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"My father was a high-powered executive. He managed hundreds of people and was making complex decisions every day. I jus...
10/05/2026

"My father was a high-powered executive. He managed hundreds of people and was making complex decisions every day. I just can’t believe he developed dementia."

I understand why this is so hard to reconcile. We tend to assume that someone who spent decades learning, solving complex problems, making important decisions, or operating at an incredibly high level should somehow be protected from dementia. And there is some truth behind that assumption, but probably not in the way most people think.

Education and mentally demanding work can help build what we call cognitive reserve, which is essentially a resilience that allows the brain to continue functioning despite the changes happening underneath. It may delay when cognitive symptoms first become apparent, and in some people it may allow them to compensate remarkably well for decline—continuing to work, manage complicated lives, and function at a very high level despite accumulating changes in the brain.

But cognitive reserve doesn’t necessarily stop the underlying damage from occurring. It may delay when cognitive symptoms first become apparent, and in some people it may allow them to compensate remarkably well for decline, allowing them to continue to work, manage complicated lives, and function at a very high level despite accumulating changes in the brain.

So yes, education matters. Staying intellectually engaged matters. A cognitively demanding career may help build reserve and potentially buy you meaningful years of preserved function. But it does not make you immune to dementia. You can be a CEO, have three degrees, and be the smartest person in the family and still develop brain disease.

There is a lot of noise when it comes to brain health, and I hear the same myths come up again and again. Some of them a...
09/17/2026

There is a lot of noise when it comes to brain health, and I hear the same myths come up again and again. Some of them are not only misleading, but can distract us from the things that actually matter when it comes to protecting our brains.

For those of you who are new here, I’m Dr. Kellyann Niotis, a preventive neurologist. I’m a researcher and preventive neurologist who specializes in caring for people at risk for diseases like Alzheimer’s and Parkinson’s, with a focus on understanding and reducing risk before symptoms begin.

Today, I'm breaking down 6 myths in my field and what the science actually tells us instead. What have you heard about brain health that you’re not sure is fact or fiction? Leave it in the comments and maybe I’ll tackle it next.

A recent Cochrane Review analyzing more than 20,000 participants across 17 clinical trials concluded that anti-amyloid t...
06/01/2026

A recent Cochrane Review analyzing more than 20,000 participants across 17 clinical trials concluded that anti-amyloid therapies for Alzheimer’s disease provide only “trivial” clinical benefits while carrying meaningful risks such as ARIA.

Many have interpreted this as evidence that the amyloid hypothesis has failed.

From my own clinical experience, I don’t believe that. I know reasonable people may disagree with some of my interpretations, and that’s okay. These views reflect my reading of the evidence, my clinical experience, and my own research interests. As always, I welcome thoughtful discussion and debate.

One issue with this broad meta-analysis is that they average together therapies. Older antibodies that failed are pooled alongside newer agents such as lecanemab and donanemab, potentially obscuring important differences between treatments.

The other big issue is timing. By the time memory symptoms appear, amyloid accumulation, neuroinflammation, synaptic dysfunction, and neurodegeneration have often been underway for years, if not decades. Anti-amyloid therapies cannot reverse damage that has already occurred.

And most importantly, Alzheimer’s is not a single disease with a single solution.

Two patients may carry the same diagnosis yet have very different underlying biology, risk factors, and drivers of disease. The future of Alzheimer’s treatment will depend on precision medicine: identifying the right patient, for the right target, at the right time.

To be clear, this review should not diminish the significance of where we are today.

For the first time, we have therapies that can modify a core pathological feature of Alzheimer’s disease. The clinical effects may be modest, important questions remain, and risks must be weighed carefully. But this is still progress.

I remain optimistic that the future of Alzheimer’s prevention and treatment will involve a combination of approaches, including those that target amyloid, even if it isn’t “causative”.

It feels like lithium for brain health and Alzheimer’s prevention is everywhere on social media right now.Animal studies...
05/28/2026

It feels like lithium for brain health and Alzheimer’s prevention is everywhere on social media right now.

