Fish Oil Fatty Acids for Aging Disorders
Healthy aging is crucial for achieving a prolonged, disease-free life span in humans. In recent years, the shift in n-6: n-3 fatty acid ratio to as high as 20:1 from an ideal ratio of about 4:1 has been found to be a major cause of chronic inflammation an
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Jyothi Maria Veigas and Gabriel Fernandes
Introduction Aging is inevitable and so is death. Aging in humans begins between the age of 40 and 50, and the survival of an organism depends on the balance between damage and processes of maintenance and repair systems of the body. Therefore, in order to achieve healthy aging, interventions aimed at strengthening body’s maintenance and repair systems rather than treating the damage [1] may help prevent or delay the damage to begin with. It is every individual’s desire, as Row and Kahn [2] would put it, to age successfully, that is, to grow older avoiding disease and disability, maintaining high physical and cognitive function, and conducting sustained engagement in social and productive activities. Exercising control over what we eat and how much we eat plays an important role in reaching this goal. Long-chain polyunsaturated fatty acids (PUFAs) such as n-3 fatty acids and n-6 fatty acids have long been known to be essential for optimal health. n-3 fatty acids can be obtained from both plant and marine sources. Biologically, active n-3 fatty acids, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) are found in marine fish, the richest sources being anchovy, herring, farmed and wild salmon, and mackerel along with other fish such as sardines, tuna, and bluefish. Certain algae also produce high levels of EPA and DHA. The chief n-3 fatty acid found in plant sources is alpha-linolenic acid (ALA) which is found mostly in walnuts, flax seed, canola, etc. In order to exert benefits similar to EPA, ALA must be first converted to EPA by a J.M. Veigas G. Fernandes Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, 78229, TX, USA e-mail: [email protected] G. Fernandes (&) 9103 Honey Creek, San Antonio, 78230, TX, USA e-mail: [email protected] J.M. Veigas Princess Margaret Cancer Center—Cancer Clinical Research Unit, 700 University Avenue, Toronto, M5G 1Z5, ON, Canada
series of elongation enzymes which only occurs to a small extent in humans. This conversion is also affected in the presence of high linoleic acid (LA), an n-6 fatty acid, in the diet which competes with these enzymes for its conversion to arachidonic acid [3] reducing the conversion of ALA by 40–50 % [4]. Arachidonic acid (AA) is a precursor of 4-series leukotrienes which is an important mediator of inflammation [5, 6]. In the past few decades, there has been an increase in the consumption of LA in the American diet which constitutes to about 7 % of daily caloric intake and 20 % of total dietary fatty acids [7]. While an n-6/n-3 ratio of 4:1 is presumed to be ideal, the current Western diet is largely deficient in n-3 fatty acids with the ratio ranging from 10:1 to 25:1 [8–10]. This higher ratio of n-6/n-3 fatty acids is recognized to be associated with chronic inflammatory disorders such as non-alcoholic fatty liver disease, cardiovascular disease, obesity, inflammatory bowel disease
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