Brain Health
Viagra and its active ingredient sildenafil may protect against Alzheimer's disease. But how does this connection work through nitric oxide and cGMP? Discover how you can naturally improve your brain circulation.
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Suffering from erectile dysfunction is certainly no pleasure for affected men. In the truest sense of the word, in such cases, (sexual) pleasure often goes missing. Unless, of course, you take the well-known blue pill to help.
Viagra, or more precisely its active ingredient sildenafil, widens the blood vessels in the erectile tissue, which as a result increases blood flow and thus improves erectile function. Simple mechanism.
But what does this have to do with the performance of our brain?
In an interesting cohort study published just last week, researchers found a link between taking Viagra for erectile dysfunction and a subsequently lower Alzheimer's risk in these men.¹
This effect was dependent on the number of prescriptions. The more often a man was prescribed Viagra, the lower his risk of developing Alzheimer's dementia.
Fun Fact: Originally, Viagra wasn't intended to improve erectile function at all—it was supposed to be a medication for high blood pressure and angina pectoris. Aha—so it's not just about the middle of the body, but about blood circulation throughout the entire body.
Blood circulation, which depends directly on the dilation of our blood vessels, is regulated in the body primarily by the gas nitric oxide. The discovery and description of this earned a Nobel Prize in Physiology or Medicine in 1998. Seems pretty important, then.
Sounds complicated, but please don't check out yet.
In our publications, we usually abbreviate explanations of NO's effects and simply say: NO works. In reality, NO activates a signaling molecule called cGMP. And that works. Because cGMP relaxes, for example, the smooth muscle found in our blood vessels.
Widened blood vessels mean lower blood pressure and better blood circulation. cGMP is naturally broken down by an enzyme called PDE. To increase the effect of NO via cGMP and thus improve blood circulation, we... give PDE inhibitors.
Viagra is one such PDE inhibitor. Aha! So Viagra inhibits this enzyme (PDE), which means the blood-flow-promoting effect of NO lasts longer.
But back to the study mentioned at the beginning. Admittedly, it has some limitations, but there's a plausible mechanism behind the observation.
Another study found, in the cerebrospinal fluid of Alzheimer's patients, not only lower cGMP levels but also more PDE compared to healthy control subjects.²
This could suggest that too little cGMP in the brain might be involved in the development of Alzheimer's. Even in animal studies, researchers have already found neuroprotective effects from administering PDE inhibitors.
So for us, this means very concretely: NO promotes blood circulation to the brain and has additional cell-protective effects—mediated through cGMP. That's why Viagra might protect the brain. But the point of this article isn't really about Viagra…
There are better ways to naturally improve cGMP levels and thus vascular health and blood circulation. We simply need good NO levels in our blood vessels. How to achieve that has been an important topic in our publications for many years. Want some examples?
This last point is particularly crucial, because arginine—citrulline is the precursor to arginine—is what your body uses to make NO. To produce enough NO, we need sufficient amounts of the amino acid arginine (or citrulline).
Did you know? Watermelon contains particularly high amounts of citrulline. With a whole melon you get a proud 5-10 g. Of course, you can simply drink a serving of our Citrulline Plus, which was specifically designed for this purpose ;-)
Whatever you do, take care of your NO metabolism!
Adesuyan, M. et al. Phosphodiesterase Type 5 Inhibitors in Men With Erectile Dysfunction and the Risk of Alzheimer Disease. Neurology 102, e209131 (2024).
Ugarte, A. et al. Decreased levels of guanosine 3', 5'-monophosphate (cGMP) in cerebrospinal fluid (CSF) are associated with cognitive decline and amyloid pathology in Alzheimer's disease. Neuropathol. Appl. Neurobiol. 41, 471–482 (2015).
