Month: March 2026

Year Six of Changing to a youthful phenotype with sprouts

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1. I’ve continued daily practices from Year Five to experience another year without being sick (if I don’t count getting MSG poisoning from Chinese food.) I consequently scheduled a doctor visit next week to get a sumatriptan prescription refilled.

2. Two modifications to what’s mentioned in 2026 diet and supplement changes:

– In that post’s comments, Ole Bisgaard Pedersen asked if I took NAD+ supplements such as NAM, NMN or NR – forms of vitamin B3 that are precursors to NAD+. I didn’t note that last year I started taking Now brand Flush-free niacin 500 mg mid-morning.

Nicotinamide riboside has the most human evidence, including a Tru Niagen clinical trial that showed improvements in peripheral artery disease. It’s too expensive for long-term use, though.

Even if I could afford it, there isn’t a magic bullet for fixing vascular system dysfunction. PAD is just one symptom of a cardiovascular system that needs to be overhauled then maintained at a healthy level. There is no clinical trial that has a logical therapeutic end point to stop treatments where a person could say, “I’ve done enough for my vascular system, my physical and cognitive functions won’t backslide.”

– 2-3 years ago, I changed from microwaving broccoli sprouts in a plastic bag to microwaving them in a small bowl with a small plate covering it to keep them from popcorning out of the bowl. I use a 1000W microwave oven on 80% power for ten seconds.

3. The two vitamin C macaque studies I’ve recently curated both ran for a human equivalent of ten years. I was encouraged that both found Nrf2 activation to be part of their causal beneficial evidence, since vitamin C wasn’t on my radar as a Nrf2 activator.

I expect that in four years I’ll write a Year Ten post on eating microwaved broccoli sprouts. I haven’t seen human evidence for broccoli extracts that bypass small intestine absorption and metabolism per Glucosinolate and isothiocyanate human interventions, or enteric capsules, or nanoformulations as suitable substitutes. Maybe studies on broccoli sprout powder or a Nrf2 activator that tops sulforaphane will be published before then, who knows.

2026 diet and supplement changes

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I switch things around pretty often, but I haven’t said much about diet and supplement changes since this time last year. Here’s what I’ve done in terms of changes that I’ve since abandoned or reduced, followed by additions or increases that I’ve kept.

Abandoned and reduced items

1. I stopped using Avena sativa oats to grow 3-day-old oats sprouts. I again ran into the same situation where I got < 10% yield.

The first time this happened in 2023, I related to the Montana farmer that degraded seed vitality was probably caused by the way that Amazon handled their oat products. I’m the customer, though, and I won’t make it my problem if the vendor can’t meet expectations.

I switched to sprouting Avena nuda oats based on Sprouting hulless oats. I’ll note that this Illinois farmer doesn’t let Amazon handle their organic Avena nuda oats, and they add on post office shipping costs. They don’t recommend sprouting, probably because of liability, although I’ve had a 91% germination rate over three days. I might have ordered Avena sativa oats directly from the Montana farmer bypassing Amazon if they were also organic.

2. I stopped taking alpha ketoglutarate. In my view, increasing tricarboxylic acid (TCA) cycle intermediate metabolites such as alpha ketoglutarate and CoQ10 should not be the primary way to improve mitochondrial electron transport chain function.

Instead of biochemical considerations, focus on photon modulation, which precedes biochemical reactions. Which means mitochondrial studies should be controlled for light exposures, and very few of them do that, although it’s the way nature works.

This past winter I increased indoor non-LED light exposure within a circadian rhythm framework. I’ll switch back to walking the beach at sunrise from being out in mid-day sun after it gets a little bit warmer.

3. I’ve taken creatine on and off during the past year. There’s a bit of literature on its use for improving methyltransferase system components like homocysteine.

Stopping creatine fits one of the overall patterns that studies demonstrate – people who are initially deficient in the studied item get a benefit, while people who are initially sufficient don’t benefit from treatment. I’ve always tested mid-range for homocysteine, which is desirable.

