Your questions,
answered.

BPC-157 (Body Protection Compound 157) is a synthetic peptide derived from a protein found in gastric juice. Pre-clinical research — primarily in rodent models — shows significant effects on tissue repair, tendon healing, and gut integrity. It appears to work by upregulating growth factor signalling and modulating nitric oxide synthesis.

The limitation is that high-quality human clinical trial data remains limited as of 2026. Most evidence is derived from animal studies, case reports, and self-reported biohacker data. This doesn't make it ineffective — it means the evidence base is immature. Phase II human trials in gastrointestinal conditions are underway.

The EMA's June 2026 regulatory update raises the compliance bar for peptide sourcing in Europe. If you are considering BPC-157, sourcing provenance and purity verification are now essential, not optional.

GHK-Cu (copper peptide) is one of the better-studied cosmetic peptides, with a mechanism involving upregulation of collagen, elastin, and glycosaminoglycan production. It also appears to have anti-inflammatory properties and may activate genes associated with tissue remodelling.

Topical application has the most evidence — particularly for wound healing and skin texture improvement. Systemic use (injectable) is less well characterised in humans. Loren Pickart's foundational research, replicated in several subsequent studies, supports its collagen-stimulating properties. More recent research suggests potential epigenetic activity, though this remains investigational.

The SELECT trial (2023–2025) was the pivot point. Semaglutide reduced major cardiovascular events by 20% in non-diabetic, overweight individuals — an effect that persisted even after controlling for weight loss. This strongly suggests mechanisms beyond metabolic control, including reduced systemic inflammation and possible direct vascular effects.

Emerging data also points to neuroprotective effects and potential reduction in Alzheimer's disease risk. The EVOKE trial results, expected in 2026, will clarify the neurological picture. For longevity clinicians, GLP-1 agonists are increasingly viewed as cardio-metabolic and inflammation-modulating tools — not merely weight loss drugs.

Tirzepatide (dual GIP/GLP-1) shows a more potent metabolic profile; early data suggests superior fat loss with preserved lean mass compared to semaglutide, which matters for longevity outcomes beyond simple body weight.

Both NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside) effectively raise NAD⁺ levels in humans. The practical differences are more nuanced than marketing suggests.

NR has more published human trial data, including work from Brenner and colleagues at University of Iowa. NMN has generated significant excitement following David Sinclair's research, and recent Keio University trials confirm bioavailability and NAD⁺ elevation in humans. A 2024 Washington University head-to-head trial found both raised muscle NAD⁺ comparably at equivalent doses, with NMN showing marginally better bioavailability in older adults.

Practically: NR is more extensively studied; NMN is increasingly well-evidenced and preferred by many longevity clinicians for older adults due to its direct conversion pathway. Dose range in trials: 250–1000mg/day. Neither has shown significant adverse effects at these doses. Timing with food appears to matter less than consistency of dosing.

NAD⁺ (nicotinamide adenine dinucleotide) is a coenzyme central to cellular energy metabolism and a required substrate for sirtuins — enzymes implicated in DNA repair, inflammation regulation, and circadian rhythm maintenance. It also feeds PARP enzymes involved in genomic stability.

By the mid-40s, tissue NAD⁺ levels have typically fallen by 40–60% from peak. The primary mechanism appears to be increased consumption by CD38 — an enzyme whose expression rises with age-related chronic inflammation. This creates a depletion spiral: more inflammation → more CD38 → less NAD⁺ → impaired sirtuin activity → more genomic instability → more inflammation.

Restoring NAD⁺ in animal models consistently shows improvements in energy metabolism, muscle function, cognitive markers, and several hallmarks of aging. The human data is directionally consistent, though effect sizes vary considerably.

Spermidine is a polyamine naturally found in wheat germ, aged cheese, mushrooms, and legumes. Its longevity relevance centres on autophagy induction — the cellular "self-cleaning" process that clears damaged proteins and organelles, which declines significantly with age.

