax, so they can fill up with blood and support erections. Apparently, nicorandil does this. Here is an article about using potassium channels for treating ED: LINK HERE.

Nicorandil has been used for years in Europe and Japan, but apparently we are behind the times here in the USA. Go figure.

See this link for an article on nicorandil from the European Heart Journal: CLICK HERE

Here is another article about increasing potassium levels for erections, using the drug phentolamine: LINK HERE. It is in theInternational Journal of Impotence Research.

Using (Blue) Light to Get Erections

10 Friday Jun 2016

Here is an interesting new therapy being developed – it uses blue light to produce cyclic guanosine monophosphate (cGMP), a chemical that contributes to erections.

Here is an article on this, from this link: ARTICLE

BLUE LIGHT TO TREAT ERECTILE DYSFUNCTION

Some men reach for the “little blue pill” to deal with erectile dysfunction. However, Viagra helps only to prolong an erection, but does not actually trigger it. Researchers have now developed a new solution: a gene therapy that triggers reliable erections.

From the age of 30, the number of men who have unsatisfactory erections or none at all increases. In the over-60 age group, more than half of all men have been affected by erectile dysfunction, a disorder in which normal sexual stimulation does not lead to an erection.

The main causes include cardiovascular disease, diabetes, hormonal imbalance, neurological disease, and the side effects of medication. Even spinal paralysis can result in patients no longer being able to have erections.

 

A gene construct that reacts to blue light is injected into the erectile tissue of the penis. As soon as it is exposed to the light, a precursor molecule (guanosine triphosphate or GTP) is converted into the second messenger cyclic guanosine monophosphate (cGMP), which exists naturally in a number of human organs.

This allows voltage-dependent calcium channels to close, thereby reducing calcium levels in the cells, which in turn relaxes muscle cells and increases blood flow to the erectile tissue. And so the penis becomes stiff.

An enzyme then slowly breaks down cGMP so that the erection wears off with time. Viagra blocks this enzyme and intensifies and prolongs the erection, but it cannot trigger one.

Thanks to the gene construct, the production of cGMP is not stimulated by sexual arousal but by exposure of the erectile tissue to blue light.

“In this way, we circumvent the usual sexual stimulation that triggers a cascade of signals in the body and ultimately leads to an erection,” says study leader Martin Fussenegger, professor of biotechnology and bioengineering at ETH Zurich in Basel.

The researchers tested their new development in male rats by injecting the gene construct into the erectile tissue—with good results. Their findings appear in Angewandte Chemie.

In most cases, the blue light acted like a switch that allowed the rats’ erection to be “turned on.” For some of the animals, the stimulation even led to ejaculation.

“The system of an erection is very similar across all mammals,” says Fussenegger. He is therefore convinced that the gene construct will also work in humans. “Even Viagra works on rats. It prolongs the erection’s intensity, just as it does in humans.”

SIDE EFFECTS?

“Injection of a gene construct should not be a barrier to potential users, as injections in the erectile tissue are already a standard treatment for erectile dysfunction these days,” says Fussenegger.

The erectile tissue is largely insensitive to pain; it is also for the most part detached from normal blood circulation, so the probability that the gene construct could reach other parts of the body is very low.

In addition, cGMP breaks down relatively quickly. As Viagra prolongs the erection, any possible gene therapy could be supplemented by this medication.

An artificially induced erection would satisfy a great need among patients suffering from erectile dysfunction, says Fussenegger. “Several doctors have confirmed this to me,” he says. In addition, not all sufferers are allowed to take Viagra, such as those with known heart disease.

Researchers worked on this gene construct for four years and for the time being it exists only as a prototype; tests in humans have yet to take place. “Before it can be used as a treatment, it requires highly expensive clinical tests,” says Fussenegger. “We are actively looking for partners to put our technology into clinical practice.”

Drugs in Development: Latest Report on BAY 41-2272

30 Wednesday Sep 2015

Here is an update on a drug in development – BAY 41-2272 (From the pharmaceutical company Bayer). Although there are some drugs in development, it is always surprising how little research there is in this field. Many drugs, such as Viagra, were discovered while studying other areas (heart disease).

Anyway, you can find this article at this link: ARTICLE LINK

Beneficial Effect of the Soluble Guanylyl Cyclase Stimulator BAY 41-2272 on Impaired Penile Erection in db/db−/−Type II Diabetic and Obese Mice

  1. Kenia Pedrosa Nunes,
  2. Cleber E. Teixeira,
  3. Fernanda B. M. Priviero,
  4. Haroldo A. Toque, and
  5. R. Clinton Webb

Abstract:

Type 2 diabetes mellitus (DM2) and obesity are major risk factors for erectile dysfunction (ED). In diabetes, increased oxidative stress leads to decreased nitric oxide (NO) bioavailability, and diabetic patients appear to be less responsive to conventional therapy with phosphodiesterase type 5 inhibitors. We investigated whether the soluble guanylyl cyclase stimulator BAY 41-2272 (5-cyclopropyl-2-[1-(2-fluoro-benzyl)-1H-pyrazolo[3,4-b]pyridine-3-yl]pyrimidin-4ylamine) is effective in improving impaired corpus cavernosum (CC) relaxation in obese DM2 mice by reducing oxidative stress. Adult db/db−/− mice or their lean db/+ littermates were used to assess vascular function, cGMP levels, antioxidant status, NADPH oxidase expression, and superoxide formation in the absence or presence of BAY 41-2272. Results showed that BAY 41-2272 (10−8 to 10−5 M) potently relaxed CC from db/+ or db/db−/− mice in a similar manner. BAY 41-2272 significantly enhanced both endothelium-dependent and nitrergic relaxation induced by electrical field stimulation (EFS), and improved the impaired relaxation to acetylcholine and EFS in the diabetic animals in a concentration-dependent manner (10−8 to 10−7 M). BAY 41-2272 increased cGMP levels and potentiated relaxation responses to exogenous NO in CC. Total antioxidant status was reduced in plasma and urine whereas expression of vascular NADPH oxidase subunits (gp91phox, p22phox, and p47phox) was increased in the CC of db/db−/− mice, suggesting a state of oxidative stress. These effects were prevented by BAY 41-2272 in a concentration-dependent manner. These results suggest that BAY 41-2272 improves CC relaxation in db/db−/− mice by increasing cGMP and augmenting antioxidant status, making this drug is a potential novel candidate to treat ED.

Spider Venom and ED Treatment

13 Thursday Aug 2015

Researchers have identified a chemical found in spider venom that causes erections in laboratory rats. It seems to work through the familiar mechanism of raising nitric oxide. Other things that appear to raise nitric oxide levels, supporting better erections: increasing HDL levels, taking arginine supplements, Viagra/Cialis/Levitra, and eating watermelon.

Here is a link to the research: LINK

Exercise and ED

13 Thursday Aug 2015

Here is a recent study with rats that shows the benefits of exercise for ED: (LINK HERE)

Summary Erectile dysfunction (ED) is a major public health problem that seriously affects the quality of life of patients and their partners and its prevalence increases significantly with ageing. In this study, we tested the hypothesis that age-associated decrease in penile endothelial (eNOS) and neuronal nitric oxide synthase (nNOS) activity in aged rats may be increased by regular exercise. A total of 28 young (4 m) and aged (24 m) male rats were divided into four equal groups: group 1 – young control; group 2 – young trained; group 3 – old control and group 4 – old trained group. Groups 2 and 4 rats were trained to swim for 30 min a day and 5 days a week, which lasted 8 weeks. At the end of 8 weeks, rats were sacrificed and penile tissues evaluated for eNOS and nNOS activities. eNOS and nNOS activities were evaluated by immunohistochemistry in paraffinized penile tissues and results assessed semiquantitatively. Results also were compared with healthy age-matched and adult (4 m) controls. Serum level of testosterone (T) was determined using ELISA kits (Beckman Coulter, Fullerton, CA, USA). In penile tissues of aged control rats, eNOS and nNOS staining were weakly positive; however in trained groups, eNOS and nNOS immunoreactivity were increased. In young control group, eNOS and nNOS activities were more intense than aged control. eNOS and nNOS activities were higher in adult trained group than control. Serum T concentrations were significantly higher in young and aged trained group than in control groups. We can suggest that regular exercise upregulates eNOS and nNOS expressions in the aged and young rat penis. Regular exercise may improve penile erection by increasing penile neurotransmitter in both young and aged rats.

How Does Viagra Work?

13 Thursday Aug 2015

Some new data suggests that Viagra (sildenafil) may have other mechanisms that support sexual function, such as an effect on dopamine levels in the brain.

Here is an interesting article (study) on this: LINK HERE from the Journal of Sexual Medicine.
Here is the abstract:
J Sex Med. 2012 Nov 15. doi: 10.1111/j.1743-6109.2012.03000.x. [Epub ahead of print]

Experimental Evidence for Sildenafil’s Action in the Central Nervous System: Dopamine and Serotonin Changes in the Medial Preoptic Area and Nucleus Accumbens During Sexual Arousal.

Kyratsas C, Dalla C, Anderzhanova E, Polissidis A, Kokras N, Konstantinides K, Papadopoulou-Daifoti Z.

Source

Department of Pharmacology, Medical School, University of Athens, Athens, Greece First Department of Psychiatry, Eginition Hospital, Medical School, University of Athens, Athens, Greece Andrology Institute of Athens, Athens, Greece.

Abstract

Introduction.  Sildenafil is the first effective oral treatment for male erectile dysfunction. Although it is generally accepted that its action is peripheral, it has been suggested that it influences central neural pathways that are involved in male sexual arousal. Recently, it was shown that local sildenafil administration enhances extracellular dopamine (DA) in the nucleus accumbens (NAcc). Aim.  The aim of this study was to determine whether sildenafil administration alters dopaminergic and serotonergic activity in the NAcc and the medial preoptic area (mPOA) during a model of sexual arousal. Methods.  An acute (2 days) or chronic (21 days) sildenafil regimen (1 mg/kg) was administered intraperitoneally to male rats. Thirty minutes after the last sildenafil injection, all males were exposed to noncontact erection sessions by the presentation of inaccessible estrous females. Half of the males had previous experience of noncontact sexual encounter and the other half were exposed for the first time. Main Outcome Measures.  Tissue levels of DA and its metabolites, 3,4-Dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), as well as serotonin (5-HT) and its metabolite 5-HIAA, were measured in the mPOA and NAcc with high-performance liquid chromatography with electrochemical detector. Dopamine ([DOPAC+HVA]/DA) and serotonin (5-HIAA/5-HT) turnovers were also calculated as indices of neurotransmission. Results.  In nontrained males, acute and chronic sildenafil treatment increased DA and 5-HT turnover rates in the mPOA and NAcc. In trained rats, acute sildenafil also increased DA and 5-HT turnover rates in both structures, whereas chronic treatment enhanced 5-HT turnover rate only in the mPOA and DA turnover rate only in the NAcc. Conclusions.  Our data confirm that sildenafil enhances dopaminergic activity in the NAcc, extend these findings to the mPOA and furthermore, reveal sildenafil-induced effects on serotonergic activity in these brain regions as well. Therefore, present findings support an effect of sildenafil on central neural pathways that are involved in the control of sexual arousal. Kyratsas C, Dalla C, Anderzhanova E, Polissidis A, Kokras N, Konstantinides K, and Papadopoulou-Daifoti Z. Experimental evidence for sildenafil’s action in the central nervous system: Dopamine and serotonin changes in the medial preoptic area and nucleus accumbens during sexual arousal. J Sex Med **;**:**-**.
© 2012 International Society for Sexual Medicine.

Increasing Nitric Oxide

13 Thursday Aug 2015

One of the keys to improved sexual function is high levels of nitric oxide. When you take Viagra/Cialis/Levitra, these increase nitric oxide levels, allowing for better erections.

So, what else can you do?

Here are some ideas, from this article (LINK)
– Eat dark chocolate
– Take L-arginine supplements (3 g/day)
– Exercise
– Take Pine Bark Extract, as described here: (LINK)

A review of the French maritime pine bark extract (Pycnogenol), a herbal medication with a diverse clinical pharmacology.

OBJECTIVES: An increasing body of evidence indicates that Pycnogenol (PYC), a standardized extract of French maritime pine bark, has favorable pharmacological properties. This is a review of studies with both PYC and components of the preparation, that have helped to elucidate target sites and possible mechanisms for activity in men.
METHODS: Studies appearing in peer reviewed literature, as well as results presented at international meetings not yet available as published papers, are included in this review. Additional data from published sources in German and French languages that are not widely available are also included.
RESULTS: Chemical identification studies showed that PYC is primarily composed of procyanidins and phenolic acids. Procyanidins are biopolymers of catechin and epicatechin subunits which are recognized as important constituents in human nutrition. PYC contains a wide variety of procyanidins that range from the monomeric catechin and taxifolin to oligomers with 7 or more flavonoid subunits. The phenolic acids are derivatives of benzoic and cinnamic acids. The ferulic acid and taxifolincomponents are rapidly absorbed and excreted as glucuronides or sulphates in men, whereas procyanidins are absorbed slowly and metabolized to valerolactones which are excreted asglucuronides. PYC has low acute and chronic toxicity with mild unwanted effects occurring in a small percentage of patients following oral administration. Clinical studies indicate that PYC is effective in the treatment of chronic venous insufficiency and retinal micro-hemorrhages. PYC protects against oxidative stress in several cell systems by doubling the intracellular synthesis of anti-oxidative enzymes and by acting as a potent scavenger of free radicals. Other anti-oxidant effects involve a role in the regeneration and protection of vitamin C and E. Anti-inflammatory activity has been demonstrated in vitro and in vivo in animals. Protection against UV-radiation-induced erythema was found in a clinical study following oral intake of PYC. In asthma patients symptom scores and circulating leukotrienes are reduced and lung function is improved. Immunomodulation has been observed in both animal models as well as in patients with Lupus erythematosus. PYC antagonizes the vasoconstriction caused by epinephrine and norepinephrine by increasing the activity of endothelialnitric oxide synthase. Dilation of the small blood vessels has been observed in patients withcardiovascular disease, whereas in smokers, PYC prevents smoking-induced platelet aggregation and reduces the concentration of thromboxane. The ability to inhibit angiotensin-converting enzyme is associated with a mild antihypertensive effect. PYC relieves premenstrual symptoms, including abdominal pain and this action may be associated with the spasmolytic action of some phenolic acids. An improvement in cognitive function has been observed in controlled animal experiments and these findings support anecdotal reports of improvement in ADHD patients taking PYC supplements.
CONCLUSIONS: There is much evidence showing that PYC has beneficial effects on physiological functions. Results from ongoing clinical research are required to confirm and extend previous observations.

Research Update: Alagebrium

13 Thursday Aug 2015

Some recent findings on a drug being developed for ED – alagebrium (more evidence that the future of ED treatments will be combination therapy (multiple drugs/mechanisms of action): (LINK)

Int J Impot Res. 2012 May-Jun;24(3):114-21. doi: 10.1038/ijir.2011.54. Epub 2011 Dec 29.

Therapeutic effect of combination of alagebrium (ALT-711) and sildenafil on erectile function in diabetic rats.

Gurbuz N, Sagdic G, Sanli A, Ciftcioglu A, Bassorgun I, Baykal A, Usta MF.

Source

Department of Biochemistry, Akdeniz University, School of Medicine, Antalya, Turkey.

Abstract

Recently, the relationship between advanced glycation end products (AGEs) and erectile dysfunction (ED) has been reported. The present study aimed to investigate whether a combination of an AGE cross-link breaker (alagebrium/ALT-711) and sildenafil could enhance the erectile capacity in streptozotocin (STZ) diabetic rats. Additionally, we assessed the effect of that treatment option on some molecules that have been suggested to have crucial roles in AGE-related ED pathways. Four groups of animals were utilized: (1) age-matched control rats, (2) STZ-induced diabetic rats (40 mg kg(-1) i.p.), (3) STZ rats+sildenafil (5 mg kg(-1) p.o.), (4) STZ rats treated with a combination of sildenafil (5 mg kg(-1) p.o)+alagebrium/ALT-711 (10 mg kg(-1) p.o.) for the final 1 month of the 2 months of diabetes period. At 2 months after i.p. injection of STZ, all animals underwent cavernosal nerve stimulation (CNS) to assess erectile function. Penile tissue AGEs, MDA (malondialdehyde), cyclic guanosine monophosphate (cGMP) (ELISA), endothelial nitric oxide (NO) synthase (eNOS), inducible NO synthase (iNOS) (western blot), nuclear factor (NF)-κB, mitogen-activated protein (MAP) kinase (immunohistochemistry) and apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling) analyses were performed in all groups of rats. STZ diabetic rats had a significant decrease in erectile function as determined by the peak intracavernosal pressure (ICP) and total ICP (area under the erectile curve) after CNS when compared with control rats.

Angiotensin-(1-7): New Treatment for ED?

13 Thursday Aug 2015

Another promising agent for treating ED is angiotensin-(1-7). The Angiotensin-renin system is believed to be involved in ED, so this chemical may help reverse the process.

This Article tells you more: ARTICLE LINK

J Sex Med. 2013 Oct;10(10):2430-42. doi: 10.1111/jsm.12262. Epub 2013 Jul 24.

An oral formulation of angiotensin-(1-7) reverses corpus cavernosum damages induced by hypercholesterolemia.

Fraga-Silva RA1, Costa-Fraga FP, Savergnini SQ, De Sousa FB, Montecucco F, da Silva D, Sinisterra RD, Mach F, Stergiopulos N, da Silva RF, Santos RA.

Author information

Abstract

INTRODUCTION:

The renin angiotensin system plays a crucial role in erectile function. It has been shown that elevated angiotensin-II levels contribute to the development of erectile dysfunction (ED). Oppositely, angiotensin-(1-7) (Ang-[1-7]) mediates penile erection by activation of receptor Mas. Recently, we have developed a formulation based on Ang-(1-7) inclusion in cyclodextrin (CyD) [Ang-(1-7)-CyD], which allows for the oral administration of Ang-(1-7).

AIM:

In the present study, we evaluated the effects of chronic treatment with Ang-(1-7)-CyD on penile fibrosis, oxidative stress, and endothelial function in hypercholesterolemic mice.

METHODS:

Apolipoprotein(Apo)E-/- mice fed a Western-type diet for 11 weeks received Ang-(1-7)-CyD or vehicle during the final 3 weeks. Collagen content and reactive oxygen species (ROS) production within the corpus cavernosum were evaluated by Sirius red and dihydroethidium staining, respectively. Protein expression of neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS), nicotinamide adenine dinucleotide phosphate (NADPH) subunits (p67-phox and p22-phox), and AT1 and Mas receptors in the penis was assessed by Western blotting. Nitric oxide (NO) production was measured by Griess assay in the mice serum. Cavernosal strips were mounted in an isometric organ bath to evaluate the endothelial function.

MAIN OUTCOME MEASURES:

The effect of Ang-(1-7)-CyD treatment on penile fibrosis, oxidative stress, and endothelial function in hypercholesterolemia-induced ED.

RESULTS:

Ang-(1-7)-CyD treatment reduced collagen content in the corpus cavernosum of ApoE-/- mice. This effect was associated with an attenuation of ROS production and a diminished expression of NADPH. Furthermore, Ang-(1-7)-CyD treatment augmented the expression of nNOS and eNOS in the penis and elevated vascular NO production. Importantly, these effects were accompanied by an improvement in cavernosal endothelial function.

CONCLUSION:

Long-term treatment with Ang-(1-7)-CyD reduces penile fibrosis associated with attenuation of oxidative stress. Additionally, cavernosal endothelial function in hypercholesterolemic mice was markedly improved. These results suggest that Ang-(1-7)-CyD might have significant therapeutic benefits for the treatment of erectile dysfunction.

Good Article on Yohimbe / Yohimbine

11 Tuesday Aug 2015

Here is a good article on yohimbe and yohimbine. They emphasize how these drugs can cause bad side effects if you are taking certain other drugs. And as I posted earlier, insomnia is a real problem with some of these herbs.

Anyway, here is the LINK.

NCX-911, a Novel Nitric Oxide-releasing PDE5 Inhibitor

10 Monday Aug 2015

Here is an article about a drug that was being developed.

I haven’t heard much about it recently, but the concept is interesting.