4. I had some cocoa powder lying around for a year or two, and I used it this past winter to improve the taste of coffee I bought on sale. Cocoa flavanols are supposed to improve various health measures. But I haven’t been provided access to the most recent human studies, so I won’t repeat their results without reading their details.

5. I saw this at Costco, and picked up a package:

A 2025 review covered pecan research, Pecans and Human Health: Distinctive Benefits of an American Nut. Eating pecans seems to have some health benefits, and they taste alright.

For me, though, the dryness of a chewed pecan bolus creates a swallowing problem that walnuts don’t have. YMMV.

6. I stopped taking 2 g magnesium L-threonate. I’ve always tested high for magnesium without using a specific supplement.

7. I reduced D3 by 25 mcg to a daily 2400 IU. Winter is over.

New and increased items

1. I curated five 2025 ergothioneine studies in Human studies of ergothioneine after stopping mushroom intake via AGE-less chicken soup. I wasn’t thrilled that none of them investigated long-term effects of persistent plasma ergothioneine levels.

This year I decided to start taking the higher 25 mg dose of the first study once a week. That should produce some benefits at a lower ergothioneine blood level than daily doses produce. I’ll check periodically for 2026 research.

2. The only paper I’ve curated on deuterium (heavy hydrogen) is Taurine and mitochondrial health. I started using Icelandic glacier water to make coffee and tea, and for just drinking.

It isn’t advertised as deuterium-depleted water, and it isn’t manufactured as such. But I think any glacier water contains less deuterium than local water. I use local filtered water for sprouting and cooking.

3. Per The return of the free radical theory of aging I started taking extra vitamin C separately from other supplements in the form of Now brand liposomal 1 gram twice daily this past winter. That study found vitamin C to be an anti-aging compound for primates.

Reference 72 of that 2026 paper is a freely available 2025 study https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(25)00339-X “Vitamin C conveys geroprotection on primate ovaries” that used the same vitamin C dose and duration in macaques to find:

“VC slowed aging in various ovarian cell types. Moreover, VC protected human ovarian endothelial and stromal cells (SCs) from aging partially via NRF2 activation. This study establishes a proof-of-concept for delaying primate ovarian aging with a single compound, and provides important insights into preventing and treating degenerative diseases related to ovarian aging.”

4. I restarted taking inulin last year, about 3 grams (a heaping teaspoon) daily after posting Inulin vs. FOS. My 2.5 year-old grandchild takes a level teaspoon daily, as inulin’s beneficial effects aren’t just for old people.

5. I started taking 12 mg astaxanthin twice in the morning. I use Nrf2 activators in the morning because Nrf2 is especially involved in the circadian cycle, as noted in papers such as Broccoli sprouts activate the AMPK pathway, Part 4.

6. I increased daily raw egg consumption from 3 eggs a day to 3 eggs twice daily.

7. This year, Ovega 3 algae oil DHA 420 mg/EPA 140 mg became no longer available AFAIK. I substituted Vegan Omega 3 algae oil DHA 300 mg/EPA 150 mg in the morning and Sports Research Omega 3 fish oil DHA 310 mg/EPA 690 mg in the afternoon.

8. I picked up this Korean seaweed in a 10-pack at Costco. The label doesn’t say what its iodine content is. I eat it as a snack whenever I get a salt craving, maybe once a week.

The return of the free radical theory of aging

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A 2026 primate study investigated effects of vitamin C:

“Here, we define a conserved iron-lipid axis driving primate aging, termed ‘ferro-aging.’ Multi-tissue profiling in humans and non-human primates reveals age-progressive iron accumulation, fueling chronic lipid peroxidation orchestrated by acyl-coenzyme A (CoA) synthetase long-chain family member 4 (ACSL 4). Distinct from acute ferroptosis, this ACSL4-mediated process promotes cellular senescence and systemic functional decline.

