Does fish oil decrease lifespan?

A new study found that giving fish oil to mice decreased their lifespan: Dietary supplementation with Lovaza and krill oil shortens the life span of long-lived F1 mice

Marine oils rich in ω-3 polyunsaturated fatty acids have been recommended as a preventive treatment for patients at risk for cardiovascular diseases. These oils also are the third most consumed dietary supplement in the USA. However, evidence for their health benefits is equivocal. We tested the daily, isocaloric administration of krill oil (1.17 g oil/kg diet) and Lovaza (Omacor; 4.40 g/kg diet), a pharmaceutical grade fish oil, beginning at 12 months of age, on the life span and mortality-related pathologies of long-lived, male, B6C3F1 mice. The oils were incorporated into the chemically defined American Institute of Nutrition (AIN)-93 M diet. An equivalent volume of soybean oil was removed. Krill oil was 3 % and Lovaza 11 % of the oil in the diets. When their effects were analyzed together, the marine oils significantly shortened life span by 6.6 % (P = 0.0321; log-rank test) relative to controls. Individually, Lovaza and krill oil non-significantly shortened median life span by 9.8 and 4.7 %, respectively. Lovaza increased the number of enlarged seminal vesicles (7.1-fold). Lovaza and krill oil significantly increased lung tumors (4.1- and 8.2-fold) and hemorrhagic diathesis (3.9- and 3.1-fold). Analysis of serum from treated mice found that Lovaza slightly increased blood urea nitrogen, while krill oil modestly increased bilirubin, triglycerides, and blood glucose levels. Taken together, the results do not support the idea that the consumption of isolated ω-3 fatty acid-rich oils will increase the life span or health of initially healthy individuals.

Seems to me that the important questions are whether the dose given to the mice was reasonable. The authors argue that it was. Hemorrhagic diathesis – bleeding into the peritoneum – appeared to be the main cause of death.

The cross-species scaling factors used to adjust dosages between animals and humans suggest that mice should receive 8 to 12 times the effective human dosage of a drug to account for species-specific pharmacodynamic and pharmacokinetic differences (reviewed in Spindler 2012). The Lovaza dose used here is approximately 9.3 times the recommended human dosage per kilogram body weight. The krill oil dosage is modest in comparison to the dosages used in mouse studies to demonstrate a beneficial effect on serum and hepatic cholesterol and triglyceride levels (Vigerust et al. 2012; Tandy et al. 2009). For example, tumor necrosis factor alpha-transgenic mice fed a high-fat diet containing 5.8 % krill oil (approximately five times the dosage used here) had lower plasma levels of triacylglycerol and cholesterol and higher levels of hepatic mitochondrial and peroxisomal fatty acid β-oxidation and carnitine turnover (Vigerust et al. 2012). High fat-fed mice receiving krill oil at 12.5 g/kg diet (approximately 10 times that used here) had reduced hepatomegaly, hepatic steatosis, triacylglycerols, and cholesterol (Tandy et al. 2009).


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Allan Folz says May 24, 2014

Thanks, that’s an interesting study.

I don’t know a thing about cross-species scaling factors, but obviously their whole paper hangs on the assumption that mice should be taking 10x the O3 to get a bio-identical dose. Color me skeptical, especially as rodents generally and mice in particular haven’t evolved feeding on O3-rich diets. I further have to wonder if the 10x factor is based on research using O6?

Nonetheless, I do take the study as reinforcement that one should be careful about over-dosing O3, especially on a long-term basis (qualitative). Unfortunately, I don’t feel this brings up any closer to knowing what those doses are (quantitative).

As for myself, I will continue giving me and mine the minimal dose that I’ve found to be necessary to effect a positive mental health outcome in each individual.

    Mangan says May 25, 2014

    Allan: Agree about the dose. Since so much of O3 effects are due to incorporation into tissues, it doesn’t seem obvious to me why the dose for a mouse should be greater than for a human. It’s not about metabolism but about tissue saturation.

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