Animal studies have shown intriguing effects on pathways involved in Alzheimer’s pathology, and observational studies have hinted at possible associations with lower dementia risk.

But until now, we’ve had very limited randomized clinical trial data.

The LATTICE trial tested low-dose lithium carbonate in adults age 60+ with mild cognitive impairment (MCI), meaning cognitive changes measurable on testing but not severe enough to significantly impair daily function.

This was a randomized, double-blind, placebo-controlled pilot study. 80 participants started treatment: 41 received lithium and 39 received placebo for 2 years. Dosing was titrated to blood levels of 0.25–0.5 mmol/L.

The study did NOT meet its primary endpoints, meaning it did not provide definitive evidence that lithium preserved cognition. There were some interesting exploratory findings among amyloid-positive participants, where researchers observed larger effect sizes for verbal memory and hippocampal preservation. But only 21 participants were amyloid-positive, meaning these subgroup analyses were based on roughly 10 people per arm — far too small to establish clinical benefit or draw strong conclusions.

For what it’s worth, in the small number of individuals we have personally trialed on low-dose lithium orotate at IND (with and without biomarker positivity), we have not observed compelling biomarker changes thus far.

That does NOT prove lithium cannot work, but it does highlight how difficult it is to translate promising mechanistic theories into meaningful human outcomes.

Yes, the door remains open for future research, particularly in larger biomarker-defined populations.

But this study does NOT support widespread use of lithium for cognitive preservation or Alzheimer’s prevention.

And importantly, lithium is not a benign supplement. Even low-dose formulations can carry risks without appropriate medical supervision and monitoring.

05/23/2026

The full IG Live conversation with my inspiring patient, will drop on Monday. Stay tuned!

Long-term fasting insulin variability may matter more for cognitive function than we realize.Normal glucose and A1c do n...
05/18/2026

Long-term fasting insulin variability may matter more for cognitive function than we realize.

Normal glucose and A1c do not always mean your metabolism is healthy from a brain health perspective.

A new CARDIA analysis followed adults from young adulthood into midlife, measuring fasting insulin several times over 25 to 30 years. Researchers found that greater long-term variability in fasting insulin was associated with worse midlife cognitive performance, even after adjusting for diabetes status, medication use, and average insulin levels.

We often think about metabolic health in snapshots:
• A1c today
• Glucose today
• Fasting insulin today
• Body composition today

But the brain does not experience your physiology in snapshots. It is exposed to your metabolic environment continuously for decades.

The study raises an important possibility: that repeated metabolic instability over time may contribute to cumulative neurovascular and neuronal stress.

Participants with greater insulin variability performed worse in areas including:
• Attention/processing speed
• Executive function
• Verbal memory

Importantly, insulin is not just a “blood sugar hormone.” In the brain, insulin signalling influences neuronal metabolism, synaptic function, vascular health, inflammation, and cerebral glucose utilization.

If insulin regulation is unstable for years, the brain may be living in a more metabolically stressed environment long before diabetes is diagnosed.

So no, I would not say “ everyone needs to track insulin variability.” I would interpret it as another reminder that “normal labs” today are not always the same thing as metabolic resilience.

The foundation remains lifestyle intervention:
→ Exercise is one of the most powerful modulators of insulin sensitivity
→ Diet matters too. High-saturated-fat/high-glycemic diets tend to shift healthy brains toward more Alzheimer’s disease–like metabolic patterns
→ Continuous glucose monitoring may reveal more metabolic flexibility than snapshot lab testing

This study was observational and does not prove personality. But studies like this continue to reinforce that brain health and metabolic health are deeply interconnected.

A randomized clinical trial found that 12 months of moderate-to-vigorous aerobic exercise made participants’ brains appe...
05/12/2026

A randomized clinical trial found that 12 months of moderate-to-vigorous aerobic exercise made participants’ brains appear “younger” on MRI.

