The information in this article is not intended as, and should not be taken as, medical advice. Interventions like exercising, dietary changes, and taking medications and supplements can have both benefits and side effects. Please consult with a medical professional about any medical concerns.

by Nils Osmar — March 2026

Preface

This article reviews 12 interventions that the evidence suggests may help protect our brains as we age. None of them is a guarantee, and the list is not exhaustive. But the Lancet Commission on Dementia has estimated that up to 40% of dementia cases could be prevented or delayed through changes like these. Here’s a quick overview:

Strong evidence: Exercise — especially strength training at least twice a week — is one of the best-supported ways to protect your brain. Not smoking and maintaining a healthy weight in midlife also have solid evidence behind them.

Good evidence, with caveats: Drinking moderate amounts of coffee (1–3 cups/day) and tea is consistently linked to lower dementia risk in large studies, though we can’t yet prove the relationship is causal. Eating fatty fish, cutting back on sugar (especially fructose from processed foods), using an air purifier to reduce particulate exposure, and avoiding head injuries are all supported by meaningful research.

Promising but preliminary: Intermittent fasting shows strong results in animal studies but limited human data. Phosphatidylserine, a supplement, has some positive trial results but the studies are small. Low-dose lithium is generating real excitement after a landmark 2025 study in Nature, but human trials are still in early stages.

The full article below goes into each of these in detail — what the research actually shows, how strong it is, and where it falls short. If you have time for only one takeaway: these protective factors appear to be additive. You don’t need to do everything on this list, but the more of them you can reasonably incorporate, the more you may be stacking the odds in your favor.

There’s no known cure for Alzheimer’s, and the treatments for it once it develops are largely ineffective. But there’s growing evidence that several lifestyle interventions may help prevent it, and may also help prevent other forms of dementia.

None of these is a guaranteed shield. But taken together, they represent a toolkit for protecting long-term brain health.

In the article below, I’ve summarized the evidence for each intervention—including both what the research shows and where it falls short. My goal is to be straightforward about both the promise and the limitations.

1. Drinking Coffee or Cocoa (With Caffeine Intact)

What the research shows: Multiple meta-analyses and large cohort studies have found that moderate coffee consumption—roughly 1 to 3 cups per day—is associated with a reduced risk of dementia. A 2024 meta-analysis encompassing 38 cohorts and over 751,000 participants found a non-linear relationship between coffee intake and dementia risk, with 1 to 3 cups daily showing the strongest protective association. A large UK Biobank study (303,887 participants aged 55+) found that caffeine intake up to 400 mg/day was significantly associated with lower dementia risk. A 2021 Australian longitudinal study following participants for over 10 years found that higher coffee intake was associated with slower cognitive decline and reduced cerebral amyloid-beta accumulation—a key hallmark of Alzheimer’s.

Proposed mechanisms include caffeine’s ability to block adenosine receptors (reducing neuroinflammation), its antioxidant properties, and the neuroprotective effects of polyphenols and other bioactive compounds in coffee and cocoa. Notably, the benefits may not come from caffeine alone—research in animal models suggests other coffee compounds also contribute to amyloid clearance.

Limitations: Nearly all the human evidence is observational, meaning it shows correlation, not proven causation. People who drink coffee may differ from non-drinkers in other ways (exercise habits, socioeconomic status, etc.). There is significant methodological heterogeneity across studies, and some research has found no benefit or even negative effects in certain populations. Very high caffeine intake can disrupt sleep, which is itself a risk factor for dementia. Randomized controlled trials specifically testing caffeine for dementia prevention are lacking.

2. Drinking Green Tea and White Tea

What the research shows: The 2024 meta-analysis mentioned above found that increased tea consumption was linearly associated with decreased dementia risk—a 4% reduction per additional cup per day. Tea also showed a protective association with Alzheimer’s specifically. Green tea may have an edge over black tea due to its higher concentration of catechins, particularly EGCG (epigallocatechin gallate), which has demonstrated anti-amyloid and anti-inflammatory properties in laboratory studies. One Japanese study found that green tea consumption, but not black tea or coffee, was associated with reduced risk of cognitive decline.

Limitations: The evidence for tea is generally less robust than for coffee. Most studies are observational and conducted in East Asian populations, raising questions about generalizability. It’s difficult to separate the effects of tea from overall dietary and lifestyle patterns. Supplement forms of EGCG have raised some liver safety concerns at very high doses, though moderate tea drinking appears safe for most people.

