Maybe this will have you performing like you did 20-30 years ago…
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Take more of this vital nutrient for stronger “rockiness”
Most people probably consider “rockiness” problems to be a natural consequence of age.
But recently, science has shown that erections problems can be at least delayed with proper dietary habits and supplements.
The main reason for erections issues could be the declining DHEA levels that occur with aging (Nawata, 2002).
This seems plausible considering that androgens are derived from DHEA…
Yet there is also reason to believe that other nutritional factors are involved in “rockiness” problems.
For instance, magnesium is absolutely essential for vasodilation (widening the blood vessels).
And magnesium has recently been shown to correlate with erections (Toprak, 2017).
This connection is intuitive anyway, because the arteries supplying the penis and cavernosal muscle must relax (not contract) for a boner to occur (Andersson, 1995).
Magnesium relaxes smooth muscles and is a fundamental vasodilator.
This notion has even more support when you consider that diabetes is a strong predictor of erections problems (Malavige, 2009).
And that diabetics on average also have low intakes of magnesium (Larsson, 2017), low plasma magnesium (Wälti, 2003), and low intracellular magnesium (Resnick, 2003).
These findings make sense in light of the role that magnesium plays in glucose metabolism (Kandeel, 1996).
Another dietary risk factor for erections problems is low vitamin C.
And that is part of the reason why smoking is associated with erections problems (McVary, 2001).
Free radicals in smoke destroy vitamin C – and it’s consistently found lower in smokers (Smith, 1987).
Deficiency of vitamin C has been shown to cause both erectile and endothelial dysfunction, two conditions that are reversible by its supplementation (Heitzer, 1996).
Vitamin C works to improve vasodilation by regenerating tetrahydrobiopterin (Patel, 2002).
An essential cofactor for NOS (nitric oxide synthase), tetrahydrobiopterin (BH4 or THB) is also involved in the synthesis of neurotransmitters, including dopamine.
Although it’s generally best to avoid high levels of nitric oxide (NO), we do need some to control blood flow.
But vitamin C can only increase nitric oxide up to a point anyway, so there’s no worry that vitamin C is going to raise NO too high.
Pathologically high amounts of NO are instead found to occur either from treatments or from an immune response that upregulates inducible‑NOS (inducible nitric oxide synthase).
Inducible‑NOS is a different enzyme from endothelial NOS (e-NOS) and neuronal NOS (n-NOS), the isoforms needed for vascular control and penile function.
Because magnesium causes vasodilation through an entirely different mechanism, it could perhaps lower the amount of NO needed for vascular response.
So, fortunately, we’re now aware of three natural and safe supplements that can reliably improve “rockiness” problems – DHEA, magnesium, vitamin C.
And recently, a fourth supplement that can improve “rockiness” has been discovered…
As of only six years ago, folate (vitamin B9) has recently been shown to do just that:
The impetus of this study was the prior clinical reports of folate improving endothelial dysfunction, a condition often found alongside “rockiness” problems.
They had also come across an epidemiological study linking ED with homocysteine (Demir, 2006), a dangerous metabolite that’s safely lowered by folate and vitamin B12.
Homocysteine is much more dangerous than methionine because it can form a stable free radical and cause lipid peroxidation (Selley, 2002).
So, folate’s has a role in lowering homocysteine and it has proven utility in treating vascular disease…
So it was only a matter of time before someone decided to examine the link between folate and “rockiness”.
Chinese Doctors Yan, Yu, Yin, Zou, and Yang recruited 133 patients for this pioneering study.
The subjects were then subdivided into four groups, assayed for serum folate, and given questionnaires to fill out.
They found a significant association between serum folate and penile function.
The “rockiness” problems-only group had a 38% lower concentration of folate than the control subjects:
The group with both “rockiness” problems and premature ejaculation together – a rather unfortunate combination – had 28% lower serum folate levels than controls.
When the two “rockiness” problem groups are combined (for greater statistical power), they had 34% less serum folate than controls.
This finding was significant…
But since it’s comparing only 67 “rockiness” problem subjects with 30 controls, it may come off as tentative to some people.
However, before you discount this association as being speculative, have a look at this Turkish study published just one year later:
These researchers had come across the Chinese study on the folate-rockiness link and decided to confirm or deny the association.
They recruited 40 controls and 120 men with “rockiness” issues, making this study a bit larger than the previous one.
The “rockiness” problem group was further subdivided into three by severity, thereby forming a total of four groups each comprised of 40 men.
