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Longevity protocols, side by side.

Every protocol profiled on variis, on the same table. Evidence level, categories, and sources, all graded and dated.

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39 of 49 protocols. Scroll horizontally on narrow screens.

Advanced lipid panel (ApoB and Lp(a))Autologous stem cell therapyBioidentical hormone therapyCollagen supplementationContinuous glucose monitoring (CGM) in non-diabeticsContrast therapyCoronary artery calcium (CAC) scoringCreatine monohydrate supplementationDEXA body composition and bone density scanningEpigenetic / DNA-methylation biological age clockExosome therapyFull-body MRI screeningGHK-Cu (copper peptide)GLP-1 receptor agonists (semaglutide, tirzepatide)Latest coverageGLP-1s and healthspan: a 2026 reader’s primerGrowth hormone (recombinant somatropin) therapyHyperbaric oxygen therapy (HBOT)Infrared saunaLow-dose naltrexone (LDN)Menopausal hormone therapy (MHT)Metformin (off-label for healthspan / metabolic optimisation)Multi-cancer early detection liquid biopsy (ctDNA)NAD+ IV infusionNicotinamide riboside (NR) supplementationNMN supplementationOmega-3 fatty acid supplementationPersonalised supplement protocol (biomarker-guided stack)Rapamycin / sirolimus (off-label, low-dose intermittent)Red light therapy / photobiomodulationSleep optimisation protocol (circadian timing, sleep tracking, home sleep studies)Spermidine supplementationStructured resistance training and strength/functional prescriptionTestosterone replacement therapy (TRT)Therapeutic plasma exchange (TPE)Thymosin alpha-1 and thymosin beta-4 (TB-500)Thyroid assessment and optimisationVitamin D supplementationVO2max / cardiopulmonary exercise testingWhole-body cryotherapyZone 2 aerobic training prescription
EvidenceClinicalCommercialCommercialCommercialCommercialCommercialClinicalClinicalClinicalCommercialCommercialCommercialCommercialClinicalClinicalCommercialCommercialPreclinicalClinicalPreclinicalCommercialCommercialMechanismMechanismClinicalCommercialPreclinicalCommercialCommercialPreclinicalClinicalClinicalCommercialPreclinicalClinicalClinicalClinicalCommercialClinical
Also known asApoB, Apolipoprotein B, Lp(a), Lipoprotein(a), Advanced lipids, Cardiovascular risk profileAdipose-derived stem cells, ADSC, Autologous MSC, Mesenchymal stem cell therapy, Adipose tissue-derived stem cell therapyBHRT, cBHT, compounded bioidentical hormones, bio-identical hormone support, body-identical hormone therapycollagen peptides, hydrolysed collagen, hydrolyzed collagen, collagen hydrolysate, bioactive collagen peptidesCGM, FreeStyle Libre, glucose sensor, metabolic monitoring, continuous glucose monitorHot-cold contrast, Contrast bathing, Nordic cycle, Contrast pools, Sauna and ice bath protocol, Contrast water therapyCT calcium score, Calcium score, CAC score, Cardiac calcium scan, Coronary calcium scoring, Agatston scorecreatine, creatine monohydrateDXA, DEXA scan, dual-energy X-ray absorptiometry, body composition scan, bone densitometryDNA methylation age, DNAmAge, epigenetic clock, biological age testing, LinAge 2.0, Horvath clock, OMICmAge, DunedinPACE, TruAgeExosomes, Extracellular vesicles (EVs), Stem cell derived exosomes, Mesenchymal stem cell (MSC) exosomes, Stem cell culture supernatant, Conditioned media / secretomeWhole-body MRI, Whole-body screening MRI, Full body scan, Full body MRI + CT chestGHK-Cu, copper tripeptide-1, GHK copper, glycyl-L-histidyl-L-lysine copper, copper tripeptide complexGLP-1 RA, semaglutide, Wegovy, Ozempic, tirzepatide, Mounjaro, GLP-1/GIP dual agonist, incretin mimeticsHGH, hGH, somatropin, somatotropin, human growth hormone therapy, recombinant human growth hormone, rhGHHBOT, hyperbaric oxygen, mild hyperbaric therapy, soft-shell chamber, hyperbaric oxygen treatmentfar infrared sauna, FIR sauna, IR sauna, infrared heat therapyLDN, naltrexone low dose, low-dose naltrexoneHRT, menopausal HRT, hormone replacement therapy, oestrogen/progestogen therapy, MHT, systemic oestrogen therapy, local vaginal oestrogenmetformin hydrochloride, biguanide, Glucophage, APO-Metformin, DiaforminMCED, circulating tumour DNA screening, LucenceINSIGHT, liquid biopsy cancer screen, Galleri, SPOT-MAS, cell-free DNA cancer screeningNAD+ drip, intravenous nicotinamide adenine dinucleotide, NAD IV therapy, IV NAD+NR, Nicotinamide riboside chloride, Niagen, NAD+ precursorNicotinamide mononucleotide, NMN, beta-nicotinamide mononucleotide, NMN drip, NAD+ precursor supplementation, NMN IV therapyFish oil, EPA/DHA, Marine n-3 fatty acids, Omega-3 index, Icosapent ethyl (prescription EPA)targeted supplementation, supplement prescription, nutraceutical protocol, biomarker-guided supplementation, personalised stackSirolimus, Rapamune, mTOR inhibitor, Low-dose intermittent rapamycinPBM, photobiomodulation, LED light therapy, low-level laser therapy, LLLT, NovoThor, red light bed, Theralightsleep hygiene programme, circadian rhythm optimisation, sleep and stress programme, home sleep study, restorative sleep pillar, QQRT sleep protocolspermidine, polyamine supplementation, spermidine trihydrochloride, wheat germ extract spermidineStrength training prescription, Resistance exercise prescription, Grip strength testing, 30-second sit-to-stand test, Exercise physiology programming, Functional capacity testingTRT, androgen replacement, androgen replacement therapy, andropause treatment, male hormone therapy, testosterone therapy, testosterone optimisationPlasmapheresis, Therapeutic plasmapheresis, Plasma exchange, TPEthymosin, Thymosin Alpha-1, Ta1, Thymalfasin, Zadaxin, Thymosin Beta-4, Tbeta4, TB-500Thyroid optimisation, TSH/T3/T4 panel, Thyroid function testing, Thyroid hormone replacement, Levothyroxine (T4), Liothyronine (T3)Cholecalciferol, Vitamin D3, 25-OH vitamin D repletion, CalciferolVO2 max, VO2max testing, CPET, cardiopulmonary exercise testing, cardiorespiratory fitness testing, maximal oxygen uptake, exercise treadmill testing with gas exchangeWBC, Cryosauna, Cryotherapy chamber, Whole-body cryostimulation, CryosuiteZone 2, Zone 2 training, aerobic base training, moderate-intensity continuous training, MICT, base endurance training
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Evidence summaryApoB and Lp(a) are among the best-evidenced biomarkers in the longevity-clinic universe. Both are supported by large human cohort studies and Mendelian randomisation work indicating causal, not merely correlational, contributions to atherosclerotic disease, and both are recognised in mainstream lipid guidelines. Two important honest limits apply. First, the evidence establishes them as risk markers and causal exposures, not as interventions: measuring ApoB or Lp(a) has not itself been shown in a randomised trial to extend healthspan or lifespan. Second, Lp(a) is at present largely non-actionable. It is minimally responsive to diet, exercise or statins, and the outcome data for the Lp(a)-lowering agents in late-stage development were not yet in hand at the time of writing, so a raised result mainly intensifies management of other modifiable risk factors. ApoB is more actionable, since it responds to established lipid-lowering therapy. A caveat on this record specifically: the live web-search budget for this session was exhausted before the primary literature and guideline sources could be retrieved directly, so the evidence characterisation above rests on the clinical consensus reflected in the clinical sources retrieved rather than on primary papers opened in this session. It should be re-verified against ESC/EAS and NLA guideline documents before publication.There is no human randomised controlled trial showing that autologous adipose-derived stem cell therapy extends healthspan, slows biological ageing, or improves any validated ageing outcome. The trial literature that clinics gesture at is largely in different products and different indications: allogeneic (donor) mesenchymal cell infusions studied in small early-phase frailty trials, and autologous cell injections studied for localised joint and wound repair. Neither supports a systemic rejuvenation claim, and allogeneic frailty data cannot be transferred to an autologous adipose product. What is genuinely established is mechanism (MSCs are immunomodulatory and paracrine-active) plus a commercial market. Claims spanning dozens of unrelated conditions, as seen on clinic pages, are a marker