Aging is biology,
not destiny.

Advancing the Science of Healthy Aging by translating cutting-edge
research into real-world longevity solutions through measurable,
trackable, and actionable insights into the biology of aging.

50%

NAD+ decline between ages 40 to 60

20y

Gap between healthspan and lifespan

85%

Reach optimal NAD+ with intervention

Nine hallmarks drive how your cells age

Nine interconnected hallmarks drive aging, where NAD+ decline, mitochondrial dysfunction, senescent cells, inflammation, and DNA damage form a cascading cycle of decline.

Genomic instability causes DNA damage to accumulate over time.

Telomere attrition shortens the protective caps at the ends of chromosomes.

Epigenetic alterations disrupt normal gene expression patterns.

Loss of proteostasis impairs the body’s ability to maintain protein quality.

Deregulated nutrient sensing disrupts metabolic signaling and cellular balance.

Mitochondrial dysfunction reduces the cell’s ability to produce energy efficiently.

Cellular senescence leads to the accumulation of aged and damaged cells.

Stem cell exhaustion diminishes the body’s capacity for tissue repair & regeneration.

Cellular communication changes weakens coordination between cells and tissues.

NAD + Levels Decline With Age

Average NAD + levels compared to age 20

aging science nad levels decline image 1

Reasons for NAD decline

NAD+ levels naturally decline with age due to a combination of factors.

Increased consumption

Cells use more NAD+ to repair accumulated damage from DNA breaks, oxidative stress, and inflammation.

Decreased Production

Enzymes that make NAD+ become less efficient. Cells can’t keep up with demand.

Active Degradation

CD38 enzyme breaks down NAD+ faster with age. By your 60s, CD38 activity can be 10x higher than in your 20s.

What low NAD+ causes

When NAD+ levels fall, every system in your body feels it.

Energy
production drops

DNA repair
slows overtime

Sirtuins stop
working properly

Mitochondria struggles
energy production

Circadian rhythm
gets disrupted

“After processing tens of thousands of NAD+ tests, we see a clear pattern. Most people over 40 are deficient. But when we restore optimal levels, the clinical improvements are remarkable.”

Dr. Jin-Xiong She

Founder

“Zombie” cells that refuse to die
create chronic problems

Damaged cells are supposed to self-destruct. Sometimes they don’t. They become senescent — stuck between life and death.

The SAAP Problem

Senescent cells release inflammatory signals, damaging proteins, and molecules that harm neighboring cells. This is called SASP (senescence-associated secretory phenotype).

The Accumulation Effect

By your 60s or 70s, senescent cells make up a significant portion of certain tissues. Each one damages surrounding cells, creating more senescent cells.

Why It Matters

Research shows clearing senescent cells extends healthspan and reduces age-related disease in animals. Human trials are underway.

Young Immune System

Clears senescent cells efficiently

Young Immune System

Clears senescent cells efficiently

Young Immune System

Clears senescent cells efficiently

Chronic inflammation accelerates
every aging process

Acute inflammation heals. Inflammaging destroys.

Why It Matters

Senescent
Cells

Release inflammatory signals constantly

Damaged
Mitochondria

Leak reactive molecules

Cellular
Debris

Activates immune pathways

Gut Barrier
Breakdown

Bacterial components enter bloodstream

Immune
Dysregulation

Body can’t shut off inflammation

The Cascade Effect

Each source makes the others worse. Inflammation damages mitochondria. Damaged mitochondria create senescent cells. Senescent cells produce more inflammation.

Clinical Impact

What You
Experience

Joint pain, brain fog,
poor recovery, fatigue.

What Bloodwork
Shows

High CRP, cytokines, and
metabolic disruption.

Cellular repair systems struggle
to keep up with damage

Your DNA takes thousands of hits daily from oxidative stress, toxins, UV radiation, and normal metabolism. The problem isn’t just damage. The problem is when repair can’t keep up.

THE DNA+ CONNECTION

100 NAD+ Molecules

Consumed per single DNA break repair

DNA repair enzymes (PARPs)

need massive amounts of NAD+.

When NAD+ drops with age, repair slows. Damage accumulates faster than it gets fixed.