We identify vitamin C (VC) as a direct inhibitor of ACSL4. Long-term VC administration in aged monkeys for over 40 months potently reduces ferro-aging signatures across tissues, attenuates multi-organ pathology, and improves neurological and metabolic functions. Multi-omic aging clocks indicate the VC-mediated reversal of biological age.

Despite decades of interest in oxidative stress, largely sparked by the free radical theory of aging, efforts to modulate it broadly with antioxidants have yielded inconsistent or neutral outcomes, highlighting the theory’s limitations and underscoring the need to identify more specific, upstream drivers. A critical challenge remains: determining whether the iron-lipid axis constitutes a core upstream driver of aging in primates and, if so, whether it is therapeutically targetable.

In this study, we bridge these gaps. We define an iron-triggered, ACSL4-governed, lipid peroxidation-driven program that escalates with age across diverse cell types and multiple organs in non-human primates.

VC treatment dose-dependently increased Nrf2 phosphorylation and activation. VC orchestrates a dual-defense strategy against ferro-aging: it directly suppresses the pro-aging lipid peroxidation driver ACSL4, while in parallel, it bolsters the cell’s intrinsic antioxidant capacity via Nrf2 pathway activation.

Middle-aged cynomolgus monkeys (12–16 years old, approximating human 40–50 years) received daily oral VC (30 mg/kg group) or a control treatment for 40 months under standardized conditions.

Structural MRI analysis demonstrated that VC intervention counteracted age-related brain atrophy. Using general linear mixed models, we found that VC restored cortical surface area in the frontal lobes of aged monkeys. Regional analysis identified enlargement in four regions of the orbital frontal cortex, an area critical for adaptive behavior.

Diffusion MRI-based connectomics revealed that, compared with young animals, aged monkeys exhibited reduced structural connectivity in 18 brain regions. VC treatment restored connectivity in 9 of these regions, which were predominantly located in the posterior parietal cortex, a hub for spatial awareness and decision-making.

VC exerted robust neuroprotective effects. It attenuated heterochromatin loss (increased H3K9me3) in the prefrontal cortex and hippocampus and reduced abnormal protein aggregates, including cytosolic aggresomes and Aβ. Additionally, VC lowered the abundance of activated microglia and astrocytes and suppressed expression of the innate immune sensor cGAS in the hippocampus.

VC supplementation reduced the estimated biological age across multiple organs. At the epigenetic level, VC lowered DNA methylation age in several tissues, including brain, brown adipose tissue, muscle, skin, aorta, and kidney. In the hippocampus, the most substantial reductions in biological age occurred in microglia, oligodendroglia, and oligodendrocyte precursor cells. In the pancreas, alpha cells, beta cells, and ductal cells showed the greatest rejuvenation.

In summary, chronic VC supplementation inhibits the ferro-aging pathway, reduces multidimensional biological age across primate organs, and ameliorates a spectrum of functional declines in nervous and metabolic systems. Our work establishes ACSL4 inhibition as a promising and translationally relevant therapeutic strategy for mitigating aging-related decline.

A long-term, 40-month intervention study in aged non-human primates is a highly translational model given their shared inability with humans to synthesize VC endogenously. The finding that a single, safe nutrient can reverse multidimensional aging clocks in a primate has profound implications for translational longevity medicine.”

https://www.sciencedirect.com/science/article/abs/pii/S1550413126000537 “Vitamin C inhibits ACSL4 to alleviate ferro-aging in primates” (not freely available) Thanks to Dr. Pradeep Reddy for providing a copy.

Grok’s take on this study:

“For humans (who, like macaques, cannot synthesize vitamin C), the Recommended Dietary Allowance (RDA) is 75–90 mg/day for adults (~1–1.5 mg/kg for a 60–70 kg person) to prevent deficiency. Upper safe intake levels are much higher: up to 2,000 mg/day (Tolerable Upper Intake Level) is considered safe for most adults, with no established adverse effects at that level from food/supplements.