of weak evidence rather than broad efficacy. Known risks include liposuction harvest complications, injection-site events, and, for unregulated preparations, contamination and inappropriate cell differentiation. Graded commercial: it is sold and marketed well ahead of the evidence."Bioidentical" is a marketing term, not a regulatory or pharmacological category, and this is the central thing to understand about it. Regulator-approved body-identical products (transdermal estradiol, micronised progesterone, testosterone) have genuine randomised evidence, but for symptom control in menopause and for treating diagnosed hypogonadism, not for extending healthspan or lifespan. Custom compounded bioidentical preparations are a separate case: the 2020 US National Academies review found a lack of rigorous safety and effectiveness evidence from well-designed or properly controlled studies, and recommended their use be restricted. The Australasian Menopause Society states it cannot endorse compounded bioidentical therapy, noting there are no data on the efficacy of compounded oestrogen for maintaining bone density, that compounded progesterone delivery has been documented as inadequate for endometrial protection with associated endometrial cancer risk, and that excipients in the preparations are unknowable. Salivary hormone testing, frequently bundled with BHRT programmes to justify dosing, is not a validated basis for titration. There is no clinical trial evidence that any bioidentical hormone regimen, compounded or pharmaceutical, extends lifespan, slows biological ageing, or improves a hard healthspan endpoint in people without a hormone deficiency. The gap between what is sold and what is shown is wide, which is why this grades commercial rather than clinical.This is a NEGATIVE FINDING for clinic coverage: a prior discovery pass across Singapore and Australian longevity clinic sites found no clinic in either market naming collagen in a published clinical protocol, and I could not extend or contradict that. What clinical trial evidence exists for collagen peptides addresses cosmetic and symptomatic endpoints, principally skin elasticity and hydration and self-reported joint pain, typically in small, short, industry-funded randomised trials. There is no human evidence that collagen supplementation extends lifespan, slows biological ageing, or improves any hard healthspan outcome such as mortality, incident disease, fracture rate, or a validated ageing biomarker. It does not act on a recognised hallmark-of-ageing pathway in any demonstrated way; the plausible account is simply that it supplies glycine, proline and hydroxyproline plus possible peptide signalling to fibroblasts, which is a nutritional argument rather than a geroscience one. Marketing volume in both markets is very high and is not evidence. IMPORTANT LIMITATION ON THIS PROFILE: my session's live web search budget was exhausted before I could run any searches of my own, so I did not independently retrieve trial-level or clinic-level sources; the only source I opened and verified live is the HSA health supplements overview. The evidence characterisation above should be treated as unverified pending a fresh search pass.CGM has strong clinical evidence in diabetes, where it improves glycaemic control and is a regulated therapeutic device. That evidence does not transfer to the non-diabetic longevity use case. In healthy people, the case rests on mechanism (glycaemic variability and post-meal spikes are associated with metabolic risk markers) plus short-term behaviour-change data, not on outcome trials. There are no trials showing that wearing a CGM as a non-diabetic extends healthspan, reduces mortality, or prevents incident diabetes. Normal-range reference data for non-diabetics is also thin, so "spikes" flagged by consumer apps often fall within ordinary physiology, and the interpretive layer (scores, rankings, food grades) is proprietary and unvalidated. The honest read: a real, well-engineered measurement device wrapped in a healthspan narrative its own evidence base does not yet support. Note also that Vively's own material states Medicare does not cover CGM for non-diabetic individuals in Australia, which is a reimbursement fact and says nothing about approval status.The human literature for contrast water therapy sits almost entirely in the sports recovery domain: short-term perceived soreness and subjective recovery after exercise. It does not demonstrate healthspan, mortality, biological-ageing or chronic-disease outcomes. Heat exposure (sauna) and cold exposure each have their own separate literatures of varying quality, but the combined contrast protocol as sold by wellness facilities has not been shown in humans to extend healthspan or alter ageing biomarkers, and the "Nordic cycle" packaging is an operator construct, not a validated clinical protocol. Important caveat on this profile: this session's live web search budget was exhausted before I could retrieve primary trial literature, so the evidence characterisation above is stated conservatively and is NOT backed by a source I opened in this session. Treat the evidence grade as a floor, not a verified finding, and re-run the literature search before publishing. Cold plunging also carries real cardiovascular risk for some users, which operator marketing typically omits.CAC is the best-evidenced item in the longevity imaging category, but the evidence is prognostic rather than interventional. Everlab cites the Multi-Ethnic Study of Atherosclerosis (Detrano et al., NEJM 2008), a large prospective cohort showing CAC independently predicts future cardiovascular events. That design is observational, not randomised: it establishes that the score stratifies risk, not that scanning asymptomatic people improves survival or healthspan. There is no live-verified randomised trial evidence retrieved here showing that CAC screening itself reduces mortality, and a zero score does not exclude non-calcified plaque. Note a correction to the discovery brief: the National Heart Foundation of Australia endorsement attributed to Everlab could not be found on either Everlab page retrieved; both the imaging page and the test index omit it, and the imaging page cites MESA instead. Treat the Heart Foundation attribution as unverified pending a direct Heart Foundation source.Creatine has one of the largest human trial literatures of any supplement, and the muscle-related findings are genuine clinical evidence: randomised trials consistently show increases in lean mass and strength when creatine is combined with resistance training, including in older adults, which is directly relevant to sarcopenia and healthspan. Cognitive effects are far weaker and inconsistent, largely confined to sleep-deprived or stressed states rather than healthy rested adults. Critically, no trial shows creatine extends lifespan or slows biological ageing in humans; the longevity framing is mechanistic extrapolation from its role in cellular energy metabolism, not an outcome that has been measured. Claims about mitochondrial output and metabolic health are mechanism-level. A caveat on this profile specifically: I was unable to run live literature searches in this session, and the clinical characterisation above rests on one retrieved clinic-authored source plus prior established knowledge, not on primary trial documents I opened. Treat the strength and lean-mass claim as well-supported but independently unverified here.The evidence base is split, and the two halves should not be conflated. For bone mineral density, DEXA is the established diagnostic reference standard, and BMD measured this way has well-documented linkage to fracture risk, which is how the WHO osteoporosis diagnostic thresholds are defined. That is a genuine clinical-grade indication with hard outcome relevance. For the body-composition and general "longevity metric" use, the evidence is materially weaker: DEXA measures body composition accurately, but accurate measurement is not the same as demonstrated benefit. There is no trial evidence that serially scanning asymptomatic adults for visceral fat or lean mass changes mortality, healthspan, or any hard outcome, and the longevity-clinic framing rests on the assumption that a better number drives better behaviour rather than on outcome data. Important caveats on this profile specifically: this session's web search budget was exhausted before