VITALIZE
Daily NAD⁺ support is a core longevity strategy; with age, NAD⁺ falls, affecting mitochondrial output, DNA repair, and sirtuin signaling.
What to know
- Human trials show oral NMN raises circulating NAD⁺ within weeks and improves gait, grip, and fatigue metrics.
- Conserving NAD⁺ (↓ CD38), supporting methylation (TMG), and directing signaling (SIRT1/AMPK via polyphenols) strengthen outcomes.
- Daytime use aligns with circadian NAD⁺/NAMPT rhythms.
VITALIZE delivers once-daily AM support for the NAD⁺ network—built for consistent, measurable replenishment.
Research & references
| Study topic | Summary of finding | Reference |
|---|---|---|
| NAD⁺ decline with age | NAD⁺ falls with age, impairing mitochondrial function and sirtuin activity. | Sinclair et al., Cell, 2013 |
| Circadian NAD⁺ rhythm | NAD⁺/NAMPT oscillate with the clock; daytime is the natural “on” window. |
Ramsey et al., Science, 2009
Peek et al., Science, 2013 |
Human studies show oral NMN raises circulating NAD⁺ within weeks and supports functional measures—daily dosing builds the reserve.
| Study topic | Summary of finding | Reference |
|---|---|---|
| Oral NMN raises NAD⁺ (human) | NMN supplementation elevated circulating NAD⁺ within weeks; well tolerated. | Irie et al., Endocr J, 2020 |
| Physical function & fatigue | ~250 mg/day NMN for 12 weeks improved lower-limb function and reduced drowsiness in older adults. | Liao et al., GeroScience, 2022 |
| Strength & walking distance (multicenter RCT) | In healthy middle-aged adults, 60 days of NMN (300–900 mg/day) increased 6-minute walk distance in a dose-dependent manner with acceptable safety; some strength measures improved in sub-analyses. | Yi et al., GeroScience, 2022/2023 |
| How NMN gets in | Slc12a8 transporter supports direct cellular uptake of NMN, providing oral bioavailability rationale. | Fang et al., Nature Metabolism, 2019 |
Age-related CD38 activity burns through NAD⁺; calming CD38 helps conserve what you make.
| Study topic | Summary of finding | Reference |
|---|---|---|
| CD38 drives NAD⁺ loss with age | Age-related CD38 upregulation is a major NAD⁺ hydrolase driving NAD⁺ decline and mitochondrial dysfunction; inhibiting or knocking out CD38 preserves NAD⁺. | Camacho-Pereira et al., Nat Med, 2016 |
| Apigenin, SASP & CD38 | Flavone apigenin inhibits CD38 and raises intracellular NAD⁺. In disease models it lowers CD38, increases NAD⁺/SIRT3 activity, and reduces inflammatory signaling related to SASP pathways. | Escande et al., FASEB J., 2013 |
Efficient methylation (e.g., TMG) recycles nicotinamide back to NAD⁺, keeping the salvage pathway running clean.
| Study topic | Summary of finding | Reference |
|---|---|---|
| TMG lowers homocysteine | Betaine (TMG) provides methyl donors and lowers plasma homocysteine in humans. Dose-dependent reductions observed across randomized controlled trials. |
Steenge et al., Am J Clin Nutr, 2001
Olthof et al., Am J Clin Nutr, 2005 |
| Methylation & NAD⁺ salvage (why methyl capacity matters) |
The NNMT pathway consumes methyl groups to clear nicotinamide. Methylation status directly interacts with NAD⁺ salvage and cellular NAD⁺ balance. Supporting methylation helps efficient recycling of nicotinamide back into NAD⁺. |
Williams et al., 2012
Bhasin et al., 2023 |
| Liver/metabolic support (TMG) | In NAFLD/NASH patients, betaine supplementation improved liver steatosis grade and key biomarkers of liver health in clinical studies. | Abdelmalek et al., Hepatology, 2009 |
Polyphenols help direct NAD⁺ toward useful programs—SIRT1/AMPK pathways linked to mitochondrial function and cellular maintenance.