Treated monkeys represent advanced aging stages (likely equivalent to human 50s–70s+ based on ‘aged’ designation and long-term intervention effects), extending the prior 12–16-year monkey range (human ~35–55) to broader anti-aging applications. While human trials are needed, the primate evidence (long-duration, systemic benefits) strengthens the case for high-dose, sustained vitamin C as a strategy against ferro-aging in humans. It elevates vitamin C from a nutrient to a targeted anti-aging compound in primates.”

Coincidentally, I started taking extra vitamin C separately from other supplements in the form of liposomal 1 gram twice daily this past winter. Can’t say that it had any effects on my intended target, avoiding sniffles and sneezing, as allergy season kicked off in early February. With this study’s findings, I’ll continue.

Eat broccoli sprouts for ALS?

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A 2026 rodent study investigated sulforaphane’s ability to affect ALS-like symptoms:

“The objective of this study was to evaluate neuroprotective efficacy and safety of sulforaphane (SUFP) in a methylmercury (MMHg⁺)-induced preclinical rat model of amyotrophic lateral sclerosis (ALS). ALS is characterized by progressive motor neuron degeneration and muscle wasting, leading to impairments in gait, swallowing, salivation, and routine motor activities.

64 animals were classified into eight groups: 1st: normal control, 2nd: vehicle control; 3rd: SUFP perse (4 mg/kg, i.p.), 4th: MMHg + (5 mg/kg, p.o.), 5th: MMHg + 5 + SUFP (2 mg/kg, i.p.), 6th: MMHg+ 5 + SUFP (4 mg/kg, i.p.), 7th: MMHg+ 5 + omaveloxolone (OVX) (30 mg/kg, i.p.), and 8th: MMHg + 5 + dimethyl fumarate (DIMT) (50 mg/kg, i.p.). Neurotoxin MMHg + was orally administered at 5 mg/kg for the first 21 days. For the next 22 days, SUFP, OVX, and DIMT were administered intraperitoneally (i.p.).

SUFP modulates neurotransmitter levels such as acetylcholine (A), dopamine (B), GABA (C), glutamate (D), and serotonin (E).

SUFP4 exerted broad neuroprotective effects in ALS pathology by restoring antioxidant proteins (Nrf2, HO-1, SIRT1), suppressing apoptotic (Bax, caspase-3, Bcl-2) and inflammatory markers (TNF-α, IL-1β), and enhancing the anti-inflammatory cytokine IL-10. It also downregulated stress-related signaling pathways (PI3K/Akt, p75NTRECD, MAPKs) associated with neurodegeneration. These molecular effects translated into meaningful functional recovery, as evidenced by improvements in grip strength, locomotor performance, spatial memory, and depressive-like behavior.

Histopathological evaluation demonstrated attenuation of demyelination and preservation of neuronal architecture including the cerebral cortex, hippocampus, striatum, midbrain, and cerebellum. Beyond central neuroprotection, SUFP exerted systemic benefits by normalizing hepatic enzymes, improving skeletal muscle integrity, restoring redox balance, stabilizing neurofilament and myelin-associated proteins, and correcting hematological alterations.

Despite limitations related to study duration and animal sex, this work strongly positions SUFP as a promising, multi-target therapeutic candidate for ALS with both neural and systemic protective efficacy.”

https://link.springer.com/article/10.1007/s12035-026-05683-5 “Sulforaphane-Mediated Multitarget Therapeutic Effects in Methylmercury-Induced ALS-Like Pathology: Comparative Analysis and Multifaceted Approach to Neuroprotection and Systemic Recovery” (not freely available) Thanks to Dr. Sidharth Mehan for providing a copy.

Unlike A Nrf2 treatment for ALS?, this study didn’t present evidence that its treatment compound was effective for preventing ALS. For one thing, currently-known disease factors involving heat shock proteins and associated genes, some of which are Nrf2 targets, weren’t investigated.

Two Nrf2 activators were used in both studies as comparators of Nrf2 activation effects. Neither omaveloxolone nor dimethyl fumarate are ALS causal treatments, though, and have undesirable side effects.

