Quick Comparison
| Ashwagandha | Omega-3 (DHA) | |
|---|---|---|
| Half-Life | 6-12 hours (withanolides) | 20-67 hours (plasma), but brain DHA turns over slowly over weeks |
| Typical Dosage | KSM-66 extract: 300-600 mg daily. Sensoril extract: 125-250 mg daily. Root powder: 3-6 g daily. Best taken with food. Can be taken morning or evening (does not cause drowsiness in most people). | Standard: 1-2 g combined EPA/DHA daily (aim for at least 500 mg DHA). For depression: 1-2 g EPA-dominant fish oil. Triglyceride form is better absorbed than ethyl ester. Take with a fatty meal. |
| Administration | Oral (capsules, powder). Standardized extracts (KSM-66 or Sensoril) are preferred over raw root powder for consistent dosing. | Oral (softgels, liquid). Triglyceride or phospholipid forms preferred over ethyl ester for bioavailability. Take with food containing fat. |
| Research Papers | 9 papers | 10 papers |
| Categories |
Mechanism of Action
Ashwagandha
Ashwagandha's withanolide compounds (withaferin A, withanolide A, withanone) modulate the hypothalamic-pituitary-adrenal (HPA) axis, reducing corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) signaling, thereby lowering cortisol production by 25-30% in stressed individuals. It acts as a GABA-A receptor positive allosteric modulator at the benzodiazepine site, producing anxiolytic effects without sedation. Ashwagandha inhibits acetylcholinesterase (AChE), raising acetylcholine levels in the hippocampus and cortex. The withanolides have anti-inflammatory properties via inhibition of NF-κB and COX-2, and antioxidant effects that reduce neuroinflammation and oxidative stress. It may support neurogenesis through upregulation of BDNF and its receptor TrkB, and modulation of the PI3K/Akt pathway.
Omega-3 (DHA)
DHA is a structural component of neuronal phospholipids (particularly phosphatidylethanolamine and phosphatidylserine in synaptic membranes), maintaining membrane fluidity which is essential for G-protein-coupled receptor function, ion channel gating, and synaptic vesicle fusion. DHA is metabolized by 15-lipoxygenase to specialized pro-resolving mediators (SPMs) including neuroprotectin D1 (NPD1), which actively resolve neuroinflammation by reducing NF-kappaB activation and pro-inflammatory cytokine production. DHA supports BDNF expression through modulation of the CREB pathway and promotes synaptic plasticity by enhancing long-term potentiation (LTP) and dendritic spine density. It also influences neurotransmitter receptor conformation and binding efficiency. Deficiency impairs membrane signaling, increases neuroinflammation, and accelerates cognitive decline.
Risks & Safety
Ashwagandha
Common
Gastrointestinal discomfort, drowsiness at higher doses, thyroid hormone elevation.
Serious
Can cause hyperthyroidism in susceptible individuals — avoid with thyroid conditions without medical oversight. Rare liver injury reports.
Rare
Vertigo, nasal congestion, sexual dysfunction.
Omega-3 (DHA)
Common
Fishy aftertaste, burping, mild gastrointestinal discomfort.
Serious
High doses (>3 g/day) may increase bleeding risk — caution with blood thinners. Fish oil quality matters — choose products tested for mercury and oxidation.
Rare
Allergic reaction in people with fish/shellfish allergy.
Full Profiles
Ashwagandha →
An Ayurvedic adaptogen used for over 3,000 years that has become one of the most popular and well-studied supplements for stress, anxiety, and cognitive function. Ashwagandha (Withania somnifera) significantly reduces cortisol levels, improves stress resilience, and enhances memory and reaction time. KSM-66 and Sensoril are the two most studied standardized extracts.
Omega-3 (DHA) →
DHA (docosahexaenoic acid) makes up approximately 40% of the polyunsaturated fatty acids in the brain and is essential for neuronal membrane structure, fluidity, and signaling. DHA deficiency is associated with cognitive decline, depression, and neuroinflammation. It is one of the few supplements with strong evidence for maintaining brain health across the lifespan.