| Study topic | Summary of finding | Reference |
|---|---|---|
| Sirtuins are NAD⁺-dependent | Sirtuins couple cellular NAD⁺ status to stress-response, metabolic, and maintenance programs. | Imai & Guarente, Nat Rev Mol Cell Biol, 2014 |
| Sirt1 → mitochondria/metabolism | Resveratrol engages SIRT1/PGC-1α pathways and improves metabolic and mitochondrial function. | Price et al., Cell Metab, 2012 |
| Pterostilbene neuro/mitochondrial benefits | Pterostilbene demonstrates greater potency than resveratrol in cognitive and aging models, including mitochondrial benefits. | Chang et al., Neurobiol Aging, 2012 |
| Resveratrol → SIRT1/PGC-1α & mitochondrial programs (preclinical) | In high-fat–fed mice, resveratrol activated SIRT1/PGC-1α signaling, improved insulin sensitivity and mitochondrial function, reduced hepatic steatosis, and increased survival compared to controls. | Baur et al., Nature, 2006 |
| Piperine boosts polyphenol exposure | Piperine inhibits glucuronidation and enhances the bioavailability of polyphenols such as resveratrol and curcumin. |
Johnson et al., Mol Nutr Food Res, 2011
Shoba et al., Planta Med, 1998 |
Reliability matters: verified identity/purity, real-world stability, and human tolerability in randomized trials.
| Study topic | Summary of finding | Reference |
|---|---|---|
| Human tolerability (NMN) | NMN is well tolerated at ~250–600 mg/day across multiple randomized controlled trials. |
Irie et al., Endocr J, 2020
Liao et al., GeroScience, 2022 Yi et al., GeroScience, 2022/23 |
| Uthever® NMN identity & purity | ≥99% β-NMN with validated identity, batch COAs, and independent third-party purity verification. | Uthever® technical dossier / COAs |
| 24-month stability (solid form) | Demonstrated solid-form stability over 24 months — the labeled dose remains accurate throughout the shelf life. | Uthever® stability data |
| Human tolerability (summary) | Broad clinical evidence shows NMN is well tolerated in long-term human use across ~250–600 mg/day dosing. | Irie 2020; Niu 2021; Liao 2022 |
RENEW
Nighttime autophagy naturally slows with age; supporting cellular “clean-up” at night helps maintain mitochondrial quality and calm inflammatory tone.
What to know
- Spermidine is a well-studied autophagy activator; human trials in older adults report memory and cognitive signal improvements.
- Curcumin (Longvida®) and EGCG help down-shift inflammatory pathways and support mitophagy/mitochondrial protection.
- PM dosing aligns with circadian repair programs (sleep window = best coverage).
RENEW delivers once-daily PM support for overnight cellular clean-up, mitochondrial upkeep, and next-day recovery.
Research & references
Autophagy is the body’s cellular clean-up program; it declines with age and is tightly linked to healthspan.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Autophagy & longevity | Autophagy — the cell’s internal clean-up and recycling system — is essential for maintaining cellular and tissue stability. Declines in autophagy with age contribute to increased risk of age-related diseases. |
Levine & Kroemer, Cell, 2019
Aman et al., 2021 |
| Nobel recognition | Discovery of the molecular machinery governing autophagy explains why “cell recycling” is a fundamental repair and longevity pathway, earning the 2016 Nobel Prize. | Ohsumi (Nobel), Nat Cell Biol, 2016 (perspective) |
Spermidine activates autophagy; in humans, higher intake links to lower mortality and RCTs in older adults show improvements on select memory measures.
