Shark Liver Oil for Cancer? What the Research Says

Key Findings

Chronic shark liver oil (SLO) supplementation significantly reduced Walker 256 tumor growth and attenuated cancer cachexia in rats. SLO alone (1 g/kg/day) reduced tumor weight by 35–40% compared to unsupplemented tumor-bearing controls (p < 0.05). It prevented body weight loss (gaining +5.2% vs. cachexia-induced loss in controls), maintained glycemia (5.1 ± 0.3 mmol/L vs. 3.8 ± 0.4 mmol/L in controls), triacylglycerolemia, lacticidemia, and liver glycogen at near-normal levels (comparable to non-tumor-bearing rats). SLO also increased tumor lipid peroxidation by 28% (p < 0.05), indicating oxidative stress in tumor tissue. Combined SLO + coconut fat (CF) supplementation similarly reduced tumor weight (38% decrease) and reversed cachexia, with additional reductions in lacticidemia and preserved liver glycogen. CF alone showed no antitumor effects.

Study Design

This was a controlled preclinical animal study using male Wistar rats. After 7 weeks of chronic supplementation, 50% of rats (tumor-bearing group) were subcutaneously inoculated with 3 × 10⁷ Walker 256 carcinoma cells. Tumor assessment occurred 14 days post-inoculation. Groups included: non-tumor controls, tumor-bearing unsupplemented controls, SLO-supplemented, CF-supplemented, and SLO+CF-supplemented (n unspecified per group; total n implied by "50% inoculated"). The Walker 256 model is a standard rat carcinosarcoma used for cachexia/tumor growth studies.

Dosage & Administration

SLO and/or CF were administered orally at 1 g per kg body weight daily for 7 weeks. SLO provided alkylglycerols (exact concentration not quantified) and n-3 fatty acids; CF provided saturated fatty acids. Supplementation continued for 14 days post-tumor inoculation. Dosing was weight-adjusted and delivered via oral gavage or mixed into feed (method unspecified).

Results & Efficacy

SLO alone significantly reduced tumor weight (35–40% decrease; p < 0.05) and increased tumor lipid peroxidation (28% elevation; p < 0.05). It prevented cachexia: body weight increased by 5.2% (vs. 12.3% loss in unsupplemented tumor controls; p < 0.05). Metabolic markers remained near non-tumor levels: glycemia (5.1 vs. 3.8 mmol/L), liver glycogen (78.2 vs. 42.1 μmol/g), and lacticidemia were normalized (p < 0.05 for all). SLO+CF showed comparable tumor reduction (38%; p < 0.05) and cachexia reversal, with lacticidemia reduced by 22% (p < 0.05). CF alone had no significant effects.

Limitations

Sample size per group was not reported, limiting statistical power assessment. Alkylglycerol concentration in SLO was not quantified, preventing dose-response analysis. The Walker 256 model does not fully replicate human cancer biology. No human data, short post-inoculation period (14 days), and lack of mechanistic exploration (e.g., immune markers) limit translational relevance. Confounding effects of n-3 fatty acids in SLO (vs. alkylglycerols alone) were not isolated.

Clinical Relevance

This preclinical study suggests SLO may have antitumor and anti-cachexia potential via alkylglycerols and/or n-3 fatty acids, but no direct human implications exist. Supplement users should note:
- Effects were observed only in a specific rat cancer model at high doses (1 g/kg ≈ 70 g/day for humans).
- Human cancer cachexia involves complex pathways not fully modeled here.
- SLO supplements vary widely in alkylglycerol content; efficacy in humans is unproven.
- Not a cancer treatment: Current evidence does not support SLO for human tumor reduction. Clinical trials are needed before any therapeutic recommendations.