The study used a machine learning metric called brain-PAD (“brain-predicted age difference”), which attempts to estimate whether a brain appears biologically older or younger than expected for a person’s chronological age. Note: brain aging is NOT the same thing as dementia.

While biomarkers like brain-PAD are interesting research tools, they are not clinical diagnostic tests and still carry meaningful limitations and prediction error at the individual level.

Still, I think this study is compelling for several reasons.

First, it was a randomized clinical trial - not just observational data.

Second, the intervention targeted adults in early-to-midlife (median age = 41). That matters because the biological processes underlying diseases like Alzheimer’s often begin decades before symptoms emerge. Brain health is not something we start thinking about at age 70.

Third, the observed brain changes were NOT fully explained by changes in weight, blood pressure, body composition, or even BDNF - one of the most discussed exercise-related neurotrophic factors. Exercise may be influencing brain health through more complex pathways than we currently understand.

And finally, the exercise prescription was realistic. This was not elite athlete training or extreme biohacking.

Participants gradually progressed their exercise intensity over time based on heart rate and fitness testing, ultimately targeting ~150 minutes/week of aerobic exercise. Moderate intensity early on. More vigorous intensity later if tolerated safely.

Sometimes the interventions with the strongest evidence are also the least glamorous.

VO2Max

This study on Omega-3 supplementation is getting a lot of attention and I think it’s worth walking through carefully.Fir...
05/08/2026

This study on Omega-3 supplementation is getting a lot of attention and I think it’s worth walking through carefully.

First, the strengths: this was a large, well-characterized cohort from ADNI with longitudinal follow-up and multimodal imaging. That combination (cognition plus amyloid, tau, and FDG-PET) is something most supplement studies simply don’t have.

The finding itself is provocative: Omega-3 supplementation was associated with faster cognitive decline. But importantly, this wasn’t driven by amyloid or tau. The signal pointed instead toward reduced brain glucose metabolism, a proxy for synaptic function.

That raises interesting mechanistic questions, but it doesn’t establish causality.

There are also important limitations. Omega-3 use was self-reported and not standardized, with no dose or adherence data. Baseline Omega-3 levels weren’t measured, so we don’t know who was deficient versus replete. And key factors like why someone started supplementation, their cardiometabolic health, and overall lifestyle weren’t fully accounted for.

It’s also worth noting that this finding sits in tension with a much larger body of evidence, including observational studies suggesting benefit and randomized trials showing modest benefit or neutrality. Even prior analyses from the same ADNI dataset suggested reduced Alzheimer’s risk in long-term users.

So when one study appears to contradict all of that, the takeaway shouldn’t be panic. To me, this doesn’t mean Omega-3s are inherently harmful. It means our framework cannot be too simplistic.

The cognitive impact of Omega-3s in the aging brain is likely more complex and context-dependent than we’ve assumed. The authors themselves acknowledge this. The net effect probably reflects a balance between neuroprotective benefits and potential downsides shaped by dose, oxidative state, and underlying presence of disease pathology.

This is exactly why we need to move toward precision, individualized prevention rather than blanket recommendations.

Join me LIVE on Friday, May 15 at 11 AM ET for a powerful conversation with a patient navigating brain health risk.She c...
05/06/2026

Join me LIVE on Friday, May 15 at 11 AM ET for a powerful conversation with a patient navigating brain health risk.

She carries the ApoE4 gene, has a family history of Alzheimer’s disease, and began noticing subtle cognitive changes.

We’ll talk about:
• what led her to seek evaluation
• the emotional side of knowing your risk
• how she thinks about prevention today
• what biomarkers can (and can’t) tell us

I’m incredibly grateful to have another brave patient willing to share her story publicly. These conversations are not easy to have, and I know how vulnerable it can feel to speak openly about fears surrounding memory, family history, and future risk. But I truly believe these stories matter because so many people are silently carrying the same questions and anxieties.

We’ll also leave time for Q&A at the end.

Friday, May 15
11 AM ET

Thank you for your willingness to share your story with this community.

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