- keep blood glucose/insulin as low as you can. Reduce non-MUFA calories when possible
- LITHIUM. Effects of lithium on oxidative stress parameters in healthy subjects
- Amazon indigenous group's lifestyle may hold a key to slowing down aging: Tsimane people are unique for their healthy brains that age more slowly -- ScienceDaily
- Consumption of coffee and tea and risk of developing stroke, dementia, and poststroke dementia: A cohort study in the UK Biobank
- Eating mushrooms may reduce the risk of cognitive decline -- ScienceDaily
- https://www.frontiersin.org/articles/10.3389/fnagi.2014.00076/full (the more calm/less active your brain is, the better). Try to get a qeeg to see if your brain is unnecessarily noisy. Meditation also slows brain decline (the studies aren’t great and don’t adjust for intensity of meditation)
- THC/cannabinoids can clear up amyloid AND they can induce sleep/deep sleep - get one of the special CBN-based formulations for it (Cannabinoids remove plaque-forming Alzheimer’s proteins from brain cells - Salk Institute for Biological Studies ). Try microdosing. I do not recommend full trippy doses. Sleep Cannabis-Infused Botanical Mints | Shop | Sava is my favorite formulation (has melatonin too!)
- https://www.pnas.org/content/117/25/13856 . Do not live within 300 yards of a major roadway (esp one w/diesel), or downtown.
- supplemental melatonin. See Doris Loh and Antioxidants | Free Full-Text | Melatonin: Regulation of Biomolecular Condensates in Neurodegenerative Disorders
- BREAKING ALZHEIMER’S – Dr. Dayan Goodenowe
- get opencures blood tests to test for plasmalogens, choline, Sphingomyelin, ceramides. Try to increase Sphingomyelin. MAKE SURE plasmalogens are high (the effect sizes are unreal)
- Plasmalogen Deficiency, Dementia, and Death with Dr. Dayan Goodenowe - Kara Fitzgerald ND Naturopathic Doctor
- REDUCE HOMOCYSTEINE (try betaine + b12, ESP if you’re taking metformin). keep folate high (https://www.frontiersin.org/articles/10.3389/fnins.2021.661198/full )
- lutein/zeaxanthin + other long-chain carotenoids (also astaxanthin - Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging ). Lutein accumulates in subcellular membranes of brain regions in adult rhesus macaques: Relationship to DHA oxidation products
- green tea (Green tea consumption is associated with annual changes in hippocampal volumes: A longitudinal study in community-dwelling middle-aged and older Japanese individuals - ScienceDirect ). Try loose-leaf organic if you can (tea bags often have microplastics or bleaching agents, and pesticide contamination in non-organic is high). Google Books
- An Hour of Light and Sound a Day Might Keep Alzheimer's at Bay - Scientific American
- flavonols - High intake of dietary flavonols tied to lower risk of Alzheimer's dementia . The Rush University study on dementia has SOOO much information
- keep high omega-3 DHA (wellnessfx.com for the omega-3 blood tests). DHA more important than EPA
- put air purifiers in all your rooms - there is no minimum safe dose of air pollution. EVEN SEATTLE-LEVELS OF POLLUTION INCREASE DEMENTIA RISK - Fine Particulate Air Pollution Associated With Higher Risk of Dementia - Neuroscience News
- get a sleep study to test for apnea (apnea can accelerate brain decline)
- wear a fan over your bed to decrease sleeping temperature (decreased body temperature helps increase deep sleep). Wear a whoop to track deep sleep (whoop/dreem are better than oura which often fails to capture deep sleep)
- HIIT, run from pt A to point B (to pt of exhaustion). Intensity of exercise matters more than hours put in. Same for weight-lifting [also impt for like stimulating blood vessel growth)
- get regular MRI scans to track brain mass over time (and do the proper interventions). Some suggest PET scans (they can measure receptor/synapse densities). They also release more radiation, which could be hormetic for some people AND brain-damaging for others.
VASCULAR AGING IS SUPER-IMPT Counteracting age-related VEGF signaling insufficiency promotes healthy aging and extends life span | Science
Google super-ager memory research
Get Nfl protein measured - https://www.frontiersin.org/articles/10.3389/fneur.2019.00338/full
neurofeedback! afvaf afaf
POSSIBLE, needs more info: Edaravone - Wikipedia
https://www.nature.com/articles/s41380-021-01159-1 also needs more evidence.’
=> bigger dendritic spines also decrease less w/age than smaller dendritic spines
Exercising + playing RTS games when older (esp Sins of a Solar Empire/Rise of Nations can help). Strategy-Based Video Games May Improve Older Adults' Brain Function | American Association for the Advancement of Science
FOLLOW ALL OF KENNETH HAYWORTH
it’s worth looking up Wallerian degeneration - Wikipedia / https://www.nature.com/articles/nrn3680 - you want to keep NMNAT2 high. Neurons tend to shrink/shrivel rather than die. They are unique from other tissue in that they don’t divide (though they do lose A LITTLE bit of telomere) and how their synaptic/axonal properties ARE affected by age in a way very different from other tissue (in particular, larger spines decline less w/age), and processes that maintain spine size/density tend not to be the same processes that affect aging process in other tissues
also note hypothalamic inflammation is one thing that often makes people unable to control their hunger over time, DON’T EAT TOO MUCH, b/c ROS from feeling full is PRECISELY what controls hypothalamic inflammation.