3. Exercising (Especially Resistance Training and HIIT)

What the research shows: Exercise is among the most well-supported interventions for dementia prevention. While aerobic exercise has traditionally received the most attention, a growing body of research highlights resistance training as particularly valuable. A 2024 narrative review of randomized controlled trials found that resistance exercise induces structural brain changes in older adults that could reduce Alzheimer’s risk, including increased hippocampal and cortical volume, improved white matter integrity, and enhanced neuroplasticity. These benefits appear to follow a dose-response pattern: at least twice per week for at least six months, with the greatest effects seen in those already experiencing some cognitive decline.

A 2025 study published in GeroScience found that just six months of twice-weekly resistance training preserved hippocampal volume and white matter integrity in older adults with mild cognitive impairment. A 2025 meta-analysis of 17 RCTs confirmed that resistance exercise significantly improved cognitive function in older adults, particularly executive function and information processing speed. Moderate-intensity training (roughly 55–70% of maximum heart rate) appears to produce the greatest cognitive benefits.

Proposed mechanisms include increased BDNF (brain-derived neurotrophic factor) production, reduced neuroinflammation, improved insulin sensitivity, enhanced cerebral blood flow, and—unique to resistance training—the release of beneficial myokines from contracting muscles. The WHO recommends resistance exercise for older adults specifically due to its dual benefits for both muscle preservation and brain health.

Limitations: While the evidence is strong by the standards of lifestyle interventions, most RCTs are relatively small and short-term (6–24 weeks). Long-term randomized data spanning years or decades is still limited. The optimal “dose”—frequency, intensity, and type of exercise—hasn’t been definitively established. And exercise may be more effective at slowing decline in people who already have mild impairment than at preventing initial onset in cognitively healthy adults, though the evidence suggests benefit for both.

4. Eating a Very Low Sugar Diet

What the research shows: A longitudinal study from Rush University Medical Center (789 older adults, average 7.3 years of follow-up) found that those in the highest quintile of total sugar intake were twice as likely to develop dementia compared to those in the lowest quintile. Fructose and sucrose showed particularly strong associations—the highest fructose consumers had a 2.8-fold increased risk. A separate analysis from the Framingham Offspring Study confirmed that higher fructose consumption was associated with increased all-cause dementia and Alzheimer’s risk.

A 2023 paper in the American Journal of Clinical Nutrition proposed an intriguing theoretical framework: that fructose metabolism activates an ancient “foraging response” that, when chronically activated by modern high-sugar diets, drives progressive brain inflammation and neurodegeneration. In animal models, prolonged fructose exposure produces tau tangles and amyloid beta deposits—the hallmark proteins of Alzheimer’s. Elevated fructose levels have also been found in the brains of Alzheimer’s patients.

Limitations: The epidemiological studies are observational and rely on food frequency questionnaires, which are imprecise measures of actual intake. The “foraging response” hypothesis, while provocative and well-argued, remains theoretical—it hasn’t been tested in human intervention trials. It’s also important to distinguish between fructose from whole fruits (which come packaged with fiber, vitamins, and phytonutrients) and fructose from added sugars and high-fructose corn syrup. The concern is primarily with the latter. The relationship between sugar and dementia may also be partially mediated by sugar’s effects on obesity, diabetes, and cardiovascular health—all of which are themselves dementia risk factors.

5. Eating Fatty Fish (Omega-3s) While Minimizing Omega-6

What the research shows: Omega-3 fatty acids, particularly DHA (docosahexaenoic acid), are major structural components of brain cell membranes. Epidemiological studies have consistently linked higher fish consumption and higher blood levels of omega-3s with better cognitive function and reduced dementia risk. Neuroimaging studies have found that people with higher omega-3 levels tend to have larger hippocampal volumes and better-preserved brain structure at midlife. The modern Western diet’s high ratio of omega-6 to omega-3 fatty acids (often 15:1 or higher, versus the historical ratio closer to 2:1) may promote chronic neuroinflammation.

Limitations: Randomized trials of omega-3 supplementation for dementia prevention have yielded mixed results. Several large trials found no significant cognitive benefit from fish oil supplements in cognitively healthy older adults. The discrepancy between observational studies (which tend to be positive) and RCTs (which are often negative) may mean that fish eating is a marker for an overall healthier diet, or that the specific form and dose of omega-3s matters, or that benefits accrue only over decades of dietary pattern rather than short-term supplementation. The recommendation to eat fatty fish like salmon, mackerel, and sardines is well-supported, but taking fish oil pills may not replicate those benefits.

