Estrogen, statins, and polyunsaturated fatty acids: similarities in their actions and benefits-is there a common link?
OBJECTIVE
To investigate whether there is any common link between estrogen, statins, and polyunsaturated fatty acids (PUFAs), which have similar actions and benefits.


METHODS
To critically review the literature pertaining to the actions of estrogen, statins, and various PUFAs.


RESULTS
Estrogen, statins, and PUFAs enhance nitric oxide synthesis, suppress the production of proinflammatory cytokines such as tumor necrosis factor(alpha), interleukin-1, interleukin-2, and interleukin-6, show antioxidant-like and antiatherosclerotic properties, have neuroprotective actions, and by themselves or their products inhibit tumor cell proliferation and improve osteoporosis. Estrogen, statins, and PUFAs not only have similar actions but also appear to interact with each other. For instance, the binding of estrogen to its receptor on the cell membrane may be determined by its lipid content, statins and PUFAs inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase activity, statins influence the metabolism of PUFAs, and PUFA deficiency enhances 3-hydroxy-3-methylglutaryl coenzyme A reductase activity. Statins and PUFAs inhibit tumor cell proliferation, suppress ras activity, and may prevent neurodegeneration and improve cognitive functions such as learning and memory. This suggests that PUFAs might be mediators of the actions of statins. Estrogen boosts cognitive performance in women after menopause and may protect against Alzheimer's disease.


CONCLUSIONS
The common link between estrogen, statins, and PUFAs may be nitric oxide. Hence, a combination(s) of estrogen or its derivatives, statins, and various PUFAs may form a novel approach in the management of various conditions such as hyperlipidemias, coronary heart disease, atherosclerosis, osteoporosis, cancer, neurodegenerative conditions, and to improve memory.
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EFA Sciences LLC, Norwood, Massachusetts 02062, USA. undurti@hotmail.com
D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D001161:Arteriosclerosis / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D016207:Cytokines / Q000096:biosynthesis; D004347:Drug Interactions; D004967:Estrogens / Q000494:pharmacology* / Q000502:physiology; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology* / Q000502:physiology; D020249:Hormone Replacement Therapy; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism*; D010024:Osteoporosis / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control
D016207:Cytokines; D004967:Estrogens; D005231:Fatty Acids, Unsaturated; D000960:Hypolipidemic Agents; D009569:Nitric Oxide