Hemodynamic Observations of Tumo Yoga Practitioners in a Himalayan Environment

Abstract Background: Few attempts have been made to evaluate the physiology of traditional Eastern health practices. The goal of this study was to evaluate the hemodynamic effects of the mysterious Buddhist practice of tumo. Tumo is a meditative practice that produces inner heat through the alleged cultivation of body energy-channels. Methods: This study was performed by members of an international expedition to the Himalayan Mountains in the Republic of India. The study was performed in an unpopulated outdoor mountainous area at an altitude of 16,400 ft with ambient temperatures between -10 and -15°C. Two (2) cohorts of subjects were studied: healthy non-yogi volunteers and tumo practitioners. All of the subjects were stripped down to their underclothes and exposed to the subzero atmospheric temperatures for 5 minutes. The volunteers were then passively rewarmed while the tumo practitioners performed tumo for up to 10 minutes. Blood pressure, heart rate, and stroke volume index (SVI) and cardiac index were measured noninvasively using a NICOMÔ hemodynamic monitor, while carotid blood flow and biventricular performance were determined echocardiographically at each stage of the experiment. The total peripheral resistance index (TPRI), left ventricular ejection fraction (LVEF), and tricuspid annular plane systolic excursion (TAPSE) were determined using standard formula. Results: Fourteen (14) subjects (six volunteers and eight tumo practitioners) completed the study. There was one female subject in each group. With cold exposure, the SVI and carotid blood flow decreased while the TPRI increased significantly in both groups. In the volunteer group, these changes retuned to baseline with rewarming. Following tumo, the cardiac index (4.8 -0.6 versus 4.0 -0.5 l/m 2 ; p < 0.01), carotid blood flow (445 -127 versus 325 -100 mL/min/m 2 , p < 0.01), LVEF (68 -5 versus 64 -7%; p < 0.05) and TAPSE (2.9 -0.4 versus 2.4 -0.5 cm; p < 0.01) were significantly higher when compared with baseline, while the TPRI was significantly lower (1786 -189 versus 2173 -281; p < 0.01). Conclusions: Tumo was associated with a hyperdynamic vasodilated state with increased biventricular performance. We postulate that tumo results in a massive increase in sympathetic activity with activation of brown adipose tissue and marked heat production. The increased heat production may explain the paradoxical vasodilatation in tumo practitioners exposed to subzero temperatures

Genetic predictors of chronic heart failure in obese patients

BACKGROUND: the study of molecular genetic markers and pathogenetic mechanisms of neurohormonal activation, as well as their importance in the formation of heart failure in obesity, is an urgent problem of modern medicine, the solution of which will allow effective prevention of cardiovascular complications, optimize treatment and improve the prognosis of obese patients. AIMS: search for genetic markers presumably involved in the pathogenesis of secondary diastolic heart failure in patients with obesity. MATERIALS AND METHODS: PCR-diagnostics of whole blood of 104 patients with obesity was carried out, which were divided into 2 groups, depending on the presence of diastolic heart failure. The following candidate genes were analyzed: angiotensinogen AGT gene (C521T and T704C), angiotensin II receptor gene of the first type AGTR1 (A1166C), angiotensin II receptor gene of the second type AGTR2 (G1675A), aldosterone synthase gene CYP11B2 (C (-344) T). RESULTS: It is shown that the development of secondary diastolic heart failure in obese individuals of both sexes is associated with the mutation of the aldosterone synthase gene CYP11B2, namely, with the replacement of the C allele at the -344 position by the T allele and the presence of the T / T genotype. The relative risk of developing the disease with the T / T genotype was 5.93 times higher in men (p = 0.008) and 4.57 times in women (p = 0.014). For men, the mutation of the angiotensinogen AGT gene, namely the replacement of the allele C at position 521 by the T allele, is important. At the same time, the relative risk of development of SDS in the T / T genotype is increased by 4.26 times (p = 0.039). Mutations of the genes of the angiotensin II receptor of the first type AGTR1 (A1166C) and the angiotensin II receptor of the second type AGTR2 (G1675A) are not associated with the development of diastolic heart failure in obese patients. CONCLUSIONS: The data presented can be used to stratify the risk of secondary heart failure in obese individuals