Phosphodiesterase type 5 (PDE5) inhibitors have reduced efficacy in treating erectile dysfunction (ED) in conditions where there is a lack of endogenous nitric oxide (NO). Therefore, NO-releasing PDE5 inhibitors have been developed. Here we report the effect of such a compound, NCX-911, on the tone and nitrergic relaxations of rabbit corpus cavernosum in the absence or presence of a NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME; 500 muM). NCX-911 was found to be as potent as sildenafil at inducing relaxation of rabbit cavernosum (EC50 values 997.8plusminus195.7 and 1000.5plusminus140.8 nM, respectively). The potency of NCX-911 was not altered, but that of sildenafil decreased five-fold in the presence of l-NAME (EC50 values 1281.2plusminus268.3 and 4959.1plusminus882.1, nM respectively, P<0.001 for sildenafil). Both compounds potentiated nitrergic relaxations with similar potencies. These results suggest that NO-releasing PDE5 inhibitors could potentially be more useful than PDE5 inhibitors in the treatment of ED in conditions where there is a lack of endogenous NO.

From this link: ABSTRACT

Poly(ADP-ribose) Polymerase Inhibition Improves Erectile Function

09 Sunday Aug 2015

Here’s an interesting article on a developing technology. I like these articles because sometimes you can find an herb that is available now that you can use.
Poly(ADP-ribose) polymerase inhibition improves erectile function by activation of nitric oxide/cyclic guanosine monophosphate pathway in diabetic rats.
Li WJ1, Peng Y, Zhou J, Li B, Wang H, Zhang J, Wang Z.
J Sex Med. 2012 May;9(5):1319-27. doi: 10.1111/j.1743-6109.2012.02666.x. Epub 2012 Mar 16.

Abstract

INTRODUCTION

Endothelial dysfunction-induced abnormalities of the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling pathway in the corpus cavernosum are thought to be the main factors involved in the pathogenesis of diabetes-induced erectile dysfunction (ED). Recent studies have shown that the poly(adenosine diphosphate ribose) polymerase (PARP) pathway plays a critical role in diabetic endothelial dysfunction.

AIM:

The aim of this study is to determine whether activation of the PARP pathway is involved in diabetic cavernosal endothelial dysfunction and abnormalities of the NO/cGMP pathway.

METHODS:

Male Sprague-Dawley rats were randomly divided into three groups: age-matched controls, diabetic controls (DM), and the 3-aminobenzamide (3-AB, a PARP inhibitor)-treated diabetic group (DM+3-AB). Diabetes was induced by intraperitoneal injection of streptozotocin. Eight weeks after inducing diabetes, the DM+3-AB group was treated with 3-AB for 4 weeks.

MAIN OUTCOME MEASURES:

Erectile function was assessed at 12 weeks after inducing diabetes by stimulating the cavernous nerve. Expression of poly(ADP-ribose), protein kinase B (Akt), phospho-Akt, endothelial nitric oxide synthase (eNOS), phospho-eNOS, and neuronal nitric oxide synthase (nNOS) were evaluated by Western blot. Cavernous NO generation and cGMP levels were also determined.

RESULTS:

The DM group showed impaired erectile function and significantly increased PARP activity. Expression of total eNOS and nNOS, phospho-Akt, and eNOS decreased significantly in the DM group compared with those in the control group. In addition, cavernous NO generation and cGMP levels decreased significantly in the DM group compared with those in the control group. Treatment with 3-AB restored erectile function and significantly reversed all molecular alterations except decreased nNOS expression.

CONCLUSION:

Overactivation of the PARP pathway in the corpus cavernosum of diabetic rats was involved in cavernosal endothelial dysfunction and abnormalities of the NO/cGMP pathway resulting in ED. These findings may be applied to develop novel therapies for patients with diabetic ED.

Simple Approach: CO2

09 Sunday Aug 2015

Carbon Dioxide – CO2 – is poisonous at high levels; but at low levels, it can support vasodilation. The nice thing about CO2 is that you produce it all the time. Just don’t exhale as much CO2 or inhale as much oxygen, and you will raise your CO2 levels. The body carefully controls these, but you may be able to get some benefit from this.

Once again, I am finding that our medical science is quite primitive, and that some ancient forms of health knowledge – such as yoga and Chinese medicine – may have answers that we are only now discovering. I support Western medicine, but when it comes to something as simple as breathing, we simply haven’t had much interest in this field. However, the more I look into breathing, the more I realize that most people either hyperventilate – breathe in too much oxygen – or don’t expand their lungs fully. So, I am researching this and will report more in the near future.

New Firm Studying Drug for ED

09 Sunday Aug 2015

It’s funny how once I start one line of research, I find a lot of promising information. I have been looking at arginine for ED. This lead to the question of what happens when we inhibit the enzyme that breaks down arginine – arginase.

Now I find that a company is developing drugs that block arginase. The company is Arginetix Inc, and it is attempting to develop arginase inhibitors for the treatment of pulmonary arterial hypertension (PAH) and erectile dysfunction (ED). They are also exploring the treatment of asthma and atherosclerosis.

A study published in The American Journal of Physiology – Heart and Circulatory Physiology demonstrated that, in a mouse model of ED, treatment with an arginase inhibitor restored the intracavernosal pressure (a measure of erection health) of aged mice to the level of young mice without affecting young mice.

While other companies have worked on arginine as a target, no other group is focusing on arginase. Inhibiting the enzyme increases production of nitric oxide, which is critical for cell signaling, and reduces the production of reactive oxygen, which can damage cells.

For more information, here is a press release from Argenitex: CLICK HERE.

Here is an article about inhibiting arginase: CLICK HERE.

If you want to create your own arginase inhibitor in your laboratory, here’s how: CLICK HERE.

On wikipedia, they have this to say about arginase:

Arginase II is coexpressed with nitric oxide (NO) synthase in smooth muscle tissue, such as the muscle in the genitals of both men and women. The contraction and relaxation of these muscles has been attributed to NO synthase, which causes rapid relaxation of smooth muscle tissue and facilitates engorgement of tissue necessary for normal sexual response. However, since NO synthase and arginase compete for the same substrate (L-arginine), over-expressed arginase can affect NO synthase activity and NO-dependent smooth muscle relaxation by depleting the substrate pool of L-arginine that would otherwise be available to NO synthase. In contrast, inhibiting arginase with ABH or other boronic acid inhibitors will maintain normal cellular levels of arginine, thus allowing for normal muscle relaxation and sexual response.[6]

Recent studies have implicated arginase as a controlling factor in both male erectile function and female sexual arousal, and is therefore a potential target for treatment of sexual dysfunction in both sexes. Additionally, supplementing the diet with additional L-arginine will decrease the amount of competition between arginase and NO synthase by providing extra substrate for each enzyme.[7]

Does Marijuana Cause ED?

09 Sunday Aug 2015

Over 60 million people in the US have tried marijuana. Millions of American men smoke marijuana regularly. What effect does it have on their sex drives? Can it cause ED?

I did some research on this question. Here is a link to an article (from 1981) in the New York Times (LINK HERE). It says that short term, the active drug in marijuana (THC) raises testosterone, which is good; however, chronic use can significantly lower testosterone, which is bad. This may be why some young men who smoke a lot of pot have a low sex drive.

Most of the other information I can find supports this view, which would affect men and women.

Acupuncture and ED

09 Sunday Aug 2015

Here is an interesting article about the use of acupuncture to raise nitric oxide levels (in reference to hypertension, which may be related to ED):

LINK HERE: 

From the American Journal of Chinese Medicine.

Does Fasting Help ED?

09 Sunday Aug 2015

Fasting – not eating – increases the sensitivity of D2 (dopamine) receptors (in rats), so this may also help in humans.

Study on this:

http://www.ncbi.nlm.nih.gov/pubmed/18305018

Dimethylarginine Dimethylaminohydrolase…

19 Sunday Jul 2015

Here’s another avenue I’m following for better erections…dimethylarginine dimethylaminohydrolase (DDAH) is an enzyme that degrades asymmetric dimethylarginine (ADMA), which inhibits the production of nitric oxide synthase. Why should you care?

Because nitric oxide synthase takes a nitrogen atom from L-arginine, producing nitric oxide (NO), so that NO can activate cGMP and cause blood vessels in the penis to relax, so blood can come in and you can get an erection.

In certain health problems – such as high levels of homocysteine (homocysteinemia) – the evil ADMA is more likely to impair the release of NO. Therefore, it is reasonable to assume these elements play a role in erectile dysfunction.

DDAH is a perfect drug for supporting erections. In a mouse model, mice with high levels of DDAH decreased levels of ADMA by 50%, which was associated with a significant increase in nitric oxide synthase activity. They also had healthier blood vessels.

Has DDAH been explored as an ED treatment? Are there any herbs that mimic the effects of DDAH? I haven’t found any.

BH4: Potential Treatment

17 Friday Jul 2015

A few years old, but interesting, as there is now a BH4 product on the market (Kuvan)

Information on BH4 (also known as tetrahydrobiopterin): http://en.wikipedia.org/wiki/Tetrahydrobiopterin

Information on Kuvan:
http://www.bmrn.com/products/kuvan.php

Here is the link to the PubMed listing to the abstract below (you can also get this complete article for free).http://www.ncbi.nlm.nih.gov/pubmed/16491266

Asian J Androl. 2006 Mar;8(2):159-67.
Evaluation of tetrahydrobiopterin (BH4) as a potential therapeutic agent to treat erectile dysfunction.
Sommer F1, Klotz T, Steinritz D, Bloch W.
Abstract
AIM: Nitric oxide (NO)-mediated smooth muscle relaxation causes penile erections. The endothelial NO synthase (eNOS) coenzyme tetrahydrobiopterin (BH4) converts eNOS-mediated catalytic activity from oxygen radical to NO production, improving endothelial function and vascular smooth muscle relaxation.
METHODS: Using quantitative immunohistochemistry, 8-isoprostane and nitrotyrosine concentrations were compared in cavernosal tissue from 17 potent and 7 impotent men, and the effect of single oral doses of BH4 on penile rigidity and tumescence was investigated. The pharmacodynamic effect of single oral doses of BH4 on penile rigidity and tumescence was investigated in a randomized, placebo-controlled, double-blind cross-over fashion in 18 patients with erectile dysfunction (ED) while receiving visual sexual stimulation.
RESULTS: 8-Isoprostane content in endothelium and smooth muscle was significantly higher in impotent patient samples; the level of nitrotyrosine was unchanged in ED patients. Relative to placebo, a single dose of 200 mg BH4 led to a mean increase in duration of > 60% penile rigidity (33.5 min [95% confidence interval (CI): 13.1-49.3] at base and 29.4 min [95% CI: 8.9-42.2] at tip). A 500-mg dose increased the relative duration of > 60% penile rigidity by 36.1 min (95% CI: 16.3-51.8) at the base and 33.7 min (95% CI: 11.4-43.9) at the tip. Treatments were well tolerated.
CONCLUSION: BH4 treatment is suggested to switch eNOS catalytic activity from super-oxide to NO formation, leading to a reduced formation of free radical reaction product 8-isoprostane without alteration of nitrotyrosine. The observed results make BH4 a suitable candidate as an ED treatment through reconstitution of altered catalytic activity of the eNOS.

Kuvan is for treating PKU – the disease that makes NutraSweet (aspartame) dangerous. Do people with ED also have a problem with aspartame? Maybe there is a common link.

Some Research Items…

17 Friday Jul 2015

Here are some interesting studies:

1. Research with the drug BAY 41-2272

Type 2 diabetes mellitus (DM2) and obesity are major risk factors for erectile dysfunction (ED). In diabetes, increased oxidative stress leads to decreased nitric oxide (NO) bioavailability, and diabetic patients appear to be less responsive to conventional therapy with phosphodiesterase type 5 inhibitors. We investigated whether the soluble guanylyl cyclase stimulator BAY 41-2272 (5-cyclopropyl-2-[1-(2-fluoro-benzyl)-1H-pyrazolo[3,4-b]pyridine-3-yl]pyrimidin-4ylamine) is effective in improving impaired corpus cavernosum (CC) relaxation in obese DM2 mice by reducing oxidative stress. Adult db/db(-/-) mice or their lean db(/+) littermates were used to assess vascular function, cGMP levels, antioxidant status, NADPH oxidase expression, and superoxide formation in the absence or presence of BAY 41-2272. Results showed that BAY 41-2272 (10(-8) to 10(-5) M) potently relaxed CC from db(/+) or db/db(-/-) mice in a similar manner. BAY 41-2272 significantly enhanced both endothelium-dependent and nitrergic relaxation induced by electrical field stimulation (EFS), and improved the impaired relaxation to acetylcholine and EFS in the diabetic animals in a concentration-dependent manner (10(-8) to 10(-7) M). BAY 41-2272 increased cGMP levels and potentiated relaxation responses to exogenous NO in CC. Total antioxidant status was reduced in plasma and urine whereas expression of vascular NADPH oxidase subunits (gp91phox, p22phox, and p47phox) was increased in the CC of db/db(-/-) mice, suggesting a state of oxidative stress. These effects were prevented by BAY 41-2272 in a concentration-dependent manner. These results suggest that BAY 41-2272 improves CC relaxation in db/db(-/-) mice by increasing cGMP and augmenting antioxidant status, making this drug is a potential novel candidate to treat ED.

Source: http://www.ncbi.nlm.nih.gov/pubmed/25740897

2. Blue-light for erections

Precise spatiotemporal control of physiological processes by optogenetic devices inspired by synthetic biology may provide novel treatment opportunities for gene- and cell-based therapies. An erectile optogenetic stimulator (EROS), a synthetic designer guanylate cyclase producing a blue-light-inducible surge of the second messenger cyclic guanosine monophosphate (cGMP) in mammalian cells, enabled blue-light-dependent penile erection associated with occasional ejaculation after illumination of EROS-transfected corpus cavernosum in male rats. Photostimulated short-circuiting of complex psychological, neural, vascular, and endocrine factors to stimulate penile erection in the absence of sexual arousal may foster novel advances in the treatment of erectile dysfunction.

Source: http://www.ncbi.nlm.nih.gov/pubmed/25788334

3. Other new drugs in development

Introduction: Erectile dysfunction adversely affects the lives of millions of men, and is the most commonly treated sexual disorder today. The erectile process has been extensively investigated, with major advances made in elucidating many of the complex molecular pathways involved. These advances have allowed researchers to design and study drug formulations that target various aspects of this complex process. The initial culmination of this research was the introduction of phosphodiesterase 5-inhibitors. While effective in many patients, they are not satisfactory for all afflicted men. As a result, researchers are developing novel drugs that target different molecular pathways. Areas covered: The paper will review these pathways, and the potential agents that target them. More specifically, first dopaminergic and melanocortin receptor agonists that act centrally will be covered. Then, the paper will examine the “second-generation” phosphodiesterase 5-inhibitors, soluble guanylate cyclases, rho-kinase inhibitors, and maxi-k channel activators that act peripherally. Expert opinion: Most of these novel drugs have yet to reach Phase III studies. However, it is likely that in years to come, patients will be selectively treated with these novel agents as a monotherapy or in combination with others acting in a synergistic manner.

Source: http://www.ncbi.nlm.nih.gov/pubmed/25740087

Autoerotic Asphyxiation

13 Saturday Jun 2015

Do you recall the news a few years back about David Carridine and autoerotic asphyxiation (AEA)? Here’s an interesting thought — readers of my website will recall that new evidence suggests that carbon dioxide and carbon monoxide are similar to nitric oxide in that they can cause vasodilation, needed for an erection. For people who practice AEA, it seems reasonable to assume that they are increasing levels of these gases, which increases erections and perhaps pleasure. This may be especially true as they get older, when nitric oxide systems decline.

This is a very sad story (I was a big fan of his work, especially in Kill Bill) but the lesson I get from this is that we need more research on sexual health. The more I research this topic (and it’s been over 3 years of intense review of the literature), the more I am surprised how little research is being done in this field. But then I am always surprised how little medical research is being done AT ALL, considering that health/life is the most important thing we have. Apparently, we have more important things to do with our money than save our own lives.

Well, I will continue to review the literature and make connections that no one else seems to be making, as one of the few objective sexual health websites that is not sponsored by anyone and not beholden to anyone but you, the reader. After all, mine is the ONLY WEB SITE that can explain WHY autoerotic asphyxiation may actually work on a scientific level. No other site uses science to explore human sexuality the way I do.

This, of course, is not an endorsement of a dangerous approach to fighting ED. In fact, many websites say that “the FBI estimates” that up to 1,000 people die each year from AEA. Of course, no sources for this number is provided, who knows? I can’t imagine that FBI really provides an annual report of AEA…Regardless, all approaches to enjoying sex should be safe and not cause you to hang yourself by accident. And we can find a healthy way to provide the CO2 without the noose…that would provide the benefit without the risk.

Research Finds a New Substance that May Lead to Treatment for ED…

23 Tuesday Dec 2014

This “gastrin-releasing peptide” may play an important role in erections. We’ll see what future research finds. Link to article on PubMed: http://www.ncbi.nlm.nih.gov/pubmed/21104362
Anat Sci Int. 2011 Mar;86(1):19-29. doi: 10.1007/s12565-010-0097-z. Epub 2010 Nov 23.

Gastrin-releasing peptide system in the spinal cord mediates masculine sexual function.

Sakamoto H

Abstract

The lumbar spinal segments are of particular interest because they are sexually dimorphic and contain several neuronal circuits that are important in eliciting male sexual responses such as erection and ejaculation. Gastrin-releasing peptide (GRP) is a member of the bombesin-like peptide family first isolated from the porcine stomach. A collection of neurons in the lumbar spinal cord (L3-L4 level) of male rats projects to the lower lumbar spinal cord (L5-L6 level), releasing GRP onto somatic and autonomic centers known to regulate male sexual reflexes. All these target neurons express and localize specific receptors for GRP. This system of GRP neurons is sexually dimorphic, being prominent in male rats but vestigial in females. The system is completely feminine in genetically XY rats with a dysfunctional androgen receptor gene, demonstrating the androgen-dependent nature of the dimorphism. Pharmacological stimulation of GRP receptors in this spinal region remarkably restores sexual reflexes in castrated male rats. Exposure of male rats to a severe traumatic stress decreases the local content and the axonal distribution of GRP in the lumbar spinal cord and results in an attenuation of penile reflexes in vivo. Administration of a specific agonist for GRP receptors restores penile reflexes in the traumatic stress-exposed male rats. This review summarizes findings on this recently identified spinal GRP system, which may be vulnerable to stress, that controls male reproductive function. The identification of a male-specific neuronal system regulating sexual functions offers new avenues for potential therapeutic approaches to masculine reproductive dysfunction.

Magnetic Stimulation – to Cause Erections.

16 Sunday Nov 2014

Here is an interesting study (LINK HERE). They used magnetic stimulation to create erections in dogs. The erections would stop when the magnetic stimulation was removed, and could be restarted any number of times. As far as I know, this has never been attempted in humans.

The article doesn’t indicate if this approach would turn you into a “chick magnet”.

Chasteberry – Too Little or Too Much? It All Depends on Dose

16 Sunday Nov 2014

Here’s an interesting finding. Chasteberry (Vitex agnus-castus) is said to bind dopamine 2 (D2) receptors. Why is that interesting? Because so does apomorphine, an ED drug.

But it gets even weirder. A low dose of chasteberry binds to D2 receptors – killing desire. But high levels of chasteberry increase desire – by reducing prolactin, the evil chemical that creates the refractory period after orgasm.

But which dose is too little and which is too much?

