Longevity Medicine in Southlake, TX

Longevity Medicine at Magnolia Functional Wellness in Southlake, TX

The longevity medicine space has a credibility problem. Supplement companies, biohacking influencers, and wellness marketers have flooded this area with products and protocols that share the vocabulary of geroscience without its rigor. Patients deserve a physician who can separate signal from noise — who reads the primary literature, understands the mechanisms, and gives an honest account of what's well-established versus what's promising versus what's being sold aggressively because the margins are good.

Dr. Farhan Abdullah is a board-certified Internal Medicine physician who approaches longevity medicine the same way he approaches every clinical decision: with attention to mechanism, evidence quality, patient selection, and realistic expectations. Here is what the evidence actually shows for the agents we offer.

Rapamycin (Sirolimus) — mTOR Inhibition

Rapamycin is an FDA-approved immunosuppressant discovered in the 1970s that has become one of the most compelling longevity candidates in biomedical research. It works by inhibiting mTORC1 — the mechanistic target of rapamycin — a central cellular nutrient-sensing pathway that regulates growth, autophagy, and cellular aging.

What the animal evidence shows: Rapamycin is the only pharmacological intervention that has consistently extended maximum lifespan in multiple mammalian species across independent studies. The NIH Intervention Testing Program has replicated lifespan extension in mice across multiple genetic backgrounds, in both sexes, even when initiated late in life (equivalent to starting treatment at 60 years old in humans). These results have been reproduced in yeast, worms, flies, and dogs.

What the human evidence shows: Human data is more limited but growing. Early clinical studies using rapamycin analogs (rapalogs) showed improved immune function and reduced respiratory infection rates in older adults. The PEARL trial — a 48-week randomized controlled trial in 114 adults aged 50–85 using low-dose intermittent rapamycin (5mg or 10mg weekly) — found the treatment was safe and well-tolerated, with improvements in lean muscle mass and quality-of-life measures. A 2025 Oxford pilot study showed low-dose rapamycin reduced senescent cell markers in immune cells of older adults and improved DNA damage resistance. Biological age modeling of existing cohort data suggests meaningful geroprotective effects.

What remains uncertain: Human lifespan extension hasn't been demonstrated — the trials haven't been long enough or large enough to show it. Optimal dosing for longevity in healthy adults isn't established. Long-term immunological effects at low intermittent doses require further study. Notably, Bryan Johnson — the tech entrepreneur who popularized rapamycin self-experimentation — ultimately discontinued use citing susceptibility to infection and impaired healing, illustrating the risks of unsupervised high-dose use. At appropriate low intermittent doses under physician supervision, the safety profile appears favorable; the risks of casual self-prescription at higher doses are real.

At Magnolia, we use: Low-dose intermittent dosing (typically 5–7mg once weekly) consistent with the protocols being studied in clinical trials, with baseline immune function assessment and regular monitoring.

Metformin — AMPK Activation & Metabolic Geroprotection

Metformin has been used clinically for over 60 years, is among the safest drugs in medicine, costs pennies per dose, and has more supporting observational evidence as a longevity intervention than any other compound. It activates AMPK (AMP-activated protein kinase) — an energy-sensing enzyme that promotes metabolic efficiency, reduces chronic inflammation, improves insulin signaling, and mimics aspects of caloric restriction at the cellular level.

What the observational evidence shows: Multiple large population studies have found that diabetic patients on metformin outlive non-diabetic patients not on metformin — a striking finding suggesting metformin's effects extend beyond glucose control. People on metformin show reduced incidence of cancer, cardiovascular disease, and cognitive decline compared to patients on other antidiabetic medications. A 2024 cynomolgous monkey trial — the closest animal model to human physiology — found metformin treatment over three years rolled back aging biomarkers by 4–6 years across multiple tissues, with improved cognitive performance and cortical brain thickness preservation.

What the TAME trial shows: The NIH-supported TAME trial (Targeting Aging with Metformin) enrolled 3,000 adults aged 65–79 to formally test whether metformin delays aging as an indication. Results show metformin delayed the onset of multiple age-related diseases simultaneously — participants experienced fewer cardiovascular events, cancers, and cognitive decline compared to placebo. While it didn't significantly extend life expectancy in this timeframe, delaying the onset of multiple major age-related diseases in a single intervention is a meaningful clinical finding. Dr. Nir Barzilai, the trial's principal investigator, notes that people on metformin are twice as likely to reach age 90 as other diabetic patients.

What remains uncertain: Whether benefits demonstrated in diabetic populations fully translate to healthy non-diabetic adults is still under investigation. Some research suggests metformin may blunt adaptations to exercise — a clinically relevant concern for active patients that needs to be weighed individually. The optimal dose and timing for longevity in non-diabetic populations hasn't been established by randomized trial.

At Magnolia, we use: Low to moderate dosing (typically 500–1500mg daily) with gradual titration to minimize GI side effects, regular B12 monitoring (metformin reduces B12 absorption), and kidney function monitoring. Metformin is typically our starting point for patients new to geroprotective medicine given its evidence base, safety profile, and cost.

Senolytics — Clearing Senescent Cells (Dasatinib + Quercetin)

Cellular senescence is one of the most clearly established hallmarks of aging. Senescent cells — often called "zombie cells" — are cells that have permanently stopped dividing but refuse to die. They accumulate throughout the body as we age and secrete a toxic cocktail of inflammatory proteins, proteases, and cytokines called the SASP (Senescence-Associated Secretory Phenotype) that drives chronic tissue inflammation, organ dysfunction, and accelerated aging in surrounding cells.