6. Eating Meat (with some caveats)

The question of red meat and dementia is a little tricky because it depends on our genetic type and on whether the meat has been processed. Recent evidence does suggest that for some people, meat consumption can be beneficial. From the study, published in JAMA:

Among 2157 older adults without dementia (mean [SD] age 71.2 [9.2] years; 1337 female [62.0%]), 1680 participants had longitudinal cognition data and 569 participants (26.4%) had APOE34/44 genotypes. During follow-up, 296 participants developed dementia and 690 died without dementia. Among participants with APOE34/44 genotypes, higher total meat consumption (top vs bottom quintile) was associated with better cognitive trajectories (β = 0.32; 95% CI, 0.07 to 0.56; P = .01) and reduced dementia risk (sHR, 0.45; 95% CI, 0.21 to 0.95; P = .04).

No associations were found in participants with APOE22/23/24/33 genotypes (cognitive trajectory: β = –0.11; 95% CI, –0.27 to 0.06; P = .20; dementia: sHR, 0.95; 95% CI, 0.57 to 1.61; P = .86). P values for APOE interaction were .004 for cognition and .10 for dementia. In the top quintile of meat consumption, dementia risk and cognitive decline were similar between APOE strata. A higher ratio of processed to total meat was unfavorably associated with dementia (sHR, 1.14; 95% CI, 1.01 to 1.29; P = .04), showing no APOE interaction and no substantial difference between unprocessed red meat and poultry. Post hoc analyses suggested concordant APOE interaction for all-cause mortality (unprocessed meat exposure, APOE34/44: HR, 0.85; 95% CI, 0.73 to 0.99; P = 0.04; P for interaction = .03).

7. Not Smoking

What the research shows: Smoking is one of the most well-established modifiable risk factors for dementia. Smokers have a roughly 30–40% higher risk of developing dementia compared to non-smokers, and the risk increases with heavier and longer smoking. Smoking accelerates vascular damage, promotes neuroinflammation, increases oxidative stress, and may directly damage brain tissue. The evidence is strong enough that the WHO and the Lancet Commission on Dementia include smoking cessation among their top recommendations.

Limitations: This is one of the less controversial items on this list. However, it’s worth noting that some older epidemiological studies (many funded by the tobacco industry) suggested smoking might be protective—a finding that has been thoroughly debunked by more rigorous, independent research. The good news: quitting smoking even in midlife significantly reduces dementia risk compared to continuing to smoke.

8. Using an Air Purifier

What the research shows: Research from USC and other institutions has found consistent associations between long-term exposure to air pollution (particularly fine particulate matter, PM2.5) and increased dementia risk. Encouragingly, USC research has also found that improvements in air quality are associated with reduced dementia incidence, suggesting the damage is at least partially reversible at a population level. Air purifiers with HEPA filters can dramatically reduce indoor particulate matter, which is significant given that most people spend the majority of their time indoors.

Limitations: While the link between air pollution and dementia is increasingly well-established, there are no randomized trials specifically testing whether air purifiers prevent cognitive decline. The evidence connecting dirty air to dementia comes from epidemiological studies of regional air quality, not from individual-level interventions like home air purifiers. Also, houseplants have been shown in controlled studies to remove negligible amounts of indoor pollutants at realistic scales—a HEPA filter is far more effective. Outdoor air quality, which you can’t control with a home purifier, also matters.

9. Losing Excess Body Fat (If Overweight or Obese)

What the research shows: Multiple large-scale studies have found that midlife obesity is associated with a significantly higher risk of dementia later in life. The mechanisms likely include chronic systemic inflammation, insulin resistance, vascular damage, and hormonal disruptions—all of which affect brain health. The Lancet Commission on Dementia lists midlife obesity as one of 12 modifiable risk factors for dementia.