any primary literature or guideline source could be retrieved live, so the clinical claims above are stated from general established radiology practice and are NOT backed by a source URL retrieved in this session. Treat the evidence grade as provisional pending a sourced pass. Only the three clinic pages listed in sources were actually opened and verified.Methylation clocks are well established as population-level correlates: they predict all-cause mortality and age-related disease risk better than chronological age in large prospective cohorts. That is association, not utility. The interventional evidence is thin and does not support the way the test is sold. The most-cited human trial is a pilot RCT in Aging (2021, n=43 healthy men aged 50-72, 8-week diet and lifestyle programme) reporting a 3.23-year reduction in DNAmAge versus controls; the authors themselves call for larger and longer trials, the cohort was narrow, and several investigators disclosed financial interests in the intervention. Critically, the outcome measured was the clock readout itself, not a healthspan or mortality outcome. As of this research there is no RCT showing that measuring a methylation clock, or acting on the number it produces, improves any hard health outcome. Practical limits compound this: clocks are not standardised between labs, test-retest variability can be on the order of years, results are not diagnostic, and there is no validated clinical protocol for what to change if the number comes back high. Reasonable use is as a research-grade engagement or tracking metric, explicitly labelled as such. It should not be presented as a clinically actionable measure of ageing.Human data exist, but not for healthspan. The largest synthesis, a 2025 systematic review and meta-analysis of 39 human clinical studies in Aesthetic Surgery Journal, reports roughly 20% wrinkle reduction, 15-23% gains in pigmentation, elasticity and texture, and 18-24% improvements in hair density and thickness. Its own limitations are decisive: most included studies were open-label or single-arm, Cochrane ROB2 risk-of-bias assessment was "often not feasible", sample sizes were small and follow-up ran only 6-12 weeks. Every endpoint was surface dermatologic or trichologic. There are no systemic outcomes, no biomarkers of ageing, no organ-function or mortality data, and no controlled human trial of exosomes for any healthspan endpoint in either market. Systemic or IV exosome use for longevity is supported by mechanism and animal work only. Product characterisation is a second problem: "exosome" preparations are not standardised between suppliers, dose is not expressed in any comparable unit, and stem cell culture supernatant is a different and less defined material again. Safety is not neutral. A 2025 case series documents four women with persistent erythema, granulomatous nodules and permanent scarring after intradermal injection of cosmetic-grade exosome formulations, none of whom fully resolved despite steroids, laser and surgery. No exosome product holds marketing approval as a medicine in Australia, Singapore, the US or the EU. This should be presented as an aesthetic adjunct with early-stage cosmetic evidence, not as a systemic longevity protocol.The evidence base does not support the healthspan claims made for whole-body MRI as a screen for asymptomatic, average-risk adults. There is no randomised trial showing that whole-body MRI screening of unselected asymptomatic adults reduces all-cause or cancer-specific mortality. Where MRI screening does have real support, it is in defined high-risk groups (for example hereditary cancer predisposition surveillance), which is a different population and a different indication from the consumer longevity product. The documented harms are substantial and well characterised: a high rate of incidental findings, most of which are benign, driving downstream imaging, biopsy, and invasive workup, plus overdiagnosis and anxiety. Everlab's own product page concedes this, stating that for average-risk individuals the research is ongoing and that the role of whole-body MRI as a broader screening tool in asymptomatic average-risk adults "remains less clearly established", and that the scan is not a reliable screen for breast, colon, or prostate cancer, with ovaries difficult to assess. Note: this profile was compiled without live literature search (the session's web search budget was exhausted), so the evidence characterisation above rests on the vendor page retrieved plus the discovery brief, not on independently retrieved trial or guideline sources. Treat the evidence grading as directionally reliable but not source-complete.The evidence base is strongly split by route of administration, and the longevity positioning rests on the weaker half. Topical/cosmetic: this is the better-supported context. There is genuine human data, including a randomised trial of topical copper tripeptide complex on CO2 laser-resurfaced skin (PubMed 16847171), and cosmetic-product RCTs reporting improvements in fine lines, skin density and pigmentation. An interventional trial of topical GHK-Cu gel for acute wound healing is registered on ClinicalTrials.gov (NCT07437586), which itself indicates the question is still open rather than settled. These are dermatological and cosmetic endpoints, not healthspan endpoints. Injectable/systemic longevity: this is where clinics market it and where the evidence is thinnest. A 2026 UNSW review of injectable anti-ageing peptides states there is "some limited evidence GHK-Cu could play a role in collagen production, and wound healing in mice" but that "these findings have not been confirmed in humans". The same review characterises the injectable peptide field generally: evidence "mostly limited to animal studies", human studies "small and short-term", and "no high-quality trials reflecting real-world use", concluding there is not enough quality evidence to support the anti-ageing claims made for peptides. What the evidence does NOT show: no human trial demonstrates that systemic or injectable GHK-Cu extends healthspan, slows biological ageing, improves any validated ageing biomarker, or produces systemic tissue rejuvenation. Much of the enthusiasm derives from gene-expression and mechanistic work (e.g. the frequently cited PMC6073405 review of GHK-Cu gene data), which is hypothesis-generating, not outcome data. Copper is also biologically active and not benign at arbitrary systemic doses, and compounded injectable product carries sterility, identity and dosing uncertainty that regulators in both markets have flagged. Graded "commercial": it is widely sold and heavily marketed for longevity, but the human outcome evidence supporting those specific healthspan claims does not exist. The topical cosmetic evidence is real but does not transfer to the systemic claim.This is the strongest human evidence base in the longevity-clinic drug universe, but the strength sits in cardiometabolic disease, not in ageing. The SELECT trial (17,604 adults with overweight or obesity and established cardiovascular disease, no diabetes; ~40 months mean follow-up) found semaglutide 2.4 mg weekly cut the composite of cardiovascular death, non-fatal MI and non-fatal stroke by 20% (HR 0.80, 95% CI 0.72 to 0.90, p<0.001), with a supportive but hierarchically untested all-cause mortality signal (HR 0.81, 95% CI 0.71 to 0.93) and mean 9.4% weight loss. Reducing MACE and incident diabetes in a high-risk population is a genuine healthspan-relevant outcome, and that is what justifies a clinical grade. What the evidence does NOT show: no trial has demonstrated that GLP-1 RAs extend lifespan, and none was designed to. Ageing-specific data is early and small. A randomised placebo-controlled study reported semaglutide slowed one validated epigenetic clock by roughly 9%, and a UC San Diego pilot reported telomere lengthening in about half of treated participants over 24 weeks; these are surrogate biomarkers, not outcomes, in small samples, and epigenetic-clock movement has never been validated as a proxy for lifespan. The first trial explicitly powered for healthspan endpoints in healthy older adults, VITAL-H (ARPA-H funded, UT Health San Antonio), was only announced in February 2026 and has not reported. Critically, essentially all outcome evidence comes from populations with obesity, diabetes or established cardiovascular disease. There is no outcome evidence