The obesity paradox predicts the second wave of COVID-19 to be severe in western countries

Funding Information: This work was funded by the Latvian Council of Science grants lzp-2018/1-0393 (I.A.K.), lzp-2018/2-0057 (T.K.), and lzp-2020/2-0271 (T.K.). Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.While COVID-19 infection and mortality rates are soaring in Western countries, Southeast Asian countries have successfully avoided the second wave of the SARS-CoV-2 pandemic despite high population density. We provide a biochemical hypothesis for the connection between low COVID-19 incidence, mortality rates, and high visceral adiposity in Southeast Asian populations. The SARS-CoV-2 virus uses angiotensin-converting enzyme 2 (ACE2) as a gateway into the human body. Although the highest expression levels of ACE2 are found in people’s visceral adipose tissue in Southeast Asia, this does not necessarily make them vulnerable to COVID-19. Hypothetically, high levels of visceral adiposity cause systemic inflammation, thus decreasing the ACE2 amount on the surface of both visceral adipocytes and alveolar epithelial type 2 cells in the lungs. Extra weight gained during the pandemic is expected to increase visceral adipose tissue in Southeast Asians, further decreasing the ACE2 pool. In contrast, weight gain can increase local inflammation in fat depots in Western people, leading to worse COVID-related outcomes. Because of the biological mechanisms associated with fat accumulation, inflammation, and their differential expression in Southeast Asian and Western populations, the second wave of the pandemic may be more severe in Western countries, while Southeast Asians may benefit from their higher visceral fat depots.publishersversionPeer reviewe

The Obesity Paradox Predicts the Second Wave of COVID-19 to Be Severe in Western Countries

While COVID-19 infection and mortality rates are soaring in Western countries, Southeast Asian countries have successfully avoided the second wave of the SARS-CoV-2 pandemic despite high population density. We provide a biochemical hypothesis for the connection between low COVID-19 incidence, mortality rates, and high visceral adiposity in Southeast Asian populations. The SARS-CoV-2 virus uses angiotensin-converting enzyme 2 (ACE2) as a gateway into the human body. Although the highest expression levels of ACE2 are found in people's visceral adipose tissue in Southeast Asia, this does not necessarily make them vulnerable to COVID-19. Hypothetically, high levels of visceral adiposity cause systemic inflammation, thus decreasing the ACE2 amount on the surface of both visceral adipocytes and alveolar epithelial type 2 cells in the lungs. Extra weight gained during the pandemic is expected to increase visceral adipose tissue in Southeast Asians, further decreasing the ACE2 pool. In contrast, weight gain can increase local inflammation in fat depots in Western people, leading to worse COVID-related outcomes. Because of the biological mechanisms associated with fat accumulation, inflammation, and their differential expression in Southeast Asian and Western populations, the second wave of the pandemic may be more severe in Western countries, while Southeast Asians may benefit from their higher visceral fat depots

Socioeconomic position, immune function, and its physiological markers

The development of costly traits such as immune function and secondary sexual traits is constrained by resource availability. The quality of developmental conditions and the availability of resources in ontogeny may therefore influence immune system functions and other biological traits. We analyzed causal pathways between family socioeconomic position, strength of immune response, and five physiological biomarkers in young Latvian men (n = 93) using structural equation modeling. Men from wealthier families had higher testosterone levels (rs = 0.280), stronger immune response (rs = 0.551), and higher facial attractiveness (rs = 0.300). There were weak, non-significant correlations between family income, body fat percentage (rs = −0.147), and fluctuating asymmetry (rs = −0.159). Testosterone partially (33.8%) mediated the effect of family income on facial masculinity. Testosterone (positively) and adiposity (negatively) partially (4%) mediated the relationship between family income and immune function. Higher facial masculinity, higher facial symmetry, and lower adiposity were reliable and independent cues of better immune function (R2 = 0.238) in a larger sample of young Latvian men (N = 146). Resource availability in ontogeny has an important role for the development of immune function and physical appearance, and it is a key parameter to be included in human eco-immunological research

Ultrastructural Changes in the Skeletal Muscle of Senile Rats with Significant Age-Dependent Motor Deficits

The anterior tibial (AT) muscle of 6 female Wistar rats aged 35-44 months, was examined by an electron microscopy. Previously, significant age-dependent functional and morphological deficits were found in these rats including [1] a strongly decreased muscle mass and force, [2] muscle stiffness, [3] spontaneous, tonic electromyographic activity, and [4] light-microscopic features of chronic denervation atrophy. In the present study diverse ultrastructural changes were found in muscle which correspond to chronic denervation atrophy. A number of already described abnormalities could be demonstrated in our material. However, sarcoplasmic reticulum (SR) tubular formations and extensive muscle fiber fragmentation have not been previously associated with senile changes in muscle. This can be explained by a very advanced age of our experimental animals and, in consequence, a more advanced denervation atrophy. Therefore it would appear that no single abnormality or set of morphological changes are characteristic of senile skeletal muscle. Key words: skeletal muscle, ultrastructure, denervation atrophy, aging. Basic Appl. Myol, 8 (3): 185-190, 1998 It is well known that both the muscle strength andniuscle mass decline with age. The morphological changes that might explain these impairments have been studied by severa

Clinical and genetic characteristics of late-onset Huntington's disease

Background: The frequency of late-onset Huntington's disease (>59 years) is assumed to be low and the clinical course milder. However, previous literature on late-onset disease is scarce and inconclusive. Objective: Our aim is to study clinical characteristics of late-onset compared to common-onset HD patients in a large cohort of HD patients from the Registry database. Methods: Participants with late- and common-onset (30–50 years)were compared for first clinical symptoms, disease progression, CAG repeat size and family history. Participants with a missing CAG repeat size, a repeat size of ≤35 or a UHDRS motor score of ≤5 were excluded. Results: Of 6007 eligible participants, 687 had late-onset (11.4%) and 3216 (53.5%) common-onset HD. Late-onset (n = 577) had significantly more gait and balance problems as first symptom compared to common-onset (n = 2408) (P <.001). Overall motor and cognitive performance (P <.001) were worse, however only disease motor progression was slower (coefficient, −0.58; SE 0.16; P <.001) compared to the common-onset group. Repeat size was significantly lower in the late-onset (n = 40.8; SD 1.6) compared to common-onset (n = 44.4; SD 2.8) (P <.001). Fewer late-onset patients (n = 451) had a positive family history compared to common-onset (n = 2940) (P <.001). Conclusions: Late-onset patients present more frequently with gait and balance problems as first symptom, and disease progression is not milder compared to common-onset HD patients apart from motor progression. The family history is likely to be negative, which might make diagnosing HD more difficult in this population. However, the balance and gait problems might be helpful in diagnosing HD in elderly patients