Most blood tests don’t measure
cellular health directly

Standard “full panels” miss the markers that matter most for aging.

Standard Blood Panel

Cellular Energy & Oxidative Stress:

Intracellular NAD+, ROM, TAC, 8-OHdG, SABG, Klotho

Inflammation & Immune Function:

hs-CRP, IL-6, IL-8, IL-1β, TNF-α, D-Dimer

Metabolic Health:

Glucose, HbA1c, GSP, Homocysteine, Insulin, C-Peptide

Cardiovascular Risk:

LDL-C, HDL-C, ApoB, Lp(a), TRIG

Liver & Kidney Function:

ALP, ALT, eGFR-Cr, eGFR-Cys, UA

Hormonal Balance:

DHEA, HGH, PRL, Total T, E2, Progesterone, SHBG, LH, FSH, TSH, Free T3, Free T4

Nutrient Status:

Vitamin D3, Folate, Vitamin B12

Muscle & Structural Health:

Iron & Protein Status:

Ferritin, ABL

Prostate Health:

Free PSA, Total PSA

The Ultimate Panel

Cellular Energy & Oxidative Stress:

Intracellular NAD+, ROM, TAC, 8-OHdG, SABG, Klotho

Inflammation & Immune Function:

hs-CRP, IL-6, IL-8, IL-1β, TNF-α, D-Dimer

Metabolic Health:

Glucose, HbA1c, GSP, Homocysteine, Insulin, C-Peptide

Cardiovascular Risk:

LDL-C, HDL-C, ApoB, Lp(a), TRIG

Liver & Kidney Function:

ALP, ALT, eGFR-Cr, eGFR-Cys, UA

Hormonal Balance:

DHEA, HGH, PRL, Total T, E2, Progesterone, SHBG, LH, FSH, TSH, Free T3, Free T4

Nutrient Status:

Vitamin D3, Folate, Vitamin B12

Muscle & Structural Health:

Iron & Protein Status:

Ferritin, ABL

Prostate Health:

Free PSA, Total PSA

NAD+ Reference Ranges

NAD+ Level (μM)	Category	Status
0-20	Severely Deficient	High dysfunction risk
20-30	Deficient	Below healthy threshold
30-40	Suboptimal	Functioning but not thriving
40-100	Optimal	Healthy cellular function
>100	Too High	No additional benefits

Only 15% of people over 40 reach optimal without intervention

From Results to Action

Testing without guidance is just data. We turn numbers into action.

Personalized Protocols

Your protocol targets your specific deficiencies, not generic recommendations.

Evidence-Based Interventions

Supplement dosing, lifestyle modifications, and retest timelines based on your results.

Clinical Support

Free consultation included with AgingSOS panels.

Test, Act, Optimize (TAO)

We measure first then personalize your protocol

Test

Measure intracellular NAD+, inflammatory markers, and metabolic health indicators. Your baseline shows where you actually are, not where you think you are.

Act

Choose interventions targeting your specific needs based on test results. Personalized dosing based on your starting point, not one-size-fits-all recommendations.

Optimize

Retest after 4-8 weeks. Adjust protocol based on results. Some people need higher doses. Others respond quickly. The only way to know is to measure.

Our Philosophy

Science-Backed Formulations

Our Approach

Multi-Pathway Targeting

Addresses multiple aging pathways simultaneously.

Research-Based Dosing

Clinically effective doses, never label fillers.

Clinical Validation

Backed by clinical data and peer-reviewed research.

Explore Our Formulations

CLIA-Certified Testing

Third-Party Verification

cGMP Manufacturing

Full Transparency

Aging is biology, not destiny.

Nine hallmarks drive how your cells age

Increased consumption

Decreased Production

Active Degradation

What low NAD+ causes

Energy production drops

DNA repair slows overtime

Sirtuins stop working properly

Mitochondria struggles energy production

Circadian rhythm gets disrupted

The SAAP Problem

The Accumulation Effect

From Results to Action

Personalized Protocols

Evidence-Based Interventions

Clinical Support

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Aging is biology,
not destiny.

Energy
production drops

DNA repair
slows overtime

Sirtuins stop
working properly

Mitochondria struggles
energy production

Circadian rhythm
gets disrupted