Low-dose aspirin slashed dementia risk by 70% in certain people, study shows. Researchers at Monash University in Australia went back to the ASPREE trial, a large study in which older adults took either a daily low-dose aspirin or a dummy pill (placebo). They analyzed the genetic data of more than 13,500 participants and gave each person a "polygenic score", a combined measure of many small gene variants, linked to how many platelets their blood makes. Platelets are the tiny cells that help blood clot. In the 20% of people with the highest platelet scores, just 1% of those on aspirin developed dementia, compared with 3.3% of those on placebo, about 70% lower risk. Earlier trials found aspirin didn't prevent dementia when everyone was considered together, so this points to a hidden group who might benefit, and to platelet biology as a new lead in dementia research. The signal wasn't tied to known Alzheimer's risk genes. But the same high-score group also had more major bleeding on aspirin, 4.4% vs 2.1% on placebo. This is a subgroup finding that still needs confirming in a dedicated trial. Do not start taking aspirin to prevent dementia on your own: daily aspirin can cause serious bleeding, so talk to your doctor first. source: Fransquet, P. D., Yu, C., Tran, C., Hussain, S. M., Brodtmann, A., Tonkin, A. M., Nelson, M. R., Ryan, J., McNeil, J. J., & Lacaze, P. (2026). Platelet count polygenic scores may modify the effect of aspirin in primary prevention of dementia. Alzheimer's & Dementia, 22(9).

WHO-grade electrolytes irrigate hypoxic tissue & improve brain perfusion. NAC is a refined, powerful stabilizer but dose + timing are complex & need calibration. For neuroinflammation cognition + mood: Lo dose nicotine patch, hydroxizine, LDN, micro/low dose Abilify, Alpha GPC.

The humble mushroom in your fridge has a hidden winter superpower: it is a biological satellite dish designed to trap the sun. Mushrooms contain a compound called ergosterol. It is virtually identical to the cholesterol in human skin. When hit by ultraviolet light, it instantly transforms into pure Vitamin D. In the summer, leaving mushrooms in the sun for 15 minutes skyrockets their Vitamin D levels by over 1,000%. They retain that potency for days in the fridge and survive the heat of a searing pan. It is a living hack for human vitality. But right now, we are in the depths of winter. The angle of the earth has locked us under a weak sky. The UV index is flatlining, and window glass completely blocks the remaining UVB rays. If you leave your mushrooms on an indoor windowsill today, nothing happens. To activate them in the winter, you have to shift the physics: 1. Slice them thin: You need maximum surface area. 2 Flip them over: The gills contain the highest concentration of ergosterol. Point them directly at the sky. 3. Go outdoors: Glass is a barrier. They need direct, unfiltered contact. 4. Extend the time: The winter sun is weak. Give them 2 hours minimum. If the sky is completely grey, hack the system. Placing a reptile UVB lamp over sliced mushrooms indoors for an hour triggers the exact same evolutionary chemistry. Nature doesn't stop operating in the dark seasons. It just requires you to understand the geometry.

He drove his wife to one of the best hospitals in America for a planned caesarean. A routine one. Her second. Charles Johnson watched her blood collect in a catheter bag for ten hours while he asked for help. Kira Johnson died at 2:22am. Cedars-Sinai, Los Angeles, 12th April 2016. Kira Johnson was 39. She spoke five languages, raced cars, ran marathons. The caesarean was scheduled. Everything about it was routine. Her son Langston was delivered at midday. By the afternoon her husband could see blood in her catheter. He told a nurse. He was told they would check. He asked again. And again. A CT scan was ordered and then not performed. He has described being told, at one point, that his wife was simply not a priority right now. He stood in a corridor for ten hours asking people to look at his wife. They took her back to theatre just after midnight. There were three litres of blood in her abdomen. She died shortly after. Her son Langston was twelve hours old. Charles Johnson has spent the decade since as one of the most effective advocates in American maternal health. He founded 4Kira4Moms. He has testified before Congress. The federal Black maternal health legislation introduced in recent years carries work he pushed for. He talks about one thing more than any other, and it is not the medicine. It is the ten hours. He was standing right there, in the building, awake, articulate, asking. And it made no difference at all.

