EPA and DHA have differing effects in men with Hyperlipidemia. DHA increased LDL particle size, increased fasting insulin, but did not increase fasting glucose.
Omeg-3, DHA and EPA, increased adiponectin production. In addition, blockade of the PPAR-gamma resulted in a reduction in adiponectin production. Thus PPAR gamma activation results in adiponectin production by adipocytes.
Rat study, but it finds that n-3, capsaicin, and curcumin can not only decrease the inflammation associatied with arthritis, but it can delay it all together.
There is a growing body of preclinical literature suggesting that ω-3 FAs, and DHA
in particular, may play a therapeutic role in mTBI
the
potential for ameliorating or possibly even preventing the complications associated with concussions
DHA is the predominant ω-3 FA present in the brain, and, consistent with this finding, DHA,
and not EPA, has been demonstrated to be critical for brain development and cognitive function throughout life
the concentration of EPA in the brain is negligible
(77–80), suggesting that EPA plays a limited role in mediating the beneficial effects of LCPUFA supplementation on mTBI pathology
the current state of the science regarding LCPUFA supplementation for the treatment of concussion
is based primarily on animal models
there is evidence that the amount of DHA in brain tissue is decreased after mTBI (65, 66), suggesting an elevated need for DHA in mTBI recovery.
the well-established role of DHA in supporting
the structure and function of the brain throughout the lifespan (26, 27, 46, 47, 53) provides encouragement that LCPUFAs may also prove beneficial in the context of concussion recovery.
no therapies are currently available to aid the recovery from this injury
Previously discussed reports outlining the use of ω-3 FAs in the recovery from severe
TBIs (reviewed in Ref. 92) described the use of very-high doses of LCPUFAs (16.2 g/d EPA plus DHA) in the recovery of these patients
Within
the context of mTBIs/concussions, translating a DHA intake used in several rat studies of mTBI recovery (40 mg ⋅ kg−1 ⋅ d−1 DHA) (57, 63, 64) using body surface area conversion methods (93) amounts to an estimated human intake of 387 mg/d DHA
Animal study finds pre-emptive DHA at 40 mg/kg reduced injury response during medically induced TBI. Not only can DHA be used with TBI, but this study suggests it can be used in a prevention mode.