Limitations: The relationship between weight and dementia is more nuanced than it first appears. Interestingly, obesity in late life (after age 65) has sometimes been associated with lower dementia risk—a phenomenon sometimes called the “obesity paradox.” This may reflect reverse causation: weight loss often precedes dementia diagnosis by years as the disease silently progresses. The strongest evidence points to midlife obesity (ages 40–65) as the critical window. Additionally, fitness level may matter more than weight per se—a person who is somewhat overweight but physically active may have lower risk than a sedentary person of “normal” weight. The goal should be metabolic health and reduction of visceral fat, not obsessing over a number on a scale.

10. Fasting and Time-Restricted Eating

What the research shows: Animal studies have consistently shown that intermittent fasting and caloric restriction protect against cognitive decline. Proposed mechanisms include enhanced autophagy (the cellular “cleanup” process that clears damaged proteins, including amyloid), improved insulin sensitivity, reduced neuroinflammation, increased BDNF production, and improved mitochondrial function. Some human studies have found cognitive improvements with time-restricted eating, particularly in metabolic markers associated with brain health.

Limitations: The human evidence for fasting and dementia prevention specifically is limited. Most of the compelling data comes from animal models, and the leap from mice to humans is significant. Long-term randomized trials of intermittent fasting for cognitive outcomes in humans are essentially nonexistent. There are also practical concerns: fasting can lead to muscle loss in older adults if protein intake isn’t adequate, and sarcopenia (muscle wasting) is itself linked to cognitive decline. Fasting protocols need to be carefully designed, especially for people over 65, to ensure adequate nutrition.

11. Taking Phosphatidylserine

What the research shows: Phosphatidylserine (PS) is a phospholipid that is abundant in brain cell membranes and plays a role in cell signaling and neurotransmitter release. It is one of the few brain supplements with a meaningful base of human trial data. A 2022 systematic review and meta-analysis found that PS had a positive effect on memory in older adults with cognitive decline. Several double-blind, placebo-controlled trials in the 1990s found modest cognitive improvements in patients with mild to moderate Alzheimer’s, particularly in verbal recall and attention. A 2024 RCT in Chinese older adults with mild cognitive impairment found that a PS-containing supplement improved cognitive function over 12 months, particularly short-term memory.

Limitations: The positive early trials used phosphatidylserine derived from bovine (cow) brain cortex, which is no longer available due to concerns about prion disease transmission. Modern supplements use plant-derived PS (from soy or sunflower), which has a different fatty acid composition, and whether it’s equally effective is uncertain. Many of the trials were small (50–150 participants), short-term (3–6 months), and some were industry-funded. Benefits appear modest and may be most noticeable in people who already have mild impairment. The Alzheimer’s Drug Discovery Foundation rates the evidence as suggestive but notes that more rigorous, larger trials are needed. Typical dosing in studies was 300 mg/day.

12. Taking Low-Dose Lithium

What the research shows: This is one of the most exciting emerging areas in dementia prevention. A landmark 2025 study published in Nature by Harvard researcher Bruce Yankner and colleagues found that lithium is the only metal significantly depleted in the brains of people with mild cognitive impairment and Alzheimer’s disease. They discovered that amyloid plaques sequester lithium, effectively creating a brain lithium deficiency as the disease progresses. In mouse models, depleting dietary lithium markedly increased amyloid deposits, tau accumulation, neuroinflammation, and cognitive decline. Conversely, low-dose lithium orotate supplementation prevented and reversed these changes in both Alzheimer’s model mice and normal aging mice.

In human clinical trials, a Brazilian study found that even a microdose of 300 micrograms of lithium per day stabilized cognitive function in Alzheimer’s patients over 15 months, while the placebo group continued to decline. A longer trial by Forlenza and colleagues found that low-dose lithium (serum level 0.25–0.5 mEq/L) appeared to cut the risk of progression from mild cognitive impairment to dementia roughly in half over 4 years. Epidemiological studies from Denmark and elsewhere have found that populations with higher naturally occurring lithium in their drinking water have lower rates of dementia. A systematic review of these studies concluded that lithium levels as low as 0.002–0.056 mg/L in drinking water were associated with reduced dementia risk.

Limitations: Despite the excitement, the human clinical trial evidence remains limited: the trials are small (34–61 participants in the key studies), and attrition was significant. The Forlenza trial’s primary endpoint for conversion to dementia narrowly missed statistical significance (p = 0.06). Lithium at standard psychiatric doses carries well-known risks to kidney and thyroid function, though the doses being discussed for dementia prevention are far lower. The safety profile of long-term low-dose lithium orotate in healthy older adults hasn’t been established in large trials. Yankner’s group has stated that a clinical trial of lithium orotate is being planned but has not yet begun. This is a space to watch closely, but it’s premature to make strong recommendations.

