Frying, Boiling, Or Barbequing Meat Can Increase Brain Inflammation

When you fry, broil, or barbecue meat, even if it's just slightly brown, there is a malar reaction, myar reaction, that can result in damaging advanced location end products. So this can happen with beef, pork, chicken, or fish. And in cheese, these are formed when it's aged. So there's not much in milk. But in hard cheese, yes, there's quite a bit of these advanced location end products.

They increase brain inflammation. They attach to the rage receptor, receptor for advanced location end products is very aptly named the rage receptor. Generate and estimate 50 times as many free radicals damaging and chilling off brain cells compared to normal proteins. These AGEs can lodge in the amulet plaque and stay there forever, showering your brain with radiation like free radical damage. Let's avoid them. Where they found?

Let's see, chicken, bacon, beef, chicken, chicken, beef, chicken, chicken, beef, chicken, turkey, chicken. Okay, you get the idea. These foods are not only sources of advanced location end product and study showing that these dietary advanced location end products when eaten about half are absorbed into the bloodstream with a transporter to the brain and damage it. It's also true that these same foods have organically pesticides by

healthy foods. Advanced location end products were 2-3 times higher in Alzheimer's brains and found to be probable causes of tau tangles. Now, tau tangles are more tightly correlated with these symptoms of Alzheimer's disease than our aminberg plaques. Hedept reduced in our trial, the dietary advanced location end products by limiting cooking methods. No barbican boiling or deep frying of meat, chicken or fish, and no hard cheeses

were allowed on our diet in there. This is difficult for people to do. We have a neuroscience nutrition foundation. All of us worked for free during the years of doing this trial and for many years afterwards. And if you would like to go to neuroscience nutrition.org and give us a donation, we'd be duly grateful and continue our work. Thank you. Now, I want to tell you

more about how these aminberg plaques are formed. They're involved in about 80% of dementia cases. The clumps of protein occur between nerve cells and look like these fuzz balls in the picture. Also, their tau tangles not shown, they're phosphorylated tau, and they also contribute to it. Now, you see a cell membrane here. And beta and gamma secretase SNP off the aminlet precursor protein labeled APP here

to form the beta aminlet peptide. This peptide goes on to form oligomers, which are highly toxic and kill off brain cells. Then they become fibrils. Also highly toxic. Then they lodge an aminlet plaque, which continue to be quietly toxic and house advanced location end products forever. Very difficult to get rid of these things. So let's see about how we can not form them. And in this

study in molecular neurobiology in 2018, they said thus preventing Alzheimer's disease. What they really meant was thus preventing the formation of aminlet beta and more aminlet plaques are to get rid of the ones that are there. They looked at people with Alzheimer's disease. They found severely low levels of SAMI in the cerebral spinal fluid at all brain regions in Alzheimer's patient.