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NAD+

The Molecule That Determines Whether Your Cells Can Execute

NAD⁺ decline is not abstract—you feel it. Energy becomes less predictable. Some days run smoothly; others fall apart under loads you used to handle without thinking. Sleep restores less. A single night of disruption creates outsized fatigue the next day. Alcohol produces disproportionate exhaustion the next morning. Recovery from workouts stretches longer. After an illness, you stay foggy and unsteady for days or weeks.

Stress tolerance drops as well. Minor challenges feel heavier. Focus is harder to sustain. Meals matter more; delayed food triggers irritability or shakiness because the system struggles to switch to fat when glucose is low. Even small injuries or normal inflammation linger longer than they should. The pattern is familiar: effort costs more, resilience costs more, and the buffer that once absorbed disruption has thinned.

These are not unrelated issues. They are what it feels like when the molecule that powers energy production, repair, stress adaptation, and immune communication is being consumed faster than it can be replaced.

That molecule is NAD⁺.

NAD⁺ is the currency your cells use to make energy and repair damage—at the same time. Every time you burn carbohydrates or fat for fuel, NAD⁺ carries electrons through the mitochondria. The same molecule is consumed when DNA is repaired, when genes are regulated for stress response and circadian rhythm, and when the immune system signals inflammation.

One pool. Four competing demands.

When that pool is full, the system runs cleanly. Energy is steady. Repair happens quietly in the background. Stress resolves. Inflammation completes its work and shuts off on time.

When the pool is low—from chronic stress, poor sleep, alcohol, illness, or simple aging—the system begins rationing. Energy becomes fragile. Recovery slows. Cognitive clarity fades early in the day. Stress responses amplify. The mechanisms that maintain long-term cellular stability quiet down because they do not have the fuel to run. The result is not a specific disease. It is a posture: a metabolism that struggles to execute at the level it used to.

By age 60, most people have lost 50–80% of their baseline NAD⁺. This decline is not pathological—it is universal. The question is not whether your NAD⁺ has fallen. It has. The question is whether restoring it changes what your system can do.

Clinical & Academic Research

NAD⁺ therapy is not fringe. Academic centers and federal institutes have studied NAD⁺ biology for over a decade, with programs spanning aging, metabolism, exercise physiology, and neurodegeneration.

Clinical Trials (U.S.-Based)

Major U.S. Institutions Leading Trials: Massachusetts General Hospital (MGH), University of Southern California (USC), University of Iowa, Washington University in St. Louis, NIH / NIA and the RECOVER Initiative.

Typical Protocols

RouteDoseFrequencyContext
Subcutaneous/IM100-250 mg2-5× per weekActive repletion, higher demand
IV infusion250-1000 mg1-2x per weekSevere depletion, clinical supervision
Oral precursors (NR/NMN)300-500 mgDailyMaintenance, general support

Exact dosing sits with the treating clinician. The goal is repletion—rebuilding a depleted pool so that energy and repair can run in parallel again.