As it says on Wikipedia (http://en.wikipedia.org/wiki/Vitex_agnus-castus):

The mechanism of action [of chastberry] is not fully understood[19] but it is assumed that it has dopaminergic effects resulting in changes of prolactin secretion. At low doses, such as might have been used in previous centuries for suppression of sexual desire, it inhibits activation of dopamine 2 receptor by competitive binding, causing a slight increase in release of prolactin. In higher concentrations, as in modern extracts, the binding activity is sufficient to reduce the release of prolactin. A study has found that treatment of 20 healthy men with higher doses of Vitex agnus-castus was associated with a slight reduction of prolactin levels, whereas lower doses caused a slight increase as compared to doses of placebo.[20] A decrease of prolactin will influence levels of Follicle-stimulating hormone (FSH) and estrogen in women ;[citation needed] and testosterone in men .[citation needed] Dopaminergic compounds (diterpenes with prolactin-suppressive effects that were almost identical in their prolactin-suppressive properties than dopamine itself) present inVitex agnus castus seem likely to be the clinically important compounds which improve premenstrual mastodynia and possibly also psycho-somatic symptoms of PMS.[21]

Here’s a study that offers a high dose of 480 mg for lowering prolactin:
http://www.ncbi.nlm.nih.gov/pubmed/9021345

From the study:

The effects of three doses of a special Agnus castus extract (BP1095E1)–extracts from 120 mg, 240 mg and 480 mg of drug per day–were examined within the framework of a placebo-controlled clinical study of tolerance and prolactin secretion in 20 healthy male subjects during a period of 14 days. There was good tolerance during the study as regards the following: adverse effects, the effects on blood pressure and heart rate, blood count, Quick’s test, clinical chemistry as well as testosterone, FSH and LH values. During each study phase the 24-hour prolactin secretion profile was measured from the penultimate to the final day, and the amount of prolactin release was monitored an hour after TRH stimulation on the last day. A significant increase in the 24-hour profile was registered with the lowest dose in comparison to placebo, the opposite being the case with the higher doses, i.e. a slight reduction. In contrast to the administration of placebo, the 1-hour AUC after TRH stimulation resulted in a significant increase with the lowest dose and a significant reduction with the highest dose. The results suggest effects of the special Agnus castus extract which are dependent on the dose administered and the initial level of prolactin concentration.

Other PDE5 Inhibitors?

16 Sunday Nov 2014

Interesting article on phosphodiesterase inhibitors, from The International Journal of PharmTech Research:

http://sphinxsai.com/ptvol4/pdf_vol4/pt=30%20(1148-1160).pdf

PHOSPHODIESTERASE INHIBITORS: THEIR ROLE AND IMPLICATIONS

such as cAMP and cGMP and thus have pivotal roles in cellular functions. PDE inhibitors such as theophylline have been employed as anti-asthmatics since decades and numerous novel selective PDE inhibitors are currently being investigated for the treatment of diseases such as Alzheimer’s disease, erectile dysfunction and many others. This review attempts to elucidate the pharmacology, applications and recent developments in research on PDE inhibitors as pharmacological agents.
Keywords: Phosphodiesterases, Phosphodiesterase inhibitors.

Melatonin – Does It Cause ED? Or Treat It?

11 Tuesday Nov 2014

Depending on what you read, melatonin – a common hormone used to help sleep – can cause ED, prevent ED, or treat ED.

Personally, I don’t want to try it, but how about you? Does anyone have ED after taking melatonin?

Anyway, here are some of the reports:

1. Melatonin causes ED:
Cell Mol Neurobiol, 2001 Dec, 21(6):605-16, “Melatonin-dopamine interactions: from basic neurochemistry to a clinical setting”

2. Melatonin prevents ED: 
Qiu XF1, Li XX, Chen Y, Lin HC, Yu W, Wang R, Dai YT. Mobilisation of endothelial progenitor cells: one of the possible mechanisms involved in the chronic administration of melatonin preventing erectile dysfunction in diabetic rats. Asian J Androl. 2012 May;14(3):481-6. doi: 10.1038/aja.2011.161. Epub 2012 Feb 27.

Abstract

Diabetes-induced oxidative stress plays a critical role in the mobilisation of endothelial progenitor cells (EPCs) from the bone marrow to the circulation. This study was designed to explore the effects of chronic melatonin administration on the promotion of the mobilisation of EPCs and on the preservation of erectile function in type I diabetic rats. Melatonin was administered to streptozotocin-induced type I diabetic rats. EPCs levels were determined using flow cytometry. Oxidative stress in the bone marrow was indicated by the levels of superoxide dismutase and malondialdehyde. Erectile function was evaluated by measuring the intracavernous pressure during an electrostimulation of the cavernous nerve. The density of the endothelium and the proportions of smooth muscle and collagen in the corpus cavernosum were determined by immunohistochemistry. The administration of melatonin increased the superoxide dismutase level and decreased the malondialdehyde level in the bone marrow. This effect was accompanied by an increased level of circulating EPCs in the diabetic rats. The intracavernous pressure to mean arterial pressure ratio of the rats in the treatment group was significantly greater, compared with diabetic control rats. The histological analysis demonstrated an increase in the endothelial density of the corpus cavernosum after the administration of melatonin. However, melatonin treatment did not change the proportions of smooth muscle and collagen in the corpus cavernosum of diabetic rats. Chronic administration of melatonin has a beneficial effect on preventing erectile dysfunction (ED) in type I diabetic rats. Promoting the mobilisation of EPCs is one of the possible mechanisms involved in the improvement of ED.

  1. Melatonin treats ED: Tavukçu HH1, Sener TE, Tinay I, Akbal C, Erşahin M, Cevik O, Cadirci S, Reiter RJ, Sener G.

Melatonin and tadalafil treatment improves erectile dysfunction after spinal cord injury in rats. Clin Exp Pharmacol Physiol. 2014 Apr;41(4):309-16. doi: 10.1111/1440-1681.12216.

Abstract

Oxidative stress plays an important role both in spinal cord injury (SCI) and erectile dysfunction (ED). The present study investigated the effects of melatonin and tadalafil treatment alone or in combination on SCI-induced ED. Male Wistar albino rats (n = 40) were divided into five groups: sham-operated control and SCI-injured rats given either vehicle, melatonin (10 mg/kg, i.p.), tadalafil (10 mg/kg, p.o.) or a combination of melatonin and tadalafil. Spinal cord injury was induced using a standard weight-drop method. On Day 7 after SCI, intracavernosal pressure (ICP) was measured and all rats were decapitated. Cavernosal tissues were obtained to examine caspase 3, nitric oxide synthase (NOS), myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, as well as cGMP, nerve growth factor (NGF), malondialdehyde (MDA) and glutathione (GSH) levels. Spinal cord injury caused oxidative damage, as evidenced by increases in MDA and cGMP levels. In addition, MPO and caspase 3 activites were increased after SCI, whereas GSH and NGF levels and SOD activity were reduced. Melatonin effectively reversed these oxidative changes. Furthermore, in rats treated with both melatonin and tadalafil, the recoveries were more pronounced than in rats given either melatonin or tadalafil alone. The ICP/mean arterial pressure value in vehicle-treated SCI rats was significantly higher than in the control group, whereas in the tadalafil- and tadalafil + melatonin-treated groups have returned this value had returned to control levels. As an individual treatment, and especially when combined with tadalafil, a well-known agent in the treatment of ED, melatonin prevented SCI-induced oxidative damage to cavernosal tissues and restored ED, most likely due to its anti-oxidant effects.

Sunscreen Cause Erectile Dysfunction — and Skin Cancer?

19 Sunday Oct 2014

Sunscreen Cause Erectile Dysfunction — and Skin Cancer?

Here is a story you won’t find anywhere else but here! But I dig into the deepest recesses of the obscure medical literature, and found a new (possible) erection blocker — sunscreen!

Plus, it may cause skin cancer.

OK, here’s the story from the journal Melanoma Research: (melanoma is a bad form of skin cancer, as you probably know):

1. Sunscreen — suntan lotion — prevent redness after skin is exposed to sun light. The more it protects against sun, the higher the SPF – sun protection factor.

2. The redness from sun exposure is caused, in part, by the action of our old friend, nitric oxide (NO) — discussed on many posts of this blog.

3. Sunscreen has been found to block NO by inhibitor the enzyme that produces NO — inducible nitric oxide synthase (iNOS).

4. Because of this, the researchers say that sunscreen may actual contribute to MORE skin cancer, because it blocks the protective effect of NO on the skin.

5. Finally — I wonder if sunscreen is absorbed and whether it blocks NO in other parts of the body. This is important because NO is needed for an erection.

Does sunscreen cause skin cancer and deflate erections? It remains to be seen.

Here is a link to the study, by Chiang et al at the VA Medical Center in Memphis, TN.

CLICK FOR LINK

Yohimbine – Not Very Impressive Results

24 Wednesday Sep 2014

THIS LINK summarizes research with yohimbine, the active chemical in the herbal product yohimbe. You can get a presciption for yohimbine from your doctor or buy the herb yohimbe on-line or at the drug store or vitamin shop.

The conclusion of a review of studies is that this drug is not very effective. It may help some people some time. My opinion is that you can use it to mildly enhance the effect when combined with Viagra or Cialis, but that by itself it doesn’t do much. I could be wrong but that has been my experience – please feel free to post your opinion.

Testosterone Supplements – Pros and Cons

18 Thursday Sep 2014

Should men take testosterone supplements – for low-T or other reasons? And what are the dangers?

A study in JAMA said users may have more heart attacks, but that study is being challenged, as described here:

A study the FDA has cited as a reason to investigate the cardiovascular safety of testosterone drugs has come under heavy fire from critics. Physicians and researchers are calling for the November paper’s retraction, citing at least two corrections that they say compromise its credibility.

As MedPage Today reports, the Androgen Study Group, comprising more than 125 doctors, has sent a letter to Howard Bauchner, editor-in-chief of the Journal of the American Medical Association (JAMA), asking that a study that linked testosterone therapy to a greater risk of death, heart attack and stroke in some patients be pulled from the publication.

With the market for testosterone therapies rapidly expanding, so-called “Low-T” drugs have landed at the heart of a safety controversy, with activists going so far as to urge the FDA to label the treatments with black-box warnings. Last year, the JAMA study raised red flags on the big-selling drugs. AbbVie ($ABBV), Eli Lilly ($LLY) and Endo ($ENDP), among others, are selling into a market expected to reach $5 billion by 2017, which critics say has been expanding as drugmakers have steered men toward using them as lifestyle treatments.

But the journal has since published two corrections to the paper, one clarifying that results were based on estimates rather than raw data, and the other–on which the Androgen Study Group’s letter centers–involving a reclassification of more than 1,000 patients excluded from the study, including 100 who were women.

“They found that almost 10% were women in an all-male study, so why should we believe any of the other data?” Harvard Medical School’s Abraham Morgentaler told MedPage Today. “These data were so off that it’s hard to believe the data for the entire study are accurate.”

Study author Michael Ho of the Eastern Colorado VA, on the other hand, says he and his colleagues “stand firmly by the results” of their study, claiming they were not altered by the changed reasons for exclusion. “Misperception about that could suppress research that raises important questions about patient safety,” he told the news source.

In the meantime, the FDA is looking into testosterone drugs itself, announcing a decision in January to reassess the safety issue. So far, the agency hasn’t reached a conclusion, a stance that has sparked the ire of those convinced the drugs are dangerous.

“In the face of this accumulating evidence, this statement is reckless and is a betrayal of the FDA’s role as an agency in the U.S. Public Health Service,” Sidney Wolfe, founder of the advocacy group Public Citizen, said in a petition last month.

Source article: (click link)

http://www.fiercepharma.com/story/critics-knock-jama-study-linking-testosterone-drugs-cardio-risks/2014-03-28?utm_medium=nl&utm_source=internal

TNF-Alpha and ED?

10 Wednesday Sep 2014

Excessive TNF-alpha levels are associated with ED – so does reducing them help fight ED?

Here is a post from another blog that might help:

A while ago I was doing some experiments taking herbal and vitamin TNF-alpha inhibitors (for anti-inflammatory purposes), and noticed that while I took these, I had the hardest erections I’d seen for ages. Sometimes just spontaneous ones, like being a teenager.

On checking this out, I found that there is a link between erectile dysfunction and high TNF-alpha:

TNF-alpha knockout mice have increased corpora cavernosa relaxation

Since TNF-alpha may arise from chronic low level infection, here we see yet again that there is a link between a human health condition — in this case erectile dysfunction — and pathogenic microbes.

Perhaps those people with higher microbial loads in their bodies will have higher TNF-alpha levels. And such people may therefore have less erection strength. Anyway, for anyone that has some underlying chronic inflammation in their body (perhaps due to an infection-linked health conditions like CFS, lupus, IBS, etc), consider that this may be causing a degree of erectile dysfunction.

Here is a list of TNF-alpha inhibitors (in no particular order) that may remedy this erectile dysfunction:

The following supplements DECREASE production of TNF-alpha:

Cat’s claw herb – a remarkably potent inhibitor of TNF-alpha production.
“5-Loxin” extract from Indian frankincense (Boswellia serrata) is a very potent inhibitor of TNF-alpha.
Acetylcholine significantly inhibits the release of TNF-alpha (L-carnitine can boost acetylcholine).
N-acetyl-L-cysteine
Astragalus
Burdock (Arctium lappa) — Arctigenin extract
Ginger
Chondroitin sulfate
Evening primrose oil (GLA converts to Prostaglandin E1, which suppresses TNF-alpha)
Devil’s claw
Curcumin
Milk thistle
Alpha lipoic acid
Allicin (from garlic)
Stinging nettle leaf (Urtica dioica)
Magnesium
Vitamin C
EGCG (green tea extract)
Vitamin E
Tea tree oil
Ashwagandha (Withania somnifera)
Rehmannia root
Coptis root
Anethole (in fennel)
Frankincense
Xylitol
Fish Oil (Omega-3)
Oxymatrine
Artesunate
Dietary fiber
Niacinamide
Andrographolide (from Andrographis paniculata)
Olmesartan (Benicar)
Quinine
Naltrexone
Deprenyl
Azithromycin
Royal jelly
Oregano
Gingko
Licorice
Clove
Q10

The following INCREASE production of TNF-alpha:
Reishi mushroom
Rhodiola rosea
Elderberry
Chlorella
Spirulina
Ginseng
Aged garlic extract
Dandelion root
Honey
Chocolate
Echinacea
Silica
Lactoferrin
Biotin deficiency up-regulates TNF-alpha production in murine macrophages

Note that in my TNF-alpha reduction experiments, I used a good 10 or 12 of these various different supplements at the same time, including the more potent ones like cat’s claw.

TNF-alpha Inhibitors

01 Friday Aug 2014

Excessive TNF-alpha levels are associated with ED – so does reducing them help fight ED?

Here is a post from another blog that might help:
A while ago I was doing some experiments taking herbal and vitamin TNF-alpha inhibitors (for anti-inflammatory purposes), and noticed that while I took these, I had the hardest erections I’d seen for ages. Sometimes just spontaneous ones, like being a teenager.

On checking this out, I found that there is a link between erectile dysfunction and high TNF-alpha:

TNF-alpha knockout mice have increased corpora cavernosa relaxation

Since TNF-alpha may arise from chronic low level infection, here we see yet again that there is a link between a human health condition — in this case erectile dysfunction — and pathogenic microbes. 

Perhaps those people with higher microbial loads in their bodies will have higher TNF-alpha levels. And such people may therefore have less erection strength. (Actually, this might not be a bad thing from an evolutionary perspective, as I guess it might tend to prevent procreation from men that have high microbial loads in their bodies — and so would not be strong and fit fathers).

Anyway, for anyone that has some underlying chronic inflammation in their body (perhaps due to an infection-linked health conditions like CFS, lupus, IBS, etc), consider that this may be causing a degree of erectile dysfunction.

Here is a list of TNF-alpha inhibitors (in no particular order) that may remedy this erectile dysfunction:



The following supplements DECREASE production of TNF-alpha: 

Cat’s claw herb – a remarkably potent inhibitor of TNF-alpha production.

“5-Loxin” extract from Indian frankincense (Boswellia serrata) is a very potent inhibitor of TNF-alpha.

Acetylcholine significantly inhibits the release of TNF-alpha (L-carnitine can boost acetylcholine).

N-acetyl-L-cysteine
Astragalus
Burdock (Arctium lappa) — Arctigenin extract
Ginger
Chondroitin sulfate
Evening primrose oil (GLA converts to Prostaglandin E1, which suppresses TNF-alpha)
Devil’s claw
Curcumin
Milk thistle
Alpha lipoic acid
Allicin (from garlic)
Stinging nettle leaf (Urtica dioica)
Magnesium
Vitamin C
EGCG (green tea extract)
Vitamin E 
Tea tree oil
Ashwagandha (Withania somnifera)
Rehmannia root
Coptis root
Anethole (in fennel)
Frankincense
Xylitol
Fish Oil (Omega-3)
Oxymatrine
Artesunate
Dietary fiber 
Niacinamide
Andrographolide (from Andrographis paniculata)
Olmesartan (Benicar) 
Quinine
Naltrexone
Deprenyl
Azithromycin
Royal jelly
Oregano
Gingko
Licorice
Clove
Q10

The following INCREASE production of TNF-alpha: 

Reishi mushroom
Rhodiola rosea
Elderberry 
Chlorella
Spirulina
Ginseng
Aged garlic extract
Dandelion root
Honey
Chocolate
Echinacea
Silica
Lactoferrin
Biotin deficiency up-regulates TNF-alpha production in murine macrophages


Note that in my TNF-alpha reduction experiments, I used a good 10 or 12 of these various different supplements at the same time, including the more potent ones like cat’s claw, and ac

For Those Who Don’t Like Beets, Beetroots, or Beetroot Juice…

12 Thursday Jun 2014

If you don’t want to bother with beets, try taking potassium nitrate. It is available online as a supplement for weight lifters.

Ask your doctor before using it, though – just to be safe.

But here is some information supporting its use:

(You can get a free PDF here)

http://hyper.ahajournals.org/content/56/2/274.full?sid=a3e944f7-ca55-4dfd-a8af-a4216aed7446

Hypertension. 2010 Aug;56(2):274-81. doi: 10.1161/HYPERTENSIONAHA.110.153536. Epub 2010 Jun 28.

Inorganic nitrate supplementation lowers blood pressure in humans: role for nitrite-derived NO.

Abstract
Ingestion of dietary (inorganic) nitrate elevates circulating and tissue levels of nitrite via bioconversion in the entero-salivary circulation. In addition, nitrite is a potent vasodilator in humans, an effect thought to underlie the blood pressure-lowering effects of dietary nitrate (in the form of beetroot juice) ingestion. Whether inorganic nitrate underlies these effects and whether the effects of either naturally occurring dietary nitrate or inorganic nitrate supplementation are dose dependent remain uncertain. Using a randomized crossover study design, we show that nitrate supplementation (KNO(3) capsules: 4 versus 12 mmol [n=6] or 24 mmol of KNO(3) (1488 mg of nitrate) versus 24 mmol of KCl [n=20]) or vegetable intake (250 mL of beetroot juice [5.5 mmol nitrate] versus 250 mL of water [n=9]) causes dose-dependent elevation in plasma nitrite concentration and elevation of cGMP concentration with a consequent decrease in blood pressure in healthy volunteers. In addition, post hoc analysis demonstrates a sex difference in sensitivity to nitrate supplementation dependent on resting baseline blood pressure and plasma nitrite concentration, whereby blood pressure is decreased in male volunteers, with higher baseline blood pressure and lower plasma nitrite concentration but not in female volunteers. Our findings demonstrate dose-dependent decreases in blood pressure and vasoprotection after inorganic nitrate ingestion in the form of either supplementation or by dietary elevation. In addition, our post hoc analyses intimate sex differences in nitrate processing involving the entero-salivary circulation that are likely to be major contributing factors to the lower blood pressures and the vasoprotective phenotype of premenopausal women. 

Beets?

31 Saturday May 2014

Some interesting things about beets. They seem to help with a lot of things, and may help with ED.

Here is some information on this: Atherosclerosis. 2013 Nov;231(1):78-83. doi: 10.1016/j.atherosclerosis.2013.09.001. Epub 2013 Sep 11.

Beetroot juice improves in overweight and slightly obese men postprandial endothelial function after consumption of a mixed meal.

Joris PJ1, Mensink RP
Abstract

BACKGROUND:

Through effects on nitric oxide (NO) bioavailability, endothelial function is improved after the intake of beetroot juice-which is rich in inorganic nitrate-, but decreased after the intake of a meal.

OBJECTIVE:

The objective of this study was to examine if beetroot juice could counteract the impairment of endothelial function associated with the ingestion of a mixed meal.

METHODS:

Twenty healthy overweight and slightly obese men with a BMI between 28 and 35 kg/m(2) received in random order a mixed meal providing 56.6 g of fat with beetroot juice or a control drink. The beetroot juice (140 mL) provided approximately 500 mg dietary nitrate. Flow-mediated dilation (FMD) of the brachial artery was measured before and 2 h after meal consumption. Blood was sampled at regular intervals.

RESULTS:

Postprandial changes in serum triacylglycerol (TAG) (P = 0.69), plasma glucose (P = 0.84) and insulin (P = 0.67) concentrations were comparable between the meals. After consumption of beetroot juice, the postprandial impairment in FMD following a standardized mixed meal was improved (P = 0.030) compared with the control drink (-0.37 ± 2.92% versus -1.56 ± 2.90%). Following beetroot juice consumption, plasma concentrations of the circulating NO pool were higher at T60, T120, and T240 (P < 0.001 at all time points).

