Ground breaking research (cited below) suggests that optimizing carnitine intake can enhance fatty acid oxidation in healthy persons who already have adequate carnitine levels. Biotin is needed for glucosemetabolism, mitochondrial function, nail and skin health. Carnitine and Biotin work together clinically for the nutritional support of the biochemical disturbances that can occur in metabolic syndrome, weight loss, and type II diabetes. While carnitine supports fat burning, it can also increase gluconeogenesis?an undesirable effect. This may lead to an increase in blood sugar and a concomitant rise in insulin and malonylCoA activity. Increased malonylCoA activity can inhibit the mitochondrial fat transporting enzyme Carnitine Palmitoyl Transferase I (CPT-1) and thereby decrease fat transport, fatburning and weight loss (J Clin Invest. 1996 Nov 15;98(10):2244-50).
Biotin has been theorized to inhibit some of the enzymes responsible for gluconeogenesis when taken in optimal amounts. Therefore, when using carnitine to support fatty acid oxidation, Crayhon Research strongly recommends taking 1 mg of biotin for every 500 mg of carnitine to keep gluconeogenesis and insulin metabolism balanced. Carnitine and Biotin are also both often found deficient in pregnancy and in patients taking valproic acid.
Research Summaries:
Kelly GS. L-Carnitine: therapeutic applications of a conditionally essential amino acid. Altern Med Rev. 1998 Oct;3(5):345-60.
A trimethylated amino acid roughly similar in structure to choline, carnitine is a cofactor required for transformation of free long-chain fatty acids into acylcarnitines, and for their subsequent transport into the mitochondrial matrix, where they undergo beta-oxidation for cellular energy production. Mitochondrial fatty acid oxidation is the primary fuel source inheart and skeletal muscle, pointing to the relative importance of this nutrient for proper function in these tissues. Although L-Carnitine deficiency is an infrequent problem in a healthy, well-nourished population consuming adequate protein, many individuals within the population appear to be somewhere along a continuum, characterized by mild deficiency at one extreme, and tissue pathology at the other. Conditions which seem to benefit from exogenous supplementation of L-Carnitine include anorexia, chronic fatigue, coronary vascular disease, diphtheria, hypoglycemia,male infertility, muscular myopathies, and Rett syndrome. In addition, preterm infants, dialysis patients, and HIV+ individuals seem to be prone to a deficiency of L-Carnitine, and benefit from supplementation. Although available data on L-Carnitine as an ergogenic aid is not compelling, undersome experimental conditions pretreatment has favored aerobicprocesses and resulted in improved endurance performance.
Cavallini G, Caracciolo S, Vitali G, Modenini F, Biagiotti G. Carnitine versusandrogen administration in the treatment of sexual dysfunction, depressed mood, and fatigue associated with male aging. Urology. 2004 Apr;63(4):641-6.Muller DM, Seim H, Kiess W, Loster H, Richter T.
Effects of oral L-Carnitine supplementation on in vivo long-chain fatty acid oxidation inhealthy adults. Metabolism. 2002 Nov;51(11):1389-91. Despite an abundance of literature describing the basic mechanisms of action of L-Carnitine metabolism, there remains some uncertainty regarding the effects of oral L-Carnitine supplementation on in vivo fatty acid oxidationin normal subjects under normal conditions. It is well known that L-Carnitine normalizes the metabolism of long-chain fatty acids in cases of Carnitine deficiency. However, it has not yet been shown that L-Carnitine influences the metabolism of long-chain fatty acids in subjects without disturbancesin fatty acid metabolism. Therefore, Crayhon Research investigated the effects of oral L-Carnitine supplementation on in vivo long-chain fatty acid oxidationby measuring 1-[(13)C] palmitic acid oxidation in healthy subjects before and after L-Carnitine supplementation (3 x 1 g/d for 10 days). The manufacturer observed a significant increase in (13)CO(2) exhalation. This is the first investigation to conclusively demonstrate that oral L-Carnitine supplementation results in an increase in long-chain fatty acid oxidation in vivo in subjects without L-Carnitine deficiency or without prolonged fatty acid metabolism. Pistone G et al. Levocarnitine administration in elderly subjects with rapid muscle fatigue: effect on body composition, lipid profile and fatigue.
Drugs Aging. 2003;20(10):761-7.AIM: Levocarnitine is an important contributor to cellular energy metabolism.
This study aims to evaluate the effects of levocarnitine supplementation on body composition, lipid profile and fatigue in elderly subjects with rapid muscle fatigue.
METHOD: This was a placebo-controlled, randomised, double-blind, two-phase study. Eighty-four elderly subjects with onset of fatigue following slight physical activity were recruited to the study. Prior to randomisation all patients entered a 2-week normalisation phase where they were given an 'ad libitum' diet, according to the National Cholesterol Education Program (Step 2). Subjects were asked to record their daily food intake every 2 days. Before the 30-day treatment phase, subjects were randomly assigned to two groups (matched for male/female ratio, age and body mass index). One group received levocarnitine 2g twice daily (n = 42) and the other placebo (n = 42). Efficacy measures included changes in total fat mass, total muscle mass, serum triglyceride, total cholesterol, high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C),apolipoprotein (apo)A1, and apoB levels. The Wessely and Powell scale wasused to evaluate physical and mental fatigue. Subjects were assessed at the beginning and end of the study period. RESULTS: At the end of the study, compared with placebo, the levocarnitine-treated patients showed significant improvements in the following parameters: total fat mass (-3.1 vs -0.5kg), total muscle mass (+2.1 vs +0.2 kg), total cholesterol (-1.2 vs +0.1mmol/L), LDL-C (-1.1 vs -0.2 mmol/L), HDL-C (+0.2 vs +0.01 mmol/L), triglycerides (-0.3 vs 0.0 mmol/L), apoA1 (-0.2 vs 0.0 g/L), and apoB (-0.3 vs -0.1g/L). Wessely and Powell scores decreased significantly by 40% (physical fatigue) and 45% (mental fatigue) in subjects taking levocarnitine, compared with 11% and 8%, respectively, in the placebo group (p < 0.001 vs place bofor both parameters). No adverse events were reported in any treatment group. CONCLUSION: Administration of levocarnitine to healthy elderly subjects resulted in a reduction of total fat mass, an increase of total muscle mass, and appeared to exert a favorable effect on fatigue and serum lipids. Koutsikos D et al. Oral glucose tolerance test after high-dose i.v. biotin administration in normoglucemic hemodialysis patients.
Ren Fail.1996 Jan;18(1):131-7.Koutsikos D, Agroyannis B, Tzanatos-Exarchou H. Biotin for diabeticperipheral neuropathy. Biomed Pharmacother. 1990;44(10):511-4.
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