A human equivalent of this study’s higher sulforaphane dose is ((4 mg x .162) x 70 kg) = 45 mg. 45 mg of sulforaphane might be too much to consistently take at one time because of unpalatability. But I documented taking an estimated 52 mg for a year during 2020-2021 by eating microwaved 3-day-old broccoli sprouts twice a day.

Nrf2 and stem cells

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A 2026 review subject was mechanisms and therapeutic potential for Nrf2 activators in combination with mesenchymal stem cells:

“Mesenchymal stromal/stem cells (MSCs) are multipotent stem cells that can be isolated from various tissues – such as bone marrow (BM), umbilical cord (UC), adipose tissue (AD), dental pulp (DP), hair follicle (HF), and placenta – and differentiated into multiple lineages under appropriate conditions. Their functional repertoire includes immunomodulation, homing, and differentiation, which collectively help establish a balanced inflammatory and regenerative niche within damaged tissues during severe inflammation. MSCs-derived extracellular vesicles (MSCs-EVs) and conditioned medium (MSCs-CM) play remarkable roles, exhibiting potent anti-inflammatory and antioxidant properties that offer novel therapeutic alternatives for inflammatory diseases.

Therapeutic capacity of MSCs in inflammatory conditions is increasingly attributed to their potent paracrine activity rather than solely to their differentiation potential. A key mechanism underlying this paracrine effect is activation of the Nrf2 antioxidant pathway.

MSCs and their secreted products including exosomes (Exos), EVs, and CM, activate Nrf2 through multi-dimensional/target mechanisms, thereby enhancing cellular antioxidant defenses, modulating immune responses, and promoting tissue repair. It is noteworthy that therapeutic efficacy of MSCs and their derivatives can be enhanced through external modulation, including pretreatment with natural compounds.

Preconditioning refers to brief treatment of MSCs or their derivatives with physical, chemical, or biological factors prior to application, aiming to enhance their ability to counteract oxidative stress and improve their therapeutic efficacy. Flavonoids precondition and prime MSCs via the direct Keap1-Nrf2 pathway or indirect PI3K-Akt pathway, which enhances cellular resilience to adverse conditions by reducing apoptosis and promoting survival. Primed MSCs, in turn, remodel the microenvironment through an altered secretory profile, releasing bioactive factors that create more favorable conditions for their own persistence.

The core logic of these strategies lies in simulating or inducing adaptive stress, such as employing specific chemical molecules or drug stimuli, or utilizing physical / microenvironmental preconditioning to mimic specific physical conditions of the in vivo injury environment. The most straightforward strategy is overexpression of Nrf2 or its key downstream effector molecules.

The majority of existing studies remain at the level of observing correlations with Nrf2 upregulation, and there is still a lack of precise causal validation regarding key upstream signals – such as specific cytokines, miRNAs, or proteins – through which MSCs or derivatives initiate Nrf2 activation. Mechanistic insights are predominantly derived from in vivo or rodent (mouse/rat) model experiments, with a notable absence of clinical validation, insufficient long-term safety and pharmacokinetic data, and a lack of standardization in administration routes and dosages, all of which hinder clinical translation.

The essential role of the Nrf2 pathway has not been rigorously confirmed, as most studies have not employed reverse genetic validation using Nrf2-knockout animals or specific inhibitors. Consequently, it remains unclear whether therapeutic effects are necessarily and exclusively dependent on Nrf2, and potential synergistic contributions from other pathways may have been overlooked.

Most natural flavonoids face challenges such as low oral bioavailability, rapid metabolism, and poor targeting. Numerous challenges remain to be addressed in order to translate these promising preclinical findings into clinical practice. Future research should focus on the following aspects:

  1. Elucidating precise upstream molecular mechanisms by which MSCs activate Nrf2;
  2. Employing more clinically relevant chronic disorder models;
  3. Systematically evaluating long-term safety, optimal delivery strategies (including dosage and route of administration), and immunogenicity of MSCs-based therapies;
  4. Validating selection criteria (optimal source), quality control, batch-to-batch consistency of MSCs, and addressing regulatory and ethical barriers to clinical translation; and
  5. Integrating molecular docking, ADMET (Absorption, Distribution, Metabolism, Excretion, Toxicity) prediction, and in vitro and in vivo validation to further elucidate regulatory effects of flavonoids and enhance understanding of their mechanisms of action.”

