Quick Comparison
| B-Complex | Phenibut | |
|---|---|---|
| Half-Life | Water-soluble; excreted daily (except B12 which is stored) | 5-6 hours |
| Typical Dosage | Standard: A quality B-complex providing 25-100 mg of B1, B2, B3, B5, B6, plus 400-800 mcg folate (as methylfolate) and 500-1000 mcg B12 (as methylcobalamin). Methylated forms preferred for B9 and B12 (folate → methylfolate, B12 → methylcobalamin). Take in the morning — B vitamins can be mildly energizing. | Standard: 250-1000 mg on an empty stomach, no more than 1-2 times per week. NEVER use daily — tolerance and dependence develop within 3-5 days of consecutive use. Onset: 2-4 hours (slow). Do not exceed 2000 mg per occasion. |
| Administration | Oral (capsules, tablets, sublingual). Methylated forms preferred for B9 and B12. Take with breakfast. | Oral (powder, capsules). Take on an empty stomach — food significantly reduces absorption. Slow onset (2-4 hours). |
| Research Papers | 10 papers | 10 papers |
| Categories |
Mechanism of Action
B-Complex
Each B vitamin serves specific neurological functions: B1 (thiamine) — cofactor for transketolase (pentose phosphate pathway), pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase; essential for glucose metabolism and ATP production in neurons. B2 (riboflavin) — precursor to FAD/FMN, cofactors for Complex I and II of the electron transport chain, and glutathione reductase. B3 (niacin/niacinamide) — precursor to NAD+/NADPH via the salvage pathway; NAD+ is substrate for sirtuins, PARP, and 400+ dehydrogenases. B5 (pantothenic acid) — component of coenzyme A, required for acetylcholine synthesis via choline acetyltransferase and for fatty acid oxidation. B6 (pyridoxine) — cofactor for AADC (5-HTP to serotonin, L-DOPA to dopamine), GABA synthesis (GAD), and homocysteine metabolism. B9 (folate) — tetrahydrofolate donates methyl groups for dTMP and purine synthesis, and for homocysteine remethylation. B12 (cobalamin) — cofactor for methionine synthase (myelin maintenance) and methylmalonyl-CoA mutase.
Phenibut
Phenibut is a structural analog of GABA with a phenyl ring that confers lipophilicity and allows blood-brain barrier penetration (unlike GABA itself). It acts as a GABA-B receptor agonist, binding to the GABAB1/GABAB2 heterodimer and activating Gi/o-coupled signaling (similar to baclofen), producing anxiolytic, muscle relaxant, and sedative effects through inhibition of adenylyl cyclase and modulation of potassium and calcium channels. Phenibut also blocks the alpha-2-delta-1 and alpha-2-delta-2 subunits of voltage-gated calcium channels, reducing presynaptic calcium influx and neurotransmitter release (similar to gabapentin/pregabalin). The dual mechanism—GABA-B agonism dampening inhibitory interneurons and calcium channel blockade reducing excitatory transmission—produces potent anti-anxiety and sleep-promoting effects. Rapid tolerance develops due to receptor downregulation.
Risks & Safety
B-Complex
Common
Bright yellow urine (harmless — riboflavin excretion), mild nausea.
Serious
Very safe at standard doses. B6 can cause peripheral neuropathy at >200 mg daily for extended periods.
Rare
Flushing from niacin (B3) if non-flush form is not used.
Phenibut
Common
Drowsiness, dizziness, nausea, tolerance with repeated use.
Serious
Physical dependence develops rapidly with daily use. Withdrawal can be severe and dangerous (anxiety, insomnia, psychosis, seizures). Respiratory depression when combined with alcohol or other CNS depressants.
Rare
Hallucinations, severe rebound anxiety, suicidal ideation during withdrawal.
Full Profiles
B-Complex →
The B vitamins (B1, B2, B3, B5, B6, B9, B12) are essential coenzymes in brain energy metabolism, neurotransmitter synthesis, and methylation reactions. Deficiency in any B vitamin impairs cognitive function. B12 and folate deficiency specifically cause irreversible neurological damage if untreated. A high-quality B-complex is foundational for any nootropic regimen, particularly for vegetarians, older adults, and those under chronic stress.
Phenibut →
A GABA-B agonist and alpha-2-delta voltage-gated calcium channel blocker developed in Russia for anxiety, insomnia, and PTSD. It crosses the blood-brain barrier (unlike GABA supplements) and produces potent anxiolytic and social confidence effects. However, it carries significant addiction and withdrawal risks — tolerance develops within days of daily use, and withdrawal can be severe.