Does it matter really? Why not aim for a certain amount of DHA and EPA per day instead of focusing on the source? [/quote]
I suppose that depends on who you ask. Since you asked me…
The mixed species oil you get with generic fish oil of can impact the O3 consistency and absorption. Some fish oil processes use excessive heat, potentially changing the structure of the oil. Many fish oil formulas totally lack antioxidants as well. My literature research over the past day or so indicates Salmon oil is superior to fish oil. I will no longer use fish oil myself. I have not found a lot of papers on krill oil until tonight.
The anti-oxidant potency of krill oil is such that when compared to fish oil in terms of ORAC values, it was found to be 48 times more potent than fish oil.
(Note: they did not directly compare Salmon and krill, just fish and krill.)
Boring stuff ahead…proceed at your own peril…
â??Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids.â??
University of California, Berkeley, California, USA.
The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are orthomolecular, conditionally essential nutrients that enhance quality of life and lower the risk of premature death. They function exclusively via cell membranes, in which they are anchored by phospholipid molecules. DHA is proven essential to pre- and postnatal brain development, whereas EPA seems more influential on behavior and mood. Both DHA and EPA generate neuroprotective metabolites. In double-blind, randomized, controlled trials, DHA and EPA combinations have been shown to benefit attention deficit/hyperactivity disorder (AD/HD), autism, dyspraxia, dyslexia, and aggression. For the affective disorders, meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function. Huntington disease has responded to EPA. Omega-3 phospholipid supplements that combine DHA/EPA and phospholipids into the same molecule have shown marked promise in early clinical trials. Phosphatidylserine with DHA/EPA attached (Omega-3 PS) has been shown to alleviate AD/HD symptoms. Krill omega-3 phospholipids, containing mostly phosphatidylcholine (PC) with DHA/EPA attached, markedly outperformed conventional fish oil DHA/EPA triglycerides in double-blind trials for premenstrual syndrome/dysmenorrhea and for normalizing blood lipid profiles. Krill omega-3 phospholipids demonstrated anti-inflammatory activity, lowering C-reactive protein (CRP) levels in a double-blind trial. Utilizing DHA and EPA together with phospholipids and membrane antioxidants to achieve a triple cell membrane synergy may further diversify their currently wide range of clinical applications.
â??Evaluation of the effect of Neptune Krill Oil on chronic inflammation and arthritic symptoms.â??
OBJECTIVES: a) To evaluate the effect of Neptune Krill Oil (NKO) on C-reactive protein (CRP) on patients with chronic inflammation and b) to evaluate the effectiveness of NKO on arthritic symptoms. METHODS: Randomized, double blind, placebo controlled study. Ninety patients were recruited with confirmed diagnosis of cardiovascular disease and/or rheumatoid arthritis and/or osteoarthritis and with increased levels of CRP (>1.0 mg/dl) upon three consecutive weekly blood analysis. Group A received NKO (300 mg daily) and Group B received a placebo. CRP and Western Ontario and McMaster Universities (WOMAC) osteoarthritis score were measured at baseline and days 7, 14 and 30. RESULTS: After 7 days of treatment NKO reduced CRP by 19.3% compared to an increase by 15.7% observed in the placebo group (p = 0.049). After 14 and 30 days of treatment NKO further decreased CRP by 29.7% and 30.9% respectively (p < 0.001). The CRP levels of the placebo group increased to 32.1% after 14 days and then decreased to 25.1% at day 30. The between group difference was statistically significant; p = 0.004 at day 14 and p = 0.008 at day 30. NKO showed a significant reduction in all three WOMAC scores. After 7 days of treatment, NKO reduced pain scores by 28.9% (p = 0.050), reduced stiffness by 20.3% (p = 0.001) and reduced functional impairment by 22.8% (p = 0.008). CONCLUSION: The results of the present study clearly indicate that NKO at a daily dose of 300 mg significantly inhibits inflammation and reduces arthritic symptoms within a short treatment period of 7 and 14 days.