Selenium and Heart Failure
Translational research focusing on synergy between lifestyle interventions and treating HF.
(Mal-)nutrition has a great impact on the human heart. An aberrant equilibrium of circulating molecules like minerals and trace elements (for example iron, iodine and zinc) in the patients’ blood are closely associated with in the development and progression of HF. It was shown that up to 50% of patients with heart failure suffer from some form of malnutrition, like micronutrient insufficiencies.
Selenium (Se) is an essential micronutrient and previous studies suggested that severe deficiency in humans is associated with cardiomyopathy (Keshan disease). This disease is characterized as a rare but fatal form of dilated cardiomyopathy (DCM) showing the same clinical characteristics as idiopathic DCM, but with strong geographic distribution (Keshan County, northeast China). Treatment with selenium mitigated the clinical manifestations in patients with the disease and the government implemented nutritional policies promoting oral selenium supplementation, virtually eliminated Keshan disease in areas where it was endemic.
Recently, we showed in a large European cohort of 2382 patients with worsening heart failure (BIOSTAT-CHF) that approximately 25% of patients with HF have a serum Se concentration below clinical reference value (<70ug/L) and that this was associated with poorer quality of life, poor exercise capacity and a worse prognosis. Se deficiency was particularly frequent in older patients and more often women who had more severe signs and symptoms of HF. Serum Se concentrations of 70-100ug/L appeared to have similar adverse associations, suggesting that values <100ug/L, found in >50% of this cohort, might be considered insufficient for the physiological requirement and thus abnormal.
“The solution for modern age diseases like HF should lie in lifestyle interventions, like improving nutrition, exercise and reducing stress.”
Regarding the potential mechanism for these observations experimental data showed that Se deficiency in isolated human cardiomyocytes disrupts mitochondrial electron transport chain function leading to less efficient production of ATP, increased production of reactive oxygen species (ROS).
It remains to be clarified whether low Se levels in heart failure patients are just a marker for poor prognosis, or causative for development and progression of heart failure. Furthermore, the pathophysiological mechanisms affected by Se deficiency are currently unknown and will be explored in depth using both clinical/biomarker studies and state-of-the-art 3D tissue engineering of human heart tissues.
People involved
International collaborations
- BIOSTAT-CHF collaborators