supporting use in metabolically healthy, normal-weight adults, which is precisely the longevity-clinic use case, and no evidence base at all for the "microdosing for longevity" protocols some clinics market. Loss of lean mass with weight loss is a real and under-discussed risk in older adults. Verdict: clinical for cardiometabolic and weight outcomes in indicated populations; mechanism-to-preclinical for any anti-ageing claim specifically.The human evidence for somatropin as an anti-ageing intervention is unusually well characterised, and it is not supportive. The definitive synthesis is Liu et al., a systematic review of 31 randomised controlled trials of GH in healthy elderly adults (Annals of Internal Medicine, 2007). It found small body-composition shifts (fat mass down about 2.1 kg, lean body mass up about 2.1 kg) with no demonstrated gain in strength, function, quality of life or survival, and significantly higher rates of soft tissue oedema, arthralgia, carpal tunnel syndrome, gynaecomastia, and new-onset diabetes or impaired fasting glucose. The authors concluded GH cannot be recommended as an antiaging therapy. Nothing since has overturned that: the frequently cited TRIIM trial (Fahy et al., Aging Cell, 2019) reported thymic regrowth and a roughly 1.5 to 2.5 year reduction in epigenetic age, but it enrolled only nine men, had no control arm, and combined rhGH with DHEA and metformin, so no effect can be attributed to GH alone and no clinical outcome was measured. Separately, the benefit in genuinely GH-deficient adults (pituitary disease, hypopituitarism) is real and is the basis of the registered indication, but that population is not the ageing population these clinics are marketing to. There is also a documented harm signal in the other direction: lower GH/IGF-1 signalling is associated with longer life in multiple model organisms and in human GH-receptor-deficiency cohorts, so the mechanistic rationale for supplementing GH to extend healthspan is contested rather than merely unproven. Chronic supraphysiological GH causes acromegaly, insulin resistance, and cardiovascular disease. Even the Singapore clinic pages advertising the treatment state plainly that HGH is not the anti-ageing miracle it is claimed to be.The evidence for HBOT splits sharply, and the split is the whole story. For its accepted medical indications the clinical evidence is genuine and long-standing. For longevity and healthspan claims it is not. The most-cited human ageing work is a small set of single-arm prospective trials from the same Israeli group (Hachmo et al., Aging 2020 on telomere length and immunosenescence; Hachmo et al., Aging 2021 on skin ageing), plus a widely circulated 2022 Frontiers in Neurology paper that is a single-subject case report (n=1). None of the longevity-outcome studies retrieved were randomised or sham-controlled, which matters acutely here because chamber sessions produce strong expectancy effects and because telomere length in isolated blood cells is a surrogate that can shift with leukocyte population changes rather than cellular rejuvenation. No trial demonstrates an effect on mortality, incident disease, or any hard healthspan endpoint. Separately, the protocols in those studies (60 sessions at ~2 ATA, pure oxygen) are not what soft-shell consumer chambers deliver, so even the weak positive findings do not transfer to most commercially sold sessions. Graded "commercial": HBOT is a real medical technology being marketed for an indication its own evidence base does not yet support.The evidence base most often quoted for "sauna and longevity" (the Finnish cohort work linking frequent sauna bathing to lower cardiovascular and all-cause mortality) is for traditional hot-air sauna, not infrared, and does not transfer: the thermal load, session temperature and exposure pattern are materially different. For infrared specifically the published human work is small, short, mostly unblinded, and centred on symptom and comfort endpoints rather than healthspan outcomes. There is no human trial evidence I could verify in this session showing that infrared sauna use changes mortality, biological ageing, or any hard longevity endpoint. Detoxification claims in particular have no credible supporting outcome data. It is a low-risk, pleasant, plausibly mildly cardiovascularly stimulating heat exposure sold on the back of somebody else's evidence base. NOTE ON THIS RECORD: my live web-search budget was exhausted before I could complete verification. I confirmed only one source by direct retrieval (TH7 Body Labs). The evidence characterisation above is therefore directional and should be re-verified against live literature before publication.There is no human trial of LDN with a longevity or healthspan endpoint. The only lifespan evidence is invertebrate: a 2024 iScience study reported a 17.6 percent median lifespan extension and improved mobility in C. elegans at 2.5 micromolar via SKN-1 (the worm NRF2 orthologue), with no benefit at high dose. That is a worm result, not a mammalian or human one. In humans the best-developed dataset is fibromyalgia pain, where a 2025 systematic review and meta-analysis of five RCTs found a significant reduction in pain scores but small samples and limited robustness. For long COVID a 2025 systematic review found zero RCTs, only four observational pre-post studies (n=155), with low certainty of evidence. A 2026 narrative review in Advances in Therapy covering 105 studies including 15 RCTs concluded that early positive uncontrolled findings were rarely replicated in placebo-controlled trials and that the literature is dominated by case reports and small feasibility studies prone to publication bias. What the evidence does NOT show: any effect on ageing biomarkers, biological age, mortality, or any healthspan outcome in humans. Anyone presenting LDN as a longevity intervention is extrapolating from a worm study and an anti-inflammatory mechanism story.MHT has genuine randomised human evidence, which is rare in this field, but the evidence supports symptom relief and bone outcomes far more strongly than it supports lifespan extension. What is well established: MHT is the most effective treatment for vasomotor symptoms, and it prevents bone loss and reduces fragility fractures. Australian Prescriber notes it is recommended regardless of symptoms in premature ovarian insufficiency to reduce osteoporosis and cardiovascular risk. The Women's Health Initiative, a randomised placebo-controlled trial in women aged 50 to 79 with an intact uterus, was stopped early in 2002 after conjugated equine oestrogen plus medroxyprogesterone acetate showed increased breast cancer incidence and an unfavourable overall benefit-risk ratio; oestrogen alone showed a different, more favourable breast cancer signal. Longer follow-up and the "timing hypothesis" literature suggest reduced all-cause mortality and coronary heart disease when MHT is started under age 60 or within 10 years of the final menstrual period, but this is largely post hoc subgroup and meta-analytic evidence, not a prospective trial designed to test longevity, and it should not be read as proof that MHT extends life. What it does NOT show: no trial has tested MHT against a primary endpoint of healthspan, biological age or all-cause mortality in the general population; benefit is age- and timing-dependent and does not transfer to late initiation; and breast cancer, VTE and stroke risks are real and dose-, route- and regimen-dependent. Separately, custom-compounded "bioidentical" hormone therapy, which several longevity clinics market, is explicitly not recommended by Australian Prescriber because of limited dose regulation and lack of safety data, and compounded products sit outside the ARTG. The evidence supporting registered MHT does not transfer to compounded formulations.Metformin has genuine human outcome evidence, but for diabetes, not for longevity. Australian Prescriber describes it as "the only glucose-lowering oral drug that has been shown to reduce mortality in patients with diabetes" (https://australianprescriber.tg.org.au/articles/safe-prescribing-of-metformin-in-diabetes.html). That finding is in people with type 2 diabetes and is a diabetes-treatment result, not evidence of an anti-ageing effect in healthy people. For healthspan specifically, the evidence base is animal and mechanistic plus observational, with no completed randomised trial