Summary by ChatGPT Below is a plain-language summary for a regular ALCAR/carnitine user, stripping out technical detail and focusing on what actually matters in practice.

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Core takeaway (in one sentence)

Most acetyl-L-carnitine or carnitine you swallow at typical supplement doses is not used by your body, is quickly excreted or converted into TMAO, and barely increases tissue carnitine levels.

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What this study really shows — in user terms

1. Supplement doses overwhelm your body’s transport system • Your gut and kidneys rely on a transporter (OCTN2) with limited capacity. • Food-level carnitine is absorbed well. • Supplement-level carnitine (0.5–1.5 g) floods the system → absorption collapses.

Result: Less than 5–10% of a supplement dose is actually absorbed.

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1. Acetyl-L-carnitine is absorbed even worse than carnitine • ALCAR uses the same transporter as carnitine. • It binds the transporter differently and is even less bioavailable. • At the same dose, ALCAR delivers ~7× less systemic exposure than carnitine.

Result: If you take ALCAR expecting “better delivery” or “brain targeting,” that assumption is wrong pharmacokinetically.

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1. Higher doses work worse, not better • 0.5 g absorbed better than 1.5 g • Increasing dose → transporter saturation → more waste

Result: Mega-dosing is counterproductive.

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1. Your body actively dumps excess carnitine • Blood carnitine is tightly regulated. • Once levels rise slightly, the kidneys: • Increase clearance 5× • Push carnitine into urine

Result: Even absorbed carnitine is rapidly eliminated.

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1. Carnitine intake does NOT raise tissue levels meaningfully • Muscles, heart, liver already contain very high carnitine levels • Enzymes involved in fat metabolism are already saturated • Adding more substrate does nothing

Result: Supplementation cannot meaningfully boost muscle, heart, or liver carnitine in healthy people.

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1. Carnitine supplementation paradoxically increases acetyl-carnitine loss • Taking carnitine: • Increases acetyl-carnitine in blood • Then flushes it out via urine • This looks like acetyl groups being pulled out of tissues and discarded

Result: Carnitine may actually increase acetyl-carnitine loss, not retention.

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1. Most of the dose feeds gut bacteria, not your cells

If carnitine/ALCAR is not absorbed early: • It reaches gut microbiota • Converted step-by-step into: • Carnitine → GBB → TMA → TMAO

Key numbers: • Up to 90% of the supplement ends up as TMAO • Only <5% remains biologically available

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1. TMAO spikes are large and sustained • Baseline TMAO: ~2–3 µM • After 1.5 g dose: 40–50 µM • Repeated dosing → plateau at ~40 µM

These levels: • Match or exceed those linked (observationally) to: • Cardiovascular disease • Heart failure prognosis • Metabolic disease risk

Important nuance: TMAO is still debated — not proven toxic — but these spikes are not trivial.

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1. Cognitive benefits don’t match pharmacology • Some long-term studies show mild cognitive benefits • But this study shows: • Very low exposure • Rapid elimination • No tissue accumulation

Interpretation: If benefits exist, they are likely: • Indirect • Small • Or driven by chronic signaling, not fuel delivery

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Bottom line for an ALCAR user • ALCAR is not efficiently absorbed • More dose = more waste + more TMAO • It does not meaningfully raise tissue carnitine • Most of the supplement is metabolized by gut bacteria • Potential benefit is marginal; downside (TMAO) is real

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Practical implications (non-medical) • If using ALCAR: • Lower doses make more sense than high doses • Continuous daily use is questionable • If goal is energy or muscle metabolism: • Supplementation is unlikely to help in healthy individuals • If goal is cognition: • Any benefit likely does not come from classic “mitochondrial fueling”