| Study topic | Summary of Findings | Reference |
|---|---|---|
| Triggers autophagy; lifespan in models | Spermidine activates autophagy (“cell clean-up”) and extends lifespan in yeast, flies, and worms. When autophagy is blocked, benefits disappear — showing autophagy is required for the effect. | Eisenberg et al., 2009 |
| Memory in older adults (pilot RCT, SCD) | In older adults with subjective cognitive decline, a small pilot RCT found improvements on select memory measures compared with placebo. | Wirth et al., 2018 |
| Memory in older adults (larger/longer RCTs; mixed outcomes) | Larger and longer RCTs found no significant improvement on the primary memory outcome. Spermidine was well tolerated. Some exploratory signals (e.g., verbal memory, inflammation markers) require confirmation at higher doses. |
JAMA Netw Open, 2022
Wirth et al., 2022 |
| Dose & safety (human) | Across human trials, oral spermidine is generally well tolerated at common supplemental doses. Mild GI symptoms are the most typical side effects. Safety results in larger RCTs were comparable to placebo. |
Schwarz et al., 2018 (tolerability study)
SmartAge RCT (safety), 2022 |
| Circadian rhythm support | Polyamine levels (including spermidine) decline with age. Restoring them in animal models helped rejuvenate and stabilize circadian timing. | Cell (journal reference; study DOI varies) |
| Higher intake ↔ lower mortality (cohort studies) | Observational population studies link higher dietary spermidine intake with lower mortality over long-term follow-up. These studies are correlational and do not prove causation. | Kiechl et al., 2018 |
Bioavailable curcumin can down-shift inflammatory pathways and support recovery; SLCP/Longvida® achieves measurable free-curcumin exposure that suits PM coverage.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Calms inflammatory signals (mechanism & human context) | Curcumin down-regulates key inflammatory pathways including NF-κB, TNF-α, and COX-2. Human studies reviewed show reductions in inflammatory markers in various conditions. | Hewlings & Kalman, Foods, 2017 (review) |
| Exercise recovery (human; Longvida®) | In active adults, Longvida® curcumin reduced post-exercise inflammation and muscle-damage biomarkers over a 4-day recovery period. |
McFarlin et al., 2016 (PubMed)
Free full text |
| Night-window suitability (PK; Longvida®) | SLCP/Longvida® technology provides sustained plasma levels of free curcumin with good tolerability, supporting its use for overnight “coverage.” | Gota et al., 2010 |
| Curcumin & autophagy (mechanistic/translation) | Curcumin can promote autophagy by modulating AMPK/mTOR signaling across cellular and translational models, according to mechanistic reviews. | Nasery et al., Molecules, 2020 (review) |
EGCG promotes autophagy via AMPK/mTOR pathways and shows improvements in cardiometabolic/inflammatory markers in human literature.
| Study Topic | Summary of Findings | Reference (click to read) |
|---|---|---|
| Inflammation balance (human evidence) | A 2024 meta-analysis of randomized trials found that green tea supplementation reduced circulating TNF-α. Effects on other inflammatory cytokines were mixed and influenced by study duration. | Meta-analysis, 2024 |
| Promotes autophagy (mechanism → pathway) | EGCG induces autophagy and autophagolysosome formation through CaMKKβ → AMPK signaling. It shifts AMPK/mTOR balance under ER-stress conditions. |
Kim et al., 2013
Holczer et al., 2018 |
| Mitochondrial / mitophagy support | Reviews highlight EGCG as a mitophagy-promoting polyphenol that helps clear damaged mitochondria and reduce oxidative stress burden. | Srivastava et al., 2023 (review) |
| Cardiometabolic markers (human) | A systematic review and meta-analysis found that green tea supplementation improved lipid markers and glycemic control in adults. | Zamani et al., 2023 |
In humans, astaxanthin can lower oxidative-stress/inflammatory markers; mechanistically it localizes to membranes and helps stabilize mitochondria (e.g., limits mPTP opening).
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Antioxidant & inflammation (human RCTs/meta) | A 2022 meta-analysis of randomized controlled trials found that astaxanthin modestly reduces oxidative-stress and inflammation biomarkers in humans, such as MDA and CRP. | Ma et al., Nutrition Research, 2022 |
| Immune balance & oxidative stress (human RCT) | A randomized, placebo-controlled trial in healthy young women showed astaxanthin reduced biomarkers of DNA damage and acute-phase inflammation, while enhancing aspects of immune function. |
Park et al., 2010 (PubMed)
Free full text (review context) |
RESET
Intermittent senolytics target accumulated senescent (“aged”) cells that drive inflammaging and tissue decline.
What to know
- Pulsed, short-duration senolytic protocols in preclinical studies—and early human pilots—lower senescent-cell signals and show functional benefits.
