The pathways that tie the research together.
Many interventions act on the same few processes. Open a mechanism to see everything that touches it.
Mitochondria & energy
She treats mitochondrial dysfunction as part of the root cause of aging: it limits cellular energy and raises oxidative stress, and immune cells are especially vulnerable to decline and 'exhaustion.'
12 interventionsGlutathione & oxidative stress
Glutathione is the cell's main internal antioxidant; she explains that glycine plus cysteine (e.g., from NAC) can restore it, countering oxidative stress tied to cognitive decline, inflammation, heart disease, and insulin resistance.
12 interventionsEpigenetics & DNA
Aging involves accumulating somatic mutations, shifts in DNA methylation that epigenetic clocks measure, and loss of organized chromatin structure; a new study showed boosting SIRT6 reversed some of these DNA changes.
12 interventionsAmyloid & tau
Amyloid-beta plaques and tau tangles define Alzheimer's, but she frames them as possibly an innate immune defense against pathogens, with blood-brain barrier leakiness, fibrinogen, and GSK3β acting upstream.
11 interventionsCellular senescence
Senescent 'zombie' cells stop dividing, which helps prevent cancer, but they pile up with age and secrete inflammatory signals that drive inflammaging; she increasingly favors restoring the immune system's own clearance over senolytics.
7 interventionsGut microbiome
Gut microbes make metabolites that can protect (bifidobacteria, 5-AVAB, arginine) or harm (imidazole propionate), shaping immune balance, heart, and brain health; modern exposures like artificial sweeteners shift the microbiome.
7 interventionsCircadian rhythm & sleep
Circadian rhythm affects about 40% of active genes and immune timing; light at night lowers melatonin, disrupting the clock gene BMAL1 increased amyloid deposition in mice, and short sleep in midlife raises later dementia risk.
7 interventionsAutophagy
Autophagy is cellular recycling of damaged proteins and components; her posts link spermidine and FOXO3 to inducing it, and she cites a mouse study where inhibiting autophagy caused neuromuscular dysfunction in old age.
6 interventionsCollagen & extracellular matrix
The extracellular matrix changes with age: AGEs crosslink and stiffen collagen in skin and vessels, escaped digestive proteases can break down matrix, and excess fibronectin scars the blood-brain barrier.
6 interventionsImmune aging & T cells
The thymus shrinks with age, weakening T cells against infection and cancer; she highlights arginine as fuel for T cell metabolism and red-light therapy as a way to support immune function.
6 interventionsMethylation & homocysteine
The methylation cycle supplies methyl groups for gene regulation and creatine synthesis (about 40% of them go to creatine); B12, B6, and folate help keep homocysteine, a heart and brain risk marker, in check.
5 interventionsGut barrier
The intestinal mucus layer shields the body from digestive enzymes and bacteria; animal studies show it thins with age and with food emulsifiers, and she considers its integrity essential to healthy aging (the autodigestion theory).
5 interventionsNLRP3 inflammasome
The NLRP3 inflammasome is an immune sensor that amyloid-beta and tau activate in microglia, setting off IL-1β-driven neuroinflammation; large medication datasets suggest blocking it may lower Alzheimer's risk.
4 interventionsLipids & membranes
Membrane lipids matter: plasmalogens act as brain antioxidant phospholipids and are very low in Alzheimer's, C15:0 is thought to stabilize cell membranes, and the omega-6 to omega-3 balance shapes inflammation.
4 interventionsStem cells
Stem cell decline limits regeneration: senescent stem cells renew poorly, microbiome shifts impaired intestinal stem cells in old mice, and adult neurogenesis drops sharply in Alzheimer's.
4 interventionsNAD+
NAD+ is a coenzyme that powers mitochondrial energy, DNA repair, and immune function; she notes levels fall 50% or more by age 60 as CD38 (inflammation) and PARP use more of it and production drops.
3 interventionsGSK3β
GSK3β drives the tau phosphorylation that forms tangles; she highlights research that lithium deficiency raises GSK3β, and that low-dose lithium inhibits it.
2 interventionsBlood-brain barrier
The blood-brain barrier controls what enters the brain; she sees its breakdown, through excess astrocyte fibronectin in APOE4 or a thinning glycocalyx, as upstream of amyloid buildup, inflammation, and pathogen entry.
2 interventionsNutrient sensing & mTOR
Animal studies suggest restricting specific amino acids (methionine, cysteine, BCAAs such as valine), rather than calories alone, drives longevity; the gut metabolite imidazole propionate activates mTORC1 and impairs insulin signaling.
2 interventions