Gamma linolenic acid (GLA) is a dietary omega-6 fatty acid found in many plant oil extracts. Commercial products are typically made from seed extracts from evening primrose (average oil content 7-14%), blackcurrant (15-20%), borage oil (20-27%) and fungal oil (25%). GLA is not found in high levels in the diet. It has been suggested that some individuals may not convert the omega-6 fatty acid linoleic acid to longer chain derivatives, such as GLA, efficiently. Thus, supplementation with GLA-containing oils, such as borage oil and evening primrose oil, is occasionally recommended to increase GLA levels in the body. GLA is available commonly as a dietary supplement and is sold over the counter in capsules or oil to treat a variety of conditions such as eczema, oral mucoceles (mucus polyps), hyperlipidemia (high cholesterol), depression, postpartum depression, chronic fatigue syndrome (CFS), psoriasis (chronic skin disease), muscle aches, and menopausal flushing. There is currently good evidence for GLA treatment in rheumatoid arthritis, acute respiratory distress syndrome, and diabetic neuropathy (nerve damage). Little or no effect has been found in treatment of atopic dermatitis, attention deficit hyperactivity disorder (ADHD), cancer prevention, menopausal flushing, systemic sclerosis, and hypertension (high blood pressure). GLA has also been used to help with the body's response to tamoxifen in breast cancer patients. Today, production and extraction of oil from evening primrose and borage is done by companies primarily in China, New Zealand, and England. Pharmaceutical licensing for GLA oil products has had only limited success worldwide.
The main function of L-carnitine is to transfer long-chain fatty acids in the form of their acyl-carnitine esters across the inner mitochondrial membrane before beta-oxidation. In humans, it is synthesized in the liver, kidney, and brain and actively transported to other areas of the body. For example, 98% of the total body L-carnitine is confined to the skeletal and cardiac muscle at concentrations approximately 70 times higher than in the blood serum. Supplementation may be necessary in rare cases of primary carnitine deficiency, which may be caused by a defect in carnitine biosynthesis, a defect in carnitine active transport into tissue, or a defect in renal (kidney) conservation of carnitine. Known conditions of secondary deficiency of carnitine (insufficiency), in which L-carnitine is effective, include chronic stable angina and intermittent claudication characterized by distinct tissue hypoxia (low oxygen levels). Another condition that may benefit from carnitine supplementation is decreased sperm motility. Although use in preterm infants suggests carnitine supplementation may aid in maintaining or increasing plasma carnitine levels and possibly weight gain, carnitine is not routinely added to preterm total parenteral nutrition (TPN). However, soy-based infant formulas are fortified with carnitine to levels found in breast milk. In 1986, the U.S. Food and Drug Administration (FDA) approved L-carnitine for use in primary carnitine deficiency. D-carnitine or DL-carnitine may cause secondary L-carnitine deficiency and should not be used.