Hemodynamic Observations of Tumo Yoga Practitioners in a Himalayan Environment

Abstract Background: Few attempts have been made to evaluate the physiology of traditional Eastern health practices. The goal of this study was to evaluate the hemodynamic effects of the mysterious Buddhist practice of tumo. Tumo is a meditative practice that produces inner heat through the alleged cultivation of body energy-channels. Methods: This study was performed by members of an international expedition to the Himalayan Mountains in the Republic of India. The study was performed in an unpopulated outdoor mountainous area at an altitude of 16,400 ft with ambient temperatures between -10 and -15°C. Two (2) cohorts of subjects were studied: healthy non-yogi volunteers and tumo practitioners. All of the subjects were stripped down to their underclothes and exposed to the subzero atmospheric temperatures for 5 minutes. The volunteers were then passively rewarmed while the tumo practitioners performed tumo for up to 10 minutes. Blood pressure, heart rate, and stroke volume index (SVI) and cardiac index were measured noninvasively using a NICOMÔ hemodynamic monitor, while carotid blood flow and biventricular performance were determined echocardiographically at each stage of the experiment. The total peripheral resistance index (TPRI), left ventricular ejection fraction (LVEF), and tricuspid annular plane systolic excursion (TAPSE) were determined using standard formula. Results: Fourteen (14) subjects (six volunteers and eight tumo practitioners) completed the study. There was one female subject in each group. With cold exposure, the SVI and carotid blood flow decreased while the TPRI increased significantly in both groups. In the volunteer group, these changes retuned to baseline with rewarming. Following tumo, the cardiac index (4.8 -0.6 versus 4.0 -0.5 l/m 2 ; p < 0.01), carotid blood flow (445 -127 versus 325 -100 mL/min/m 2 , p < 0.01), LVEF (68 -5 versus 64 -7%; p < 0.05) and TAPSE (2.9 -0.4 versus 2.4 -0.5 cm; p < 0.01) were significantly higher when compared with baseline, while the TPRI was significantly lower (1786 -189 versus 2173 -281; p < 0.01). Conclusions: Tumo was associated with a hyperdynamic vasodilated state with increased biventricular performance. We postulate that tumo results in a massive increase in sympathetic activity with activation of brown adipose tissue and marked heat production. The increased heat production may explain the paradoxical vasodilatation in tumo practitioners exposed to subzero temperatures

Dissecting the role of cadmium, lead, arsenic, and mercury in non-alcoholic fatty liver disease and non-alcoholic steatohepatitis

The objective of the present study was to review the existing epidemiological and laboratory findings supporting the role of toxic metal exposure in non-alcoholic fatty liver disease (NAFLD). The existing epidemiological studies demonstrate that cadmium (Cd), lead (Pb), arsenic (As), and mercury (Hg) exposure was associated both with an increased risk of NAFLD and altered biochemical markers of liver injury. Laboratory studies demonstrated that metal exposure induces hepatic lipid accumulation resulting from activation of lipogenesis and inhibition of fatty acid β-oxidation due to up-regulation of sterol regulatory element-binding protein 1 (SREBP-1), carbohydrate response element binding protein (ChREBP), peroxisome proliferator-activated receptor γ (PPARγ), and down-regulation of PPARα. Other metabolic pathways involved in this effect may include activation of reactive oxygen species (ROS)/extracellular signal-regulated kinase (ERK) and inhibition of AMP-activated protein kinase (AMPK) signaling. The mechanisms of hepatocyte damage during development of metal-induced hepatic steatosis were shown to involve oxidative stress, endoplasmic reticulum stress, pyroptosis, ferroptosis, and dysregulation of autophagy. Induction of inflammatory response contributing to progression of NAFLD to non-alcoholic steatohepatitis (NASH) upon toxic metal exposure was shown to be mediated by up-regulation of nuclear factor κB (NF-κB) and activation of NRLP3 inflammasome. Moreover, epigenetic effects of the metals, as well as their effect on gut microbiota and gut wall integrity were also shown to mediate their role in NAFLD development. Despite being demonstrated for Cd, Pb, and As, the contribution of these mechanisms into Hg-induced NAFLD is yet to be estimated. Therefore, further studies are required to clarify the intimate mechanisms underlying the relationship between heavy metal and metalloid exposure and NAFLD/NASH to reveal the potential targets for treatment and prevention of metal-induced NAFLD.Fil: Tinkov, Alexey A.. Yaroslavl State University; RusiaFil: Aschner, Michael. Albert Einstein College of Medicine; Estados UnidosFil: Santamaria, Abel. Universidad Nacional Autónoma de México; MéxicoFil: Bogdanov, Alfred R.. Russian State Social University; RusiaFil: Tizabi, Yousef. Howard University College of Medicine; Estados UnidosFil: Virgolini, Miriam Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Zhou, Ji Chang. Sun Yat-sen University; ChinaFil: Skalny, Anatoly V.. Yaroslavl State University; Rusi