CONCLUSION:

In healthy overweight and slightly obese men a single dose of beetroot juice attenuates the postprandial impairment of FMD following a mixed meal, possibly through increases in plasma NO concentrations.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Arginine for ED — Worked for Me!

25 Tuesday Mar 2014

Here’s an easy thing you can do that might work.

I read that 4 grams (4,000 mg) of arginine can help with ED. I have tried arginine in the past but never at this high a dose. But then I read this again, from a reliable medical source, so I tried it last night.

For experimental purposes, I try taking things at night and seeing if there is an effect when I wake up. If I wake up like a regular middle-aged man, then that means no effect. If I wake up like a 16-year-old, then that means it has had an effect.

This morning, after taking 4 grams of arginine last night, I woke up like a 16-year-old.

I can’t say for sure it was the arginine; it may just be a coincidence; it may have been the garlic I have been eating (2 cloves/day, crushed). It may be the exercise I have been doing, or the new sunlamp I use. It may just be springtime. Or all combined. Who knows? But it seemed I had a dramatic benefit from taking a large dose of arginine – the precursor of nitric oxide – right before bedtime.

So, I will try this again tonight, and see if I have the same effect.

In the past, I find sometimes thing work, and then they stop. Maybe I need a higher dose. 5 grams?

In any case, this is something you can try. It’s safe, does not require a prescription, and easy to do. There is even research to back up this approach.

If you try this, let me know what happens.

Here’s an article that studied 5 grams of arginine for ED:

http://www.ncbi.nlm.nih.gov/pubmed/10233492

BJU Int. 1999
Feb;83(3):269-73.
Effect of oral
administration of high-dose nitric oxide donor L-arginine in men with organic
erectile dysfunction: results of a double-blind, randomized, placebo-controlled
study.
Chen J1, Wollman Y,
Chernichovsky T, Iaina A, Sofer M, Matzkin H.
Abstract
OBJECTIVES:
To determine, in a
prospective randomized, double-blind placebo-controlled study, the effect of 6
weeks of high-dose (5 g/day) orally administered nitric oxide (NO) donor
L-arginine on men with organic erectile dysfunction (ED).
PATIENTS AND
METHODS:
The study included
50 men with confirmed organic ED who were randomized after a 2-week placebo
run-in period to receive L-arginine or placebo. A detailed medical and sexual
history, O’Leary’s questionnaire, a specially designed sexual function
questionnaire and a sexual activity diary were obtained for each patient. All
participants underwent a complete physical examination including an assessment
of bulbocavernosus reflex and penile haemodynamics. Plasma and urine nitrite
and nitrate (designated NOx), both stable metabolites of nitric oxide, were
determined at the end of the placebo run-in period, and after 3 and 6 weeks.
RESULTS:
Nine of 29 (31%)
patients taking L-arginine and two of 17 controls reported a significant
subjective improvement in sexual function. All objective variables assessed
remained unchanged. All nine patients treated with L-arginine and who had
subjectively improved sexual performance had had an initially low urinary NOx,
and this level had doubled at the end of the study.
CONCLUSIONS:

 

Oral administration
of L-arginine in high doses seems to cause significant subjective improvement
in sexual function in men with organic ED only if they have decreased NOx
excretion or production. The haemodynamics of the corpus cavernosum were not
affected by oral L-arginine at the dosage used.

More on Sunlight and ED

13 Thursday Mar 2014

This is from the “Sunlight Institute” and this link: SUNLIGHT INSTITUTE

(you have to check the original article if you want the reference articles)

Could Sunlight Deficiency lead to erectile dysfunction (ED)? Could sunlight exposure or exposure to a tanning bed be as effective as Cialis?

Submitted by Sunlight Institute
on Sunday, October 7, 2012
By: Marc Sorenson, Sunlight Institute
Earlier this year I published, with the assistance of Dr. William B Grant, a paper entitled “Does Vitamin D Deficiency Contribute to Erectile Dysfunction (ED)?”[i] In that paper, we made the point that low levels of vitamin D correlated to increased risk of cardiovascular diseases including heart attacks, strokes and heart failure. For example, Giovannucci and colleagues showed that men with the lowest levels of serum vitamin D had a 2.4-times-increased risk of heart attack.[ii] ED is often an important indicator of cardiovascular disease (CVD) and a powerful early marker for asymptomatic CVD. Erection is a vascular event, and ED is often a vascular disease caused by endothelial damage and subsequent inhibition of vasodilation—the expansion of arterial width that is necessary for optimal blood flow throughout the body, including the penis.

One of the interesting findings of the literature search was the fact that sunlight stimulates vasodilation through a mechanism that has nothing to do with vitamin D. That mechanism is the production of nitric oxide (NO) by exposure to another spectrum of light, the non-vitamin-D-producing light called UVA. (NO is a well-known, potent vasodilator). Whole-body irradiation with UVA has been shown to lower blood pressure by stimulating NO production in the skin, which then significantly lowers blood pressure. These increased NO levels are accompanied by increased vasodilation and blood flow in the brachial artery.[iii] It is likely that such vasodilation may also enhance sexual function in men by increasing vasodilation and blood flow in the penile arteries, thereby reducing ED. If sunlight exposure causes vasodilation that lowers blood pressure, there is no reason to doubt that it would be a tremendous asset to men with ED. Both sunlight and tanning beds produce high quantities of UVA light. Perhaps research should be conducted to see whether Cialis or UVA exposure would cause the quickest relief of the ED condition. :)

One of our guests at our health resort (National Institute of Health and Fitness, http://www.nihf.com/ spent four weeks with us and sunbathed almost every day. His blood pressure decreased from 159/97 to 125/54 and leveled off at 115/70 when he returned home. I believe that the UVA light in the sunlight, and the subsequent production of NO, was greatly responsible for his blood pressure normalization. Now, I’m curious about his love life but probably won’t discuss it with him unless he volunteers!

At our health resort, we consider safe sun an integral part of our program. Call me at 888-798-6443 if you’d like to discuss this and other health benefits such as weight loss and reversal of diabetes.

– See more at: http://sunlightinstitute.org/could-sunlight-deficiency-lead-erectile-dysfunction-ed-could-sunlight-exposure-or-exposure-tanning#sthash.4hlBFxjl.dpuf

More on UV Light and Nitric Oxide

04 Tuesday Mar 2014

OK, there seems to be something here. UV light releases nitric oxide from the skin. Who knew?

So, I’m starting some tanning today!

Here is some information from this link (the reference numbers can be found in the article from this link):
http://www.vitamindwiki.com/tiki-index.php?page_id=2929

Beneficial Roles of UVA-induced Nitric Oxide (NO•) on Human Health
A few years ago it was demonstrated that nitric oxide (NO•), a gaseous free radical, is non-enzymatically induced in skin by UVA.128–130 However, UVA-induced NO• and its influence on human physiology and pathophysiology are not so well studied as the influence of NO• produced enzymatically by NO synthases.131 NO• is able to diffuse rapidly across cell membranes, and, depending on the conditions, is able to diffuse more than several hundred microns. The biological half-life of NO• is in the range from 1 ms to 2 sec, depending on superoxide (O2•-), antioxidants and oxygen concentrations.2 The biological effects of NO• are mediated through the reaction of NO• with a number of targets, such as haem groups, cysteine residues and iron and zinc clusters. This wide range of targets for NO• helps to explain the multiple roles it plays, including vasodilatation, immune defense, neurotransmission, regulation of cell death (apoptosis) and cell motility. Due to the importance of NO•, abnormal regulation of the concentration of UV-induced NO• may affect a number of important biological processes.
The rapid release of NO• following UVA exposure suggests the existence of latent stores. It is well known that part of the endogenously produced NO• is converted into nitrite (NO2-), nitrate or nitrosothiols. Earlier it was thought that these compounds are inert end products of endogenous NO• metabolism. In 2003 Rodriguez et al.132 demonstrated that in rat vascular tissue NO2- and nitrosothiols, but not nitrate, are converted back to NO• under UVA exposure

Protective effects of UV-induced NO•

Low concentrations of NO• protect cultured keratinocytes and skin from oxidative stress and UVA-induced apoptosis.130,131,134 The mechanism and the required concentrations for this protective action in skin are still unknown. Induction of Bcl-2 expression and inhibition of caspase activation have been suggested in some studies,130 but this fails to explain the rapid timescale of the response. It is possible that UVA-induced NO• may protect skin against solar radiation induced damages within 20–30 min, depending on UVA dose. Two independent studies have demonstrated that UVA exposure of human skin specimens leads to non-enzymatic NO• formation which reaches a maximum after 20 min (320–400 nm, 40 J/cm2) or after 30 min (350–400 nm, 30 J/cm2).128,133
In 2009 Oplander et al. demonstrated that irradiation of healthy individuals with biologically relevant doses of UVA lead to a sustained reduction in blood pressure.129 In 2010 it was proposed that many of the beneficial effects of sunlight related to cardiovascular health may be mediated by mechanisms that are independent of vitamin D and exposure to UV alone, but through UVA-induced NO• and nitrite.135 NO2-, for a long time considered biologically inert at low concentrations, is now known, not only to dilate blood vessels in its own right, but also to protect organs against ischemia/reperfusion damage.136 Hemoglobin, myoglobin, xanthine oxidoreductase, cytochrome P-450, and mitochondrial enzymes can all generate NO• from NO2- under hypoxic conditions.135,137 In adults, skin and blood are of comparable weight and volume. The total amount of NO2- in the epidermis is around 135 µM, while the total amount of NO2- in blood rarely exceeds 13–15 µM.133,135 Thus, mobilization of only a fraction of the relatively large epidermal pool of NO2- by sunlight is likely to be sufficient to increase plasma NO2- concentrations transiently. Thus, Feelisch et al. suggested that NO2- can be delivered to the systemic circulation and exert coronary vasodilator and cardioprotective as well as antihypertensive effects.135 NO-containing gas is effective in tissue disinfection and regulating inflammatory processes associated with acute and chronic wounds.138–140 It has been proposed that UVA-induced NO• may also have antimicrobial effects, be involved in cutaneous wound healing as well as have antitumor activity.130,141
UVA-exposure of human skin releases NO• into the circulation. In the bloodstream, NO• can reach the nervous system.129 In this way, UVA can influence transmission of nerve signals indirectly.38
However, NO• can represent, not only beneficial effects, but also toxicity, and, due to this, it is known as a Janus molecule.130 Many of the local and systemic UV-induced responses, including erythema and edema formation, inflammation, premature aging and immune suppression, can be influenced by UVA-produced NO•. Its role in the induction and in the progression of skin cancer remains uncertain. The direct toxicity of NO• is modest, but is greatly enhanced by reactions with superoxide (O2•-) to form the powerful oxidant peroxynitrite (ONOO-), which can promote oxidative damage to blood vessels and skin. Under normal conditions O2•- is rapidly removed by superoxide dismutases (SOD). NO• is quickly removed by its rapid diffusion through tissues into red blood cells where it is converted to nitrate and nitrite by a reaction with oxyhemoglobin. This limits the biological half-life of NO• in vivo to less than a second.

Increase Nitric Oxide With…Sunlight?

04 Tuesday Mar 2014

We ALL know that it’s good to increase our ol’ friend, nitric oxide. Well, here’s one I’ve never heard before. You might be able to increase nitric oxide levels in your body by exposure to…sunlight. Beyond its effect on vitamin D, sunlight is also claimed to increase levels of nitric oxide release, which flows throughout the body in a healthy way.

It sort of makes sense, actually. Animals in the wild would be healthy from walking around in the sun. It would also suggest a nitric oxide/health benefit from tanning/sunbooths/UV rays. However, this is just speculation, and the sun and tanning do have health risks.

Decide for yourself. Here is an article about it, which include a reference to an abstract from a conference. Not exactly a major study but worth a look, if you are interested.

Source:
http://www.medicalnewstoday.com/articles/260247.php

Scientists at the University of Edinburgh in the UK suggest that the heart-health benefits of sun exposure may outweigh the risk of developing skin cancer.

In the landmark study, the researchers found that when sunlight touches our skin, a compound called nitric oxide that helps lower blood pressure, is released into our blood vessels. Richard Weller, Senior Lecturer in Dermatology, and colleagues, say the effect is such that overall, sun exposure could improve health and even prolong life, because the benefits of reducing blood pressure, cutting heart attacks and strokes, far outweigh the risk of getting skin cancer.

The proof-of-principle study is being presented this week in Edinburgh at International Investigative Dermatology 2013, the world’s largest gathering of skin experts.

The abstract was published online in the Journal of Investigative Dermatology on 15 April.

The researchers note that rates of high blood pressure and cardiovascular disease rise in winter and are tied to geographic latitude (for instance they are higher in northern Europe than in southern Europe). Also, estimates show that in northern Europe, for every death from skin cancer, about 60 to 100 people die of stroke and heart disease linked to high blood pressure.

This new study is important because until now it was thought that sunlight’s only benefit to human health was production of vitamin D, which rises after exposure to the sun. Previous studies have found that while increased vitamin D levels link to lower cardiovascular disease, oral supplements do not have an effect on this.

Weller and colleagues found that the body’s production of nitric oxide is separate from production of vitamin D.

For their study they invited 24 volunteers to sit under sunlamps for two 20 minute sessions while they examined their blood pressure. In one session, they exposed the volunteers to both ultra-violet (UV) rays and heat from the lamps. In the other session, they only exposed them to the lamps’ heat and blocked the UV rays. The results showed that the volunteers’ blood pressure fell and their heart rate rose in the session where they were exposed to both UV and heat, but not when they were exposed to heat only. The reduction in blood pressure lasted for about 50 minutes.

Human skin contains large stores of nitrite (NO2) and nitrate (NO3). The researchers note that while nitrate is “biologically inert”, the action of sunlight can reduce it to active nitrite and nitric oxide (NO). They found that circulatory nitrate fell and nitrite rose during UV and heat exposure, but not during exposure to heat only. There was no difference in vitamin D levels.

Weller says in a statement that:

“We suspect that the benefits to heart health of sunlight will outweigh the risk of skin cancer. The work we have done provides a mechanism that might account for this, and also explains why dietary vitamin D supplements alone will not be able to compensate for lack of sunlight.” He and his team now want to look at the relative risks of skin cancer and heart disease in people who have received different amounts of exposure to sunlight. “If this confirms that sunlight reduces the death rate from all causes, we will need to reconsider our advice on sun exposure,” says Weller.

There have also been suggestions that exposure to the sun can help prevent infectious disease. For example, in 2011, Phil Rice, a virologist at St George’s Hospital, University of London, suggested that the sun’s UV rays inactivate the chickenpox virus on the skin.

Written by Catharine Paddock PhD

Here’s the actual abstract, from The Journal of Investigative Dermatology:

1247
UVA lowers blood pressure and vasodilates the systemic arterial vasculature by mobilisation of cutaneous nitric oxide stores

D Liu,1 BO Fernandez,3 NN Lang,2 JM Gallagher,4 DE Newby,2 M Feelisch3 and RB Weller1,5 1Dermatology, University of Edinburgh, Edinburgh, United Kingdom, 2Cardiology, University of Edinburgh, Edinburgh, United Kingdom, 3Medicine, University of Southampton, Southampton, United Kingdom, 4Leithmount Surgery, Edinburgh, United Kingdom and 5Centre for Inflammation Research, University of Edinburgh, Edinburgh, United Kingdom
The incidence of hypertension and cardiovascular disease (CVD) correlates with latitude and rises in winter. Population vitamin D levels inversely correlate with CVD, but oral supplementation does not alter CVD rates. Skin contains large stores of nitrite(NO2) and nitrate(NO3). Nitrate is biologically inert, but can be photo-reduced to active NO2 and nitric oxide (NO). The dermal vasculature enables rapid systemic dispersal of NO2 and NO.We hypothesised that ultraviolet A (UVA) mobilises NO bioactivity from skin to circulation to exert beneficial cardiovascular effects. Vit’ D is a marker for sunlight exposure. 24 healthy volunteers were sham (temp’ control) irradiated then actively irradiated with 20 J/cm2 UVA. Mean arterial pressure (MAP) fell and heart rate rose during active but not sham irrad’n (3.50±0.73 mmHg vs 2.80±0.98). The MAP fall was sustained for 50 mins in the active group only. Temperature rise was the same in both groups. Circulatory nitrite rose (0.50±0.04 μM to 0.72±0.04 μM p/

min of the NOS antagonist L-NMMA was infused to the brachial artery. FBF rose during active but not sham irradiation (23.7±6.5 % over baseline vs no change p<.0002). Physiological levels of UVA irradiation cause systemic vasodilation and lower BP in a vitamin D and NOS independent manner. Deaths from CVD and stroke are 60 to 100 times higher than from skin cancers in northern Europe. This study provides a mechanistic explanation for the inverse correlation between sunlight exposure and CVD mortality. Sunlight has beneficial effects independently of vitamin D synthesis.

Link:
http://www.nature.com/jid/journal/v133/n1s/full/jid2013104a.html

Grapefruit Juice: Increases Viagra Levels?

02 Sunday Mar 2014

Is it OK to combine grapefruit juice and Viagra (sildenafil)? How about Cialis or Levitra? Until it is clear what the effect is, I would say no. And because the effect of grapefruit juice lasts for 24 hours, until the effect on Viagra/Cialis/Levitra is clear, you should probably stay clear of grapefruit juice – period.

But here’s the evidence. I must admit I am a bit confused by this first study. It seems that the grapefruit juice — taken with Viagra — raises the levels of the drug. Isn’t that a good thing (assuming it doesn’t reach toxic levels)?

If I’m reading this correctly — and these pharmacokinetic studies are always tough to understand — (what exactly is area under the curve? ), it seems that this is the opposite of the pummelo study, which decreased sildenafil (Viagra) levels.

So, if I understand this, then taking Viagra with grapefruit juice should increase the levels — and possibly the effect — of Viagra in the body. I can’t advocate this, because I don’t what the effect would be, but it’s an interesting concept.

Here’s the abstract:

Clin Pharmacol Ther.
2002 Jan;71(1):21-9.
Effects of grapefruit
juice on the pharmacokinetics of sildenafil.
Jetter A1,
Kinzig-Schippers M, Walchner-Bonjean M, Hering U, Bulitta J, Schreiner P,
Sörgel F, Fuhr U.

Abstract

BACKGROUND ANDOBJECTIVES: Because of extensive first-pass metabolism, oral bioavailability of sildenafil reaches only 40%. Formation of the primary metabolite, N
-desmethylsildenafil, is mainly mediated by the cytochrome P450 enzyme CYP3A4.
In this study we investigated the influence of grapefruit juice, containing inhibitors of intestinal CYP3A4, on the pharmacokinetics of sildenafil and N-desmethylsildenafil.

METHODS: In a randomizedcrossover study, 24 healthy white male volunteers received single 50-mg doses of sildenafil. Two doses each of 250 ml grapefruit juice or water, respectively, were administered 1 hour before and together with the drug. Plasma concentrations of sildenafil and N -desmethylsildenafil were determined up to 24 hours post dose by use of liquid chromatography-tandem mass spectrometry (limit of quantification, 1 ng/ml).

RESULTS: Grapefruit juice changed the area under the sildenafil plasma concentration-time curve from time zero to infinity [AUC(0-infinity) from 620 [1.53] ng/ml x h to 761 [1.58] ng/ml x h (geometric mean with geometric standard deviation), corresponding to a 23% increase (90% confidence interval, 13%-33%). N-Desmethyl sildenafil AUC(0-infinity) increased by 24% (90% confidence interval, 17%-32%). Maximum plasma concentrations (C(max)) of sildenafil and N -desmethylsildenafil were essentially unchanged. There was a trend toward a prolonged time to reach C(max) during the grapefruit juice period (from a median of 0.75 hour to a median of 1.13 hours), corresponding to an increase by 0.25 hour (90% confidence interval, 0-0.63 hour). Interindividual variability was pronounced
in both periods.

CONCLUSIONS: Grapefruit juice increases sildenafil bioavailability and tends to delay sildenafil absorption. Sildenafil pharmacokinetics may become less predictable with grapefruit juice. Although patients usually will not be endangered by
concomitant use of grapefruit juice, it seems advisable to avoid this
combination.