2026 update: From a JAMA article:

Preclinical and epidemiological research suggests that lithium, a mood stabilizer used to treat bipolar disorder since the mid-19th century, might at least slow the progression of Alzheimer disease, the most common cause of dementia.

13. Avoiding Falls and Concussions

What the research shows: Traumatic brain injury (TBI), including concussions, is a well-established risk factor for dementia. Even a single moderate-to-severe TBI can significantly increase the lifetime risk of Alzheimer’s disease and other forms of dementia. Repeated mild TBIs (as seen in contact sports and military service) are associated with chronic traumatic encephalopathy (CTE). For older adults specifically, falls are the leading cause of TBI, making fall prevention an important dementia-prevention strategy. This is yet another reason why resistance training (which improves balance and reduces fall risk) is so valuable.

Limitations: The relationship between head injury and dementia is complex and may involve both the direct damage from the injury and the inflammatory cascade that follows. Not everyone who experiences a TBI develops dementia, and genetic factors (particularly APOE4 status) appear to modulate the risk. Also, the threshold of injury severity that meaningfully increases dementia risk isn’t precisely defined—it’s clear that severe TBI increases risk, but the role of very mild concussions is less certain.

The Big Picture

No single intervention on this list is a magic bullet. Dementia is a complex, multifactorial disease influenced by genetics, age, environment, and decades of accumulated biological damage. But the research increasingly suggests that these risk factors are additive—and so are the protective factors. Someone who exercises regularly, eats well, doesn’t smoke, manages their metabolic health, and protects their brain from injury is stacking the odds meaningfully in their favor.

The Lancet Commission on Dementia has estimated that up to 40% of dementia cases could theoretically be prevented or delayed by addressing modifiable risk factors. That’s not a guarantee for any individual, but it’s a powerful statement about the degree to which our daily choices shape our cognitive futures.

Medical Disclaimer

This article is not intended as, and should not be taken as, medical advice. I’m not advising that people follow any particular regimen, eat any particular diet, or take any particular supplements—just sharing information about what the research currently shows. All supplements can have side effects; it is important to research both possible benefits and side effects before starting on any supplementation regimen, and to consult with a qualified healthcare provider.

Bibliography

Coffee, Tea & Caffeine

Eskelinen MH, Kivipelto M. Caffeine as a protective factor in dementia and Alzheimer’s disease. Journal of Alzheimer’s Disease. 2010;20(Suppl 1):S167–S174.

Santos C, Costa J, Santos J, Vaz-Carneiro A, Lunet N. Caffeine intake and dementia: systematic review and meta-analysis. Journal of Alzheimer’s Disease. 2010;20(Suppl 1):S187–S204.

Cornelis MC et al. Caffeine consumption and dementia: Are Lewy bodies the link? Annals of Neurology. 2022;91(6):834–846.

Gardener SL et al. Higher coffee consumption is associated with slower cognitive decline and less cerebral Aβ-amyloid accumulation over 126 months. Frontiers in Aging Neuroscience. 2021;13:744872.

Li F, Liu X, Jiang B, Li X, Wang Y, Chen X, Su Y, Wang X, Luo J, Chen L, Li J, Lv Q, Xiao J, Wu J, Ma J, Qin P. Tea, coffee, and caffeine intake and risk of dementia and Alzheimer’s disease: a systematic review and meta-analysis of cohort studies. Food & Function. 2024;15(16):8330–8344.

Noguchi-Shinohara M et al. Consumption of green tea, but not black tea or coffee, is associated with reduced risk of cognitive decline. PLoS One. 2014;9(5):e96013.

Schreiner TG, Popescu BO. Impact of caffeine on Alzheimer’s disease pathogenesis—protective or risk factor? Life. 2022;12(3):330.

Exercise & Resistance Training

Nicola L, Loo SJQ, Lyon G, Turknett J, Wood TR. Does resistance training in older adults lead to structural brain changes associated with a lower risk of Alzheimer’s dementia? A narrative review. Ageing Research Reviews. 2024;98:102356.

Ribeiro IC, Teixeira CVL, de Resende TJR et al. Resistance training protects the hippocampus and precuneus against atrophy and benefits white matter integrity in older adults with mild cognitive impairment. GeroScience. 2025;47(3):5267–5286.