The results turned out to be nearly identical to the Chinese study…
The group with severe “rockiness” issues had 33% less serum folate and the group with moderate “rockiness” problems had 34% less:
In this study, folate was more predictive than smoking, age, or testosterone, which (surprisingly) weren’t related to penile dysfunction at all.
- The moderate-rockiness problem group had the highest testosterone
- The severe-rockiness problem group smoked the least
- And the severe-rockiness problem group were also the youngest on average
So the folate-rockiness link is getting stronger by the year, with each study.
If we combine the two studies, the same result emerges – but with more statistical power:
Severe to moderate “rockiness” problems are associated with 34% lower serum folate levels compared to controls.
Here is yet another study, an Italian study – published two years after the first:
This study included only one “rockiness” problem group and one control group, each consisting of 31 men.
Although this study had fewer participants than the others, it did measure homocysteine in addition to folate.
This parameter is useful as it helps to pinpoint the mechanism behind the effect of folate.
Again, we get essentially the same result – 35% lower serum folate in the “rockiness” problems group:
They also reported that homocysteine was higher in the “rockiness” problems group, just as you’d expect with lower folate.
But folate had a stronger correlation with erectile function than with homocysteine, perhaps implying a different mechanism behind folate’s effect.
This is supported by the observation that folate has been shown to increase blood flow within a couple of hours, long before significant reductions of homocysteine have time to occur (Doshi, 2002).
This was verified years later when infused folate relaxed blood vessels within 60 to 90 minutes, an effect shown to be the result of increased nitric oxide (Stanhewicz, 2015).
For reasons such as this, folate is now seen as acting mainly by enhancing tetrahydrobiopterin (BH4) levels – not by lowering homocysteine.
“The present study adds further weight to the notion that the salutary effects of folate on vascular function are not mediated solely through changes in plasma homocysteine levels.” (Antoniades, 2006)
The evidence for this is now strong enough that all previous associations between homocysteine and vascular disease could actually be reinterpreted as actually being caused by low folate.
To put it another way, homocysteine may be a risk factor for endothelial dysfunction because endothelial dysfunction is caused by low folate – the actual cause.
But not because of any inherent activity in itself.
Perhaps the study that really sheds light on this is the one shown below.
This is also the study that happens to be the first reporting increased THB with folate supplementation:
This study tested relaxations induced by 5-methyltetrahydrofolate (5−MTHF) – the most biologically active form of folic acid – on veins removed from 117 patients.
When I speak of “folic acid” in this newsletter, I am speaking of this type of folate, NOT the folic acid “fortified” in foods, which may be harmful.
So back to this study…
Some of the patients had also been given folate by I.V. beforehand.
(This wasn’t much of an inconvenience since all of them were undergoing bypass surgery anyway.)
And the results showed that 5−MTHF is capable of causing relaxation – induced by both acetylcholine (a neurotransmitter) and bradykinin (a peptide that causes blood vessels to dilate) – in a dose-dependent fashion after 45 minutes.
Increased relaxation was also observed in the I.V. folate group, even without adding any more folate after the veins were removed.
Relaxations induced by acetylcholine were increased twofold compared with placebo (43.2% vs. 19.4%).
Yet the responses to sodium nitroprusside (SNP) were identical.
SNP is a nitric oxide-releasing agent, so this result indicates that folate was acting through nitric oxide.
The notion that this might be the mechanism was given additional support by corresponding increased levels of THB, the cofactor for e-NOS.
This was found to be increased three-fold in the saphenous vein and two-and-a-half-fold in the mammary artery, thus leaving little reason to look further for the explanation.
So, in this order, folate increases:
(1) Tetrahydrobiopterin (BH4)
(2) Nitric oxide
But how does it do it?
Many mechanisms have been proposed in an attempt to explain just this.
But perhaps the most realistic is its ability to upregulate dihydrofolate reductase (DHFR) (Gao, 2009).
DHFR is an important enzyme because it can create tetrahydrobiopterin (BH4) from inactive dihydrobiopterin (BH2).
BH4 is a very sensitive molecule. It is easily destroyed by peroxynitrite, a common oxidant found within cells.
It also has a delicate role within the e-NOS enzyme, which means that a stray electron at the wrong time can convert it into an inactive form.
For this reason, enzymes have evolved to regenerate dihydrobiopterin (BH2) back into active tetrahydrobiopterin (BH4).