However, this article says that grapefruit juice REDUCES Viagra levels, because it blocks absorption.

https://www.riverpharmacy.ca/faq/does-grapefruit-juice-affect-viagra-and-cialis-what-about-orange-or-apple-juice

A nutraceutical is a food or part of a food that allegedly provides medicinal or health benefits, including the prevention and treatment of disease. Grapefruit juice has been touted as containing many compounds that can reduce hardening of the arteries (atherosclerosis) and even the risk of cancer. Grapefruit juice can, therefore, be justifiably referred to as a classic nutraceutical. However, for many
persons taking certain medications, grapefruit juice might actually better be
termed a “nutrapollutical!”

It turns out that grapefruit juice can directly or indirectly interact in important ways with a number of medications. This is especially important since grapefruit juice is consumed by approximately one fifth of Americans for breakfast – a time of the day when medications also are commonly taken.

Grapefruit juice blocks special enzymes in the wall of the small intestine that actually destroys many medications and prevents their absorption into the body. Thus, smaller amounts of the drugs get into the body than are ingested. When the
action of this enzyme is blocked, more of the drugs get into the body and the
blood levels of these medications increase. This can lead to toxic side effects
from the medications.

Amazingly, this remarkable food-drug interaction was discovered completely by accident over a decade ago! Researchers were investigating whether alcohol could interact with felodipine (Plendil) and used a solution of alcohol with grapefruit juice to mask the taste of alcohol for the study. Researchers discovered that blood levels of felodipine were increased several fold more than in previous studies. This
increased blood level caused an increase in the effect and side effects of felodipine.
Further research revealed that the grapefruit juice itself was actually increasing the amount of the study drug in the body.

Research about the interaction of grapefruit juice with drugs suggests that compounds in grapefruit juice, called furanocoumarins (for example, bergamottin), may be responsible for the effects of grapefruit juice. Researchers believe that
furanocoumarins block the enzymes in the intestines that normally break down
many drugs. One glass of grapefruit juice could elicit the maximum blocking
effect, and the effect may persist for longer than 24 hours. Since the effects
can last for such a prolonged period of time, grapefruit juice does not have to
be taken at the same time as the medication in order for the interaction to occur.
Therefore, unlike similar interactions, where the interaction can be avoided by
separating the administration of the two interacting agents by a couple of
hours, administration of grapefruit juice with susceptible drugs should be
separated by 24 or more hours to avoid the interaction. Since this is not
practical for individuals who are taking a medication daily, they should not
consume grapefruit juice when taking medications that are affected by
grapefruit juice.

 

BH4: Future Treatment for ED?

02 Sunday Mar 2014

A few years old, but interesting, as there is now a BH4 product on the market (Kuvan)

Information on BH4 (also known as tetrahydrobiopterin): http://en.wikipedia.org/wiki/Tetrahydrobiopterin

Information on Kuvan:
http://www.bmrn.com/products/kuvan.php

Here is the link to the PubMed listing to the abstract below (you can also get this complete article for free). http://www.ncbi.nlm.nih.gov/pubmed/16491266

Asian J Androl.
2006 Mar;8(2):159-67.
Evaluation of
tetrahydrobiopterin (BH4) as a potential therapeutic agent to treat erectile
dysfunction.
Sommer F1, Klotz T,
Steinritz D, Bloch W.
Abstract
AIM: Nitric oxide
(NO)-mediated smooth muscle relaxation causes penile erections. The endothelial
NO synthase (eNOS) coenzyme tetrahydrobiopterin (BH4) converts eNOS-mediated
catalytic activity from oxygen radical to NO production, improving endothelial
function and vascular smooth muscle relaxation.
METHODS: Using
quantitative immunohistochemistry, 8-isoprostane and nitrotyrosine
concentrations were compared in cavernosal tissue from 17 potent and 7 impotent
men, and the effect of single oral doses of BH4 on penile rigidity and
tumescence was investigated. The pharmacodynamic effect of single oral doses of
BH4 on penile rigidity and tumescence was investigated in a randomized,
placebo-controlled, double-blind cross-over fashion in 18 patients with
erectile dysfunction (ED) while receiving visual sexual stimulation.
RESULTS: 8-Isoprostane
content in endothelium and smooth muscle was significantly higher in impotent
patient samples; the level of nitrotyrosine was unchanged in ED patients.
Relative to placebo, a single dose of 200 mg BH4 led to a mean increase in
duration of > 60% penile rigidity (33.5 min [95% confidence interval (CI):
13.1-49.3] at base and 29.4 min [95% CI: 8.9-42.2] at tip). A 500-mg dose
increased the relative duration of > 60% penile rigidity by 36.1 min (95%
CI: 16.3-51.8) at the base and 33.7 min (95% CI: 11.4-43.9) at the tip.
Treatments were well tolerated.
CONCLUSION: BH4
treatment is suggested to switch eNOS catalytic activity from super-oxide to NO
formation, leading to a reduced formation of free radical reaction product
8-isoprostane without alteration of nitrotyrosine. The observed results make
BH4 a suitable candidate as an ED treatment through reconstitution of altered
catalytic activity of the eNOS.

Kuvan is for treating PKU – the disease that makes NutraSweet (aspartame) dangerous. Do people with ED also have a problem with aspartame? Maybe there is a common link.

Juice Decreases Viagra 60%!

01 Saturday Mar 2014

You won’t hear about it (anywhere else but here), but I’m starting to uncover research that shows some things can lower Viagra levels. In this article from the European Journal of Clinical Pharmacology (at this PubMed link: www.ncbi.nlm.nih.gov/pubmed/19830413), it was reported that adults drinking pummelo juice (similar to grapefruit juice) had a 60% drop in Viagra availability. That’s a pretty significant drop!

I’ll research to see if there are other things, and also find out what pummelo juice is. I think it’s something they drink in the Middle East, because the study was done in Jordan.

Article citation and abstract:

Eur J Clin Pharmacol. 2010 Feb;66(2):159-63. doi: 10.1007/s00228-009-0738-0. Epub 2009 Oct 15.

The effects of pummelo juice on pharmacokinetics of sildenafil in healthy adult male Jordanian volunteers.

Al-Ghazawi MA, Tutunji MS, AbuRuz SM.

Abstract

PURPOSE:

The main purpose of this work was to investigate the effect of pummelo juice on the pharmacokinetics of sildenafil after oral administration.

METHODS:

This was a comparative, randomized, two-period, two-treatment, two-sequence, single dose, crossover study investigating the effect of pummelo juice on the pharmacokinetics of sildenafil citrate tablets (equivalent to 50 mg sildenafil) in healthy male participants under fasting conditions compared with water as a control. Six healthy normal adult males were administered 50 mg sildenafil with pummelo juice or water at two different periods in a crossover study.

RESULTS:

Study results showed that pummelo juice reduced the rate and extent of sildenafil bioavailability to around 60% [maximum plasma concentration (C(max)); from 212.44 ng/ml to 134.07 ng/ml, 90% confidence interval (90% CI) 44.70-89.11, and area under the plasma concentration time curve from zero to infinity (AUC(infinity)); from 564.51 ng.hr/ml to 336.87 ng.hr/ml, 90% CI 39.17-90.92]. This interaction was opposite to that expected and is speculated to be due to either an effect on transporters or a physicochemical interaction between sildenafil and some components of the juice.

CONCLUSION:

Patients should be advised not to drink pummelo juice before or immediately after taking sildenafil.

 

Nitroglycerin Dilates Blood Vessels…So, Does It Help Erections?

01 Saturday Mar 2014

I started researching this question and found an interesting first hand account by an adventurous fellow who ground up tablets of nitroglycerin and applied them to his penis with an ointment.

The result was that he absorbed the drug, and had relaxed blood vessels throughout his body. This was more bothersome than erotic, and he says the experiment was a failure.

Other studies — from the pre-Viagra period – explored the use of nitroglycerin for ED. Here are some:

1. J Urol. 1989 Mar;141(3):546-8. Topical nitroglycerin: a potential treatment for impotence.Owen JA1, Saunders F, Harris C, Fenemore J, Reid K, Surridge D,Condra M, Morales A.

 Abstract
The effect of 2 per cent nitroglycerin paste applied to the penile shaft of impotent subjects was evaluated in a placebo controlled double-blind study under laboratory conditions. After application of nitroglycerin paste or a placebo ointment base, penile tumescence was recorded through a strain gauge transducer while subjects viewed an erotic video presentation. Relative to the placebo paste the number of subjects demonstrating an increase in penile circumference after nitroglycerin (18 of 26) was significantly different than all other outcome possibilities (p less than 0.05). Noninvasive vascular assessment by ultrasonography demonstrated an increase in diameter and blood flow in the cavernous arteries after application of nitroglycerin paste. Nitroglycerin paste increases blood flow in the cavernous arteries and improves tumescence after erotic stimulation. This agent may represent a new therapy for impotence.

2. J Urol. 1991 Jul;146(1):50-3. Minoxidil versus nitroglycerin: a prospective double-blind controlled trial in transcutaneous erection facilitation for organic impotence. Cavallini G.

Abstract

A new type of topically applied drug (minoxidil) to facilitate erection is presented. Minoxidil acts directly on arterial smooth muscles via relaxation. This drug (1 ml. of a 2% solution) was studied under strict laboratory conditions in a double-blind controlled trial on 33 patients (4 with neurogenic plus arterial, 10 with neurogenic and 19 with arterial impotence) and compared to placebo and nitroglycerin (2.5 gm. of a 10% ointment). The application sites were the penile shaft (nitroglycerin) or glans penis (minoxidil and placebo). Increases in diameter and rigidity were measured with the RigiScan device and arterial flow was evaluated by conventional Doppler sonography. Side effects were considered as well. This drug proved to be more active than nitroglycerin and placebo in increasing diameter, rigidity and arterial flow of the penis. The highest activity proved to occur in neurogenically impotent patients. Fewer side effects also were found with minoxidil than with nitroglycerin. For these reasons minoxidil is proposed as a long-term therapeutic agent for organic impotence.

Events Needed for Erection

27 Thursday Feb 2014

Tags

Cialis, erections, l-arginine, sexual function

Sep. 26, 2012 — For two decades, scientists have known the biochemical factors that trigger penile erection, but not what’s needed to maintain one. Now an article by Johns Hopkins researchers, scheduled to be published this week by the Proceedings of the National Academy of Sciences (PNAS), uncovers the biochemical chain of events involved in that process. The information, they say, may lead to new therapies to help men who have erectile dysfunction.

“We’ve closed a gap in our knowledge,” says Arthur Burnett, M.D., professor of urology at Johns Hopkins Medicine and the senior author of the study article. “We knew that the release of the chemical nitric oxide, a neurotransmitter that is produced in nerve tissue, triggers an erection by relaxing muscles that allow blood to fill the penis. We thought that was just the initial stimulus. In our research, we wanted to understand what happens next to enable that erection to be maintained.”
In a study of mice, Burnett and his colleagues found a complex positive feedback loop in the penile nerves that triggers waves of nitric oxide to keep the penis erect. He says they now understand that the nerve impulses that originate from the brain and from physical stimulation are sustained by a cascade of chemicals that are generated during the erection following the initial release of nitric oxide. “The basic biology of erections at the rodent level is the same as in humans,” he says.
The key finding is that after the initial release of nitric oxide, a biochemical process called phosphorylation takes place to continue its release and sustain the erection.
In a landmark study published in the journal Science in 1992, Burnett and his Johns Hopkins co-author, Solomon S. Snyder, M.D., professor of neuroscience (who is also an author on the current study), showed for the first time that nitric oxide is produced in penile tissue. Their study demonstrated the key role of nitric oxide as a neurotransmitter responsible for triggering erections.
“Now, 20 years later, we know that nitric oxide is not just a blip here or there, but instead it initiates a cyclic system that continues to produce waves of the neurotransmitter from the penile nerves,” says Burnett.
With this basic biological information, it may be possible, according to Burnett, to develop new medical approaches to help men with erection problems caused by such factors as diabetes, vascular disease or nerve damage from surgical procedures. Such new approaches could be used to intervene earlier in the arousal process than current medicines approved to treat erectile dysfunction.
In particular, Burnett says, “The target for new therapies would be the protein kinase A (PKA) phosphorylation of neuronal nitric oxide synthase (nNOS). Now that we know the mechanism for causing the ‘activated’ form of nNOS in penile nerves, we can develop agents that exploit this mechanism to help with erection difficulties.”
One of the agents studied by the researchers was forskolin, an herbal compound that has been used to relax muscle and widen heart vessels. They found that forskolin also ramps up nerves and can help keep nitric oxide flowing to maintain an erection.
“It has been a 20-year journey to complete our understanding of this process,” says Snyder. “Now it may be possible to develop therapies to enhance or facilitate the process.”
The new study, “Cyclic AMP Dependent Phosphorylation of Neuronal Nitric Oxide Synthase Mediates Penile Erection,” was funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), under grant number RO1DK067223.
In addition to Burnett and Snyder, the study article’s authors are K. Joseph Hurt from the University of Colorado, Sena F. Sezen, Gwen F. Lagoda and Biljana Musicki from Johns Hopkins, and Gerald A. Rameau from Morgan State University

SOURCE: LINK HERE

Activation of Dopamine D4 Receptors: Another Type of ED Drug

25 Tuesday Feb 2014

There was some information about this new drug, from the pharmaceutical company Abbott, that showed some promise, but I haven’t heard anything recently. The drug, called ABT-724, is similar to the ED drup apomorphine, which is sold in Europe as Uprima. However, Uprima hits a lot of dopamine receptors, including those that control nausea, so its use is limited. ABT-724, however, targets only one type of dopamine receptor, D4, which is involved in erection. So…it looked promising. Anyone heard about it? Let me know.

Here’s an article on it (LINK HERE) from The Proceedings of the National Academy of Sciences USA. Here is an article from Nature about ABT-724 (LINK HERE).

Erections…From Magnets…(Why Not?)

24 Monday Feb 2014

Here is an interesting study (LINK HERE). They used magnetic stimulation to create erections in dogs. The erections would stop when the magnetic stimulation was removed, and could be restarted any number of times. As far as I know, this has never been attempted in humans.

The article doesn’t indicate if this approach would turn you into a “chick magnet”.

Dopamine and Erection

11 Tuesday Feb 2014

Which dopamine receptor is involved in erections? It seems that the D2 receptor is important. Apomorphine – a drug used in Europe – is a D1/D2 receptor agonist. (Agonists stimulate receptors, antagonists block them…)

This is important because if you can trigger a receptor, you can get the effect. Here is some research in this area (from PubMed)L

Behav Brain Res. 2012 May 1;230(2):355-64. doi:
10.1016/j.bbr.2012.02.033. Epub 2012 Feb 25.

Dopamine agonist-induced penile erection and yawning:
differential role of D₂-like receptor subtypes and correlation with nitric
oxide production in the paraventricular nucleus of the hypothalamus of male
rats. Sanna F, Succu S, Melis MR, Argiolas A.
Abstract
The dopamine D₃ preferring agonist pramipexole (50 ng) induced penile erection and yawning when injected into the paraventricular nucleus of the hypothalamus of male rats, like the mixed D₁/D₂-like agonist apomorphine (50 ng), while the D₄ agonist PD 168,077 (100 ng), induced penile erection only. These responses lasted for 45-60 min and occurred with an increase of NO₂- and NO₃- concentrations in the dialysate obtained from the paraventricular nucleus by intracerebral microdialysis. Pramipexole and apomorphine responses were reduced by the D₂ preferring antagonist L-741,626 (5 μg), but not by the D₃ preferring antagonist SB-277011A (10 μg), or the D₄ preferring antagonist L-745,870 (5 μg), injected into the PVN before the dopamine agonist. In contrast, PD 168,077 responses were reduced by L-745,870, but not by L-741,626 or SB 277011A. Pramipexole, apomorphine and PD 168,077 effects were also reduced by the nitric oxide synthase inhibitor S-methyl-L-thiocitrulline (20 μg) and the N-type voltage-dependent Ca²⁺ channels blocker ω-conotoxin (5 ng), given into the paraventricular nucleus, and by the oxytocin antagonist d(CH₂)₅Tyr(Me)²-Orn⁸-vasotocin (2 μg), given intracerebroventricularly but not into the paraventricular nucleus before dopamine agonists. These results suggest that stimulation of D₂, but not D₃ or D₄ receptors, by pramipexole or apomorphine increases Ca²⁺ influx in cell bodies of oxytocinergic neurons. This increases the production of nitric oxide, which activates oxytocinergic neurotransmission in extra-hypothalamic brain areas and spinal cord, leading to penile erection and yawning. However, the stimulation of D₄ receptors by PD 168,077 also increases Ca²⁺ influx/nitric oxide production leading to penile erection, but not yawning.

What About Other PDEs?

15 Wednesday Jan 2014

Interesting article on phosphodiesterase inhibitors, from The International Journal of PharmTech Research:

http://sphinxsai.com/ptvol4/pdf_vol4/pt=30%20(1148-1160).pdf

PHOSPHODIESTERASE INHIBITORS: THEIR ROLE AND IMPLICATIONS

such as cAMP and cGMP and thus have pivotal roles in cellular functions. PDE inhibitors such as theophylline have been employed as anti-asthmatics since decades and numerous novel selective PDE inhibitors are currently being investigated for the treatment of diseases such as Alzheimer’s disease, erectile dysfunction and many others. This review attempts to elucidate the pharmacology, applications and recent developments in research on PDE inhibitors as pharmacological agents.
Keywords: Phosphodiesterases, Phosphodiesterase inhibitors.

Impaza for ED

15 Wednesday Jan 2014

Here is a recently published study on Impaza:

Effects of chronic treatment with the eNOS stimulator Impaza on penis length and sexual behaviors in rats with a high baseline of sexual activity

Abstract

Endothelial nitric oxide synthase (eNOS) has an important role in erection, and it also affects aspects of sexual behavior. In this experiment, we determined whether a compound enhancing the activity of eNOS, Impaza, could stimulate any aspect of sexual behavior and increase penis length in rats with a high baseline of sexual activity. For comparison, the PDE5 inhibitor sildenafil was included. Male rats were orally treated with Impaza or sildenafil for 28 days. Impaza (3 ml kg−1) was given daily while sildenafil (3 mg kg−1) was given twice weekly. Tests for sexual incentive motivation and copulatory behavior were performed just before drug treatment and at days 7, 14 and 28 of treatment. In addition, the length of the protruding penis at mount, intromission and ejaculation was measured. Impaza but not sildenafil increased penis length at mount after 14 and 28 days of treatment. The compounds failed to modify sexual incentive motivation or copulatory behavior. It is suggested that Impaza enhanced intracavernous pressure, as such a pressure increase is the most likely explanation for enhanced penis length at mount. This effect, together with an absence of motivational actions, suggests that Impaza may be the most valuable treatment for erectile dysfunction.
Link to article:
http://www.nature.com/ijir/journal/v26/n1/full/ijir201312a.html

Angiotensin II – the Erection Blocker?

09 Thursday Jan 2014

In addition for combing the medical literature for overlooked techniques for SUPPORTING erections (eg, HGW, nitric oxide, oysters, etc), I am also checking things the BLOCK erections – with the idea that it may be possible to BLOCK the BLOCKERS.

Of course, you don’t want to do this TOO much, or you can cause priapism – an erection that won’t go away. This happens with some drugs and in some people who have sickle cell anemia. This is because it is actually the natural state of the penis to be erect, but various factors keep it flacid. Remove those factors, and the penis fills with blood and become erect until these factors return, and the penis become flacid once more.

So, what if these relaxing factors (actually, vasoconstricting factors, because they cause blood vessels in the penis to constrict) are a little too overacting with age? Would it be possible to block these erection blockers a bit, therefore supporting the natural erection process?

One candidate for this is angiotensin II, a common chemical in the body that increases with many conditions. I found an old article (1997) which says that angiotensin II supports contraction of tissue in the penis, and that this effect is blocked by an angiotensin II receptor blocker (often called an “ARB”). So, drugs (such as ARBs) and perhaps foods and herbs may be able to improve erections by reducing/blocking angiotensin II.

For more information on this article, from The International Journal of Impotence Research, CLICK HERE.

Reduce Refractory Period?

06 Friday Dec 2013

I’m looking into reducing the refractory period through prolactin manipulation.

Here is one study with some suggestions: (LINK)

J Endocrinol. 2003 Dec;179(3):357-65.

Effects of acute prolactin manipulation on sexual drive and function in males.

