Background
One of the consequences of the stress response is abdominal fat cell growth  and  loss of muscle
mass, a scenario that obviously leads to insulin resistance and obesity. It is a complex set of
events orchestrated by the adrenal hormone cortisol released as a result of the stress response
that is ultimately responsible for the fact that stress promotes weight gain. Cortisol is also a
contributing factor in the blood glucose roller coaster so many suffer from. It has the exact
opposite effect of insulin; cortisol raises blood sugar levels. elevated cortisol levels are
associated with increased appetite, cravings for sugar and weight gain.

Fish Oils as a Weight Loss Aid

the long-chain omega-3 fatty acids eicosapentaenoic acid (ePa) and docosahexaenoic acid (DHa) have
been shown  to exert a number  of effects that indicate they are of value in improving metabolism
and helping with weight loss. In animal studies, feeding fish oils led to significantly lower total
body fat stores versus diets rich in other fatty acids. the exact mechanism(s) responsible for this
phenomenon are not completely understood, but there are several possible explanations:
• ePa and DHa are very effective at suppressing the synthesis of lipids in the body.
• ePa and DHa increase the oxidation of lipids as a result of an increase in carnitine
acyltransferase I activity.
• ePa can increase mitochondrial lipid oxidation indirectly as well.
• ePa and DHa can increase thermogenesis.
• ePa and DHa can increase lean body mass.

New Data

a new mechanism for ePa and DHa for promoting weight loss is lowering cortisol levels. Volunteers
in a double- blind study were given either 4 g/d of safflower oil or 4 g/d of fish oil supplying
1,600 mg/d ePa and 800 mg/d DHa for six weeks. Results demonstrated that ePa/DHa significantly
increased lean body mass and decreased fat mass. these changes were significantly correlated with a
reduction in salivary cortisol following ePa/DHa treatment. these results indicate that fish oils
may exert an effect on central mechanisms that control the release
of cortisol.

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