/sci/ - Science & Math

>>14518576
It's me anon.
In that post I aptly described they hypothalmic inflammation model of metabolic disorder.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5199695/
In short inflammation in the periphery and within the brain leads to defects in mitochondrial function and cell viability through reducing insulin transport to the brain from the periphery by promoting inflammation in a population of cells within the cerebellum that are responsible for promoting insulin uptake into the brain. saturated fats, and endotoxins reduce neuronal insulin sensitivity making brain cells degrade and this is especially true in the hypothalamus which participates in controlling most endocrine functions in the body. Declines in neuronal insulin sensitivity reduces hypothalmic metabolism of neurosteroids like pregnenolone from cholesterol and this allows cholesterol, and ceramides to accumulate in the lipid rafts of our neurons, endothelial cells and organs.
https://pubmed.ncbi.nlm.nih.gov/35108514/
Metabolic disorder and neurological disorders are both tied to the decline of insulin sensitivity and that reduces the viability of gabaergic cells such as somatostatin interneurons.
https://pubmed.ncbi.nlm.nih.gov/34430981/
Declines of these interneuron populations leads to decline of sensory encoding as well as control of metabolic functions controlled by somatostatin and leads to the disinhibition of insulin release in the periphery sensitization of autoimmunity due to reduced tolerance to inflammation and creating a hyperactive environment for your immune cells to be activated which attack your joints, promote calcification of your arteries and promotion of atherosclerosis. Inflammation in the periphery and in the brain from cortisol or endotoxins increases glutamate release which increases the production of the neurosteroid allopregnanolone which increases gabaergic tone and reduces surface expression of gaba a receptors promoting hpta axis dysfunction through chronic mild stress.