A clinical discipline focused on slowing the biological processes that drive age-related disease — cardiovascular dysfunction, metabolic decline, muscle loss, cognitive impairment, and immune dysregulation — before they become clinically apparent.
Anti-Aging Medicine: Evidence-Based Treatments for Biological Aging
A clinical discipline focused on slowing the biological processes that drive age-related disease — cardiovascular dysfunction, metabolic decline, muscle loss, cognitive impairment, and immune dysregulation — before they become clinically apparent.
Anti-aging medicine, when practiced properly, is not about cosmetic concerns or recapturing youth. It is a clinical discipline focused on slowing the biological processes that drive age-related disease — cardiovascular dysfunction, metabolic decline, muscle loss, cognitive impairment, and immune dysregulation — before they become clinically apparent. At Advanced Vitality Group, every anti-aging intervention we offer is grounded in evidence from peer-reviewed clinical trials, and we maintain a clear distinction between what science supports and what is marketing.
The core concept is biological age. Your chronological age — the number of years since you were born — tells us relatively little about your current health trajectory. Biological age, measured through validated biomarkers including epigenetic markers, inflammatory proteins, hormonal levels, and metabolic indicators, tells us how fast your body is actually aging. And unlike chronological age, biological age can be influenced.
How Biological Age Is Measured
Several methods are used in clinical practice to estimate biological age. Epigenetic clocks — algorithms that analyze DNA methylation patterns — are among the most sophisticated tools currently available and are increasingly accessible through specialty laboratories. Simpler but still clinically meaningful approaches include panels of biomarkers such as hs-CRP (high-sensitivity C-reactive protein), IGF-1, fasting insulin, testosterone, and GDF-15 — all of which shift in predictable ways with aging and can be measured with a standard blood draw.
At Advanced Vitality Group, we begin every anti-aging program with a comprehensive biomarker baseline. This gives us a functional picture of your biological age across multiple systems, identifies which aging pathways are most active, and establishes the foundation for an individualized treatment plan.
Core Anti-Aging Interventions
Hormone Optimization
Correcting age-related hormone decline using Endocrine Society and AUA guidelines
NAD+ Therapy
Restoring cellular energy and DNA repair through NMN/NR supplementation
Senolytic Therapy
Clearing dysfunctional senescent cells that drive inflammation and aging
Metformin Protocols
Off-label AMPK activation mimicking caloric restriction benefits
Biomarker Monitoring
Regular lab panels to confirm interventions produce intended changes
Lifestyle Medicine
Structured exercise, dietary optimization, and sleep protocols
Hormone Optimization: Correcting Age-Related Decline
One of the most consistently documented changes in aging is the progressive decline of key hormones — testosterone, DHEA, IGF-1, and thyroid hormones among them. This is not a minor inconvenience. Hormonal decline drives a cascade of downstream effects: loss of muscle mass and bone density, increased adiposity, metabolic slowdown, cognitive fog, reduced cardiovascular protection, and diminished quality of life.
Testosterone replacement therapy (TRT) in men with documented hypogonadism is one of the most thoroughly studied interventions in age-related medicine. The Testosterone Trials (TTrials) — a coordinated set of seven randomized controlled trials conducted in men aged 65 and older with low testosterone — demonstrated significant improvements in sexual function, physical capacity, bone mineral density, and anemia with testosterone treatment (Snyder PJ et al., New England Journal of Medicine, 2016). The American Urological Association and the Endocrine Society both provide clinical guidelines for TRT, and at Advanced Vitality Group, we follow these guidelines rigorously.
Beyond testosterone, thyroid optimization, DHEA assessment, and IGF-1 monitoring are evaluated for each patient based on laboratory findings. Hormone therapy at Advanced Vitality Group is never initiated without clinical indication confirmed by laboratory data.
NAD+ Precursor Therapy: Cellular Energy and DNA Repair
NAD+ (nicotinamide adenine dinucleotide) is a coenzyme essential to cellular energy production, DNA repair, and the activation of sirtuins — a family of proteins that regulate cellular stress response and longevity-related gene expression. The problem is that NAD+ levels decline significantly with age. Research shows approximately a 40–60% reduction in NAD+ between early adulthood and age 60, a change that impairs multiple biological systems simultaneously.
Clinical trials have begun to establish the effect of NAD+ precursor supplementation in humans. A randomized controlled trial published in Science in 2021 (Yoshino M et al.) found that NMN (nicotinamide mononucleotide) at 250 mg per day increased skeletal muscle NAD+ levels and improved muscle insulin sensitivity in postmenopausal women with prediabetes. A Phase 1 trial in healthy adults confirmed that oral NMN is safe and measurably raises blood NAD+ levels (Irie J et al., Endocrine Journal, 2020). Nicotinamide riboside (NR), the other major NAD+ precursor, has similarly been shown to safely elevate NAD+ in healthy middle-aged and older adults at doses of 250–1,000 mg per day (Martens CR et al., Nature Communications, 2018).