reporting a longevity or healthspan endpoint. The TAME trial (Targeting Aging with Metformin), the study designed to test exactly this question, has NOT reported: as of 2026 no efficacy results have been published, and primary outcomes are not expected before 2027 to 2028 (https://www.stackingyears.com/blog/tame-trial-metformin-2026-status-update). Note for the record that at least one low-quality source (imedic.health) circulates a claim that TAME has reported positive results; that claim is contradicted by better sourcing and should not be repeated. Rodent lifespan data are inconsistent and strain-dependent, and a recognised counter-signal exists in humans: metformin blunts the adaptation response to exercise training, which is a plausible healthspan negative in an otherwise healthy user. Vively's own consumer content concedes the drug "is not approved in Australia or the United States specifically for weight loss" and that any off-label prescribing "must be based on individual clinical assessment" (https://www.vively.com.au/post/can-you-use-metformin-for-weight-loss). Bottom line: well-characterised, cheap, and safe enough at the population level, but the healthspan proposition remains unproven in humans.The evidence base is commercial rather than outcome-proven. No multi-cancer early detection assay has published randomised controlled trial evidence that screening reduces cancer mortality. The largest trial, NHS-Galleri, has a published design paper only; its primary endpoint is the incidence of stage III and IV cancers at 3 to 4 years, and the authors state plainly that the trial "was not primarily powered to assess mortality reduction, as it would likely require at least 6 years follow-up." The same paper flags the relevant cautionary precedent from ovarian cancer screening, where a 10.2% reduction in late-stage incidence attenuated to a non-significant 4.4% reduction in disease-specific mortality, so a stage-shift result would not by itself establish benefit. Material harms are not hypothetical: because these tests are applied to asymptomatic populations with low pre-test probability, even high specificity yields a meaningful absolute number of false positives, each triggering a diagnostic workup (imaging, biopsy, sometimes invasive procedures) with its own cost, risk and anxiety. Overdiagnosis of indolent disease is a further unquantified harm. A negative result also carries no assurance, since sensitivity is low for early-stage disease across all assays. Two corrections to the discovery brief are worth recording. First, the Singapore offering is Lucence, not GRAIL's Galleri; I found no retrieved source confirming Galleri is commercially available in Singapore, and the marketed "up to 50 cancer types" figure applies only to the top LucenceINSIGHT 50 tier (SGD 3,800), not to the LucenceINSIGHT Core (SGD 600) bundled into NOVI's assessment, which covers six cancers. Second, on clinics: I verified NOVI Health directly from its own site. Mount Elizabeth is reported to offer a Multi-Cancer Early Detection Screen using LucenceINSIGHT, but its site returned HTTP 403 to every retrieval attempt, so I have not confirmed it and have deliberately left it out of offeredBy. DA MedSuites (Doctor Anywhere) was verified as naming LucenceINSIGHT in its top-tier Sequoia package but is not on the supplied clinic list. I found no evidence of MCED liquid biopsy at any named Australian clinic, and SPOT-MAS was not verified in either market. Two caveats on this research pass: the session's web search budget was fully exhausted before I began, so I could work only from direct URL retrieval, and both the HSA and TGA sites failed to return content (timeouts and blocks). Regulatory status is therefore null in both markets, not because it is unknowable but because I could not reach an authoritative source, and it should be re-verified before publication.The evidence base does not support the healthspan claims made for it. There is no human randomised controlled trial showing any longevity, healthspan or biological-ageing outcome from IV NAD+. The most relevant retrieved human data is a retrospective real-world pilot (PMC12907335) comparing IV NAD+ with IV nicotinamide riboside: it enrolled only 6 NAD+ recipients versus 8 NR recipients, was uncontrolled and unblinded, and was authored by staff of the commercial clinic delivering the treatment. It assessed tolerability and 30-day safety only, explicitly not efficacy. Notably, its findings cut against the marketing: the NAD+ arm reported moderate to severe abdominal cramping, diarrhoea, nausea, vomiting and chest pressure, while NR caused only minor tingling, and NAD+ infusions took 97 minutes versus 37. Metabolic readouts were exploratory only, and the authors could not even detect NAD+ concentration changes. The rationale for the intervention therefore rests on mechanism and on rodent work, not on demonstrated human outcomes. A candid signal: Artisan Regenerative's own service page describes NAD+ IV as "an unrecognized medical drug" and concedes limited clinical trial data, while simultaneously listing benefit claims spanning cognition, immunity, cardiovascular, liver, kidney and muscle function. REGULATORY, IMPORTANT LIMITATION: neither market's status was verified and both are returned as null rather than guessed. The TGA website timed out on four separate fetch attempts, so a safety alert that search results indicate exists at tga.gov.au titled "NAD, NAD+, NADH or NMN medicines sold in Australia" could not be opened or quoted; it is the single highest-priority follow-up and should be retrieved before any regulatory claim is published. No HSA source was successfully opened either. Search-result summaries suggested that NAD/NAD+/NADH are not permitted ingredients in Australian listed medicines and that Singapore restricts IV therapy outside licensed healthcare institutions, but both are secondhand search-engine paraphrases of non-authoritative pages and are deliberately excluded here. CLINICS: only Artisan Regenerative Centre is confirmed from its own site. Australian Longevity Clinic's homepage returned no service detail on fetch, so it is not listed despite the discovery note. Biogenix Australia was confirmed offering "NAD+ Therapy" from its own site but is not on the supplied AU clinic list, so it is excluded from offeredBy while still evidencing genuine AU availability.The mechanism is real and the pharmacology is settled: oral NR reliably and dose-dependently raises blood NAD+ in humans, and it has a good short-term safety record across multiple placebo-controlled trials. What the evidence does NOT show is that raising NAD+ translates into any healthspan or longevity benefit. Human RCTs to date have largely failed to demonstrate consistent improvements in muscle function, insulin sensitivity, cardiovascular endpoints, cognition, or any ageing-relevant clinical outcome, and no trial has tested mortality or disease incidence. The impressive lifespan and healthspan results come from mice and cell models, not people. The only NR-specific study surfaced in this research round is a retrospective, non-randomised chart review of 14 patients (6 NAD+ IV, 8 NR IV) at a single US commercial wellness clinic, which found IV NR was much better tolerated than IV NAD+ (37 versus 97 minute infusions; minor tingling versus moderate-to-severe cramping, nausea and vomiting) with exploratory and variable metabolic signals. Its own authors call for adequately powered randomised placebo-controlled trials to determine effectiveness. That is a tolerability observation, not efficacy evidence. Graded "mechanism" rather than "clinical" because the human trial literature establishes a biomarker change (NAD+ elevation) without an accompanying healthspan outcome. NR is also routinely conflated with NMN in marketing; they are distinct molecules with distinct regulatory treatment, and evidence for one should not be read across to the other.NMN reliably does the one thing it is mechanistically supposed to do: multiple placebo-controlled human trials show oral NMN raises circulating NAD+ concentrations dose-dependently and is safe and well tolerated at doses up to 900mg daily. Beyond that, the evidence thins out sharply. Small randomised trials report scattered functional signals: improved walking distance at 30 and 60 days, increased muscle insulin sensitivity in prediabetic women (Yoshino 2021), enhanced aerobic capacity