THIS IS WHY I STOPPED EATING MEAT

[Anonymous No.14658452]

Loss of insulin transport and insulin sensitivity in the brain provokes cognitive decline and neurological disorders as well as a metabolic syndrome as the brain controls most of our endocrine functions in the hypothalamus. Inflammation within the hypothalamus promotes cerebral insulin resistance and this reduces brain glucose metabolism and blood flow throughout the brain. Iron accumulates within our brain cells aggravated by neuroinflammation triggering the release of hepcidin by our astrocytes, heme oxygenase breaking down bilirubin and promoting iron uptake into microglial cells, endolysosomal deacidification and glutamatergic disinhibition provoking iron accumulation in our brain cells and this provokes oxidative stress, defects in autophagy and ultimately excitotoxicity and neurodegeneration. Reducing insulin sensitivity within the brain and promoting inflammation increase the tone of cortisol expression which increases endocannabinoid signaling to mitigate the effects of chronic mild stress.
Directly increasing neuronal insulin sensitivity increases metabolic homeostasis and BCAA catabolism. The failure of BCAA catabolism aggravates organ fibrosis, cancer growth, etc.

Saturated fats further promote dysfunction in the gastrointestinal barrier leading to a leaky gut, allowing bacterial endotoxins into our bloodstream. These molecules promote inflammation throughout the body through actions on TLR4. Endotoxins promote the breakdown of the blood-brain barrier allowing kynurenic acid and quinolinic acid into the brain.
Increased inflammation within the brain changes the neurotrophic activities of growth factors like BDNF to favor the production of microglial cells over that of neurons.

[Anonymous No.14658505]

Works in my body

[Anonymous No.14658575]

>>14658452
None of what you just said is real.

[Anonymous No.14658605]

>>14658452
>amino acids fucks insulin sensitivity
wrong
>meat provokes cognitice decline
wrong it's actually the opposite
>saturated fats leads to inflammation
Totally depends on the structure and length of the fat, and usually whether it will lead to oxidized forms(attacks tissue).
>saturated fats allows endotoxins to enter plasma
That's quite a chain of events.
>Endotoxins promote the breakdown of the blood-brain barrier
That's also quite a stretch.

I think you need to take your pills.

[Anonymous No.14658614]

>>14658605
post the studies first

[Anonymous No.14658616]

>>14658452
>Loss of insulin transport and insulin sensitivity in the brain provokes cognitive decline and neurological disorders as well as a metabolic syndrome as the brain controls most of our endocrine functions in the hypothalamus. Inflammation within the hypothalamus promotes cerebral insulin resistance and this reduces brain glucose metabolism and blood flow throughout the brain.
Those are arguments against grains and beans and for keto, Epilepsy is treated with keto or MIT's modified Atkins.
>Reducing insulin sensitivity within the brain
Glycation in the brain etc. Not le sensitivity. That's upstream from that in a scenario where you eat carbs. Vegetarian diets are high carb.
>Saturated fats further promote dysfunction in the gastrointestinal barrier leading to a leaky gut, allowing bacterial endotoxins into our bloodstream.
some epidemiological study with false correlations

[Anonymous No.14658619]

>>14658614
>posts a torrent of gobbledygook, no sources, would prob call for a dozen links
>sees someone says anything running counter to his shit
>"WHERE DA SUTIDEZ, AH-DURRR"

[Pax No.14659580]

>>14658619
It's demonstrated in ICV streptozotocin models in mice Alzheimers can be rapidly induced which shows a direct connection to amyloid beta induced insulin resistance within the brain aggravated by iron dysbiosis from LPS stimulation.
These effects can be replicated in mouse models where LPS is the smoking gun of cognitive decline in dementia and it's shown that Alzheimers does not occur in mice with TLR4 knockout.
https://www.frontiersin.org/articles/10.3389/fnins.2020.602508/full
https://www.sciencedirect.com/science/article/pii/S0969996120300474
https://pubmed.ncbi.nlm.nih.gov/11248117/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612444/
https://www.nature.com/articles/41792
>Here we report that insulin causes the type A γ-aminobutyric acid (GABAA) receptor, the principal receptor that mediates synaptic inhibition in the CNS8, to translocate rapidly from the intracellular compartment to the plasma membrane in transfected HEK 293 cells, and that this relocation requires the β2 subunit of the GABAA receptor. In CNS neurons, insulin increases the expression of GABAA receptors on the postsynaptic and dendritic membranes. We found that insulin increases the number of functional postsynaptic GABAA receptors, thereby increasing the amplitude of the GABAA-receptormediated miniature inhibitory postsynaptic currents (mIPSCs) without altering their time course. These results provide evidence for a rapid recruitment of functional receptors to the postsynaptic plasma membrane, suggesting a fundamental mechanism for the generation of synaptic plasticity
https://onlinelibrary.wiley.com/doi/full/10.1111/j.1471-4159.2004.02841.x
These effects are replicated in mouse models of intracerebral pancreatic islet transplantation. The effects of insulin on gaba receptor surface expression and inhibition are directly in opposition to amyloid beta