Post-covid T2DM is a way of body to compensate for the loss of metabolic rate. A cell uses 3 main substrates to produce energy: glucose, lipids, and oxygen. Whe

Post-covid T2DM is a way of body to compensate for the loss of metabolic rate. A cell uses 3 main substrates to produce energy: glucose, lipids, and oxygen. When metabolic rate is low, the brain subconsciously registers that condition and tries to "increase" the ATP yield by increasing the amount of substrates in the blood. The glucose concentration gets increased by gluconeogenesis, the oxygen gets increased by hyperventilation. In parallel, increased levels of insulin are produced to increase glucose transport function. The aim of the brain is to satisfy the energy demand, and all those compensatory actions are effective to some degree. However, the cells cannot consume all that glucose despite the massive insulin presence due to a wrecked metabolic machinery of mitochondria, and the body remains hanging in a diabetic, insulin-resistant state of T2DM. If ATP demand is still not met, hyperventilation eventually reaches its peak state, and the individual starts experiencing shortness of breath. If this state of unmet homeostasis lasts for some longer time, the signs of pathological tissue hypoxia start to kick in, causing the appearance of neurological symptoms, which are then followed by metabolic panic attacks (crashes) when left untreated. After that, a more serious cognitive impairment may follow: slurred speech, partial vision loss, problems with spatial navigation, photophobia, etc. All those symptoms correspond to a border-line dementia and may signify the close proximity of a point of no return.