Krüger TH, et al. Source
Department of Medical Psychology, University of Essen, Hufelandstrasse 55, 45122 Essen, Germany. tillmann.krueger@web.de

Abstract

The neuroendocrine response to sexual activity in humans is characterized by a pronounced orgasm-dependent increase of plasma levels of prolactin. In contrast to the well-known inhibitory effects of chronic hyperprolactinemia on sexual drive and function, the impact of acute prolactin alterations on human sexual physiology is unknown. Therefore, this study was designed to investigate the effects of acute manipulation of plasma prolactin on sexual behavior. Ten healthy males participated in a single-blind, placebo-controlled, balanced cross-over design. Prolactin levels were pharmacologically increased to high levels (protirelin, 50 micro g i.v.) or reduced to low physiological concentrations (cabergoline, 0.5 mg p.o.). Sexual arousal and orgasm were then induced by an erotic film and masturbation. In addition to continuous neuroendocrine and cardiovascular recordings, the quality and intensity of the acute sexual drive, arousal, orgasm and refractory period were assessed by extensive psychometric measures. Administration of cabergoline decreased prolactin levels and significantly enhanced all parameters of sexual drive.

No Refractory Period

28 Thursday Nov 2013

Here is a report from Nature (LINK HERE) about a man with no refractory period, because he lacks the hormone prolactin:

 

Case Report
Absence of orgasm-induced prolactin secretion in
a healthy multi-orgasmic male subject
P Haake1, M S Exton1, J Haverkamp1, M
Krämer1, N Leygraf2, U Hartmann3, M
Schedlowski1 and T H C Krueger1
1Department of Medical
Psychology, University Clinic of Essen, Essen, Germany

2Department of Forensic
Psychiatry, University Clinic of Essen, Essen, Germany

3Department of Clinical
Psychiatry, Hannover Medical School, Hannover, Germany
Correspondence to: M S Exton, Department of Medical
Psychology, University Clinic of Essen, Hufelandstr. 55, 45122 Essen, Germany.
E-mail: michael.exton@uni-essen.de
Abstract
In several studies we have recently demonstrated that orgasm induces prolactin secretion in healthy males and females. This suggests that prolactin may form a feedback regulator of the refractory period following orgasm. To examine this position we investigated the prolactin response of a healthy multi-orgasmic male subject. Blood was drawn continuously during  masturbation-induced orgasm. The prolactin response of the case-subject was compared with that of nine healthy adult men with a normal refractory period. The case-subject showed no prolactin response to three orgasms. Data from this
multi-orgasmic subject support the hypothesized role of plasma prolactin in contributing to sexual-satiation mechanisms.

International Journal of Impotence Research (2002) 14, 133-135. DOI:10.1038/sj/ijir/3900823
Keywords
sexual arousal; prolactin; multi-orgasmic; model; refractory period;
neuroendocrinology
Introduction

Sexual dysfunction is a commonly reported side effect of psychiatric medication, underscoring the importance of neuroendocrine
mechanisms in regulating sexual competence.1,2 Thus, we recently designed a continuous blood sampling technique and sexual arousal paradigm to investigate endocrine mechanisms regulating sexual arousal. This series of studies demonstrated
substantial increases in plasma prolactin following orgasm in both men and women,3,4,5 but unaltered prolactin levels following sexual arousal without orgasm.6 Further, plasma prolactin concentrations were elevated for at least 60 min following orgasm. Due to the known impact of prolactin on sexual drive and function, these data suggest that prolactin may contribute to a feedback control of the refractory period following orgasm. To investigate this position, we examined the prolactin response to orgasm of a
healthy man who reported a short refractory period, thereby fulfilling the criteria for multi-orgasmic and multi-ejaculatory males.7

Methods
The case subject (aged 25 y) reported an average refractory period of 3 min, whereby erection remains following orgasm in approximately 50% of all episodes. Sexual appetence remains high following initial orgasm, with a second orgasm usually possible in the absence of strong sexual stimulation. Every orgasm is
followed by an ejaculation. The ability to reach at least two orgasms shortly after each other was noticed by the subject in adolescence. [I bet it was] The case subject was both psychologically and physically healthy, as confirmed by psychiatric and medical examination. TRH-test confirmed normal thyreotropic and lactotropic function.
Nine healthy male volunteers, aged 26±1 y were used
as a reference group. Participants reported a refractory period of at least 10 min, and as a group disclosed an average refractory period of 19±2 min. Erection is lost after orgasm in each participant. All subjects participated following written informed consent. The experimental session was conducted as described

previously.3,4,5,6 Briefly, whilst viewing a documentary film blood
was drawn continuously from participants and divided into 10 min intervals. The film switched to erotic scenes after 20 min and again after 60 min, with subjects required to masturbate until orgasm at these times.

Results

All control participants experienced orgasm following masturbation after 30 and 60 min. Consequently, increases of plasma
prolactin concentrations were observed in each control subject. Collectively, an increase in plasma prolactin concentrations were observed following the first orgasm, with further increases following the second orgasm (Figure 1). In contrast, the case subject experienced two orgasms at 30 min, separated by 2 min, and a further orgasm at 60 min. Additionally, unaltered sexual appetence following orgasm was accompanied by unchanged concentrations of plasma prolactin in the case subject.

Discussion

These data demonstrate a clear absence of the orgasm-induced prolactin surge in a healthy male exhibiting multiple orgasms and
short refractory period. This contrasted with control participants, who each displayed a regular refractory period and associated prolactin surge following orgasm. These data support the hypothesis that orgasm-induced prolactin secretion may be one mechanism regulating peripheral and central effectors of the refractory period.4,5,6,8 Indeed, the short refractory period of the case subject may result from a combination of both peripheral and central processes, as the absent prolactin surge is accompanied by both maintenance of erection and ejaculation capacity, as well as preservation of sexual desire. Hyperprolactinemia is associated with marked depression of libido and sexual function.1,2,9 Clearly, the changes in prolactin observed following orgasm are of lower magnitude and duration than those observed in hyperprolactinemia. Nevertheless, animal data suggest that acute low-level increases of peripheral prolactin are also capable of inhibiting sexual drive.10 Thus, the prolactin response to orgasm is one candidate as a peripheral regulator of the refractory period.

In summary, a male subject displaying low refractoriness following orgasm demonstrated a clear absence of the typical prolactin surge following orgasm. These data suggest that the prolactinergic response may be one potential focus for therapeutic approaches to dysfunctional sexual drive and function.

Other Pathways to Vasodilation

14 Wednesday Aug 2013

Erection is an event associated with vasodilation. Much of the focus has been on the nitric oxide pathway, in part because of the discovery that Viagra supports erections by blocking phosphodiesterase type 5 (PDE5), the enzyme that reverses the effects of nitric oxide in vasodilation.

But there is another pathway – the prostacyclin pathway. In this pathway, arachidonic acid is broken down into prostaglandin I2 (prostacyclin), which then has vasodilatory and antiproliferation properties.
This is another avenue of research, especially for amateurs like me, because of the many herbs that work on this pathway. More on this approach in the near future, when I have time.
Some information on this pathway:
http://www.nutriguard.com/NADPHox-ED.pdfA useful inhibitor that might help with this pathway is APOCYNIN, similar to vanilla.

Described here: http://en.wikipedia.org/wiki/Apocynin

Hydrogen for ED?

28 Thursday Feb 2013

Here’s another line of research for treating ED – hydrogen-rich saline (HRS). This study from China found that HRS helps fight ED in the diabetic rat model.

J Urol. 2012 Dec 4. pii: S0022-5347(12)05812-0. doi: 10.1016/j.juro.2012.12.001. [Epub ahead of print] Protective Effects of Hydrogen-rich Saline against Erectile Dysfunction in a Streptozotocin-Induced Diabetic Rat Model.

Source: Department of Urology, the Third Affiliated Hospital of Soochow University, Changzhou 213000, Jiangsu Province, China.

OBJECTIVE:

Hydrogen has anti-oxidative-stress and anti-inflammatory effects. In the present study, we investigated the effect of hydrogen on erectile dysfunction (ED) in streptozotocin (STZ)-induced diabetic rats. Rats with diabetes mellitus (DM) in the hydrogen-rich saline (HRS) group were fed saturated hydrogen saline by intragastric administration (5 ml/kg/d) for 8 weeks (n = 8).

MATERIALS AND METHODS:

Diabetes was induced in Sprague–Dawley rats by a single intravenous injection of STZ. The diabetic rats were then randomized into a DM group and a DM hydrogen saline group; the latter were fed saturated hydrogen saline by intragastric administration (5 ml/kg/d) for 8 weeks (n = 8). At the end of week 8, erectile function was assessed by measuring the rise in intracavernous pressure (ICP) following cavernous nerve electrostimulation. Nitric oxide synthase (NOS) activity, malondialdehyde (MDA) content, 8-hydroxydeoxyguanosine (8-OhdG), and nitrite and nitrate (NOx) levels were measured in corpus cavernosum tissues. Immunolocalization of the endothelial NO synthase (eNOS) protein in corpus cavernosum tissues was detected using immunohistochemistry. Protein expression of eNOS, Bcl-2, and Bax was determined by Western blotting. eNOS, Bcl-2, and Bax mRNA levels were determined using real-time reverse transcription polymerase chain reaction methods.

RESULTS:

Oxidative stress is involved in the pathophysiological mechanism of ED. Maximum ICP in diabetic rats decreased significantly compared to that in controls. Maximum ICP increased significantly compared to that in untreated diabetic rats after treatment with HRS. Decreased levels of NOS activity, NOx and eNOS expression, as well as elevated levels of 8-OhdG and MDA were found in the DM group compared with those in the control group. HRS treatment improved NOS activity and MDA, NOx, and 8-OHdG levels in the corpus cavernosum of diabetic rats. Decreased eNOS expression in diabetic rats was ameliorated by HRS treatment. In addition, apoptosis in the diabetic rat corpus cavernosum was enhanced significantly compared with that in the control group. HRS therapy may reduce apoptosis in corpus cavernosum tissues. Furthermore, HRS ameliorated ED in diabetic rats by inhibiting oxidative stress and apoptosis.

CONCLUSIONS:

HRS treatment effectively improved erectile function in a STZ-induced diabetic rat ED model.

So How Does Viagra Actually Work?

26 Wednesday Dec 2012

Some new data suggests that Viagra (sildenafil) may have other mechanisms that support sexual function, such as an effect on dopamine levels in the brain.

Here is an interesting article (study) on this: LINK HERE from the Journal of Sexual Medicine. Here is the abstract:
J Sex Med. 2012 Nov 15. doi: 10.1111/j.1743-6109.2012.03000.x.

Experimental Evidence for Sildenafil’s Action in the Central Nervous System:
Dopamine and Serotonin Changes in the Medial Preoptic Area and Nucleus Accumbens During Sexual Arousal.

Kyratsas C, Dalla C, Anderzhanova E, Polissidis A, Kokras N, Konstantinides K, Papadopoulou-Daifoti Z.

Source

Department of Pharmacology, Medical School, University of Athens, Athens,
Greece First Department of Psychiatry, Eginition Hospital, Medical School,
University of Athens, Athens, Greece Andrology Institute of Athens, Athens,
Greece.

Abstract

Introduction.  Sildenafil is the first effective oral treatment for male
erectile dysfunction. Although it is generally accepted that its action is
peripheral, it has been suggested that it influences central neural pathways
that are involved in male sexual arousal. Recently, it was shown that local
sildenafil administration enhances extracellular dopamine (DA) in the nucleus
accumbens (NAcc). Aim.  The aim of this study was to determine whether
sildenafil administration alters dopaminergic and serotonergic activity in the
NAcc and the medial preoptic area (mPOA) during a model of sexual arousal.
Methods.  An acute (2 days) or chronic (21 days) sildenafil regimen (1 mg/kg)
was administered intraperitoneally to male rats. Thirty minutes after the last
sildenafil injection, all males were exposed to noncontact erection sessions by
the presentation of inaccessible estrous females. Half of the males had previous
experience of noncontact sexual encounter and the other half were exposed for
the first time. Main Outcome Measures.  Tissue levels of DA and its metabolites,
3,4-Dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), as well as
serotonin (5-HT) and its metabolite 5-HIAA, were measured in the mPOA and NAcc
with high-performance liquid chromatography with electrochemical detector.
Dopamine ([DOPAC+HVA]/DA) and serotonin (5-HIAA/5-HT) turnovers were also
calculated as indices of neurotransmission. Results.  In nontrained males, acute
and chronic sildenafil treatment increased DA and 5-HT turnover rates in the
mPOA and NAcc. In trained rats, acute sildenafil also increased DA and 5-HT
turnover rates in both structures, whereas chronic treatment enhanced 5-HT
turnover rate only in the mPOA and DA turnover rate only in the NAcc.
Conclusions.  Our data confirm that sildenafil enhances dopaminergic activity in
the NAcc, extend these findings to the mPOA and furthermore, reveal
sildenafil-induced effects on serotonergic activity in these brain regions as
well. Therefore, present findings support an effect of sildenafil on central
neural pathways that are involved in the control of sexual arousal.

Another Potential ED Drug

05 Wednesday Dec 2012

Here is another future ED drug in development – TMEM16A. But, of course no one is willing to put any money into researching this, so don’t expect anything to be developed soon. Oh well. Article here: (LINK)

Int J Impot Res. 2012 Nov;24(6):211-6. doi: 10.1038/ijir.2012.22. Epub 2012 Jun 21.

Calcium-activated chloride channels in the corpus cavernosum: recent developments and future of a key cellular component of the erectile process.

Linton DJ, Lau LC, Adaikan PG. Department of Anaesthiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada.

Abstract

Calcium-activated chloride channels (CaCCs) are one of five families of chloride channels, ubiquitously expressed, and essential for a host of biological actions. CaCCs have key roles in processes as diverse as olfactory transduction and epithelial secretion, and also CaCCs are essential in smooth muscle contraction. The corpus cavernosum is a vascular smooth muscle that must relax to facilitate erections. Parasympathetic activation produces relaxation of the corpus cavernosum through a nitric oxide-dependent pathway, and sympathetic stimulation in both preventing and terminating erections by contracting the corpus cavernosum. Both these pathways affect activity of CaCCs. The past 5 years produced many successes in CaCC research. One key area of success was the identification of the elusive ‘molecular candidate’ of CaCCs, as the TMEM16A protein (dubbed anoctamin-1) and potentially other members of the anoctamin family of transmembrane proteins. However, enthusiasm has been somewhat tempered because of evidence that this family of proteins may not be responsible for calcium-activated chloride currents in certain epithelial tissues. Several studies identified specific inhibitors of CaCCs as well as specific inhibitors for anoctamin-1. Despite the number of recent achievements in this field there are many details that still need to be elucidated. Of particular value would be more details on the identity of the CaCCs in corpus cavernosum smooth muscle, using new inhibitors to gain insight into the signalling pathway, and the evaluation of whether inhibition of CaCCs provides any specific benefit in different models of ED.

Combination Therapy: Viagra + MUSE

09 Sunday Sep 2012

This is an old study, but that is because MUSE got crushed when Viagra came out and the company that makes it gave up on it. But it is a good product.

Please note these doses described below are high and we do not recommend them. Discuss the use of all medications with your physician before trying them. We are not doctors.

By the way, I predict that this is the future of ED treatments – combination therapy. Multiple mechanisms of action.

AUA MEETING: Viagra And Muse More Effective When Combined In Some Patients 

DALLAS, TX — May 4, 1999 — Researchers from the world-renowned Mayo Clinic presented results from the first-ever combination study of erectile dysfunction treatments — Janssen-Ortho Inc.’s Muse(R) (alprostadil) and Pfizer Canada Inc.’s Viagra(TM) (sildenafil citrate) — at the 94th annual meeting of the American Urological Association in Dallas today.
Patients who had been unable to achieve an erection sufficient for intercourse when treated with either drug individually were given a combination of the treatments that resulted in erections sufficient for intercourse for all patients. The results were based on patient questionnaires.
“Though this is a small study group, these results are very promising, especially for patients in a similar situation where they may not have had hope for using effective, non-invasive treatment options,” said Dr. Ajay Nehra, consultant, department of urology at the Mayo Clinic and lead investigator of the study.
Of the 16 patients enrolled in the open-label study 11 had suffered from erectile dysfunction as a result of a radical prostatectomy (surgery for prostate cancer) and five had a diagnosis of organic erectile dysfunction.
“By and large, this is the most difficult patient study group because of the extent of nerve damage, yet we were still able to generate a successful response which is very encouraging, because it means that future studies can examine combination therapy in a wider variety of patients,” Dr. Nehra said.
To enter the study, patients had to have failed an initial trial of either 100mg of Viagra and/or 1,000 micrograms of Muse. This is the highest dose for each drug. Combination therapy was initiated using 100mg of Viagra 60 minutes prior to intercourse and a lower dose of Muse consisting of 500 micrograms immediately before intercourse.
“All patients were able to generate tumescence [some rigidity] before combination therapy on both drugs,” Dr. Nehra said. “However, this tumescence was not sufficient for penetration.”
According to Dr. Nehra, the rationale for choosing to combine the treatments was straight forward. “First of all, none of these patients were interested in intracavernosal injection therapy,” Dr. Nehra explained. “In addition, we know that Muse has worked well in some patients who have had a radical prostatectomy and that Viagra is less efficacious in this subset of patients.
“Since the two drugs work through different pathways, it made sense to try them together.”
In addition to being administered differently, Muse and Viagra also have different mechanisms of action. Muse contains alprostadil, a synthetic version of prostaglandin E(1) which directly causes vasodilation of blood vessels and smooth muscle relaxation through a chemical messenger called cyclic AMP (cAMP), leading to an erection. Patients do not need to have intact nerve pathways from the brain in order for Muse to work.
This differs from Viagra which works by breaking down a chemical messenger called cyclic GMP (cGMP), a compound that causes smooth muscle relaxation. Cyclic GMP is made available through the release of the neurotransmitter nitric oxide, which only works if the neuropathways from the brain are intact and if they receive some sort of sexual stimulus to do so. As such, men must have some erectile function in order for Viagra to work.
“The failure of MUSE may be due to high doses of PGE(1) which can cause contraction of the smooth muscle [instead of relaxation] by interacting with other receptors,” he said. “The failure of Viagra may be due to the nerve damage in patients. However, since they act by two different pathways, together they provide enough relaxation for an erection.”
For Dr. Nehra, he plans to continue recruitment for the study. “Given the success rate at the six month duration, our plans are to expand this study to men with diverse causes of erectile dysfunction.”

Here is a link to the source: LINK

Beta Blocker Helps Viagra

22 Sunday Jul 2012

When I say Viagra, I mean the drug class, of course.

If you use one beta blocker, it helps Viagra; another, it hurts.

So, which one do you use?

This article suggests you use nebivolol.

Here a link to the article: CLICK HERE

When I find something like this, I ask: Is there an herb that does the same thing?

As always, talk to your physician before doing anything. I am not a doctor, just a reporter of information.

Here is the abstract:

INTRODUCTION:

Traditional beta-blockers have sometimes been associated with erectile dysfunction (ED). Nebivolol is a cardioselective β(1)-adrenoceptor antagonist that promotes vasodilation through a nitric oxide (NO)-dependent mechanism.

AIM:

We evaluated the effects of nebivolol on the NO/cyclic guanosine monophosphate (cGMP) signaling pathway, on erectile function and dysfunction, and in human penile vascular tissues.

METHODS:

Erectile response to cavernosal nerve electrical stimulation in control and diabetes-induced ED rats were evaluated, along with serum nitrite/nitrate (NOx) concentration and plasma/tissue cGMP levels. Endothelium-dependent and sildenafil-induced relaxation of isolated human corpus cavernosum (HCC) and human penile resistance arteries (HPRA) were also determined.

MAIN OUTCOME MEASURES:

The effects of nebivolol on erectile function and dysfunction and on NO/cGMP-mediated responses.

RESULTS:

Treatment with nebivolol significantly potentiated erectile response in control rats, regardless of its effects on blood pressure. Nebivolol increased NOx and plasma cGMP by 3-fold and 2.75-fold, respectively, and significantly augmented the elevation of plasma cGMP produced by sildenafil. Nebivolol enhanced endothelium-dependent and sildenafil-induced relaxations of HCC tissue, and produced endothelium-dependent vasodilation of HPRA. Nebivolol, but not atenolol, significantly improved erectile response in diabetic rats (51.6%, 53.2%, and 87.1% of response at 3 Hz in nondiabetic rats, for vehicle-treated, atenolol-treated, and nebivolol-treated diabetic rats, respectively); after sildenafil administration, ED was completely reversed in nebivolol-treated diabetic rats (69.6% and 112% for diabetic rats treated with sildenafil and nebivolol plus sildenafil, respectively). Accordingly, nebivolol restored systemic NOx levels and cGMP content in penile tissue from these animals.