- Fisetin and quercetin (phytosome form for higher exposure) are dietary senolytics; luteolin and piperine support the stack.
- A monthly 2-day pulse mirrors the evidence on “hit-and-run” senolytics while avoiding continuous daily dosing.
RESET provides a 2-day-per-month senolytic pulse designed to dial down senescence signals and support tissue resilience.
Research & references
Intermittent, high-dose (“hit-and-run”) senolytic pulses can lower the burden of senescent cells and SASP signals without continuous daily dosing.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Senolytics & intermittent dosing for healthy aging | Short, intermittent high-dose senolytic protocols selectively clear senescent cells while sparing healthy tissue in preclinical models. Research shows improved tissue function and reduced inflammation, forming the rationale for non-daily senolytic schedules. | Kirkland et al., J Intern Med, 2020 |
| SASP (senescence-associated secretory phenotype) & inflammation | Senescent cells secrete inflammatory SASP factors that drive chronic, systemic inflammation. Reducing senescent cell burden in models (e.g., fisetin or quercetin-based senolytics) dampens SASP signaling and improves tissue environment. | Childs et al., Aging Cell, 2015 |
Early human studies with D+Q show that pulsed senolytics can lower senescent-cell signals and are feasible/tolerable; fisetin-based human Human pilots used D+Q (dasatinib + quercetin) to prove the principle of intermittent senolytics in people—short pulses can reduce “aging” (senescent) cell markers and show small functional gains. RESET applies the same intermittent idea using dietary senolytics (primarily fisetin plus quercetin in a high-exposure phytosome form, supported by luteolin and piperine) to aim for a consumer-appropriate monthly 2-day pulse. (D+Q ≈ “proof of concept”; RESET ≈ “nutraceutical implementation”).
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| D+Q in lung fibrosis (pilot, open-label) | Short, intermittent (“hit-and-run”) D+Q dosing was feasible in patients with idiopathic pulmonary fibrosis. Participants showed improvements in walk and chair-stand performance and reductions in senescence markers. |
Justice et al., EBioMedicine, 2019 (Full text)
PubMed link |
| D+Q in diabetic kidney disease (human adipose biopsy) | Intermittent D+Q reduced senescent-cell markers in adipose tissue and lowered SASP inflammatory signals in adults with diabetic kidney disease. |
Hickson et al., EBioMedicine, 2019 (Full text)
PubMed link |
| D+Q randomized IPF pilot (feasibility & tolerability) |
Single-center, placebo-controlled pilot trial showed intermittent D+Q was feasible and generally well tolerated in idiopathic pulmonary fibrosis — groundwork for larger efficacy trials. |
Nambiar/Kellogg/Justice et al., EBioMedicine, 2023 (PubMed)
Journal full text |
| Fisetin in humans (registered RCTs, ongoing) |
Several ongoing clinical trials are evaluating intermittent fisetin in older adults (frailty) and in knee osteoarthritis. Results are pending. |
AFFIRM Frailty Trial
Fisetin in Knee Osteoarthritis |
| Quercetin Phytosome® (Quercefit®) bioavailability (human) | Phytosome quercetin showed ~10–20× higher systemic exposure than standard quercetin and improved antioxidant biomarkers — supporting its use in pulsed senolytic protocols. | Di Pierro et al., Minerva Med, 2019 |
Fisetin is a well-studied senolytic in models—reducing senescent burden and improving tissue/function outcomes.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Lowers senescent cell burden; extends healthspan (mice) | High-dose, intermittent fisetin reduced senescent-cell burden across multiple tissues in aged mice and improved several healthspan and lifespan metrics. Supports senolytic potential and pulsed-dosing rationale. | Yousefzadeh et al., EBioMedicine, 2018 (Full text) |
| Anti-inflammatory / antioxidant signaling | Preclinical evidence shows fisetin increases glutathione, reduces inflammatory cytokines, and provides metabolic and neuroprotective benefits. Mechanistic signals align with its senolytic activity. | Review context (PubMed search) |
Quercetin is a core senolytic partner (with dasatinib in discovery work) and, in phytosome form (Quercefit®), shows substantially higher human oral exposure—useful for monthly, pulsed protocols.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Quercetin is a senolytic (discovery paper) | Foundational work identified dasatinib + quercetin (D+Q) as a senolytic combination. Quercetin alone selectively cleared certain senescent cell types (e.g., endothelial). D+Q reduced senescent burden in vivo and produced rapid functional improvements in aged mice. |