ADHD in older adults raised the odds of later cognitive impairment more than fourfold. Higher daytime light cut dementia risk. The shared axis is sunrise light on solar time. It advances the master clock, sets the nocturnal melatonin window, and times the mitohormetic ROS pulse that restores mitochondrial membrane potential. Miss that cue and the repair window for high-flux attention and memory circuits compresses. ADHD liability (clinical or genetic) marks lower tolerance for the mismatch. The light study showed larger protection precisely where the margin is already narrow—evening chronotypes, high nighttime light, APOE ε4. Pair it with darker nights, especially in winter. Absolute risks stay modest. Both studies are observational. The numbers keep pointing to the same daily contrast. Head to my bio for 1 on 1 consultation

Over the last two decades, ordinary U.S. citizens have come to see themselves in different struggles when in fact we all face the same challenges. In this essay, I present how we got to where we are, and the foundation of the solution. We have more in common than not. Read free!

Things that are connected: US live-streaming the firing squad execution of a paraplegic in a wheelchair. The public calling CPS on celeb parents with disabled babies & demanding their removal. US states bringing back forced institutionalization in private equity-owned institutions. US removes disability protections & cuts off disability services, as we’re systematically disabled by unmitigated pandemics & no one can afford healthcare. US/Canada euthanizing the disabled, poor, & mentally ill. Netherlands just euthanized a baby. Very obvious increases in ableist content, beliefs & behaviors, after we learned cognitive disabilities in the US have increased by over 40% since 2019 & the RECORD disability we’ve ignored since 2020 continues to increase. There is no funding & no help for the rapidly increasing disabled population, which is YOUNG & GROWING YOUNGER, only institutionalization to enrich private equity & certain premature death. Human life has been fully devalued. Bad things are upon us & even worse things are coming. All together now: This is a Business Model. In the end, they’re going to kill us.

BREAKING: my latest test finds that 8g of vitamin B5 per day dropped post-ruck lactate from over 656 to 23 in two weeks WHILE DOUBLING THE WORKLOAD. B5 also improved: - Pyruvate (-96%) - Alanine (-76%) - less pyruvate spillover - Citrate (undetectable → in range) - Kreb cycling working better - Hippuric acid (23x higher) - better benzoic acid clearance - Orotic acid (-88%) - less ammonia

