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Theobromine Science
By David Tolson

Theobromine (3,7-dimethylxanthine) is a compound similar in structure to caffeine and a major component of cocoa and a minor component of coffee and tea. When ingested, about 11% of caffeine is metabolized into theobromine via 1-N-demethylation, making it the second major metabolite after paraxanthine. Like caffeine, orally administered theobromine is highly bioavailable and excreted primarily as metabolites. Theobromine has a longer half-life than caffeine, around 7-8 hours.

Theobromine is marketed in many products as a weight loss aid and sometimes as a stimulant. However, there is little reason to believe that it is superior to caffeine in any way. Although theobromine has diuretic properties similar to those of caffeine, it is only a weak adenosine antagonist, and has only minor CNS stimulant effects. This is reflected in a dose discrimination study in humans, in which not all of the subjects were able to discriminate theobromine from placebo, and those that were were only able to do so at much higher doses than caffeine (in the range of 100-560 mg for theobromine compared to 1.8-178 mg for caffeine). In rats, theobromine is not as effective at reducing food intake as caffeine, but has a similar level of toxicity. Additionally, in an in vitro study, theobromine was less effective than caffeine at stimulating lipolysis in adipocytes. Theobromine does have therapeutic use in the treatment of some conditions, such as high blood pressure (because of vasodilating properties) and cardiac failure (because of diuretic properties), but the present evidence is against the use of theobromine for fat loss when compared to other options.

If you have any questions or comments regarding this article, please email dvdtlsn@bulknutrition.com.


No part of this article may be reproduced in any form without the permission of David Tolson or Mike McCandless.


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References
Acta Pharmacol Toxicol (Copenh). 1984 Jan;54(1):64-71. The effect of alkylxanthines and other phosphodiesterase inhibitors on adenosine-receptor mediated decrease in lipolysis and cyclic AMP accumulation in rat fat cells. Fredholm BB, Lindgren E.

Br J Clin Pharmacol. 1986 Aug;22(2):177-82. Comparative pharmacokinetics of caffeine and its primary demethylated metabolites paraxanthine, theobromine and theophylline in man. Lelo A, Birkett DJ, Robson RA, Miners JO.

Eur J Pharmacol. 1990 Jan 10;175(2):203-5. Caffeine inhibits forskolin-stimulated cyclic AMP accumulation in rat brain. Mante S, Minneman KP.

Food Chem Toxicol. 1984 May;22(5):365-9. Comparative toxicities of dietary caffeine and theobromine in the rat. Gans JH.

Food Chem Toxicol. 2001 Jul;39(7):667-80. Uncertainty factors for chemical risk assessment: interspecies differences in the in vivo pharmacokinetics and metabolism of human CYP1A2 substrates. Walton K, Dorne JL, Renwick AG.

Pol J Pharmacol. 2001 Nov-Dec;53(6):615-21. Effects of phenothiazine neuroleptics on the rate of caffeine demethylation and hydroxylation in the rat liver. Daniel WA, Syrek M, Rylko Z, Kot M.

Psychopharmacology (Berl). 1994 Jun;115(1-2):1-8. Discriminative stimulus and subjective effects of theobromine and caffeine in humans. Mumford GK, Evans SM, Kaminski BJ, Preston KL, Sannerud CA, Silverman K, Griffiths RR.






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