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Arachidonic acid

Arachidonic acid (AA) is a polyunsaturated omega-6 fatty acid.

 

Arachidonic acid is a polyunsaturated fatty acid present in the phospholipids of membranes of the body’s cells, and is abundant in the brain, muscles, and liver. 

 

 

Skeletal muscle is an active site of arachidonic acid retention, accounting for roughly 10-20% of the phospholipid fatty acid content typically.

 

 

AA  is involved in cellular signaling as a lipid second messenger in the regulation of signaling enzymes.

 

 

Arachidonic acid is a key inflammatory intermediate and can also act as a vasodilator.

 

 

Arachidonic acid in the body usually comes from dietary animal sources such as meat, eggs, or is synthesized from linoleic acid.

 

 

It is not an essential fatty acid, however, it does become essential if a deficiency in linoleic acid exists or if an inability to convert linoleic acid to arachidonic acid occurs. 

 

Linoleic acid is a precursor to arachidonic acid with its elongation and saturation.

Arachidonic acid  is the precursor to some prostaglandins, leukotrienes and thromboxane (TXA).

 

 

Arachidonic acid is freed from phospholipid by hydrolysis, catalyzed by the phospholipase A2 (PLA2).

 

 

Arachidonic acid for signaling purposes appears to be derived by the action of phospholipase A2.

 

 

Inflammatory arachidonic acid is generated by the action of a low-molecular-weight secretory PLA2.

 

 

It is a precursor to a range of eicosanoids.

 

 

The enzymes cyclooxygenase-1 and -2 convert arachidonic acid to prostaglandin G2 and prostaglandin H2, which in turn may be converted to various prostaglandins, to prostacyclin, to thromboxanes, and to the 17-carbon products of thromboxane metabolism.

 

 

The enzyme 5-lipoxygenase catalyzes the oxidation of arachidonic acid to various leukotrienes.

 

 

Arachidonic acid promotes the repair and growth of skeletal muscle tissue via conversion to prostaglandin PGF2alpha during and following physical exercise.

 

 

PGF2alpha promotes muscle protein synthesis through the Akt/mTOR pathway.

 

 

Arachidonic acid is one of the most abundant fatty acids in the brain, and is present in similar quantities to docosahexaenoic acid (DHA). 

 

 

The two account for about 20% of the brain’s fatty-acid content.

 

 

Neurological health is reliant upon sufficient levels of arachidonic acid and DHA.

 

 

It helps to maintain hippocampal cell membrane fluidity.

 

 

It protects the brain from oxidative stress by activating peroxisome proliferator-activated receptor gamma,and activates syntaxin-3 (STX-3), a protein involved in the growth and repair of neurons.

 

 

Arachidonic acid is also involved in early neurological development: infants given supplemental arachidonic acid for 17 weeks demonstrated significant improvements in intelligence, as measured by the Mental Development Index.

 

 

Disturbed metabolism of ARA may contribute to neuropsychiatric disorders such as Alzheimer’s disease and bipolar disorder, with alterations in the conversion of arachidonic acid to other bioactive molecules in these conditions.

 

 

Supplementation of arachidonic acid (1,500 mg/day for 8 weeks)  increases lean body mass, strength, and anaerobic power in experienced resistance-trained men. 

 

 

ARA supplementation can positively augment adaptations in strength and skeletal muscle hypertrophy in resistance-trained men.

 

 

Arachidonic acid is metabolized to both proinflammatory and anti-inflammatory eicosanoids during and after an inflammatory event, and after physical activity to promote growth. 

 

 

Through the  cyclooxygenase pathway it produces thromboxane, prostacyclin and prostaglandin D, E and F. 

 

 

Through the lipoxygenase enzyme pathway in leukocytes and in macrophages it synthesizes leukotrienes.

 

 

It plays a central role in inflammation related to injury and many diseased states. 

 

 

How AA is metabolized in the body dictates its inflammatory or anti-inflammatory activity. 

 

 

Individuals suffering from joint pains or active inflammatory disease may find that increased arachidonic acid consumption exacerbates symptoms, presumably because it is being more readily converted to inflammatory compounds.

 

 

High arachidonic acid consumption is not advised for individuals with a history of inflammatory disease, or who are in compromised health. 

 

 

ARA supplementats do not appear to have proinflammatory effects in healthy individuals, but it may counter the anti-inflammatory effects of omega-3 fatty acid supplementation.

 

 

Arachidonic acid supplementation is well tolerated with no significant side effects, and no reported changes  in kidney and liver function, serum lipids, immunity,and platelet aggregation.

 

 

Arachidonic acid in muscle tissue may be correlated with improved insulin sensitivity.

 

 

Arachidonic acid supplementation of the diets of healthy adults appears to offer no safety risk.

 

 

Arachidonic acid supplementation in sedentary subjects have failed to find changes in resting inflammatory markers.

 

 

However, strength-trained individuals are reported to have  a significant reduction in resting inflammation marker IL-6 with supplements.

 

 

There is a significantly reduced risk of heart disease with higher levels of EPA and DHA (omega-3 fats), as well as the omega-6 arachidonic acid.

 

 

American Heart Association recommends individuals follow a diet that consists of at least 5–10% of calories coming from omega-6 fats, including arachidonic acid. 

 

 

ARA is not a risk factor for heart disease, and may play a role in maintaining optimal metabolism and reduced heart disease risk. 

 

 

Maintaining sufficient intake levels of both omega-3 and omega-6 fatty acids, therefore, is recommended for optimal health.

 

 

Arachidonic acid is not carcinogenic, but 

 

it remains integral to the inflammatory and cell growth process, and supplementation is not recommended.

Metabolites particularly prostaglandins participate in normal and abnormal growth, including carcinogenesis.

Cyclooxygenase (COX) aids in the conversion of arachidonic acid to formation of prostaglandin E2.

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