https://link.springer.com/article/10.1186/s13287-026-04925-6 “Activation of Nrf2 with natural flavonoids and mesenchymal stromal/stem cells: mechanisms and therapeutic potential for inflammatory diseases” (click pdf)

This paper was overly long at 127 pages, so I focused on the later sections. None of these treatments are currently ready for clinical trials.

I also didn’t mention specific flavonoids as Nrf2 activators. It’s beyond a reviewer’s task to rank Nrf2 activators, and a study’s researchers seldom address why they used a poorly-activating flavonoid instead of a higher-ranked natural plant compound such as sulforaphane.

Polling vs. propaganda

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An anonymous doctor’s perspective on what’s permitted to be publicly discussed regarding vaccine injuries:

“Only one polling organization independently investigated it, Rasmussen Reports (a conservative polling organization which has a reputation for getting accurate results due to them having listeners punch answers in response to an automated voice rather than directly talking to someone who may bias them). For American adults, they found:

  1. July 2021: 32% believed public health officials were lying about the safety of COVID-19 vaccines.
  2. December 2022: 56% of 1000 respondents believed the vaccines were effective, 57% were concerned the vaccines had major side effects. Most importantly, 34% of those vaccinated reported minor side effects and 7% reported major side effects (e.g., those seriously impairing their quality of life).
  3. January 2023: 49% believed it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths and 28% personally knew someone whose death may have been caused by side effects of the COVID-19 vaccines. 57% wanted Congress to investigate how the CDC handled assessing vaccine safety (presumably since many suspected the CDC had covered up the dangers of the COVID vaccination program).
  4. March 2023: 11% of those surveyed reported that they believed a member of their household died from COVID-19, while 10% believed a member of their household died and that their death may have been due to a side effect of the vaccine.
  5. September 2023: 47% of those surveyed stated they did not believe the vaccines were safe and 34% did not believe they were effective. As before, these results also politically stratified as Democrats were less likely to believe the vaccines were unsafe (14% D vs. 51% R) or ineffective (17% D vs. 57% R).
  6. November 2023: 24% personally knew someone they believe died from a COVID vaccine, and of those individuals, 69% would be likely to join a class action lawsuit against the pharmaceutical companies.
  7. January 2024: 53% believe it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths and 24% personally knew someone whose death may have been caused by side effects of COVID-19 vaccines.
  8. September 2024: 55% surveyed believe it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths – including 30% who say it’s very likely.
  9. November 2025: 26% reported they had minor side effects from the vaccine and 10% reported major side effects. Additionally, 46% believed it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths – including 25% who say it’s very likely.

In short, the data shows you aren’t crazy, and while the news is not reporting it, the majority of people are seeing exactly the same thing you are. There is no getting around the fact a lot of people were harmed by these vaccines.”

https://www.midwesterndoctor.com/p/polling-reveals-a-profound-shift “Polling Reveals A Profound Shift on Vaccines: We Can’t Let Pharma Bury It”

I knew two women who died in mid-2022 in their late sixties who probably had vaccine injuries contributing to their shortened lives. The subject wasn’t allowed to be discussed earlier this decade, and it largely still isn’t.

Everything this article says about covid vaccine injuries is applicable to the childhood vaccines. I found out at a house party earlier this week that both subjects are verboten, especially with women who have preschool children, despite their libertarian orientation.

Don’t know what will change public acknowledgement of vaccine harms. Isn’t it obvious that we were and are being lied to? Why still trust untrustworthy professions?

I thought at the beginning of this decade that people would soon see through the propaganda, but that didn’t happen. I also thought that public punishments for crimes against humanity would penetrate people’s awareness that we’d been duped, but the guilty still run free.