A recent study has confirmed the findings of earlier research which indicates people who regularly take erectile dysfunction medication—particularly Viagra—have a lower risk of developing Alzheimer’s Disease.
Why the drugs appear to lessen the occurrence of Alzheimer’s is unknown. However, one theory is that the medication increases blood flow to all parts of the body, including the brain.
The results of the latest research appeared in Neurology. Scientists looked at the health records of 269,725 men in the UK. Aged over 40, the average age was 59.
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They all had a diagnosis of erectile dysfunction between the years of 2007 and 2017. Doctors prescribed medication to many of them. This typically included sildenafil (Viagra) or tadalafil (Cialis). Others received advice on lifestyle changes.
Five years later, the men were checked to see if they had developed any symptoms of Alzheimer’s. Of the original number, 1,119 were newly diagnosed with AD. There was a marked difference between those who had regularly been taking ED medication (more than 20 or 50 prescriptions throughout the study), and those who did not take the medication.
Men who regularly take Viagra were almost 20% less likely to show any symptoms of Alzheimer’s. This was more pronounced in men who took it more often. The effect was less apparent for those taking tadalafil or vardenafil (Levitra and Staxyn).
“We desperately need treatments”
These are exciting results for those working in the field. There has been a recent focus on treatments to clear the amyloid plaques on brain cells that cause Alzheimer’s. However, this is not a cure but another way to slow down the development of the disease. Anything that halts the disease appearing in the first place is cause for celebration.
“Although we’re making progress with the new treatments for Alzheimer’s disease that work to clear amyloid plaques in the brain for people with early stages of the disease, we desperately need treatments that can prevent or delay the development of Alzheimer’s disease,” said lead author Ruth Brauer, lecturer at University College London.
“More research is needed to confirm these findings, learn more about the potential benefits and mechanisms of these drugs and look into the optimal dosage.
“A randomised, controlled trial with both male and female participants is warranted to determine whether these findings would apply to women as well.”
Dr Leah Mursaleen, head of research at Alzheimer’s Research UK, welcomed the findings
“Developing drugs for diseases like Alzheimer’s is a costly process and can take many years,” she told the Daily Mail. Being able to repurpose drugs already licensed for other health conditions could help accelerate progress and open up new avenues to prevent or treat dementia-causing diseases.”
National Viagra Day
Viagra (sildenafil) was first approved by the FDA as an oral medication for erectile dysfunction on March, 27, 1998. Because of this, March 27 is designated annually as ‘World Viagra Day’, or ‘National Viagra Day’ in the US.
The medication was first developed to treat high blood pressure. However, trial subjects soon reported an unexpected side effect. It significantly improved erections in men experiencing ED. Its arrival marked the first oral, fast-acting treatment for ED.
In recent years, scientists have explored using Viagra to treat other conditions. There is mounting evidence that it might help maximize the efficiency of chemotherapy drugs to target lung, breast, colon and bladder cancers.
Related:
Viagra linked to unexpected and beneficial long-term side effect
This could be good news for anyone who takes the erectile dysfunction drug.
Promising research finds this common HIV drug might also help beat Alzheimer’s
Any treatment for Alzheimer’s is to be welcomed — especially if it’s an expensive drug already in use for another condition.
ZzBomb
Anyone else surprised to hear that there is a National Day for Medically Induced Erect Penis?
ZzBomb
Or is Medically Induced Penis Erection?
Whatever!
Stay Hard Everyone!?
abfab
All while simultaneously banning abortion.
Chrisk
Anything that gets us closer to curing this is great news. My Mom died from Alzheimer’s a few years ago and I wouldn’t wish it on my worst enemy.
There’s other things like Citrulline or L-Arginine or just beet juice that boost nitric oxide levels as well though.
abfab
Very sorry, Chrisk.
bachy
@Chrisk: so sorry for your loss.
I just started reading about Citrulline. Do you take the supplement? Very curious to hear your impressions.
Kangol2
I’m sorry to hear this, ChrisK. You have my sympathies. Thanks for the recommendations. Also, getting enough sleep is crucial.
dbmcvey
And I forgot to send cards!
MaritimeNerd
I would interpret with reservation as it doesn’t pass the smell test if you drill down further, including into the reams of supplementary data appended.
For the first 14 years (circa 2000-13) the Alzheimer’s (AD) number-at-risk ratio based on subgroup denominators was 3:1, loaded for PDE5i use, and there was an apparent scramble to equalize the ratio over the final 3-4 years to an eventual number-at-risk ratio that landed at 1.2:1 AFTER the Kaplan-Meier incidence curves trended to merging, thus having shown at that 14 year point no difference in Alzheimer’s incidence between PDE5i users and non-users. Hence the average follow-up period was about 6 years for PDE5i users, twice the period length compared to that of non-users because the majority of non-users with ED in the database were chased down closer to the end of the retrospective study period.
Moreover, the average age of non-users was 78 at date of AD diagnosis, 2 years older than that of PDE5i users at their date of diagnosis, so PDE5i users were diagnosed at a younger age. However, one would not be inclined to say PDE5i use predisposed to younger AD onset UNLESS wanting to put forward a finding as specious as the actual biased published results.
Non-users diagnosed with AD had higher rates of comorbidities (on all 18 conditions measured, and with comorbidity prevalence differentials much greater than that of AD incidence comparing the subgroups!) [comorbidities are associated with AD] as well as higher rates of illness medication treatments compared to PDE5i users. They were older and sicker and these factors alone could explain a higher rate of Alzheimer’s Disease using the person-years denominator over the shorter period of time assessed for that subgroup. For mid-70’s age range the AD incidence curve begins to rise more steeply, for example age 78.5 compared to age 76.5 within the general population. Based on age standard deviation values depicted, 68% of PDE5i users at time of AD diagnosis were age 69.5-83.7 while 68% of non-users were age 71.6-85.4
Since PDE5i’s are widely used for ED the reality that uptake was nil in spite of ED diagnosis supports the notion that the importance and pursuit of sexual function may have been secondary for them in the context of worse health overall. More meds, more drug interaction, more onerous dosage adjustment considerations, less incentivizing for PDE5i uptake. These factors suggest the possibility of reverse causation; an association between the prodomal stage of AD and PDE5i non-prescribing as opposed to causative directionality where no uptake predicts AD and uptake is protective against AD.
In sum, there would be no more reason to conclude PDE5i uptake confers Alzheimer’s risk reduction than to assert it lowers incidence of the 18 comorbidities tracked. The non-users had higher vulnerabilities to cognitive decline but never having popped Viagra or other PDE5i’s was not convincingly one of them. Latent mining the UK national database for men with ED not taking PDE5i’s in order to round out the investigative study comparator data simply yielded older and less healthy males within that subgroup.