TTFD is one of the best things for fixing many gut issues, brain fog and chronic fatigue, but it needs cofactors to work properly. If cofactors are missing, it can hurt you in the long term. Here is the exact architecture to unlock the therapeutic power of TTFD without precipitating functional collapse👇 1. The Transporter-Independent Bypass Standard water-soluble thiamine salts rely on rate-limiting active transport proteins (SLC19A2 and SLC19A3) that downregulate under inflammation and hypoxia. TTFD possesses a lipid-soluble mercapturic structure that bypasses these transport gates entirely. It diffuses passively across cell membranes, penetrates the blood-brain barrier, and saturates intracellular compartments independent of metabolic friction. 2. The Clinical Upstream Leverage Once inside the cell, TTFD targets the primary rate-limiting enzymes of bioenergetic metabolism: Pyruvate Dehydrogenase (PDH), converting glycolytic pyruvate into Acetyl-CoA to clear cellular lactic acidosis. Alpha-Ketoglutarate Dehydrogenase (KGDH), unlocking the rate-limiting turn of the Krebs cycle. Transketolase, driving the Pentose Phosphate Pathway to generate NADPH for antioxidant defense and myelin synthesis. Acetylcholine synthesis via the PDH axis, directly rebooting vagus nerve motor output, gastric motility, the migrating motor complex (MMC), and resolving chronic dysautonomia or POTS. 3. The Glutathione Extraction Trap: To release free thiamine into the cytoplasm, TTFD requires the cleavage of its prosthetic disulfide bond. This enzymatic cleavage consumes reduced intracellular glutathione (GSH). In an internal system already burdened by oxidative stress, high-dose TTFD acutely strips the remaining GSH pool, triggering immediate mast cell destabilization, chemical sensitivity, and sudden detox flares. 4. The Phosphorylation Stall Free thiamine is biologically inert. It must be converted into active Thiamine Pyrophosphate (TPP) by the enzyme Thiamine Pyrophosphokinase (TPK1). TPK1 is strictly dependent on intracellular magnesium. If magnesium is depleted, TTFD accumulates as an unphosphorylated intermediate, stalling cellular energy production while accelerating systemic receptor agitation. 5. The Intracellular Ion Shift (Refeeding Dynamics) Unlocking a paralyzed PDH complex forces immediate, high-velocity glucose oxidation. Rapid glycolysis drives circulating potassium and phosphorus out of extracellular fluid and directly into cells. Without potassium repletion, patients experience functional hypokalemia: severe muscle weakness, ectopic heartbeats, resting tachycardia, and autonomic panic. 6. The Obligate Cofactor Architecture Chelated Magnesium Magnesium is the non-negotiable coenzyme required for TPK1 to synthesize active TPP. It stabilizes ATP within the mitochondrial matrix and buffers NMDA receptor channels against sudden glutamate flux. Administer bioavailable magnesium hours before escalating TTFD. Active Riboflavin (B2 / R5P) Riboflavin in its active Flavin Adenine Dinucleotide (FAD) state is required by Glutathione Reductase to recycle oxidized glutathione back into reduced GSH. Saturating the FAD pool ensures the disulfide cleavage of TTFD does not deplete cellular antioxidant defenses. You can also add GlyNAC for extra Glutathione. Potassium Repletion Dietary and supplemental potassium buffers the sudden intracellular electrolyte shift driven by accelerated glucose metabolism. Maintaining serum potassium prevents cardiac palpitations and terminates paradoxical adrenaline dumps. Balanced Methylation and B-Complex Support Unlocking transketolase and downstream dehydrogenase enzymes spikes consumption of Niacin (NAD+) and methyl donors. A fully methylated, balanced B-complex ensures secondary metabolic pathways do not bottleneck downstream. Other Cofactors: Molybdenum (Sulfite Clearance) and Selenium (Glutathione Peroxidase Axis). 7. The Unresolved Gap Supplying magnesium, potassium, and riboflavin buffers the TTFD entry pathway, but it does not address why your baseline bioenergetic engine failed initially. If your cellular respiration is paralyzed by heavy metal displacement, peripheral thyroid resistance, chronic endotoxemia, or electron transport chain Complex I/IV stall, forcing pyruvate into the mitochondria with TTFD will merely build up upstream pressure against a locked metabolic door. Treating downstream coenzyme deficiencies while ignoring the primary systemic bottleneck guarantees persistent functional collapse. - Chronic fatigue, gut issues and brain fog all trace back to stalled mitochondrial respiration and nutrient deficiencies. DM me 'PROTOCOL' with your biggest bottleneck and what you’ve already tried. I will break down the exact step-by-step pathway to fix it.

Search for root causes. Bear in mind low volume + thickness may worsen baseline & block recovery. That's why saline IVs give relief to some. Chugging water throws off gut & more. Retail sodium-glucose electrolytes using SGLT1 (w/potass.) may help.

Good news re vision, means it can improve further. Neuroinflammation may be factor. What's thickening the blood? Eg, if fibrinogen, antiplatelet meds may not help (or worse). Is there low blood volume (common in POTS Long Covid ME/CFS)? It concentrates the blood + impedes flow.

Look into Vit. E. Nature's warfarin. Linked to cancer. Use diagnostically: good response to hi-dose 1-2 days may imply high vonWillebrand + platelet-adhesion (vessel walls). Tried toxic 1800mg once & came to life for hours, helped pinpoint medications for morbid viscosity.

The top 0.1% of US households now own 15% of all household wealth, a record high. Meanwhile, the bottom 50% own just 2%. The wealth gap has never been wider.

Would this include rhodiola, ashwagandha and huperzine a?

This has been known for several years. Several doctors treat long Covid AND vaccine injury by a complex dance involving several blood thinners and anti-coagulants. Sharyl Attkinson has featured a couple on her show including follow-up stories.

A striking 54% increase in excess deaths in young adults aged 18 -44 in 2021. Middle-aged adults were ~26% above, and all ages were ~18% above in 2021. From 2022 onward, the excess deaths in children aged 0-17 from disease ranged ~12-17% above baseline, through 2024. According to mECfS IACC PAIS distortionists, these DEAD CHILDREN are NOTHING NEW.