Senolytics are agents that selectively eliminate senescent cells by disabling their pro-survival pathways — forcing them into the apoptosis (cell death) they're avoiding. The most studied senolytic combination is Dasatinib (a tyrosine kinase inhibitor FDA-approved for leukemia) combined with Quercetin (a plant flavonoid), which target complementary survival pathways to address the heterogeneity of senescent cell populations across different tissues.

What the preclinical evidence shows: In aged mice, intermittent D+Q administration reduced senescent cell burden across multiple tissues and improved insulin sensitivity, cardiac function, exercise endurance, and lifespan. The effects are achieved with intermittent rather than continuous dosing — consistent with senescent cells taking weeks to re-accumulate after clearance.

What the human evidence shows: A Phase 1 pilot study in patients with diabetic kidney disease showed D+Q reduced senescent cell markers in adipose tissue within 11 days. A study in idiopathic pulmonary fibrosis — a senescence-driven disease — showed improved physical function (walking distance and speed) with D+Q treatment. A 2025 pilot study in older adults at risk for Alzheimer's disease showed significant improvement in cognitive assessment scores following D+Q. Dasatinib has been shown to penetrate cerebrospinal fluid, supporting neurological applications. The evidence base in humans is earlier-stage than rapamycin or metformin but is progressing meaningfully.

Important note on Dasatinib: This is a prescription cancer medication with real risks including decreased blood counts and, rarely, cardiovascular complications. It is not appropriate for unsupervised self-prescription. At the intermittent doses used in longevity protocols (typically 2-day cycles every 2–4 weeks, rather than daily oncology dosing), the safety profile is favorable — but this requires physician oversight, baseline blood counts, and monitoring.

At Magnolia, we use: Intermittent D+Q protocols consistent with clinical trial dosing, with baseline complete blood count, liver function, and careful patient selection. We discuss whether the evidence supports this intervention for your specific situation and risk profile.

NAD+ Precursors — Mitochondrial Support (NMN/NR)

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme essential for mitochondrial energy production and DNA repair, and its levels decline significantly with age — by approximately 50% between young adulthood and midlife. Declining NAD+ is linked to reduced mitochondrial function, impaired DNA damage repair, increased inflammation, and reduced sirtuin activity (sirtuins being NAD-dependent enzymes with established roles in aging biology). Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) are NAD+ precursors that raise intracellular NAD+ levels.

What the evidence shows: Human trials have demonstrated that NMN and NR supplementation consistently and meaningfully raises blood NAD+ levels — the pharmacokinetics are established. The more important question is whether raising NAD+ produces meaningful biological outcomes in humans. Small human trials have shown improvements in muscle function, insulin sensitivity, blood pressure, and inflammatory markers. A 2023 trial showed NMN improved muscle insulin sensitivity in postmenopausal women. Evidence for cognitive benefits is emerging but earlier-stage. The evidence base is less mature than rapamycin or metformin, but the mechanistic rationale is solid and the safety profile is favorable.

At Magnolia: We discuss NMN/NR in the context of your overall protocol, particularly for patients with significant mitochondrial function concerns, metabolic dysfunction, or those using it as a complement to other geroprotective agents.

Evidence-Supported Adjuncts

Creatine Monohydrate

Creatine deserves mention here because it's one of the most extensively studied compounds in human performance research — and its relevance to aging biology is increasingly well-supported and often underappreciated by patients who think of it only as a gym supplement.

Creatine is a naturally occurring compound synthesized in the liver and kidneys that serves as a rapid energy substrate for ATP regeneration in muscle and brain tissue. Endogenous production declines with age, and dietary intake from meat drops significantly in patients eating less animal protein. The clinical relevance to aging is threefold.

Muscle preservation: Skeletal muscle loss (sarcopenia) is one of the most consequential physical changes of aging — driving frailty, falls, metabolic decline, and loss of independence. Multiple meta-analyses show creatine supplementation combined with resistance training produces greater lean mass preservation and strength gains in older adults than resistance training alone. For patients on GLP-1 medications, rapamycin, or any intervention producing significant weight loss, creatine becomes clinically relevant for protecting lean mass during the weight reduction process.

Cognitive function: The brain is an energy-intensive organ and creatine supports neuronal ATP availability. Human trials have shown creatine supplementation improves working memory and cognitive performance, particularly in older adults and in conditions of metabolic stress or sleep deprivation. The cognitive aging angle is generating growing research interest.

Safety profile: Creatine monohydrate has one of the most favorable long-term safety profiles of any widely studied compound. Decades of research have not produced evidence of kidney damage in healthy individuals at standard doses despite persistent myths to the contrary.

The standard evidence-based protocol is 3–5g of creatine monohydrate daily — not the high loading doses historically recommended for athletic performance. For older adults, the evidence actually supports the lower end of this range taken consistently rather than cyclically.

We include creatine as an adjunct recommendation in longevity medicine consultations because it's inexpensive, exceptionally safe, and addresses muscle and cognitive aging through mechanisms that are genuinely relevant — not because it has the same geroprotective evidence base as rapamycin or metformin, which it doesn't. That distinction matters and we'll always tell you where something sits on the evidence spectrum.

How We Approach Protocol Design

The longevity medicine field moves fast, is full of hype, and involves real medications with real effects that require real physician judgment. Dr. Abdullah designs protocols individually — starting with the best-evidenced agents for your specific situation, monitoring your response with objective markers, and adding or adjusting based on clinical data rather than enthusiasm.

We serve patients from Southlake, Westlake, Keller, Colleyville, Trophy Club, Grapevine, Flower Mound, and throughout the Dallas-Fort Worth area who want physician-supervised longevity medicine — not a supplement subscription.