Obesity as Disorder of CO2 Respiration: Role of Allergen Exposure in Enhancing Lung Capacity and CO2 Exchange
While it has been understood for some time that the process of eliminating fat is one of unlocking and eliminating from the body carbon dioxide stored in fat, just how important lung function is to this process is likely being understated in medical literature and treatment protocols for obesity.
Taking into consideration the staggering disparity of obesity rates between states that are in lower-lying parts of the United States such as those in the deep south and states such as Colorado that lie in the higher elevations, it seems clear that the common link in many cases of obesity is reduced lung function. Both regular exercise and relocating to higher elevations share in common that they serve to improve lung capacity. A pair of lungs must, of course, work harder to acquire needed oxygen at higher elevations and in so doing, improve their capacity vis a vis an increase in their total surface area and thus gain an enhanced capability to passively eliminate CO2 from the blood.
I propose conducting a study into the role of outdoor allergens in what may be termed healthy lung inflammation. Both muscle growth and healthy expansion of lung capacity depend upon a process of slightly damaging tissue which must go through a process of brief inflammation which must then be turned off, followed by a period of growth and healing. For those living sedentary lifestyles, living in sterile (in the sense that outdoor allergens are not present) indoor environments eliminates a stimulus that had in the past served to expand lung capacity, in this author’s view.
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Neuropathology and virus in brain of SARS-CoV-2 infected non-human primates
>Neurological manifestations are a significant complication of coronavirus disease (COVID-19), but underlying mechanisms aren’t well understood. The development of animal models that recapitulate the neuropathological findings of autopsied brain tissue from patients who died from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are critical for elucidating the neuropathogenesis of infection and disease. Here, we show neuroinflammation, microhemorrhages, brain hypoxia, and neuropathology that is consistent with hypoxic-ischemic injury in SARS-CoV-2 infected non-human primates (NHPs), including evidence of neuron degeneration and apoptosis. Importantly, this is seen among infected animals that do not develop severe respiratory disease, which may provide insight into neurological symptoms associated with “long COVID”. Sparse virus is detected in brain endothelial cells but does not associate with the severity of central nervous system (CNS) injury. We anticipate our findings will advance our current understanding of the neuropathogenesis of SARS-CoV-2 infection and demonstrate SARS-CoV-2 infected NHPs are a highly relevant animal model for investigating COVID-19 neuropathogenesis among human subjects.