CONCLUSIONS:

Nebivolol in vivo activated the NO/cGMP pathway, enhanced erectile response and reversed ED in diabetic rats. Moreover, nebivolol in vitro potentiated NO/cGMP-mediated relaxation of human erectile tissues. These effects may account for the low incidence of ED in nebivolol-treated hypertensive patients. Nebivolol therefore may have utility in the treatment of ED, particularly ED associated with diabetes.

Exercise Reduces ED.

20 Friday Apr 2012

Here is a recent study with rats that shows the benefits of exercise for ED: (LINK HERE)

Summary Erectile dysfunction (ED) is a major public health problem that seriously affects the quality of life of patients and their partners and its prevalence increases significantly with ageing. In this study, we tested the hypothesis that age-associated decrease in penile endothelial (eNOS) and neuronal nitric oxide synthase (nNOS) activity in aged rats may be increased by regular exercise. A total of 28 young (4 m) and aged (24 m) male rats were divided into four equal groups: group 1 – young control; group 2 – young trained; group 3 – old control and group 4 – old trained group. Groups 2 and 4 rats were trained to swim for 30 min a day and 5 days a week, which lasted 8 weeks. At the end of 8 weeks, rats were sacrificed and penile tissues evaluated for eNOS and nNOS activities. eNOS and nNOS activities were evaluated by immunohistochemistry in paraffinized penile tissues and results assessed semiquantitatively. Results also were compared with healthy age-matched and adult (4 m) controls. Serum level of testosterone (T) was determined using ELISA kits (Beckman Coulter, Fullerton, CA, USA). In penile tissues of aged control rats, eNOS and nNOS staining were weakly positive; however in trained groups, eNOS and nNOS immunoreactivity were increased. In young control group, eNOS and nNOS activities were more intense than aged control. eNOS and nNOS activities were higher in adult trained group than control. Serum T concentrations were significantly higher in young and aged trained group than in control groups. We can suggest that regular exercise upregulates eNOS and nNOS expressions in the aged and young rat penis. Regular exercise may improve penile erection by increasing penile neurotransmitter in both young and aged rats.

More on “Breaks”: Things That Prevent Erections

14 Wednesday Mar 2012

A prime candidate for the “villian” causing men to have weaker erections as they age is endothelin-1. As noted in the wikipedia description of this compound (LINK), which increases with age:

In a healthy individual, a delicate balance between vasoconstriction and vasodilation is maintained by endothelin and other vasoconstrictors on the one hand and nitric oxide, prostacyclin and other vasodilators on the other. Overproduction of endothelin in the lungs may cause pulmonary hypertension, which can sometimes be treated by the use of an endothelin receptor antagonist, such as bosentan, sitaxentan or ambrisentan. The latter drug selectively blocks endothelin A receptors, decreasing the vasoconstrictive actions and allowing for increased beneficial effects of endothelin B stimulation, such as nitric oxide production. The precise effects of endothelin B receptor activation depends on the type of cells involved.

Hmmm. The quote refers to pulmonary hypertension but I believe the same applies to erectile dysfunction. “Endothelin receptor antagonist”…I like the sound of that.

Musings on MUSE (Aprostadil)

10 Saturday Mar 2012

I have good things to say about MUSE (alprostadil), which is a small, waxy pellet that you insert into your urethra. It is not pleasant poking a small plastic tube into the opening of your penis, but once you get used to this you may find this is a pretty interesting product. My insurance company pays for it and it is pretty cheap (although pharmacies don’t have it in stock – they have to order it).

I started with 125 mcg – the smallest dose – and then went up to 250 mcg. A “mcg” is a microgram – one thousandth of a gram – so 250 mcg is .25 grams. Sounds like a small amount but that means it is very potent. You can go up to 1000 mcg (1 gram), if necessary.

Alprostadil is a chemical that is apparently the same as prostaglandin E1. This is a chemical in your body that causes the blood vessels in your penis to expand. This is important because:

  • In the flacid (non-erect) state, the penis is blocked from being erect because chemicals in the penis keep tiny muscles on blood vessels contracted (small), so that the blood vessels do not fill up with blood.
  • When a man is sexually stimulated, his brain triggers his penis to release chemicals the remove this block, so that the tiny mucles relax, the blood vessels expand, and blood fills the blood vessels; this causes an erection. After sex, the blocking chemicals come back and the blood vessels constrict (contract) again, and the erection ceases.
  • While there are many other factors involved (and some are not even fully understood), two well known systems involved in the blood-vessel relaxation are the nitric oxide system and the prostaglandin system.
  • Nitric oxide, a gas, is released during arousal, which causes cGMP to make blood vessels relax and fill with blood. Viagra, Cialis, and Levitra work by blocking an enzyme, PDE5, that reduces cGMP levels. Viagra was originally studied for patients with heart disease, because they have problems with their blood vessels. But many patients reported that the drug increased erections, so Viagra was discovered somewhat by accident.
  • The other system the increases blood vessel relaxation uses prostaglandin E1. By inserting MUSE into your urethra, you are causes the blood vessels to relax and blood to fill the penis using this second system.

The interesting thing about MUSE is that it is the only product I have found that actually CAUSES an erection, unlike Viagra, which only SUPPORT an erection following sexual stimulation. Another good thing about MUSE is that it can be used WITH Viagra, because they use different mechanisms. In the future, some sort of combination product will no doubt be available, using multiple systems.
The only question I have about MUSE is if there is a long-term benefit from using it. There is some research that suggests that taking Viagra every night will help your penis. This is because you should have several erections at night (nocturnal tumescence), which increase blood flow to the penis at night and presumably are healthy. So, taking Viagra at night will support this process and help your penis health. Is the same thing true for MUSE? Will taking MUSE every night result in more blood flow to the penis, and support improved penis health (or at least prevent penis health decline?) Or will it somehow use up chemicals in the penis, actually causes a decline in sexual function? As far as I know, there is no research on this question.

But Honey…I Just Want You to Be Happy!

05 Monday Mar 2012

Tags

antidepressant, Condoms

Important research all men should know about! Women who do not use condoms are happier than women who do, because semen appears to be a natural antidepressant, according to published research.

Here’s some links about this research: CLICK HERE and CLICK HERE Here is the original study: CLICK HERE.

Epimedium – Icariin – Horny Goat Weed…

03 Saturday Mar 2012

It goes by many names – Epimedium brevicornum (the plant), icariin (the active chemical), Horny Goat Weed (the commercially available product). I have purchased this from Physicians Formulas and found that it is like a weak Viagra. Of course, with herbs, you never know what you are getting – there is no FDA regulation or quality standards with herbal products – but there is definitely a weak effect.

Now there is a study from the Department of Pharmacological Sciences, University of Milan, which says that altering icariin, the active chemical in Epimedium, can produce a chemical that is as active as Viagra. Here is the link to the recently published study: (CLICK HERE).
One of the authors on the study also showed, in another study, that red wine and the extracts from grape skin inhibit PDE5, the same enzyme that Viagra inhibits. For study: (CLICK HERE).Please note: I have found a recent study that shows that combining HGW with Viagra (and presumably other PDE5Is) is not a good idea, and that HGW can reduce levels of Viagra by up to 60%! See my post on this.

Here is a link to that study:
http://www.mdpi.com/1420-3049/18/6/7323

ED and Asthma: Is There a Connection?

14 Thursday Apr 2011

Tags

arginine, erectile dysfunction, supplement

I’ve been reading some interesting research on asthma (which I developed after a cold last year) and it’s relationship to L-arginine. Reading about it, I noticed that this problem seems to involve the same players at erectile dysfunction – L-arginine, nitric oxide, and others.

So, while we usually look at ED as a vascular disease, perhaps it is a disease associated with an imbalance in the L-arginine-nitric oxide system.

In one study, high doses of L-arginine reduced asthma systems, presumably by restoring the balance to this system and increasing nitric oxide production.

So, I’m wondering if I take high levels of L-arginine (available in any pharmacy or vitamin shop), whether that will help my asthma and my ED. I believe I’ve seen studies that give up to 30 g (grams) of L-arginine per day. However, I can’t recommend that as safe. Talk to your doctor or do more research before taking a high dose (above 1-2 g).

Anyway, here is a link to a study in mice that found benefits with high doses of arginine:

CLICK HERE FOR STUDY.

Here’s a Treatment You Can Do Yourself: SOD

30 Wednesday Mar 2011

An interesting study showed that taking SOD — superoxide dismutase — an enzyme that clears up free radicals that can contribute to erectile dysfunction — has some benefit (at least in rats).

Read it here: LINK to article.

The good thing about SOD is that you can buy it at a health food store. The bad news is that SOD breaks down in your digestive tract; so you have to buy a version that is absorbed without being digested. They have these at health food stores. This is one of the supplements I take every night, by the way.

Here’s the experiment I would like: take all of these supplements, and try them one at a time with rats. For example, which would be better – arginine, Viagra, SOD, etc etc.

Fish Oil for ED?

29 Tuesday Mar 2011

OK, here’s a new line of reasoning:

1. Erectile dysfunction results from problems in blood vessels – they don’t dilate (relax) the way they are supposed to, so they don’t hold the blood in them to stay rigid.

2. What helps blood vessels relax is potassium ion (K+) channels in blood vessels.

3. Something that improves K+ channels may help blood vessels to support erections.

So far, simple enough. So, it turns out that DHA- – an omega-3 fatty acid found in seafood and fish oil supplements — improves K+ channels in a dose-dependent manner (at least in rat tissue). Dose-dependent means that the more DHA you use, the more effect you have.

Now, whether this means that fish oil with DHA will help erectile dysfunction is something I will have to research. If there is a benefit, the question is what dose should be taken? One person I know who takes fish oil (for something other than ED) takes about 5 times the normal dose. However, fish oil seems to be a very healthy product, so there is certainly no problem with taking it. My other suggestion is that you take it in the morning, as it may make it hard to sleep at night, because it can give you a caffeine-like buzz.

Anyway, here is a link to an article about this (LINK HERE). I’ll see what else I can find!

Exciting Research With BH4

20 Sunday Mar 2011

Imagine Viagra with a boost – that is what you may get in the future with chemical called tetrahydrobiopterin (BH4). This is the chemical in your body that helps nitric oxide relax blood vessels (a process that is supported by Viagra and similar drugs).

This line of research opens up a whole new field for treating ED, and is very promising. I’ve found one study (see THIS LINK for the PubMed citation) in which BH4 was studied in a small group of patients with good results, as reported in The Asian Journal of Andrology.

It is possible that BH4 deficiencies are what is causing ED in the first place. Lower levels of BH4 are seen in such conditions as diabetes, which is also associated with ED and other vascular (blood vessel) disorders.

Here’s Something you Can Try: L-Citrulline

20 Thursday Jan 2011

Erections need nitric oxide, which comes from L-arginine – so taking L-arginine should boost nitric oxide levels and improve erections, right? Except it doesn’t usually work.

Part of the reason is that some of the arginine may be sent on another pathway. So, what’s the alternative?

There is L-citrulline. I always thought L-citrulline was downstream of arginine, but the study below suggests it may be better than arginine. I guess you have to read the article to find out why.

This is -as far as I know – a pretty safe (non-toxic) product that is easily available (my ideal criteria), so it is something you can try. The study below says that it can help. Presumably, it would be a good product to add on to Viagra.

Here is the abstract of the study (you can send the author an email asking for a copy of the article for free):

Cormio L, et al. Oral L-citrulline supplementation improves erection hardness in men with mild erectile dysfunction. Urology. 2011 Jan;77(1):119-22.

Department of Urology and Renal Transplantation, University of Foggia, Foggia, Italy. luigicormio@libero.it

Abstract
OBJECTIVES: To test the efficacy and safety of oral L-citrulline supplementation in improving erection hardness in patients with mild erectile dysfunction (ED). L-arginine supplementation improves nitric oxide-mediated vasodilation and endothelial function; however, oral administration has been hampered by extensive presystemic metabolism. In contrast, L-citrulline escapes presystemic metabolism and is converted to L-arginine, thus setting the rationale for oral L-citrulline supplementation as a donor for the L-arginine/nitric oxide pathway of penile erection.

METHODS: In the present single-blind study, men with mild ED (erection hardness score of 3) received a placebo for 1 month and L-citrulline, 1.5 g/d, for another month. The erection hardness score, number of intercourses per month, treatment satisfaction, and adverse events were recorded.

RESULTS: A total of 24 patients, mean age 56.5 ± 9.8 years, were entered and concluded the study without adverse events. The improvement in the erection hardness score from 3 (mild ED) to 4 (normal erectile function) occurred in 2 (8.3%) of the 24 men when taking placebo and 12 (50%) of the 24 men when taking L-citrulline (P < .01). The mean number of intercourses per month increased from 1.37 ± 0.93 at baseline to 1.53 ± 1.00 at the end of the placebo phase (P = .57) and 2.3 ± 1.37 at the end of the treatment phase (P < .01). All patients reporting an erection hardness score improvement from 3 to 4 reported being very satisfied. CONCLUSIONS: Although less effective than phosphodiesterase type-5 enzyme inhibitors, at least in the short term, L-citrulline supplementation has been proved to be safe and psychologically well accepted by patients. Its role as an alternative treatment for mild to moderate ED, particularly in patients with a psychologically fear of phosphodiesterase type-5 enzyme inhibitors, deserves further research.

Minoxidil for Erections?

19 Wednesday Jan 2011

Someone in 1994 took out a patent on the use of minoxidil for causing erections. Here’s the LINK. The person taking out the patent claims that it is effective as a topic medicine (on the skin). I don’t recommend trying this, but it would be interesting if it works, because this is an easily available product.

This might work because minoxidil raises nitric oxide levels.

Once again – information only available on my site!

 

Study Shows Some Effect From Maca

18 Tuesday Jan 2011

This study (LINK HERE) reports that an easy-to-get herb, Maca (Lepidium meyenii), has some mild benefit in humans. Men with ED received 2400 mg of Maca or placebo. The investigators reported that “a small but significant effect of Maca supplementation on subjective perception of general and sexual well-being in adult patients with mild ED.”

 

It’s nice to report on actual data.

 

My personal (subjective) experience with Maca is that it has some effect on mood; I feel the world looks a little better when I take Maca regularly. I don’t know if this translates into any sexual benefits.
For more information on this and other herbs, please send $5 to my Paypal account (menznews@yahoo.com) and I will send you my e-book on Men’s Sexual Health.

New Research Update

25 Saturday Dec 2010

For those of you who follow ongoing research in the ED field, here is a good article about some new drugs in development, from Advances in Pharmacological Sciences: LINK HERE for free article.

It includes updated information on such new treatments as sGC stimulators/activators, Rho-kinase inhibitors, and sodium nitrite.

Aspirin: Friend or Foe?

25 Saturday Dec 2010

Does aspirin cause erectile dysfunction – or reduce it? If you follow this blog, you will see that I have gone back and forth on this question, as I’ve read many different view points. Now I’ve found some evidence that suggests that it does both. Let me explain.

Short term, aspirin has effects – like raising nitric oxide levels – that should help men have better erections. However, long-term, it can reduce levels of chemicals in your body, such as prostanoids, so that could make it harder to have an erection.

So, if you take aspirin every day, and you suspect that it may be associated with a worsening of your erectile dysfunction, you may be right. I assume this concern is widespread, as this is the most searched for question that brings men to my site.
Take a look at this article: LINK HERE. It suggests that aspirin may also increase arthritis – again, long-term. Interesting stuff.
As usual, we are all pretty much on our own when it comes to understanding what we need for our bodies. Many doctors do not read original research – only the guidelines that experts panels conclude based on their interpretation of the research. So, you may be right if you suspect aspirin is a problem. Talk to your doctor before doing anything, but you may be able to find healthier alternatives.

Updates on Avanafil – New ED Drug in Development

25 Saturday Dec 2010

VIVUS, the company that is testing the new ED compound avanafil, annouced that they have had some good results in a recent phase III study. Up to 80% of men with ED had a good response, some within 15 minutes after taking avanafil.

 

The drug is similar to Viagra (sildenafil) but acts faster. Hopefully it will be priced lower.
For more information on this recent study, go to this LINK.

New Company Studying Treatment for ED

19 Sunday Dec 2010

It’s funny how once I start one line of research, I find a lot of promising information. I have been looking at arginine for ED. This lead to the question of what happens when we inhibit the enzyme that breaks down arginine – arginase.

Now I find that a company is developing drugs that block arginase. The company is Arginetix Inc, and it is attempting to develop arginase inhibitors for the treatment of pulmonary arterial hypertension (PAH) and erectile dysfunction (ED). They are also exploring the treatment of asthma and atherosclerosis.

A study published in The American Journal of Physiology – Heart and Circulatory Physiology demonstrated that, in a mouse model of ED, treatment with an arginase inhibitor restored the intracavernosal pressure (a measure of erection health) of aged mice to the level of young mice without affecting young mice.

While other companies have worked on arginine as a target, no other group is focusing on arginase. Inhibiting the enzyme increases production of nitric oxide, which is critical for cell signaling, and reduces the production of reactive oxygen, which can damage cells.

For more information, here is a press release from Argenitex: CLICK HERE.

Here is an article about inhibiting arginase: CLICK HERE.

If you want to create your own arginase inhibitor in your laboratory, here’s how: CLICK HERE.

On wikipedia, they have this to say about arginase:

Arginase II is coexpressed with nitric oxide (NO) synthase in smooth muscle tissue, such as the muscle in the genitals of both men and women. The contraction and relaxation of these muscles has been attributed to NO synthase, which causes rapid relaxation of smooth muscle tissue and facilitates engorgement of tissue necessary for normal sexual response. However, since NO synthase and arginase compete for the same substrate (L-arginine), over-expressed arginase can affect NO synthase activity and NO-dependent smooth muscle relaxation by depleting the substrate pool of L-arginine that would otherwise be available to NO synthase. In contrast, inhibiting arginase with ABH or other boronic acid inhibitors will maintain normal cellular levels of arginine, thus allowing for normal muscle relaxation and sexual response.[6] Recent studies have implicated arginase as a controlling factor in both male erectile function and female sexual arousal, and is therefore a potential target for treatment of sexual dysfunction in both sexes. Additionally, supplementing the diet with additional L-arginine will decrease the amount of competition between arginase and NO synthase by providing extra substrate for each enzyme.[7]

Some Things That Raise Nitric Oxide

14 Tuesday Dec 2010

You may have heard that Viagra works by raising levels of nitric oxide, which helps erections. But there are other ways of raising nitric oxide levels. Here are some ways to raise nitric oxide levels, which will presumably help your blood vessels and improve erections:

  • Take a sauna. Several articles (THIS LINK) show that saunas can raise nitric oxide levels. A hot bath may do the same thing. I found that taking a bath every day helped me after 1 week!
  • Get acupuncture, which some authors suggest raises nitric oxide levels in areas near to where acupuncture needles are used (LINK HERE). My guess is that massage would have the same effect.
  • Take fish oil (omega 3) (LINK HERE).
  • Drink green tea (LINK HERE)
  • Take vitamin C

A lot of this research was done in people or animals with blood vessel problems due to conditions such as obesity, high blood pressure, or diabetes. What is interesting is that a lot of tradition approaches – such as saunas – seem to have a scientific reason for improving health. As with all advice on this site, talk to your doctor before you try anything.

Aspirin: It May Be Good for Blood Vessels

13 Monday Dec 2010

I have covered the pros and cons of aspirin use. Is it good for erections, or bad? This is an important topic, because it is a very commonly used drug.

I found a recent study that suggests that aspirin is a good product for erections. I say this based on the finding of the study — done with pig blood vessels — which showed that aspirin (used at doses equivalent to what people use therapeutically) increased levels of nitric oxide in the endothelium — the tiny muscles that make blood vessels expand (vasodilate) and get smaller (vasoconstrict).

The authors of the report, Dr. D. Taubert and colleagues (from Halle, Germany) suggest that aspirin stimulates release of nitric oxide from the endothelium by increasing its formation.

Of course, one study in pig blood vessels doesn’t prove anything, but it does suggest that aspirin may not be harmful to sexual health.