This is accomplished primarily by the enzymes dihydrobiopterin (BH2) reductase, sepiapterin reductase (SPR), and dihydrofolate reductase (DHFR).
“It is, therefore, likely that net tetrahydrobiopterin (BH4) bioavailability within the endothelium reflects the balance between…BH4 synthesis, loss of BH4 by oxidation to BH2, and the regeneration of BH4 by DHFR.” (Crabtree, 2009)
The ability of DHFR to regenerate both folate and BH4 had been demonstrated forty years ago (Matthews, 1980).
Scientists are certainly not surprised by this today.
And they were not back then either, because it’s readily believable after noting their similarities:
The same core ring structure (pterin) is common to both molecules.
The only difference is that the shorter propylene glycol “tail” of biopterin is replaced by the longer p −aminobenzoyl glutamate tail characteristic of folate.
On account of this similarity, folate had even been proposed as a cofactor for e-NOS, interchangeable with tetrahydrobiopterin.
Later, it was shown to bind to the enzyme’s (e-NOS) active catalytic domain:
“We demonstrate that 5-methyltetrahydrofolate (5−MTHF) binds the active site of nitric oxide synthase and mimics the orientation of tetrahydrobiopterin.” (Hyndman, 2001)
Yet binding doesn’t necessarily translate into activity, with folate being shown later to have zero effect on biopterin‑free e-NOS (Stroes, 2000).
Folate doesn’t appear to increase tetrahydrobiopterin synthesis either, as total biopterin levels remain unchanged by folate administration during the time needed for it to take effect.
The only real change during this time is the tetrahydrobiopterin to dihydrobiopterin (BH4 to BH2) ratio (Chalupsky, 2015).
This observation is best explained by an upregulated dihydrofolate reductase (DHFR).
Twice, this upregulation by folate has been shown to occur – first by Ling Gao and then again by Mark Crabtree.
And the idea that it would occur seems obvious.
This enzyme (DHFR) is the only thing capable of converting folic acid into tetrahydrofolate (THFA) – the only active form of folate.
So it’s absolutely required for folate to have any effect at all.
Folate is a trace vitamin – the small amounts we ingest need to be constantly regenerated.
The idea that folic acid could control enzyme expression is strengthened by the finding that folate receptor-alpha (FRα) has recently been shown to do just that.
Within minutes after folic acid incubation, FRα has been observed to travel to the nucleus and induce gene transcription (Boshnjaku, 2014).
This was an important finding because, prior to this study, FRα had been known simply as a membrane transporter incapable of doing anything else.
“The results of FRα immunoblots using mouse monoclonal antibody on nuclear extracts showed that FRα translocates to the nucleus within 15 minutes of folic acid incubation.” (Boshnjaku, 2014)
They also characterized the folate receptor’s response element, which is the specific sequence of DNA the receptor binds to.
Because the dihydrofolate reductase (DHFR) gene has multiple FRα response elements, its upregulation by folic acid can be understood.
So the results, when taken together, indicate that folic acid binds to FRα to induce transcription of DHFR.
Again, DHFR is an enzyme that regenerates the tetrahydrobiopterin (BH4 ) needed for nitric oxide synthesis.
Folic acid has also been shown to reverse “rockiness” problems.
Folic acid in combination with tadalafil (Cialis, etc) increased IIEF-5 (International Index of Erectile Function) scores from 11.65 to 16.80 (Hamidi, 2013), a 44% increase in erectile function .
Scores in the tadalafil-only group only increased by 13%…
So you can be sure that folic acid was mostly responsible. Again, realize this is folate, not the typical folic acid from added to “fortified” foods, which may actually be harmful.
Folate is also safe, affordable, and necessary for other things anyhow.
Folate and vitamin B12 work together to lower homocysteine and to synthesize acetylcholine, melatonin, and epinephrine.
They do this by increasing S‑adenosylmethionine, an important cofactor used for methylation (a process involved with DNA and genes).
Folate is also required to help synthesize three of the four DNA nucleotides – thymine, guanine, and adenine – so its importance in cognitive function cannot be understated.
Pump up your performance with these 3 simple solo activities
Next time you’re home alone, I want you to try one of these simple solo activities…
It only takes 30 seconds, and it will increase your stamina, so you can last as long as you want in bed.
Men say it’s extremely pleasurable to do and that it starts working immediately.
So you can do it while she’s in the bathroom, and by the time she comes out naked and ready for you…
…you will be rigid and stay that way for 30 minutes or more.
Here’s what Nate says about using this simple solo activity: