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Polyunsaturated fatty acids which have a carbon-carbon double bond in a specific (ω-3) position are collectively called omega-3 fatty acids. Important in human nutrition omega-3 fatty acids are: alpha-linolenic (ALA, 18:3), eicosapentaenoic acid (EPA, 20:5) and docosahexanoic (DHA, 22:6) acids. The human body can obtain EPA and DHA from ALA via elongation and desaturation reactions. ALA, however, cannot be synthesized from saturated fatty acids, monounsaturated omega-9, or polyunsaturated omega-6 fatty acids. Humans lack a specific enzyme that inserts a double bond at the C-15 position of a fatty acid carbon chain.[1]

Evidence for the necessity of omega-3 fatty acids for humans was first observed in a 7-year-old girl maintained on a total parenteral nutrition formula that contained safflower oil. When the formula was changed by substituting soybean oil (a source of ALA) for safflower oil, the sensory neuropathy and visual problems that had been observed were reversed.[2]

The National Institute of Medicine currently recommends dietary intake for ALA as 1.6 g/d for men and 1.1 g/d for women in the general population aged 19–50 years. In addition, up to 10% of the ALA can be provided by EPA or DHA. Most experts, however, consider these amounts of EPA and DHA insufficient. In fact, a number of countries as well as the World Health Organization recommend daily consumption of EPA and DHA between 0.4 and 1.0 g/day for the general healthy population, and 1.1 g/day for people with special dietary consideration. Similar recommendations (1g/day of EPA+DHA) have been issued by the American Heart Association and European Society of Cardiology for people with high risk or existing coronary heart disease. It is alerting that the average combined intake of EPA and DHA omega-3 fatty acids in the United States today is only 0.1-0.2 g/day. This continues to be a constant and growing concern of nutritional experts today.[2,3]

The link between consumption of omega-3 fatty acids DHA and EPA and the risk of cardiovascular disease has been thoroughly supported by epidemiological and intervention clinical studies. The FDA has now recognized this connection and allowed a “supportive although not conclusive” health claim outlining this link for dietary supplements providing both EPA and DHA.

Fate and function of different omega-3 fatty acids in the body varies depending on the structure. ALA does not play any physiological function in the body other than to serve as a precursor for synthesis of EPA and DHA. EPA is the precursor of anti-inflammatory and anti-thrombotoc omega-3 eicosanoids and series 5 leukotrienes, which have been linked to the coronary heart disease preventative effect4. DHA serves as a component of all cellular membrane structural lipids including the ones in the nervous tissue and retina.

Dietary intakes of EPA and DHA result in decreased tissue concentrations of arachidonic acid and increased concentrations of EPA and DHA, respectively. Arachidonic acid (AA, 22:4) is a member of the omega-6 polyunsaturated fatty acid family. The parent fatty acids of the omega-6 series are linoleic acid (LA, 18:2) and gamma-linolenic acid (GLA, 18:3). AA is found primarily in the cellular membrane phospholipids. Unlike omega-3 fatty acids that serve as precursors of anti-inflammatory eicosanoids and leukotriens, omega-6 fatty acids, more specifically AA, lead to formation of predominantly pro-inflammatory messengers5. However, one should recognize that omega-6 fatty acids are also essential. Deficiency symptoms such as scaly dermatitis and skin lesions may occur in special dietary situations such as prolonged parenteral nutrition (although rare under normal circumstances).

After absorption, all dietary polyunsaturated fatty acids essentially compete for the same desaturation and elongation enzymes and later for inclusion in structural membrane phospholipids. Because the preference is given to omega-3 fatty acids, high intake of the latter reduces AA concentration in the tissues.

Both EPA and AA serve as precursors for eicosanoids - omega-3 or omega-6 type, respectively. Once again, the same enzymes are utilized in this conversion, but depending on the substrate used, the finished product varies by structure and function. Because of this phenomenon, high intakes of omega-3 fatty acids not only reduce tissue concentration of AA, but also AA-derived omega-6 eicosanoids (e.g., thromboxane A2, prostacylcin, and leukotriene B4) that are pro-inflammatory and pro-thrombotic in nature. EPA-derived omega-3 eicosanoids (e.g., thromboxane A3, prostaglandin I3, and leukotriene B5) result in a less thrombotic and atherogenic state than AA-derived eicosanoids. This is the most up to date explanation behind the cardioprotective mechanisms of dietary omega-3 fatty acids.[3]

This brings us to the critical issue of the optimal omega-6 to omega-3 ratio in the diet. In recent years there has been a shift in the relative proportions of different fatty acids in the diet. Reductions in saturated fat, mostly animal-derived have been counterbalanced, in part, by increases in omega-6 polyunsaturated fatty acid from vegetable oils. As a result, the value for omega-6 to omega-3 fatty acid ratio has increased from historical estimates of approximately 4:1 to current estimates of between 10:1 and even 20:1. This shift in the omega-3 to omega-6 ratio explains, at least partially, the increase in cardiovascular disease in the US in the last several decades. Epidemiological studies point out that low rates of heart disease in Japan, compared with the United States, are attributed by and large to a healthy ratio of omega-3 to omega-6 fatty acids in the Japanese diet rich in fish and marine vegetables.[6]

Another significant contribution of omega-3 fatty acids to human health is related to their role in supporting healthy neurological and brain function. DHA is a primary component of membrane phospholipids in the brain. Higher levels of DHA are found in the more metabolically active areas of the brain, including cerebral cortex, mitochondria, synaptosomes, and synaptic vesicles. Supplementation with EPA and DHA has been shown to support both development as well as cognitive and emotional longevity of the brain.[3,7,8]

Sources of EPA and DHA in Omega-3 A.D include cod liver and fish oils. Since heavy metals and other environmental pollutants such as PCBs are of a great concern, these oils have been subjected to the strictest panel of tests and undergo quality control measures that assure that heavy metals, dioxins and other contaminants are within minimal limits.

Fish oils are also invaluable sources of fat-soluble vitamins. The recommended daily amount of Omega-3 A.D.(3 capsules) provides 1000 IU of vitamin A in the form of naturally occurring retinol and 200 IU of vitamin D in the form of naturally occurring vitamin D3.

Vitamin A is important for the function of every cell and is required for proper gene expression, reproduction, embryonic development, growth, and immune function. In the eye retinol is used for transferring light into neural signals. Vitamin A is also required for the integrity of epithelial cells throughout the body including digestive tract mucosa, skin and hair, epithelium of the respiratory system, etc.

Vitamin A is necessary for the maintenance of healthy immune function, which depends on cell differentiation and proliferation in response to various stimuli. It is needed to generate adequate level of circulating natural killer cells, support non-specific phagocytic activity and to allow production of the mediators of the immune response.

Vitamin A deficiency is still a problem in developing countries where it contributes to increased mortality from infection among young children. In adults living in Western countries several factors including diets low in fat, eating disorders, certain liver conditions and gastric bypass surgery may lead to vitamin A deficiency.[7,9]

Pure vitamin A deficiency leads to xerophthalmia that includes night blindness and eye dryness. Another symptom of vitamin A deficiency is follicular hyperkeratosis. In the immune system, lack of adequate amounts of retinol is associated with a reduction in the number of lymphocytes and natural killer cells, and decline in antigen-specific immunoglobulin responses.

A recent epidemiological study conducted in the US in postmenpausal women 50 to 74 years of age revealed that about 19% of these women had serum level of vitamin A below accepted levels. Both low and high serum vitamin A concentrations in postmenopausal women are associated with an increased risk of hip fracture due to osteoporosis.[10]

Vitamin D is a fat soluble vitamin found in very few food sources (milk, egg yolks). However, it can be synthesized in the skin under exposure to solar UV light. Its major biologic function in humans is to maintain serum calcium and phosphorus concentrations within the normal range by enhancing the efficiency of the small intestine to absorb these minerals from the diet and to support healthy bone structure. Vitamin D function in the body is also carried out through vitamin D receptor present in the small intestine, colon, osteoblasts, activated T and B lymphocytes, insulin producing beta-islet cells, and most organs in the body, including brain, heart, skin, gonads, prostate, breast, and mononuclear cells. In these tissues vitamin D supports normal cell proliferation.[11]

The skin normally has a significant capacity to produce vitamin D following UV exposure. However, time of the day, season, and latitude play a major role in its production. For example, very little if any vitamin D is produced in the skin during winter months above 37° latitude (approximately the latitude of San Francisco). Topical sunscreens work by absorbing solar radiation before it enters the skin. A sunscreen with a sun protection factor (SPF) of 8 reduces the capacity of the skin to produce vitamin D by 95%. Sunscreen with a SPF of 15 reduces the capacity by 98%.[12] Aging also significantly decreases the capacity of human skin to produce vitamin D, therefore, this group is considered at risk of vitamin deficiency. Taking certain medications (cholestyramine) and malabsorption, such as in the case of steatorrhea due to age-related pancreatic insufficiency can also result in vitamin D deficiency.

Most nutritional experts agree that vitamin D deficiency might be more prevalent in the general population than originally thought. A recent (2004) evaluation of blood levels of vitamin D conducted in primary care patients in Boston (aged 11-18) during a routine blood draw revealed that 24.1% of adolescents were vitamin D deficient.[13]

Vitamin D deficiency is characterized by abnormalities in both calcium and phosphorus metabolism and inadequate mineralization or demineralization of the skeleton. A recent study also suggests a strong link between hypovitaminosis D and persistent, nonspecific musculoskeletal pain.[14] In another epidemiological study, people that have low plasma vitamin D concentration have been demonstrated to have a greater risk of developing colon cancer. There is a possible connection between lack of vitamin D due to inadequate UVB exposure and developing an autoimmune condition known as multiple sclerosis.[12,15] Vitamin D deficiency may result in beta-cell dysfunction and glucose intolerance, which may be corrected by vitamin D supplementation.

Research suggests that vitamin D deficiency could be an avoidable risk factor for syndrome “X” comprising of impaired glucose metabolism, dyslipidaemia, hypertension and obesity. Supplementation with vitamin D has been shown to support already healthy insulin sensitivity and glucose metabolism.[16]

In the body vitamin D is stored in the adipose tissue. However, individuals with large amounts of fat in the body are not protected from vitamin D deficiency by their vitamin D depot. It has been demonstrated that for obese individuals, the fat can be an ”irreversible sink” for vitamin D, thus increasing the risk of this nutrient deficiency.[12]

In addition to omega-3 fatty acids and naturally occurring vitamin A and D, Omega-3 A.D. contains small amounts of other beneficial oils: extra virgin olive oil (a source of monounsaturated omega-9 oleic fatty acid), butter oil (a source of palmitic, caprylic and conjugated linoleic acids) and cold pressed grape seed oil (a source of proanthocyanidins and natural tocopherols). Natural mixed tocopherols in the formula help to prolong shelf-life and improve stability of polyunsaturated fatty acids in the product.

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