also too much calcium is bad. Mg/Ca ratio is good to increase. Diffuse axonal injury - Wikipedia
POSSIBLY interesting (but not the most important thing): https://elifesciences.org/articles/62048
Repair of Mitochondrial Recycling Defect Linked to Parkinson’s Disease - Neuroscience News
ALCOHOL is INTERESTING. higher levels are undoubtedly bad, but lower levels can promote glymphatic clearance - Alcohol promotes waste clearance in the CNS via brain vascular reactivity - PubMed (needs more info)
https://academic.oup.com/aje/article/164/9/898/87190 possibly, tho effect size is not large
Supplementation with ProdromeNeuro was observed to elevate blood DHA-plasmalogen levels. The increase in blood DHA-plasmalogens correlated with a decrease in malondialdehyde levels (r=-0.5, p=7.2e-07) and an increase in catalase activity (r=0.28, p=0.008). Superoxide dismutase activity was increased in persons with low baseline activity (p=0.017).
To access the FREE seminars with full presentations and videos please visit Dr. Goodenowe’s resource site here. This is the article for seminar C106, Supplements (Series C).
ProdromeNeuro is a plasmalogen supplement designed to specifically elevate DHA plasmalogen levels. An escalating dose study was performed in 22 persons (11M/11F) diagnosed with various degrees of cognitive impairment to determine the optimal dose for elevating blood plasmalogen levels.
In addition to clinical evaluations of cognition and mobility, blood samples were collected at baseline and after each month of supplement dosing for biomarker analyses.
The escalating dosing of ProdromeNeuro was performed as follows:
Month 1 – 1ml/day (900mg/day – one bottle of ProdromeNeuro)
Month 2 – 2ml/day (1800mg/day – two bottles of ProdromeNeuro)
Month 3 – 2ml/day (1800mg/day – two bottles of ProdromeNeuro)
Month 4 – 4ml/day (3600mg/day – four bottles of ProdromeNeuro)
Month 5 – 0ml/day (0mg/day – zero bottles of ProdromeNeuro)
Blood DHA-Plasmalogen levels were observed to be increased in all participants in a dose-dependent manner. After month 1 there was a 30% increase, after months 2 and 3 there was a 60% increase and after month 4 there was a 90% increase in the target DHA-plasmalogen levels. Persons with low baseline DHA-plasmalogen levels (quartiles 1 and 2) experienced a greater increase in blood DHA-plasmalogen levels (50%, 90%, and 120%, respectively). When blood DHA-plasmalogen levels were expressed relative to an endogenous non-DHA phosphatidylethanolamine, the relative increase in the target DHA plasmalogen levels was more pronounced.
The oxidative stress cascade begins with the formation of the superoxide radical resulting from a cellular insufficiency in recycling NADH back to NAD by the mitochondrial electron transport chain. A build-up of NADH beyond the intracellular capacity to recycle NADH by alternative, non-oxidative, anaerobic mechanisms leads to the export of free electrons to the extracellular environment by NAD(P)H oxidase (NOX). These electrons combine with molecular oxygen to form the superoxide radical. Superoxide is neutralized to molecular oxygen and hydrogen peroxide by superoxide dismutase both inside and outside of the cell. Hydrogen peroxide, in turn, is neutralized into molecular oxygen and water by multiple mechanisms such as catalase, glutathione peroxidase or by chemical neutralization by plasmalogens. The failure of the antioxidant system to neutralize hydrogen peroxide results in hydrogen peroxide reacting with superoxide to form the hydroxyl free radical. The hydroxyl free radical reacts with polyunsaturated fatty acids in biological membranes to form lipid peroxides. These lipid peroxides are the primary chemoattractants for inflammatory immune cells. Malondialdehyde is a biomarker of lipid peroxidation and thus represents and quantifies the oxidative stress load on biological systems. In order to assess the effect of elevating blood DHA-plasmalogens on the oxidative stress load on the participants in the trial, malondialdehyde levels, catalase and superoxide dismutase activity and C-reactive protein levels were measured in all participants at baseline and at the end of months 3-5. Although these biomarkers are quantitatively measured, they each have biological floor levels that represent a “healthy state” which cannot reasonably be improved upon. Accordingly, in addition to evaluating the effect of ProdromeNeuro on all participants, participants were also grouped into either low (Q1,Q2) or high (Q3,Q4) subgroups and evaluated accordingly.
ProdromeNeuro supplementation reduced malondialdehyde levels in all participants by 32% (p=0.028) and by 46% (p=0.002) in persons with high baseline malondialdehyde levels. Overall, malondialdehyde levels were negatively correlated with blood DHA-plasmalogen levels (r=-0.5, p=7.2e-07)
ProdromeNeuro supplementation increased catalase activity to 186% (p=0.014) of baseline levels in participants and to 240% (p=0.02) in persons with low baseline catalase activity. Overall, catalase activity was positively correlated with blood DHA-plasmalogen levels (r=0.28, p=0.008)
ProdromeNeuro supplementation increased superoxide dismutase activity (p=0.017) only in persons with low baseline superoxide dismutase activity.
Of the 22 participants, only 4 had baseline C-reactive protein levels greater than 1.0. All four of these participants had low baseline DHA-plasmalogen levels. All four of these participants exhibited a decrease in CRP by greater than 0.5 units and in two of the participants CRP levels decreased to less than 0.5.
The results of the oxidative stress biomarker analyses indicate that increasing blood DHA-plasmalogen levels using ProdromeNeuro has a profound positive effect on oxidative stress biomarkers.
ProdromeNeuro was well tolerated at all dosages and no adverse reactions were observed or reported.