To read the study yourself, go here for a free copy (pdf) of the article: CLICK HERE

HDL-Cholesterol and Sexual Health

13 Monday Dec 2010

The first thing you realize when you study sexual health and erectile dysfunction is that a lot is simply not known. So, a person who want to have a healthy sex life into his 50s, 60s, and beyond needs to do a lot of research on his own. That’s why I started this blog (because no one else is running a web site with the type of information I want to read on this subject!)

Here’s another interesting piece of the puzzle: the relationship between low HDL-cholesterol (the so-called “good” cholesterol) and erection problems. Apparently, men with high HDL-cholesterol levels (greater than 60 mg/dL) have a much lower rate of sexual problems than those with HDL-cholesterol less than 30 mg/dL).

It also appears that HDL-cholesterol helps increase levels of nitric oxide, the gas that helps blood vessels relax (so you have have an erection).

So how can you raise HDL-cholesterol levels (which will, supposedly, increase sexual health)? Here are some ways:

  • Exercise (especially intense exercise)
  • Quite smoking
  • Eat more soluble fiber
  • Switch to the Mediterranean diet and eat lots of olive oil
  • Cut back on sugar
  • Loose weight

You know you should be doing these things anyway. But now you can do it for better sexual health!

If you want to read some medical articles about this topic, click on the links below:

From Circulation Research.

From Journal of Biological Chemistry. (use this link for a free pdf)

From Trends in Cardiovascular Medicine.

Simple Idea: Take a Sauna for Sexual Health!

28 Friday May 2010

Here’s an idea for improved sexual health: Take a sauna! I’ve found an article that describes how “sauna therapy” — that is, regularly taking a sauna — raises levels of a chemical in the body called BH4 (tetrahydrobiopterin), which is a key factor in the release of nitric oxide from arginine.

So, if you want healthier blood vessels (and healthier erections) — take a sauna regularly!

Link to this article: CLICK HERE.

For more information on BH4 and blood vessels, read this: CLICK HERE.

Possible Bad News for Pot Smokers

16 Sunday May 2010

If you are a “habitual” smoker of cannabis (pot), then you should consider the fact that you may be damaging your blood vessels (and thus causing erectile dysfunction). I had addressed the question of whether long-term use of marijuana causes a decrease in testosterone; this is a different issue.

The authors also say that habitual smoking of cannabis can also cause problems with insulin (insulin resistance).

Here’s the link to a summary of the article – you decide for yourself. (CLICK HERE).

Emerging Drugs for Erectile Dysfunction

08 Saturday May 2010

In a recent article in Expert Opinion on Emerging Drugs — not a top-tier journal, but presumably reputable — the authors (from the University of San Francisco, Department of Urology) describe emerging research on new drugs to support penile erection. They describe drugs that work through two pathways: both centrally (clavulanic acid, dopamine and melanocortin receptor agonists) and peripherally (novel PDE5I, soluble and particulate guanylil cyclase activators, rho-kinase inhibitors and maxi-K channel openers).

The melanocortin receptor agonists include bremelanotide, the drug formerly known as PT-141, which was in the news but never made it through clinical development, because of FDA concerns about side effects. Perhaps this drug is back in play.

In case you are interested, “centrally” refers to the central nervous system (the brain and spinal cord), while “peripherally” refers to the peripheral nervous system (all nerves that are not the brain and spine). So, the centrally acting drugs work on the brain, and the peripherally acting drugs work at the local level, usually in the penis (like Viagra does).

Because there are two different for these two types of drugs, future therapy may involve using both pathways in combination.

The article is not available for free but you can try sending the author a request for a free reprint, as I have done. If I get it, I’ll see if I can post it.

Anyway, here is the link to the abstract: CLICK HERE.

Pycnogenol – Any Good?

17 Wednesday Mar 2010

I am always ragging on herb/supplement companies that don’t do any research…so I have to report on a study that was actually done, with the supplement Prelox. You can read about it at THIS LINK, in an article that seems actually legitimate. The supplement has two ingredients – pycnogenol and arginine. I’ve been looking at pycnogenol for a while, but have seen some mixed data. This study says that the combination of these two substances helps men.

Now, you can buy these two ingredients separately, get higher doses, and save a lot of money. Worth a try? I don’t know. But the article appeared in International Journal of Impotence Research, which is presumably a decent journal.

UPDATE: I have been trying pycnogenol (50 mg, 3x day), with L-arginine, and I feel it has some slight benefit. This is subjective, of course, but it reminds me of the feeling I get from taking Horney Goat Weed – a sexual buzz. I have added it to my daily supplement list.

New Research: AGE Inhibitors

02 Tuesday Mar 2010

It’s been found that some of the problems associated with erectile dysfunction may be caused by things called advanced glycosylated endproducts (or AGEs). Now, research into drugs that block AGES – AGE inhibitors – are showing promise. For more information on these, check out this article: CLICK HERE.

Chinese Herb “Cnidium”. Any Good?

16 Tuesday Feb 2010

According to an article on the Internet, a good herb for men — which raises nitric oxide levels, important for healthy sexual behavior — is Cnidium. But I’d like to know what the medical literature says before I spend my hard-earned cash for this unknown herb.

So, I check www.PubMed – the National Library of Medicine – and search for Cnidium. There are a few studies – mostly from China, where they study herbs – which suggest benefits from cnidium.

Here is an abstract from one:

PURPOSE: We investigated the cavernosal relaxant effect of osthole, a coumarin isolated from Cnidium monnier (L.) Cusson which has been long used in China as a herbal medicine to improve male sexual dysfunction. MATERIALS AND METHODS: Strips of rabbit corpus cavernosum were precontracted with phenylephrine. Corporal relaxation evoked by osthole was then determined in the absence and presence of nitric oxide synthase inhibitor (L-NAME), soluble guanylate cyclase inhibitor (ODQ), cyclooxygenase inhibitor (indomethacin), tetradotoxin, and after endothelium deprivation. RESULTS: Corpus cavernosal strips showed relaxation in response to osthole (0.1 approximately 30 microM) in a dose-dependent manner. These effects were reduced partially but significantly by pretreatment with L-NAME, ODQ and by endothelial disruption. However, they were not affected by indomethacin and tetradotoxin treatment. Osthole pretreatment (from 1 to 30 microM) enhanced the sodium nitroprusside (0.3 microM)-induced relaxation of corpus cavernosum in a dose-dependent manner to a maximum of 3 times the pretreatment level at 30 microM osthole. However, this effect was abolished in the presence of zaprinast. Additionally, a higher concentration of osthole (30 microM) also enhanced forskolin-induced relaxation. CONCLUSION: The data suggested that osthole possesses a relaxant effect on rabbit corpus cavernosal tissues which is attributable to the release of NO from sinusoidal endothelium and to the potentiation of the cGMP and/or cAMP signal mediating relaxation of cavernosal smooth muscle by inhibiting phosphodiesterase.

Source (click on this link): J Urol. 2000 Jun;163(6):1975-80.

New Research on Sialorphin

26 Tuesday Jan 2010

I just stumbled on some research that is worth investigating. There is a chemical called sialorphin that appears to play an important role in sexual behavior. The research below is especially interesting because it was conducted on aging rats.

More about sialophin at these links:

http://www.sciencedaily.com/releases/2009/09/090918181456.htm

http://www3.interscience.wiley.com/cgi-bin/fulltext/118508324/PDFSTART

ROCK Star – Y-27632

13 Friday Nov 2009

Tags

erectile dysfunction

The chemical Rho-associated protein kinase (ROCK) helps keep blood vessels in your penis contracted, so that they don’t fill up with blood — until you get an erection. Blocking this enzyme, such as with the experimental drug Y-27632, should presumably help erections.

It appears to do this using non-nitric oxide pathways. This is significant because it suggests an approach for treating ED in patients who do not respond to Viagra. However, its effect on other blood vessels in your body (your heart, your eyes, your brain, etc) is not known at this point. However, if it can be used safely, it may someday be used in combination therapy with Viagra. To use a car analogy, it will be like hitting the gas (Viagra, which increases blood vessel relaxation) AND taking your foot off the breaks (because ROCK inhibitors will reduce contraction of blood vessels).

For information on Y-27632, go to THIS LINK.

Here is another article about inhibition of ROCK: THIS LINK.

Fighting ED at the Atomic Level…

25 Sunday Oct 2009

If you want to know what happens with a successful ED drug at the most basic level – the atomic level – it seems that drugs like Viagra and herbs like Horny Goat Weed cause small muscles in blood vessels to relax by opening potassium ion (K+) channels.

So can K+ channel drugs help fight ED? One such drug is called NS11021. By the way, it’s full chemical name is: (1-(3,5-Bis-trifluoromethyl-phenyl)-3-[4-bromo-2-(1H-tetrazol-5-yl)-phenyl]-thiourea). Scientists is Denmark reported in a recent issue of the British Journal of Pharmacology (LINK HERE) that NS11021 was as effective as sildenafil (Viagra) at causing rat erections.

One good thing about this type of research is that it may lead to combination therapy – where you can take two or three drugs that work at different sites to support erections. My prediction is that the future of ED treatment will consist of combination drugs. You can actually do this today if you combine Viagra with MUSE (alprostradil).

Combination herbs, on the other hand, are generally not tested. Most are probably a waste of money.

Yohimbine + Viagra = Good for Your Rat’s Sex Life

28 Monday Sep 2009

Here is some recent research that shows combining yohimbine with sildenafil (Viagra) produces a better effect than taking Viagra alone.

Here is the study: CLICK HERE.

A few comments are in order here. First of all, we are talking about the DRUG yohimbine – which can only be obtained with a prescription in the United States (I don’t know about other countries). So, we are not talking about the HERB yohimbe – this is a pure drug version.

Second, my experiences with yohimbe (the herb) have been very bad. I had all sorts of unpleasant side effects, including a racing heart, agitation, and insomnia. So, I am not suggesting that anyone try yohimbe. However, this study (in rat tissue) suggests that the effect of Viagra may be improved by adding the pharmaceutical drug yohimbine. Worth a try, because these two drugs have different mechanisms of action, so using them together may be complimentary.

Choline – For Erections

25 Friday Sep 2009

The latest supplement I’ve tried is choline, an “organic compound” usually grouped as a B vitamin. Increasing choline use should increase levels of acetylcholine, a neurotransmitter involved in erections.

I have been starting with small doses (500 mg, 2x daily) but I feel like it may have some benefit, when I take it with pycnogenol, folic acid, vitamin C, and other supplements.

Here’s some links about using choline and the role of acetylcholine in erection: LINK, LINK, and LINK.

David Carradine and Autoerotic Asphyxiation

06 Saturday Jun 2009

Just a quick comment about David Carridine and autoerotic asphyxiation (AEA) — readers of my blog will recall that new evidence suggests that carbon dioxide and carbon monoxide are similar to nitric oxide in that they can cause vasodilation, needed for an erection. For people who practice AEA, it seems reasonable to assume that they are increasing levels of these gases, which increases erections and perhaps pleasure. This may be especially true as they get older, when nitric oxide systems decline.

This is a very sad story (I was a big fan of his work, especially in Kill Bill) but the lesson I get from this is that we need more research on sexual health. The more I research this topic (and it’s been over 3 years of intense review of the literature), the more I am surprised how little research is being done in this field. But then I am always surprised how little medical research is being done AT ALL, considering that health/life is the most important thing we have. Apparently, we have more important things to do with our money than save our own lives.
 
Well, I will continue to review the literature and make connections that no one else seems to be making, as one of the few objective sexual health websites that is not sponsored by anyone and not beholden to anyone but you, the reader. After all, mine is the ONLY WEB SITE that can explain WHY autoerotic asphyxiation may actually work on a scientific level. No other site uses science to explore human sexuality the way I do.
 
That reminds me — please buy a copy of my e-book, which goes into more depth on these issues. All I ask is a contribution of $1 or more to my Paypal account (menznews@yahoo.com) . One reader sent me $100. I don’t expect that from everyone but it was very thoughtful, and I am still amazed by his generosity!

From Swingin’ Saudi Arabia – A New Sex Herb.

02 Tuesday Jun 2009

The Saudis, apparently, like to research herbs as alternatives to Viagra. Here is an abstract describing their experience with extracts from the plant Casimiroa edulis (I never heard of it, either). But if you are ever in Saudi Arabia, maybe you can score some. Let me know how it goes.

Here’s the link: (LINK HERE).

There is also information on IslamOnline.net (LINK HERE) about ED. They recommend various herbs, including Horny Goat Weed.

Please support my research, and send $1 to my Paypal account (menznews@yahoo.com).

Alfuzosin: Another Strategy for ED?

11 Monday May 2009

A recent study – not yet published (only “epublished” in the British Journal of Urology International) describes a possible CAUSE of ED called partial bladder outlet obstruction (PBOO). I believe that this is an enlarged prostate. It apparently causes a reduction in erections (in lab rats) because it lowers levels of nitric oxide synthase, the enzyme that helps release nitric oxide, which supports erections by causing blood vessels to dilate (expand) so they can fill with blood.

I have often felt there was a link between BPH and ED; this suggest that is true.

Anyway, when the investigators gave rats with PBOO the alpha-adrenoreceptor antagonist alfuzosin, the erections improved and blood flowed better. The investigators concluded that combining an alpha-adrenorecptor antagonist with a PDE5 inhibitor (ie, Viagra, Cialis) could provide better treatment than a PDE5 inhibitor alone.

There are some alpha-adrenorecptor antagonist herbs that are available, such as yohimbe (this is an alpha-2 blocker, while alfuzosin is an alpha-1 blocker; not that different, as I understand it). Although I don’t recommend yohimbe, another mechanism always offers amateur sleuths like me (and perhaps you) new options to explore.

Here’s a link to the study: (CLICK HERE)

(I just checked and alfuzosin is a drug marketed for BPH [benign prostatic hypertrophy – an enlarged prostate]. In the US, it is sold as Uroxatral and elsewhere under the tradename Xatral. Alfuzosin was approved by the FDA for treatment of BPH in June 2003. )

So, Uroxatral would have 2 benefits: it would shrink the prostate, removing the problem caused by PBOO, and it might have a direct effect on receptors, helping erections. Might be worth asking your doctor about this!

Forget Nitric Oxide – Hello Carbon Monoxide!

12 Thursday Feb 2009

The more you dig into the science of ED, the crazier things get. Now, they are saying that carbon monoxide (CO – a carbon atom and an oxygen atom) is involved in erections.

You probably have heard about the role of nitric oxide…it causes blood vessels to dilate, so they can fill with blood during an erection. Viagra works using this system. But now researchers are finding out that carbon monoxide may do the same thing. This opens up a lot of interesting possibilities, which I will be exploring in the next few weeks. However, please note that CO is also poisonous, so don’t try using it as an aphrodisiac!

Why am I the only web site that finds out this stuff?

Anyway, here is an article on Pubmed on this topic, if you want to explore further: (CLICK HERE).

Don’t forget to send me an e-mail (menznews@yahoo.com) so I can send you my free e-book on men’s sexual health. And please send $1 (or more) to my Paypal account, which is the same as my e-mail (menznews@yahoo.com) so that I can continue this research!

Is Atherosclerosis the Link Between Sleep Apnea and ED?

02 Monday Feb 2009

An interesting study suggests that the reason men with sleep apnea may have a higher rate of ED is that they have atherosclerosis – sometimes called “hardening of the arteries” – a condition in which plaque forms on the arteries. What is fascinating about this study is that they demonstrated the treatment for sleep apnea – called CPAP (continuous positive airway pressure) actually can REDUCE atherosclerosis in men with sleep apnea.
Whether this is true for men with ED was not tested, but it may explain why some studies have shown that CPAP can reduce ED in men with sleep apnea.

Here is a link to the study: LINK HERE

Another New Drug: MT-II

02 Monday Feb 2009

Tags

erectile dysfunction

Another drug being developed, which is similar to bremelanotide (PT-141), is melanotan-II (MT-II). It works by a different mechanism than Viagra/Cialis/Levitra. Here are some reports on MT-II:

First article: by Francois Guiliano, a major researcher: (LINK HERE) [Note: For some reason, the author retracted this article…not sure why.]

Second article: Also by Dr. Guiliano; you can download a pdf of the article, which is from Journal of Andrology (2004): (LINK HERE) It is pretty complicated and not for the non-medical person, but it suggests this class of drugs will be useful in the future.

Third article: This study goes back to 2000. There are some side effects with MT-II (eg, severe nausea), which may be why they haven’t developed it. (LINK HERE)

Anti-Hypertensive Medication and Erections

10 Saturday Jan 2009

Here’s a statement on the use of ARBs (angiotensin-receptor blockers) and their effect on erections:

From: CLICK FOR LINK

Recent drugs known as angiotensin-receptor blockers (ARBs), also known as angiotensin II receptor antagonists are being used to lower blood pressure in men with hypertension. In one study after 12 weeks of treatment with an ARB called losartan (Cozaar), 88% of hypertensive males with sexual dysfunction
reported improvement in at least one area of sexuality. The number of men reporting impotence declined from 75.3% to 11.8%. Other ARBs include candesartan (Atacand), telmisartan (Micardis), and valsartan (Diovan).

Traditional African Herbs

01 Thursday Jan 2009

Microdesmis keayana, an African plant used for ED by traditional medicine providers, has been shown to be associated with factors that raise nitric oxide levels (the same pathway that Viagra uses). Is it any good – or even available? I don’t know – first I’ve heard of it. For the study, CLICK HERE. Here’s another Africa herb that seems to relax blood vessels. CLICK HERE.

Another Traditional Aphrodisiac: Montanoa tomentosa

01 Saturday Nov 2008

I’ve been hearing a bit about this herb – Montanoa tomentosa – which is from Mexico. I can’t tell you if it is any good but here is an article about it from a peer-reviewed journal (CLICK HERE). The investigators say that it appears to be helpful for making rats frisky.

Topigland: Another Erectile Dysfuntion Product in Development

09 Friday May 2008

Tags

erectile dysfunction

Using the same drug found in MUSE, this is a gel you rub on: Topigland. It is currently being developed by MacroChem. Not sure what stage of development.

What Causes ED?

06 Tuesday May 2008

While I have found some approaches that help reduce ED, there is another question that I am researching – what causes ED? I am coming to the conclusion that it has something to do with the same nitric oxide system that is involved in erection, the system that is supported by Viagra.

This is a very important question, because while Viagra and other approaches may reverse the damage, they don’t stop the process from moving forward. This process, I am increasingly convinced, has to do with nitric oxide by-products, such as highly reactive peroxinitrate, that are produced as a result of a disorder in the nitric oxide system.

If so, the “treatment” of ED would involve two steps: reversing the effects of damage to blood vessels, with drugs such as Viagra, so that you can have sex; then, blocking further damage to your system, by using agents that reduce the amount of peroxinitrite in your system. Such agents exist, which I will describe in future posts.

This is all, of course, theoretical, and no one is really looking at this question, as far as I can tell. If there is someone, then please let me know! I am familiar with a Dr. Pall, who is investigating this question, but in terms of chronic diseases, such as fibromyalgia. I have also seen this system associated with various types of cardiovascular disease.

For information on Dr. Pall’s theories, CLICK HERE.

Update From the Sexual Medicine Society

15 Sunday Oct 2006

Tags

blog, blood vessels, Cialis, erectile dysfunction, future, sexual function

Sexual function is still only partially understood; but there is a lot of progress in the research of this subject. An update on recent research is found on the Sexual Medicine Society web site (LINK HERE). There is an interesting study that shows the benefits of combining Viagra with the new drug PT-141, which is sprayed in the nose. Taken together, they are very effective therapy and may be beneficial for people who do not respond to Viagra alone.

I discussed PT-141 in an early post – it looks very promising for men AND women. Here is a link (LINK HERE) with more information on PT-141, also called bremelanotide.

What Causes ED? Low Testosterone?

14 Saturday Oct 2006

Tags

ED, erectile dysfunction, Testosterone

A recent study (2003) found that men with testosterone levels in the low-normal range who do not respond to Viagra have a good response when they take Viagra combined with testosterone-raising treatments.

This would suggest that the slow but steady decline in testosterone in men contributes to the decrease in sexual function, and that drugs and herbs that increase testosterone should be taken with Viagra for optimal sexual funtion.

Here is the link to the study – (LINK HERE). In case the link doesn’t work for you, here is the study information: Aversa A, Isidori AM, Spera G, Lenzi A, Fabbri A. Androgens improve cavernous vasodilation and response to sildenafil in patients with erectile dysfunction. Clin Endocrinol (Oxf). 2003 May;58(5):632-8.

This graph shows the decline in testosterone with age:

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