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The clinical use of HMG CoA‐reductase inhibitors and the associated depletion of coenzyme Q 10 . A review of animal and human publications
Author(s) -
Langsjoen Peter H.,
Langsjoen Alena M.
Publication year - 2003
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520180212
Subject(s) - statin , medicine , hmg coa reductase , adverse effect , reductase , drug , pharmacology , cholesterol , heart failure , animal studies , dose , biology , enzyme , biochemistry
The depletion of the essential nutrient CoQ 10 by the increasingly popular cholesterol lowering drugs, HMG CoA reductase inhibitors (statins), has grown from a level of concern to one of alarm. With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ 10 deficiency is increasing noticeably. An estimated 36 million Americans are now candidates for statin drug therapy. Statin‐induced CoQ 10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials. This drug‐induced nutrient deficiency is dose related and more notable in settings of pre‐existing CoQ 10 deficiency such as in the elderly and in heart failure. Statin‐induced CoQ 10 deficiency is completely preventable with supplemental CoQ 10 with no adverse impact on the cholesterol lowering or anti‐inflammatory properties of the statin drugs. We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide‐spread deficiency of a nutrient critically important for normal heart function.