Wu J, Huang C. A systematic review and meta-analysis of the effects of resistance exercise on cognitive function in older adults. Frontiers in Psychiatry. 2025;16:1708244.

Sepúlveda-Lara A, Sepúlveda P, Marzuca-Nassr GN. Resistance exercise training as a new trend in Alzheimer’s disease research: from molecular mechanisms to prevention. International Journal of Molecular Sciences. 2024;25(13):7084.

Sugar, Fructose & Diet

Ford CN et al. Dietary sugar intake associated with a higher risk of dementia in community-dwelling older adults. Journal of Alzheimer’s Disease. 2023;95(4):1417–1425.

Zhang S, Xiao Y, Cheng Y et al. Associations of sugar intake, high-sugar dietary pattern, and the risk of dementia: a prospective cohort study of 210,832 participants. BMC Medicine. 2024;22:298.

Yan J et al. Fructose consumption is associated with a higher risk of dementia and Alzheimer’s disease: a prospective cohort study. Journal of Prevention of Alzheimer’s Disease. 2023;10(2):186–192.

Johnson RJ, Tolan DR, Bredesen D, Nagel M et al. Could Alzheimer’s disease be a maladaptation of an evolutionary survival pathway mediated by intracerebral fructose and uric acid metabolism? The American Journal of Clinical Nutrition. 2023;117(3):455–466.

Phosphatidylserine

Kang EY, Cui F, Kim HK et al. Effect of phosphatidylserine on cognitive function in the elderly: a systematic review and meta-analysis. Korean Journal of Food Science and Technology. 2022;54(1):52–58.

Crook T, Petrie W, Wells C, Massari DC. Effects of phosphatidylserine in Alzheimer’s disease. Psychopharmacology Bulletin. 1992;28:61–66.

Kato-Kataoka A et al. Soybean-derived phosphatidylserine improves memory function of the elderly Japanese subjects with memory complaints. Journal of Clinical Biochemistry and Nutrition. 2010;47(3):246–255.

Cenacchi T, Bertoldin T, Farina C et al. Cognitive decline in the elderly: a double-blind, placebo-controlled multicenter study on efficacy of phosphatidylserine administration. Aging (Milano). 1993;5(2):123–133.

Jia Z et al. Effects of a food supplement containing phosphatidylserine on cognitive function in Chinese older adults with mild cognitive impairment: a randomized double-blind, placebo-controlled trial. Journal of Affective Disorders. 2024;367:197–206.

Low-Dose Lithium

Aron L, Ngian ZK, Qiu C et al. Lithium deficiency and the onset of Alzheimer’s disease. Nature. 2025;645(8081):712–721.

Andrade Nunes M et al. Microdose lithium treatment stabilized cognitive impairment in patients with Alzheimer’s disease. Current Alzheimer Research. 2013;10(1):104–107.

Forlenza OV et al. Clinical and biological effects of long-term lithium treatment in older adults with amnestic mild cognitive impairment: randomised clinical trial. British Journal of Psychiatry. 2019;215(5):668–674.

Kessing LV, Gerds TA, Knudsen NN et al. Association of lithium in drinking water with the incidence of dementia. JAMA Psychiatry. 2017;74(10):1005–1010.

Baethge C. Low-dose lithium against dementia. International Journal of Bipolar Disorders. 2020;8:25.

Duthie AC et al. Trace lithium levels in drinking water and risk of dementia: a systematic review. International Journal of Bipolar Disorders. 2024;12:30.

General & Reviews

Livingston G, Huntley J, Sommerlad A et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020;396(10248):413–446.

Alzheimer’s Drug Discovery Foundation. Cognitive Vitality Reports: Phosphatidylserine. Available at: alzdiscovery.org/cognitive-vitality/ratings/phosphatidylserine.

Donations welcome

• Donations make this website possible.
• To donate using Buymeacoffee, please click here.

More from Nils Osmar

• Anti-Aging Youtube channel Pathways to Longevity
• Anti-Aging Facebook group: Anti-Aging and Life Extension
• Rekindle School classes in Seattle: Rekindl.e School
• My personal website: My articles, art and more: Nilsosmar.com
• Exploring possible consciousness in Claude.AI and other LLMs: AI Consciousness
• Donations make this website possible. To donate using Buymeacoffee, please click here