Intersection between Obesity, Dietary Selenium, and Statin Therapy in Brazil

Abstract

Obesity is among the most alarming health concerns, impacting public health and causing a socioeconomic challenge, especially in developing countries like Brazil, where approximately one quart of the population presents obesity. As an established risk factor for numerous comorbidities with a multifactorial etiology, obesity is a consequence of energy-dense overfeeding, however with significant undernourishment, leading to excessive adipose tissue accumulation and dysfunction, dyslipidemia, and micronutrient deficiencies. About 60% of patients with obesity take statins, a cholesterol-lowering medication, to curb dyslipidemia, with ~10% of these patients presenting various myopathies as side effects. Statins act upon the rate-limiting enzyme of cholesterol biosynthesis in the liver, which is a pathway providing intermediates to the synthesis of selenoproteins, i.e., enzymes containing the micronutrient selenium. Statins have been postulated to negatively impact selenoprotein synthesis, particularly in conditions of selenium deficiency, and potentially implicated in the myopathies occurring as side effects of statins. The Brazilian population is prone to selenium deficiency, hence could be considered more susceptible to statin side effects. This review examines the specific consequences to the Brazilian population of the harmful intersection between obesity development and concomitant micronutrient deficiencies, particularly selenium, combined with statin treatment in the context of nutrition in Brazil.

Keywords: Brazil; obesity; selenium; statins.

Figure 1

Interconnection between the cholesterol biosynthesis pathway, statins mode of inhibition of the HMG-CoA reductase step, and its consequential reduction in downstream products such as isopentenyl pyrophosphate (PP), which is necessary for the maturation of the tRNA for selenocysteine (Sec-tRNA).

Figure 2

Development of statin-associated muscle symptoms (SAMS), in which the cells of the skeletal muscle enhance its cycling of creatine (Cr)/phosphocreatine (pCr) and its cell membrane permeability, facilitating the release of creatine kinase (CK) to the circulation.