in amateur runners (Liao 2021), and maintained walking speed with improved sleep quality in older adults (Morifuji 2024). These are individually small, short, largely unreplicated, and conducted in heterogeneous populations. Critically, no trial has measured a longevity or a composite healthspan endpoint, and no trial has demonstrated that raising NAD+ produces the downstream ageing benefits the mechanism predicts. The bulk of the compelling ageing-reversal data remains in mice. Singapore's own Centre for Healthy Longevity (Prof. Brian Kennedy and Prof. Andrea Maier, NUHS) has explicitly framed its NMN work around the still-open question of whether supplementation is needed at all in a given individual and what dose makes the NAD+ change clinically meaningful, which is a fair statement of where the field actually sits. Chi Longevity's own copy concedes that "clinical outcomes vary significantly between individuals" and that "generalised supplementation might not produce beneficial results". Intravenous NMN and NAD+ drips rest on a materially weaker footing again: there is no meaningful controlled human outcome evidence for the IV route, and the pharmacokinetic rationale for bypassing oral dosing is not established. Treat oral NMN as a well-characterised NAD+-raising agent in search of a demonstrated clinical benefit, and the drip form as commercial.Human RCT evidence exists but is genuinely contested, and none of it measures lifespan or healthspan. VITAL randomised over 25,000 adults to 1 g/day marine n-3 and found no reduction in major cardiovascular events (HR 0.92) and no reduction in cancer (HR 1.03); the authors concluded supplementation did not lower incidence of either. STRENGTH, in 13,000+ statin-treated high-risk patients with high triglycerides and low HDL, found no difference versus corn oil (12.0% vs 12.2%, HR 0.99). REDUCE-IT is the main positive trial, but it tested prescription icosapent ethyl (high-dose purified EPA), not ordinary fish oil, in statin-treated patients with elevated triglycerides, cutting the primary endpoint from 22.0% to 17.2% (HR 0.75); its mineral-oil comparator remains debated. So: for a general, well-nourished population taking over-the-counter fish oil, the best evidence is null. For a specific high-risk, high-triglyceride, statin-treated subgroup, a specific prescription drug showed benefit. What is NOT shown: any effect on mortality-as-longevity, biological ageing markers, or healthspan endpoints. Observational associations between higher blood omega-3 and life expectancy (cited by Everlab) are not causal and should not be presented as trial evidence. Two caveats on this profile: the TGA website was unreachable across repeated fetch attempts this session, so the Australian regulatory field is returned null rather than guessed; and Melbourne Functional Medicine's blog returned HTTP 403, so its omega-3 recommendation could not be verified and it is excluded from the clinic list. Advantage Medical Group (Singapore) does recommend omega-3s on its own site, but it is not in the supplied SG clinic universe, so it is likewise excluded from offeredBy.The bundled offering has no outcome trials. There is no published RCT testing whether biomarker-guided supplement selection, as a strategy, improves mortality, morbidity, or any validated healthspan endpoint versus standard care or versus untargeted supplementation. Correcting a genuine, measured deficiency (vitamin D, B12, iron) is established clinical medicine, but that is deficiency treatment, not life extension, and evidence for supplementing people who are already replete is largely null or in some trials harmful. Individual components differ sharply in support and should not inherit credibility from the testing wrapped around them. The personalisation itself is the unevidenced claim: measuring a marker, acting on it, and remeasuring demonstrates that the marker moved, not that the patient will live longer or better. Notably, Everlab's own article stresses it does not sell or prescribe named products and matches supplements to test results, which is a more restrained framing than the category norm. Graded commercial because the marketing promise (healthspan extension through a personalised stack) substantially exceeds what the evidence base establishes.The lifespan case rests on animal data, not humans. Rodent evidence is genuinely robust and reproducible, which is why rapamycin is taken seriously by ageing biologists rather than dismissed. Human evidence is far thinner. A 2025 review in Aging identified fewer than a dozen trials of low-dose rapamycin or analogues in healthy participants, and concluded that human data "has yet to establish that rapamycin, or its analogues, is an effective seno-therapeutic to delay aging in healthy older adults." The human trials that exist are small, short, and measure surrogate endpoints rather than ageing outcomes: Kraig 2018 dosed 25 adults aged 70 to 95 with 1 mg/day for 8 weeks; Mannick's work used the analogue everolimus and RTB101 for immune and respiratory-infection endpoints, and the phase 3 results failed to replicate the earlier phase 2b signal. Kaeberlein's 333-user cohort is observational and unblinded, so it cannot support causal claims. No human trial has demonstrated extended healthspan or lifespan. Documented adverse findings in these studies include raised triglycerides and HbA1c, reduced plasma albumin and haemoglobin, elevated TNF-alpha, oral ulcers, and increased anxiety at some doses, so this is not a low-consequence intervention and it carries genuine immunosuppression risk requiring baseline and ongoing bloodwork. Grading this as preclinical rather than clinical is deliberate: human RCTs exist, but none establish the healthspan outcome the protocol is sold on.IMPORTANT VERIFICATION GAP: this session's web search budget was exhausted (200/200) before any search could be run, and two direct fetches of tga.gov.au timed out. The only source successfully retrieved live was HSA's general medical device regulatory overview. Nothing below should be treated as independently re-verified this session, and the regulatory fields are deliberately null. On the evidence itself, stated conservatively: PBM has a genuine, well-characterised biological mechanism and a real clinical literature for narrow indications, principally dermatologic endpoints (wrinkle depth, collagen density), musculoskeletal pain, and oral mucositis in oncology. What it does NOT have is human outcome evidence for any longevity or healthspan endpoint. There is no RCT evidence that PBM extends lifespan, alters biological age markers, improves all-cause mortality risk, or produces durable systemic metabolic benefit. Trials that exist are typically small, short, heterogeneous in wavelength, dose, and irradiance, frequently industry-linked, and rarely blinded adequately given the obvious sensory nature of the exposure. Dosing is also non-monotonic (a biphasic dose response is repeatedly described), which means device-to-device and protocol-to-protocol results do not transfer cleanly, and consumer full-body beds are not equivalent to the devices used in published trials. Graded "commercial" rather than "clinical": the modality is heavily sold in the SG/AU recovery market, but the marketed healthspan and longevity claims are extrapolated from mechanism and from adjacent-indication trials, not demonstrated for healthspan outcomes in humans. Safety profile appears benign at typical consumer doses, with eye protection the main practical caution, but even that is an inherited rather than freshly verified claim here. Provision: per discovery, AU availability is well attested across multiple independent operator sites; SG availability rests on a single media listing rather than the operator's own site and should be treated as caveat-grade. Note also that none of the discovery-identified providers appear on either supplied clinic list, so offeredBy is empty by design rather than by omission.The offering is well documented; the healthspan claims made for it are not, at least not from anything I retrieved this session. My web search budget was exhausted before I could run any literature queries, so every source below is a clinic's own marketing page reached by direct fetch. On that basis I can evidence that these clinics sell the protocol and roughly what it contains, and nothing more. I have deliberately NOT graded this "clinical" — the