Thx, I forwarded your article to my eye doc and he shared this related paper:
“Biomarkers from retinal OCTA images can provide useful information for clinical decision-making and diagnosis of AD and MCI.”
Apparently he has been taking OCTA images on my eyes (who knew!?!). He has been doing it with the idea that once he acquires the ability, he will go back to our past results and use AI algorithms to pick up early signs of dementia.
Today I had the back of my eyes and retinas photographed - small healthy blood vessels - nothing out of place. No cateract development, optic nerve great. Cost was $39. Cheap.
After seeing this article on eye exams - glad I paid the small extra for pics over the free look - drops to dialate and look. Like having a record for any future changes is great…
Glad you had the test and that is an excellent price!
Also, PSA: I had not had my eyes dilated in many years, but I actually met someone who had eye cancer and then passed… a simple eye exam would have found it early.
My doc found a tiny spot on my eye and sent me to Stanford just to make sure it was nothing, and now I go every year.
Regarding the article “More than simply leftovers: a new link between remnant cholesterol and dementia” posted by @A_User, I wanted to see where my lipids put me, compared to the people in this study. In case anyone else is interested in doing this, below is the information that I used.
When the population was stratified by remnant-C quartiles, higher remnant-C concentrations were incrementally associated with higher risks of developing all-cause dementia, Alzheimer’s disease, and vascular dementia after adjusting for age, sex, and additional confounders such as income level, BMI, comorbidities, statin and fibrate use, and total cholesterol concentration.
Remnant cholesterol corresponds to all cholesterol not found in high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C). It is calculated as total cholesterol minus HDL-C and LDL-C.
In most cholesterol panels, LDL-C is estimated as Total - HDL - Triglycerides/5. This means remnant cholesterol is the same as Triglycerides/5 and hence a proxy for Triglyceride levels.
The best way to lower Triglycerides is to raise Omega-3, so it is not suprising this corelates with risk of dementia.
Claim in one line: The video argues that Viagra (sildenafil) might lower Alzheimer’s risk, but current evidence is observational and not proof of causation.
Key evidence #1 (2021): A Cleveland Clinic–led analysis of ~7.2M U.S. insurance records linked sildenafil use with a 69% lower Alzheimer’s incidence over ~6 years; mechanistic lab work suggested effects on tau pathology.
Key evidence #2 (2024): A UCL–led cohort of ~270k U.K. men with ED found those prescribed PDE5 inhibitors had an 18% lower Alzheimer’s risk; the association strengthened with more prescriptions.
Drug-specific nuance: Some analyses report the signal mainly for sildenafil rather than for the whole PDE5I class.
Proposed mechanisms: PDE5 inhibition raises cGMP, improving cerebrovascular function; preclinical work hints at effects on tau/amyloid pathways and neuronal health.
Limits & biases: All human data so far are observational—susceptible to confounding (e.g., health-seeking behavior, ED severity, comorbidities). No randomized prevention trials yet; results don’t prove Viagra prevents Alzheimer’s.
Generalizability: Evidence mainly involves men with erectile dysfunction; relevance to women or to people without ED is unknown.
Safety considerations (if anyone considers off-label use): Never combine with nitrates, as this may increase the risk of hypotension. Rare reports of hearing or vision loss; interactions with alpha-blockers/strong CYP3A inhibitors warrant caution—discuss with a clinician.
Bottom line: Sildenafil is a promising repurposing candidate for Alzheimer’s prevention, but clinical trials are needed before recommendations can be made.
There are some interesting observations in the video that are not covered in the summary.
Most of the readers of this thread are already aware of the contents.
FWIW:
Among PDE5I medications, only sildenafil use was associated with significant risk reduction (most likely because of the small sample size for the other 2 drugs, tadalafil and vardenafil).
Sweeteners found in yoghurts and fizzy drinks can damage people’s ability to think and remember, and appear to cause “long-term harm” to health, research has found.
People who consumed the largest amount of sweeteners such as aspartame and saccharin saw a 62% faster decline in their cognitive powers – the equivalent to their having aged 1.6 years, researchers say.
They concluded: “Our findings suggest the possibility of long-term harm from low- and no-calorie sweeteners (LNCs) consumption, particularly artificial LNCs and sugar alcohols, on cognitive function.”
The study published in Neurology examined the diets of more than 12,700 adults in Brazil, and found that those who consumed the highest amounts of low- or no-calorie sweeteners experienced faster declines in memory and thinking skills over an eight-year period.
Paywalled Paper:
Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline - An 8-Year Prospective Study
To determine whether rescuing inflammatory phenotypes within the AD gut could constitute a potential therapeutic, we utilized the dietary supplement, inulin. Inulin is a soluble prebiotic fiber and, in our study, altered serum levels of bioactive metabolites, including SCFAs,119 bile acids,36 and IPA,39 correlating to an increase in Actinobacteria phyla and Bifidobacteriaceae family species among some others. […] Overall, inulin diet rescued some parameters of AD, likely via multiple mechanisms acting on the gut, the brain, and the peripheral immune cells. […] Through this investigation, we provide further evidence for the importance of the gut-brain axis, including the role of gut immune cells, and reveal possible dietary and therapeutic interventions to target inflammation in AD."
@DrFraser@John_Hemming: example of a neuroprotective intervention (in mice) that does not cross the BBB.
I have my own cocktail that I use for sweetening. Its a mix of stevia, inulin, and malic acid (helps with the aftertaste). I avoid other sweeteners like the plague; with the exception of small amounts of fructose from berries.
Important to note that tagatose did not have the negative effect noted in the study above. It also has 90% of the sweetness of sucrose (“sugar”) and apparently tastes qualitatively the most like sugar of any substitute. I’ll be trying it for the first time today. Only downsides appear to be price and it still has 1.5 kcal/gram.
I don’t think you can draw conclusions from that sweetener study.
people are notoriously horrible at reporting what they eat/drink
sweetener had no effect on people >60 which doesn’t really make sense. Less cognitive reserve generally makes a person more vulnerable to a neurotoxin.
sweetener intake is likely a surrogate for overall diet quality. Health conscious people generally try to avoid artificial sweeteners, probably exercise more, don’t smoke, may have different socioeconomic status, etc. There are numerous variables that could account for the difference and even though they try they can’t control for them all.
Not saying to go crazy with sucralose, but I highly doubt a diet soda every once in a while is going to be the cause of someone’s dementia if they are doing everything else right.
If you don’t mind me asking what is your Apoe genotype? I got the test done with Labcorp, I’m E3/E3 which means I’m at normal risk for Alzheimer’s. But I did a contact sport for 12 years so I have some brain damage and issues I’m dealing with today.