What it is
Nicotinic acid is the flushing form of vitamin B3. That matters because "niacin" can also refer to non-flushing forms like niacinamide, which do not have the same lipid-marker profile. For this experiment, the flush is intentional and confirms exposure to nicotinic acid, but it does not prove that Lp(a) is moving.
Why Lp(a)
My Lp(a) has been elevated on multiple measurements: 83 mg/dL on October 18, 2019, and 189 nmol/L on January 2, 2026, verified by repeat analysis. The older mg/dL result is not directly convertible to nmol/L because Lp(a) particle size varies, but both results sit in an elevated range.
Risk context
Current lipid guidance commonly treats Lp(a) at or above 125 nmol/L, or about 50 mg/dL, as a risk-enhancing marker. My 189 nmol/L result is above that threshold. I am treating it as a reason for more careful risk management, not as a single lab number that should drive reckless self-experimentation.
What the literature suggested
Nicotinic acid can lower Lp(a) as a lab marker in some people, often discussed around the 20 percent range. If my response were near that average, 189 nmol/L would still likely remain above the 125 nmol/L high-risk threshold. My before-and-after bloodwork did not reproduce that expected marker effect.
Outcome evidence
The hard part is that moving lipid markers is not the same as proving fewer cardiovascular events. Modern niacin outcome trials did not show a clear cardiovascular benefit when added to effective statin-based care, and guidelines do not recommend niacin as an Lp(a)-lowering therapy. That is the main reason this stays filed as an experiment rather than a recommendation.
Safety boundary
At supplement doses, nicotinic acid behaves more like a drug than a simple vitamin. The risks I care about most are severe flushing with dizziness or low blood pressure, persistent gastrointestinal symptoms, liver enzyme changes, glucose or A1c worsening, uric acid or gout issues, and any symptom that suggests liver stress.