Zhu et al., Aging Cell, 2015 (PubMed)
Wiley Full Text |
| Quercetin in human “D+Q” pilots (supports intermittent dosing) |
Short, pulsed D+Q courses in early human studies were feasible, well tolerated, and showed reductions in senescence markers along with small functional improvements. These findings support the intermittent senolytic dosing paradigm used by RESET-style protocols. |
Justice et al., EBioMedicine, 2019 (IPF)
Hickson et al., EBioMedicine, 2019 (DKD / adipose tissue) |
| Quercefit® bioavailability (human) | Quercetin Phytosome® (Quercefit®) demonstrated ~10–20× higher systemic exposure versus standard quercetin and improved antioxidant markers — relevant for achieving effective senolytic pulse levels. | Di Pierro et al., Minerva Medica, 2019 |
| Quercetin: clinical effects (supportive human data) |
Meta-analyses of RCTs suggest quercetin can improve CRP, lipid markers, and recovery after muscle damage. These are not senolytic outcomes, but support quercetin’s broader anti-inflammatory and metabolic benefits. |
Mirza et al., 2023 (review/meta)
Rojano-Ortega et al., 2023 (meta-analysis) |
Luteolin modulates SASP-related pathways and complements fisetin/quercetin in preclinical
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Senescence / inflammation pathways (preclinical) | Luteolin reduced pro-inflammatory cytokines, inhibited SASP-related signaling pathways, and demonstrated neuroprotective effects in multiple preclinical models. |
Luo et al., Front Aging Neurosci, 2017
Supporting PubMed search |
| SASP / inflammation pathways (overview) | Reviews highlight luteolin’s modulation of NF-κB, TNF-α, and broader anti-inflammatory mechanisms that intersect with cellular senescence and SASP biology. | Ntalouka et al., Front Pain Res, 2023 (review) |
Piperine can enhance the oral exposure of several polyphenols (e.g., curcumin; evidence also with resveratrol), supporting intermittent pulse coverage.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Piperine enhances curcumin exposure (human PK) | Co-administration with piperine increased oral curcumin bioavailability by ~2000% in humans, demonstrating strong inhibition of metabolic clearance. | Shoba et al., Planta Med, 1998 |
| Polyphenol uptake (mechanistic / PK) | Piperine inhibits glucuronidation pathways, increasing exposure and plasma levels of several flavonoids, including quercetin-class polyphenols. | Johnson et al., Mol Nutr Food Res, 2011 (PubMed search) |
With age, senescent cells accumulate in human skin, and their SASP (inflammatory enzymes/cytokines) is linked to collagen breakdown and dermal matrix decline.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Human skin shows more senescent cells with age | Human skin biopsies show higher levels of p16INK4a-positive cells (a core senescence marker) in aged skin compared with young skin. | Waaijer et al., Aging Cell, 2012/2015 analysis |
| Dermal fibroblast senescence drives skin aging | Reviews show senescent dermal fibroblasts accumulate with age and contribute to visible skin aging through SASP-mediated matrix breakdown, impaired repair, and chronic inflammation. |
Wlaschek & Scharffetter-Kochanek, J Invest Dermatol, 2021 (PDF)
Elsevier/JID page |
| SASP → collagen & ECM degradation | Senescent fibroblasts secrete SASP factors—including MMPs and inflammatory cytokines—that degrade collagen and weaken the extracellular matrix, accelerating dermal aging. | Pilkington et al., J Invest Dermatol, 2021 |
| Causality: fewer senescent dermal fibroblasts → better skin (models) | Selective removal of senescent dermal fibroblasts in human-skin and mouse-chimera models improved skin aging markers, supporting a causal role for senescent cells in visible aging. |
Lämmermann et al., NPJ Aging Mech Dis, 2018
Aging-US (human-skin/mouse chimera) |
| Big-picture syntheses (context) | Broad reviews conclude senescent cells accumulate in aging skin, disrupt homeostasis and repair, and are emerging as a therapeutic target for skin rejuvenation and barrier restoration. |
Chin et al., Front Physiol, 2023
Zhang et al., J Clin Invest, 2022 |
BOOST
Skin is renewed from the inside out—circulating nutrients reach the dermis to back collagen, elasticity, hydration, and antioxidant defense.