broader sleep literature does contain human randomised evidence for behavioural sleep interventions such as CBT-I, and observational evidence linking sleep duration and regularity to cardiometabolic and cognitive outcomes, but I could not open a single one of those papers here and citing them from memory would be exactly the stale-recall error to avoid. Treat the "clinical" framing in the discovery brief as unconfirmed rather than refuted. Separately, even where trial evidence for CBT-I is strong, it does not transfer automatically to these packages: none of the pages I read presents outcome data for its own programme, and the step from "better measured sleep" to "extended healthspan" is asserted commercially, not demonstrated. A re-run with search budget available should target CBT-I meta-analyses and sleep-regularity cohort studies, and would likely justify upgrading the component evidence to clinical while leaving the clinic-programme claims at commercial.The headline longevity claims rest on model organisms: spermidine extends lifespan and induces autophagy in yeast, worms, flies and mice. Human data is thinner and largely null. The SmartAge randomised controlled trial gave 0.9 mg/day of spermidine to 100 older adults with subjective cognitive decline for 12 months and did not demonstrate the hoped-for cognitive benefit. Separately, two pharmacokinetic studies found that oral spermidine, even at 40 mg/day (over 40 times the SmartAge dose), has minimal effect on circulating plasma and salivary polyamine levels, which raises a basic question about whether oral supplementation reaches tissues at all. Remaining human work is small pilot or blend-formulation studies, including a 2026 pilot on immune senescence and vaccine response, none of which are confirmatory. Supportive observational data on dietary polyamine intake is confounded by overall diet quality. In short: strong mechanism, strong animal data, no demonstrated human healthspan outcome, and unresolved bioavailability.Resistance training is one of the few longevity-clinic offerings with a genuine human outcome base: randomised trials support gains in muscle mass, strength and physical function in older adults, and grip strength and sit-to-stand performance are well-established prognostic markers associated with all-cause mortality and disability. Two honest limits apply. First, grip strength and sit-to-stand are validated as predictors, not as targets, so improving the test score has not been shown to deliver the mortality benefit the association implies. Second, no randomised trial has shown that resistance training extends lifespan; the outcome evidence is for function, strength, falls and sarcopenia, plus observational mortality association. The clinic-specific layer, that a proprietary personalised prescription outperforms standard public-health strength guidance, is unsupported and commercial. IMPORTANT CAVEAT ON THIS PROFILE: this session's live web-search budget was exhausted before any primary literature or regulatory page could be searched, so the evidence characterisation above rests on background knowledge rather than sources retrieved live in this session. Only the clinic-offering claims and the HSA remit statement were verified against pages actually opened. The TGA site was unreachable across four fetch attempts (timeouts and connection resets), so the Australian regulatory field is returned as null rather than guessed.TRT has genuine randomised human evidence, which puts it well ahead of most longevity clinic offerings, but the evidence supports narrower claims than the marketing does. TRAVERSE (n=5,246 men aged 45 to 80 with hypogonadal symptoms, testosterone under 300 ng/dL, and existing or high cardiovascular risk; NEJM 2023) found daily 1.62% testosterone gel non-inferior to placebo for major adverse cardiac events (7.0% vs 7.3%; HR 0.96, 95% CI 0.78 to 1.17). That is a safety result, not a benefit result: TRAVERSE showed TRT does not appear to raise MACE risk in that population, while also recording small excesses of atrial fibrillation, pulmonary embolism and fracture. The Australian T4DM trial (Wittert et al., Lancet Diabetes & Endocrinology 2021; n=1,007 men aged 50 to 74 with impaired glucose tolerance or new type 2 diabetes and testosterone at or below 14.0 nmol/L, explicitly WITHOUT pathological hypogonadism) found that two years of testosterone undecanoate added to a lifestyle programme cut two-year type 2 diabetes incidence by roughly 40%, with fat loss and strength gains. Notably, T4DM's own lead investigator cautioned that testosterone is not a substitute for lifestyle intervention, and follow-up reporting indicates the diabetes-prevention effect was not durable once treatment stopped. What the evidence does NOT show: no trial has demonstrated that TRT extends lifespan, reduces all-cause mortality, slows biological ageing, or improves any validated healthspan endpoint. There is no RCT evidence supporting testosterone in men with normal testosterone levels, and the long-term effects of decades-long supraphysiological or "optimisation" dosing outside diagnosed deficiency are untested. Fertility suppression is a real and sometimes irreversible consequence. The honest grade is: strong clinical evidence for symptom and metabolic outcomes in confirmed deficiency, no evidence for the longevity claim itself.TPE has decades of genuine clinical evidence for established medical indications (myasthenia gravis, demyelinating disease, thrombotic thrombocytopenic purpura, hyperviscosity syndromes, anti-GBM disease), which is why HSA's Blood Services Group runs it as a hospital service in Singapore. That evidence does not transfer to healthy ageing. The best longevity-specific data is a single randomised, single-blinded, placebo-controlled trial of 42 adults over 50 (Fuentealba et al., Aging Cell, 2025), with four arms: biweekly TPE plus IVIG, biweekly TPE alone, monthly TPE, and placebo. The TPE-IVIG arm showed rejuvenation on 15 epigenetic clocks versus placebo (FDR < 0.05), alongside coordinated shifts in proteomic, metabolomic, glycomic, and immune-cell markers. Every one of these endpoints is a molecular surrogate. The trial measured no functional, disease-incidence, healthspan, or mortality outcome, so it does not show that anyone lived longer or better. It is also small (n=42), single-blinded rather than double-blinded, and industry-linked (run with a commercial TPE provider). Two further honest caveats: the effect was largest in the arm that added IVIG, meaning the plasma exchange alone is not clearly the active ingredient; and TPE is not risk-free, carrying citrate reactions, hypotension, vascular access complications, and albumin/immunoglobulin depletion. A material correction to earlier scoping: Monash House Private Hospital in Melbourne does explicitly list "Healthy Longevity" among the indications for which its doctors may recommend TPE, so this is being marketed for longevity in Australia, not only for medical indications. However Monash House is a private hospital, not one of the named longevity clinics, and no clinic on either the Singapore or Australia list was confirmed to offer TPE. Net: real clinical drug for real diseases, surrogate-only and commercially promoted as a longevity protocol.The two peptides sit at very different points on the evidence curve, and neither has longevity evidence. Thymosin alpha-1 has a real clinical trial record, but in infectious disease and oncology adjunct settings, not healthspan. The most decisive recent datapoint is negative: the TESTS trial (BMJ, 2025), a multicentre double-blind placebo-controlled phase 3 study in 1,106 adults with sepsis, found 28-day all-cause mortality of 23.4% on thymosin alpha-1 versus 24.1% on placebo (HR 0.99, 95% CI 0.77-1.27, P=0.93) and did not meet its primary endpoint. Earlier meta-analyses in sepsis and COVID-19 suggested a possible mortality benefit, but those were built on smaller, mostly single-country trials and are outweighed by the adequately powered phase 3 result. Thymosin beta-4 is weaker still: its human data come from RegeneRx's phase 2 programme in dermal wound healing and dry eye disease (topical/ophthalmic RGN-259), and no completed phase 2 or phase 3 RCT has tested systemic injectable thymosin beta-4 or TB-500 for tendon, ligament or muscle injury, which is the use most buyers are actually seeking. Regeneration and anti-ageing claims for TB-500 rest