Biotech Values

[biomaven0]

Is there a thesis for why krill oil is better than other sources of Omega-3?

Perhaps. The fatty acids in krill oil are bound to phospholipids (primarily phosphatidycholine) instead of triglycerides or methyl esters in fish oil.

First, it's likely more potent:

Lipids. 2010 Nov 2. [Epub ahead of print]
Metabolic Effects of Krill Oil are Essentially Similar to Those of Fish Oil but at Lower Dose of EPA and DHA, in Healthy Volunteers.

Ulven SM, Kirkhus B, Lamglait A, Basu S, Elind E, Haider T, Berge K, Vik H, Pedersen JI.

Faculty of Health, Nutrition, and Management, Akershus University College, 2001, Lillestrøm, Norway, [e-mail].
Abstract

The purpose of the present study is to investigate the effects of krill oil and fish oil on serum lipids and markers of oxidative stress and inflammation and to evaluate if different molecular forms, triacylglycerol and phospholipids, of omega-3 polyunsaturated fatty acids (PUFAs) influence the plasma level of EPA and DHA differently. One hundred thirteen subjects with normal or slightly elevated total blood cholesterol and/or triglyceride levels were randomized into three groups and given either six capsules of krill oil (N = 36; 3.0 g/day, EPA + DHA = 543 mg) or three capsules of fish oil (N = 40; 1.8 g/day, EPA + DHA = 864 mg) daily for 7 weeks. A third group did not receive any supplementation and served as controls (N = 37). A significant increase in plasma EPA, DHA, and DPA was observed in the subjects supplemented with n-3 PUFAs as compared with the controls, but there were no significant differences in the changes in any of the n-3 PUFAs between the fish oil and the krill oil groups. No statistically significant differences in changes in any of the serum lipids or the markers of oxidative stress and inflammation between the study groups were observed. Krill oil and fish oil thus represent comparable dietary sources of n-3 PUFAs, even if the EPA + DHA dose in the krill oil was 62.8% of that in the fish oil.

Second, there are some preclinical studies that show differences. Here's a rat study that purports to show a difference between fish oil and krill oil:

J Nutr. 2009 Aug;139(8):1495-501. Epub 2009 Jun 23.
Endocannabinoids may mediate the ability of (n-3) fatty acids to reduce ectopic fat and inflammatory mediators in obese Zucker rats.

Batetta B, Griinari M, Carta G, Murru E, Ligresti A, Cordeddu L, Giordano E, Sanna F, Bisogno T, Uda S, Collu M, Bruheim I, Di Marzo V, Banni S.

Dipartimento di Scienze e Tecnologie Biomediche, Università di Cagliari, Cagliari 09100, Italy.
Abstract

Dietary (n-3) long-chain PUFA [(n-3) LCPUFA] ameliorate several metabolic risk factors for cardiovascular diseases, although the mechanisms of these beneficial effects are not fully understood. In this study, we compared the effects of dietary (n-3) LCPUFA, in the form of either fish oil (FO) or krill oil (KO) balanced for eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) content, with a control (C) diet containing no EPA and DHA and similar contents of oleic, linoleic, and alpha-linolenic acids, on ectopic fat and inflammation in Zucker rats, a model of obesity and related metabolic dysfunction. Diets were fed for 4 wk. Given the emerging evidence for an association between elevated endocannabinoid concentrations and metabolic syndrome, we also measured tissue endocannabinoid concentrations. In (n-3) LCPUFA-supplemented rats, liver triglycerides and the peritoneal macrophage response to an inflammatory stimulus were significantly lower than in rats fed the control diet, and heart triglycerides were lower, but only in KO-fed rats. These effects were associated with a lower concentration of the endocannabinoids, anandamide and 2-arachidonoylglycerol, in the visceral adipose tissue and of anandamide in the liver and heart, which, in turn, was associated with lower levels of arachidonic acid in membrane phospholipids, but not with higher activity of endocannabinoid-degrading enzymes. Our data suggest that the beneficial effects of a diet enriched with (n-3) LCPUFA are the result of changes in membrane fatty acid composition. The reduction of substrates for inflammatory molecules and endocannabinoids may account for the dampened inflammatory response and the physiological reequilibration of body fat deposition in obese rats.

(There are a couple more rat studies along the same lines).

Finally, there is the too-good-to-be-true study done by Neptune that showed dramatic increases in HDL:

http://www.thorne.com/altmedrev/.fulltext/9/4/420.pdf

Never been reproduced (to my knowledge) and so skepticism is appropriate.

Would there be a risk of getting too much Omega-3

I have no clue - this nutritional stuff is always frustratingly murky. The fact that Lovaza is safe tends me in the direction that there are not likely to be obvious side effects from too much omega-3, but who knows what subtle effects there may be.

FWIW, I recently had a talk with an internist friend who has a job summarizing evidence-based medicine topics for a well-known service, and he says he personally isn't convinced by the various studies showing a cardiac benefit for fish oil. He felt there just wasn't the consistency across different studies that you would expect to see if the effect was for real.

Peter