What to know
- SkinAx²™ (grape polyphenols + melon SOD + zinc + vitamin C) shows improvements in elasticity, firmness, radiance, and under-eye appearance in clinical data.
- REGGENERATE™ eggshell membrane provides collagen/elastin/HA peptides with human data for skin elasticity and hydration at comparatively low doses.
- Astaxanthin and oral hyaluronic acid support moisture, oxidative-stress balance, and visible texture/elasticity outcomes.
BOOST is a once-daily inside-out skin formula to support collagen, elasticity, hydration, and a healthier-looking glow.
Research & references
Oral actives reach the dermis via circulation and have human data for wrinkles, elasticity, hydration, and oxidative balance—a deeper layer that topicals don’t always reach. Use inside-out + outside-in together.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Collagen peptides — RCTs | Placebo-controlled trials show significant reductions in wrinkle volume and improvements in skin elasticity and hydration within 8–12 weeks of daily oral collagen peptide supplementation. | Proksch et al., Skin Pharmacol Physiol, 2014 (PubMed) |
| Collagen peptides — meta-analysis | Meta-analyses of randomized controlled trials confirm significant improvements in skin elasticity and hydration compared with placebo groups. | Multiple RCTs (meta-analysis summary) |
| Hyaluronic acid (oral) — RCTs | Daily oral hyaluronic acid (120–240 mg) improved skin hydration, increased elasticity, and reduced wrinkle appearance within 12 weeks. | Multiple RCTs (ha-oral intake studies) |
| Astaxanthin (oral) — RCTs | Human trials show improvements in skin elasticity, moisture, and wrinkle parameters (especially crow’s-feet) along with reductions in oxidative-stress markers. | Multiple RCTs (astaxanthin skin studies) |
| Eggshell membrane peptides (ESM) | Daily ESM supplementation (300–450 mg) improved skin elasticity, hydration, and crow’s-feet appearance in 4–12 weeks. | Kalman et al., 2020 — ⚑ link (PubMed / journal) |
| Vitamin C (systemic) role | Vitamin C is an essential co-factor for pro-collagen hydroxylation and supports antioxidant defense, helping maintain collagen structure and dermal integrity. | Pullar et al., Nutrients, 2017 — ⚑ link (PMC) |
Branded complex with 8-week human data and mechanistic support (collagenase inhibition); some evidence is manufacturer-sponsored.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| 8-week clinical (women 40–65) | 150 mg/day improved skin elasticity (~13%), firmness (~16.5%), radiance, and reduced under-eye dark circles by ~18% in 8 weeks. | SkinAx²™ clinical summary / spec sheet (⚑ verify) |
| Collagenase inhibition (ex vivo / mechanistic) | Demonstrated ~66% reduction in collagenase activity, supporting protection against collagen breakdown and dermal matrix degradation. | CTS-0094_A2 (⚑ verify) |
| With marine collagen (combo) | Combination of SkinAx²™ + marine collagen produced greater improvements in elasticity and wrinkle depth compared with collagen alone. | CTS-0094_A2 (⚑ verify) |
| Oxidative stress markers | Reduced systemic oxidative-stress markers; supports more even skin tone and improved resilience. | SkinAx²™ brochure (⚑ verify) |
Low-dose ESM peptides show skin elasticity/hydration improvements in small RCTs; mechanism supports bioactive collagen/ECM building blocks.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| 12-week randomized trial | Daily 300–450 mg improved skin elasticity, hydration, and dermal thickness compared with placebo in 12 weeks. | Kalman et al., 2020 (PubMed / journal link) ⚑ verify |
| Absorption / bioavailability | Eggshell-membrane–derived peptides demonstrate oral bioavailability and deliver collagen- and elastin-relevant components into circulation. | REGGENERATE™ technical sheet (⚑ verify) |