A landmark 2018 observational study found that higher spermidine intake in diet correlated with reduced all-cause mortality. Animal studies show consistent lifespan extension via autophagy induction. Human trials are ongoing, with the most promising data in cognitive protection — a 2021 trial from Charité Berlin showed improved memory performance in older adults with subjective cognitive decline.

Food sources provide meaningful amounts; supplementation doses typically range from 0.5–3mg/day of pure spermidine. It is generally well-tolerated with a benign side-effect profile in available trial data.

Magnesium deficiency is widespread — estimates suggest 40–60% of Western populations fail to meet RDA, contributing to impaired sleep, elevated cortisol, muscle dysfunction, and cardiovascular risk. But form matters considerably for outcome.

Magnesium L-threonate is the only form shown to cross the blood-brain barrier efficiently — the most studied form for cognitive outcomes and sleep quality. Magnesium glycinate offers the best bioavailability for general repletion with minimal GI side effects. Magnesium malate is preferred for energy and muscle recovery. Magnesium oxide is cheap and commonly sold but has very poor bioavailability (~4%) — largely ineffective.

For a longevity protocol: magnesium glycinate at 200–400mg before bed addresses deficiency, improves sleep quality, and supports muscle recovery. Adding magnesium L-threonate (145mg elemental) adds cognitive and neuroprotective benefit.

Vitamin D3 deficiency is extremely common in northern Europe, particularly at latitudes above 45°N during winter months. Blood levels below 30 ng/mL (75 nmol/L) are associated with increased risk of immune dysfunction, cardiovascular disease, depression, and several cancers. Optimal range for longevity purposes is generally considered 50–80 ng/mL.

Supplementation needs depend on baseline levels — which you should test before dosing. Common maintenance doses range from 2,000–5,000 IU/day. Obese individuals and those with malabsorption conditions may need significantly more to reach optimal levels.

Vitamin K2 (specifically MK-7 form) is recommended alongside D3 because higher D3 increases calcium absorption, and K2 directs calcium to bones and teeth rather than arterial walls. The evidence for D3+K2 co-supplementation in reducing arterial calcification is growing. 90–200mcg MK-7 daily is a commonly used dose alongside D3.

A meaningful longevity baseline goes well beyond a standard annual check. The markers that give you real signal on your biological age trajectory include: ApoB (better cardiovascular risk predictor than total cholesterol or LDL-C), fasting insulin and HOMA-IR (early metabolic dysfunction), hs-CRP and IL-6 (chronic inflammation), HbA1c (3-month glucose control), IGF-1 (growth hormone axis, relevant for cellular repair), Lp(a) (genetic cardiovascular risk, largely unaffected by lifestyle), free testosterone and SHBG, DHEA-S, vitamin D 25-OH, ferritin, and a full thyroid panel (TSH, free T3, free T4).

For a more advanced picture: APOE genotype (Alzheimer's risk stratification), methylation-based epigenetic age testing (Horvath clock, GrimAge), and continuous glucose monitoring (CGM) for 2 weeks provides far more information than fasting glucose alone.

Repeat core biomarkers every 3–6 months when actively optimising. The data only becomes powerful when you track trends, not individual snapshots.

Biological age testing uses DNA methylation patterns to estimate how fast your cells are aging relative to your chronological age. The leading algorithms — Horvath's original clock, PhenoAge, GrimAge, and DunedinPACE — each weight different CpG sites and have different correlations with health outcomes.

GrimAge is currently considered the strongest predictor of mortality and disease risk among the established clocks. DunedinPACE measures the pace of aging rather than a fixed age, making it useful for tracking the effect of interventions over time — this is increasingly preferred in longitudinal optimisation contexts.

Is it worth doing? Yes, with appropriate expectations. It gives you a meaningful additional data point — not a definitive prognosis. Combining epigenetic age with ApoB, HOMA-IR, VO2max, and grip strength gives a substantially more complete picture of biological trajectory than any one marker alone.