on rodent and in-vitro work plus mechanism. Two further caveats: TB-500 is a fragment and is not pharmacologically interchangeable with the full-length thymosin beta-4 used in the trials, and compounded peptide supplied outside the ARTG carries no assurance of identity, purity or dose. Thymosin beta-4 is also banned in sport at all times by WADA under the growth factors category, which matters for any athletic client.Two claims must be separated. First, testing and treating genuine thyroid disease is established standard of care with decades of clinical evidence, and thyroid panels are ordinary pathology, not a longevity innovation. Second, the "optimisation" claim, treating euthyroid or subclinically hypothyroid people to feel better or age slower, is not supported. The TRUST randomised, double-blind, placebo-controlled trial (737 adults aged 65+ with persistent subclinical hypothyroidism, NEJM 2017) found no benefit of levothyroxine on hypothyroid symptoms or tiredness scores, and pooled analysis with a second RCT found no cardiovascular benefit. An ancillary TRUST analysis found no effect on depressive symptoms. AACE/ATA guidance explicitly states thyroid hormone should not be used to treat obesity in euthyroid patients, nor for depression. No RCT shows that pushing thyroid hormone within the normal range extends healthspan, improves body composition durably, or reduces mortality. Known harms of over-replacement are real and dose-dependent: Singapore's HSA has issued a safety communication on levothyroxine and fracture risk, and long-term suppressive dosing is associated with reduced bone mineral density and atrial fibrillation risk. IMPORTANT UNVERIFIED CLAIM: I confirmed that clinics in both markets include thyroid markers in longevity panels, but I could not verify from any clinic's own site that they prescribe thyroid hormone for optimisation in euthyroid patients. Treat the treatment side as unverified. Net position: the assessment is legitimate and cheap; the optimisation narrative is a commercial construct that the best available human RCT evidence contradicts.Correcting genuine deficiency is well-supported: vitamin D with calcium has long-standing human trial evidence for bone density and fracture risk in deficient and institutionalised older populations, and severe deficiency causes rickets and osteomalacia. That is the clinical floor, and it is real. What the evidence does NOT show is a healthspan or lifespan benefit in people who are already replete. Large randomised trials in generally sufficient populations (notably VITAL) found no reduction in cancer incidence or major cardiovascular events from supplementation; this is widely reported but I was unable to re-open the primary trial sources live in this session, so treat the specific VITAL result as directionally reliable rather than independently re-verified here. The telomere-maintenance framing used in Everlab's marketing rests on a secondary/ancillary analysis, which is hypothesis-generating, not proof of slowed ageing. Advantage Medical Group's own reported figure, that more than 50% of those it tests show levels below 30 ng/mL, is clinic-internal data with no published methodology, and the 30 ng/mL threshold is itself contested (some authorities use 20 ng/mL as sufficiency). Net position: clinical evidence for treating deficiency and for bone outcomes; commercial framing for anti-ageing, longevity or healthspan extension. High-dose intermittent regimens have signals of harm (increased falls/fractures in some trials), so "more is better" is not supported.Cardiorespiratory fitness is among the most robustly evidenced predictors of all-cause mortality in humans. A retrospective cohort of 122,007 adults undergoing exercise treadmill testing at the Cleveland Clinic (JAMA Network Open, 2018, median follow-up 8.4 years) found an inverse, graded relationship between fitness and mortality, with elite performers at an adjusted hazard ratio of 0.20 versus low performers and no observed upper limit of benefit. The 2016 American Heart Association scientific statement concluded that low CRF is associated with high cardiovascular and all-cause mortality risk, is potentially a stronger predictor than smoking, hypertension, dyslipidaemia or type 2 diabetes, and significantly improves risk reclassification. What this does NOT show: the evidence establishes fitness as a modifiable exposure and a prognostic marker, not that the act of measuring VO2max changes outcomes. There is no trial demonstrating that VO2max testing itself extends lifespan or healthspan; the causal arm of the evidence rests on exercise training trials, and no RCT randomises people to being tested. Clinic-quoted effect sizes (for example Everlab's "for every 10-point increase in VO2 Max, there is a 17 per cent lower risk of death from cancer and an 11 percent reduction in overall mortality") are observational associations presented without a cited source and should not be read as causal. VO2max is also effort-dependent and protocol-dependent, so values are not directly comparable across providers, and estimated (submaximal or wearable-derived) VO2max is a weaker measure than a true maximal test with gas exchange.The human literature is real but narrow and short-horizon. Published trials are dominated by small athletic-performance and recovery studies and by inflammatory-disease cohorts (notably ankylosing spondylitis), measuring surrogate markers such as proinflammatory cytokines, lipid peroxidation products and antioxidant capacity over days to weeks. Several studies are confounded because cryotherapy is bundled with an exercise or kinesiotherapy programme, so the intervention cannot be isolated. Critically, none of this extends to longevity or healthspan endpoints: there are no trials showing that whole-body cryotherapy reduces mortality, slows biological ageing, prevents age-related disease, or produces durable functional benefit. Some of the supporting mechanistic work (for example thermogenesis and antioxidant-system effects) is animal or in-vitro. Marketed healthspan and "reverse ageing" claims are not supported by the evidence base; the defensible reading is short-term subjective recovery and transient biomarker change. Safety is a live concern: liquid-nitrogen chambers carry asphyxiation, frostbite and cold-burn risk, and the modality is unsuitable for people with uncontrolled hypertension, cardiac disease, Raynaud's, cryoglobulinaemia or pregnancy.The underlying intervention is one of the best-evidenced things in the longevity field, but the branded framing is not. Regular aerobic exercise raising cardiorespiratory fitness has extensive human RCT and large prospective cohort support for reduced all-cause and cardiovascular mortality, and VO2 max is among the strongest single predictors of mortality risk. That is the clinical layer, and it is real. What the evidence does NOT show is the specific claim doing the marketing work: that Zone 2 in particular is uniquely or optimally longevity-promoting compared with other aerobic intensities. Head-to-head trials of moderate-intensity continuous training versus higher-intensity interval training generally show interval work produces equal or greater VO2 max improvement for less time, and no trial has randomised people to zone-2-specific versus intensity-matched-alternative prescriptions with a healthspan or mortality endpoint. The mitochondrial biogenesis and fat-oxidation rationale for zone 2 is mechanistic and physiological, extrapolated from exercise-physiology substrate-utilisation data rather than from outcome trials. Total weekly aerobic volume, and simply doing the exercise consistently, are almost certainly the operative variables rather than precision zone targeting. Practical caveat for the clinic offering: the value added by a paid VO2 max test is zone precision, and for most people zone 2 can be approximated by the talk test at far lower cost. Graded "clinical" for aerobic training improving fitness and mortality risk; the zone-2-uniqueness layer is mechanism only. Note on completeness: this profile's clinic and dose claims were each verified by opening the pages cited; the regulatory framing was not verified against live HSA or TGA sources in this session because the search budget was exhausted, so it is stated as a category judgement rather than a retrieved finding.
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Not medical advice.