| Formulation comparison | In HSN formulas, the ingredient matched or exceeded bovine-collagen outcomes while using a lower dose. | Internal dossier, 2023 (⚑ verify) |
| Potency vs bovine collagen | Demonstrated comparable improvements in firmness and hydration at significantly lower mg-per-day doses, supporting ingredient efficiency. | OfferActiveInside 2024 brochure (⚑ verify) |
Human RCTs report wrinkle, elasticity, and moisture improvements and lower oxidative-stress markers with oral astaxanthin.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Women’s RCT (~6 mg/day; 6 weeks) | Daily astaxanthin (~6 mg) improved skin elasticity, crow’s-feet appearance, moisture, and reduced age-spot area and intensity within 6 weeks. | Tominaga et al., 2012 (PubMed) ⚑ verify |
| Anti-wrinkle RCT | Daily astaxanthin reduced wrinkle depth and improved overall texture and smoothness compared with placebo. | Ito et al., 2018 (PubMed) ⚑ verify |
| Oxidative-stress markers | Astaxanthin lowered MDA and other oxidative-stress biomarkers and strengthened skin’s resistance to environmental and UV-related oxidative challenges. | Yamashita, 2006 (PubMed) ⚑ verify |
Oral HA has human data for skin hydration/elasticity and is detectable systemically; results depend on molecular weight and dose.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| 12-week RCT (≥120 mg/day) | Daily ≥120 mg oral HA improved skin hydration and elasticity compared with placebo in adults with dry skin over a 12-week period. | Oe et al., 2017, J Clin Biochem Nutr (PubMed) ⚑ verify |
| Dose-range RCT (120–240 mg/day) | HA supplementation improved moisture retention, skin texture, and overall hydration metrics, with good tolerability across the 120–240 mg/day range. | Takahashi et al., 2009 (journal / PubMed) ⚑ verify |
| Systemic exposure | Evidence from oral HA absorption studies shows HA is absorbed and distributed systemically, supporting its water-binding and dermal-hydration roles. | PK review / absorption overview (your preferred source) ⚑ verify |
RCTs show reduced wrinkle volume, higher elasticity/hydration, and increased dermal collagen density; human PK confirms peptide appearance in blood.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| 8-week RCT (~10 g/day) | Daily ~10 g collagen peptides reduced wrinkle volume and increased skin elasticity and hydration compared with placebo within 8 weeks. | Proksch et al., 2014, Skin Pharmacol Physiol (PubMed) ⚑ verify |
| 12-week RCT | Collagen peptide supplementation increased dermal collagen density and improved skin smoothness and texture over 12 weeks. | Choi et al., 2019, Nutrients (PubMed / MDPI) ⚑ verify |
| Human PK | Collagen-derived dipeptides and tripeptides appeared rapidly in plasma after ingestion, supporting systemic bioavailability and mechanism of action for skin benefits. | Iwai et al., 2005, J Agric Food Chem (PubMed) ⚑ verify |
Vitamin C is essential for collagen hydroxylation and provides antioxidant support; human data link higher C intake to fewer wrinkles/better skin aging measures.
| Study Topic | Summary of Findings | Reference |
|---|---|---|
| Collagen synthesis (review) | Vitamin C is required for pro-collagen hydroxylation. Deficiency impairs dermal structure, collagen formation, and skin repair capacity. | Pullar et al., 2017, Nutrients (PMC) ⚑ verify |
| Dietary vitamin C & photoaging (population data) | Higher dietary vitamin C intake was associated with fewer wrinkles and reduced skin dryness in a large U.S. cohort, suggesting protective effects against photoaging. | Cosgrove et al., 2007, Am J Clin Nutr (PubMed) ⚑ verify |
| Antioxidant synergy (context) | Vitamin C works synergistically with polyphenols and carotenoids to support antioxidant defenses, helping counteract oxidative stress relevant to skin aging and collagen preservation. | Antioxidant network review (peer-reviewed) ⚑ verify |