These compounds are not FDA-approved drugs — they are available as dietary supplements and used under physician supervision at Advanced Vitality Group, with clear communication about the current state of evidence and the fact that large Phase 3 trials remain ongoing.
Senolytic Therapy: Clearing Dysfunctional Cells
One of the more compelling recent developments in anti-aging medicine is the clinical investigation of senolytics — agents that selectively eliminate senescent cells. Senescent cells are cells that have permanently stopped dividing but resist normal programmed cell death. They accumulate with age and secrete a pro-inflammatory cocktail known as the SASP (senescence-associated secretory phenotype), which damages surrounding tissue and drives systemic inflammation.
The most studied senolytic combination is dasatinib plus quercetin (D+Q). In a pilot study at the Mayo Clinic, D+Q reduced senescent cell markers in adipose tissue and skin, and decreased circulating inflammatory proteins including IL-6 and MMP-9 (Kirkland JL et al., EBioMedicine, 2019). A subsequent randomized controlled trial in patients with idiopathic pulmonary fibrosis showed that D+Q improved six-minute walk distance and physical performance scores (Justice JN et al., EBioMedicine, 2019). A Phase 2 trial published in Nature Aging in 2023 demonstrated that D+Q crosses the blood-brain barrier and reduces CNS senescence markers in Alzheimer's patients (Gonzales MM et al.).
Senolytics are not FDA-approved for anti-aging indications. At Advanced Vitality Group, these protocols are discussed on an individualized basis with full disclosure of the evidence level and investigational status.
Metformin and the TAME Trial
Metformin — the most widely prescribed diabetes medication in the world — has attracted significant attention in geroscience for its effects beyond glucose control. It activates AMPK, an enzyme that mimics some of the cellular effects of caloric restriction, and inhibits mTOR, a key regulator of cellular aging. Epidemiological data from a large UK cohort study found that diabetic patients on metformin monotherapy had lower all-cause mortality than matched non-diabetic controls not taking any such drug — suggesting a geroprotective effect beyond its primary indication (Bannister CA et al., Diabetes, Obesity and Metabolism, 2014).
The Targeting Aging with Metformin (TAME) trial — the first FDA-approved clinical trial designed to target aging itself as a primary endpoint — is currently underway in 3,000 non-diabetic adults aged 65–79 at 14 US sites. Results are anticipated in the mid-2020s. At Advanced Vitality Group, off-label metformin use for longevity is considered on an individualized basis, with full informed consent, after reviewing contraindications and patient goals.
Key Biomarkers We Track
| Biomarker | Target Range | Why It Matters for Anti-Aging |
|---|---|---|
| hs-CRP | < 1.0 mg/L (low risk) | Marker of systemic inflammaging; predicts cardiovascular and all-cause mortality risk |
| IL-6 | < 3.0 pg/mL | SASP component; rises with senescent cell accumulation |
| Fasting insulin | < 8 mIU/L | Insulin sensitivity; elevated insulin is a primary metabolic aging driver |
| Total testosterone (men) | 500–900 ng/dL | Anabolic capacity; muscle, bone, metabolism, cognition |
| IGF-1 | 100–250 ng/mL (age-adjusted) | Growth factor; tissue repair; correlates with biological vitality |
| Vitamin D (25-OH) | 40–60 ng/mL | Deficiency accelerates multiple aging pathways; gene expression regulator |
| NAD+ (blood) | Track from baseline | Cellular energy and DNA repair capacity; declines ~50% with age |
Reference ranges based on AHA, Endocrine Society, and peer-reviewed clinical literature.
Frequently Asked Questions
Scientific References
- Snyder PJ, et al. “Effects of testosterone treatment in older men.” NEJM. 2016;374(7):611–624.
- Yoshino M, et al. “Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women.” Science. 2021;372(6547):1224–1229.
- Martens CR, et al. “Chronic nicotinamide riboside supplementation is well-tolerated and elevates NAD+.” Nature Communications. 2018;9:1286.
- Justice JN, et al. “Senolytics in idiopathic pulmonary fibrosis.” EBioMedicine. 2019;40:554–563.
- Gonzales MM, et al. “A pilot study of senolytic therapy in Alzheimer's disease.” Nature Aging. 2023;3:161–174.
- Bannister CA, et al. “Can people with type 2 diabetes live longer than those without?” Diabetes, Obesity and Metabolism. 2014;16(11):1165–1173.
- Barzilai N, et al. “Metformin as a Tool to Target Aging.” Cell Metabolism. 2016;23(6):1060–1065.
- López-Otín C, et al. “Hallmarks of aging: An expanding universe.” Cell. 2023;186(2):243–278.
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