Protect Your Brain with Real Food

Energy consumption raises GIP and GLP1 in the proximal and distal intestine respectfully. 

Processed foods  that are nearly completely absorbed in proximal intestine raise GIP and reduce GLP1.

Unprocessed foods and low glycemic foods raise both GIP and GLP1.

Fruit juice (processed) raises GIP but fruit with peel and fiber raises first GIP and later raises GLP1.

 GLP1 is neuroprotective. GIP added to GLP1 is even more protective.

They have developed dual agonist for disease state protection.

A smart strategy is to eat real food that has low glycemic index and fiber to feed gut bacteria primarily and secondarily  via fermentation products to raise GLP1 in the distal ileum.

https://www.sciencedirect.com/science/article/pii/S0028390818300406

abstract

In animal models of neurodegenerative disorders, they show superior neuroprotective effects.

Type 2 diabetes is a risk factor for several chronic neurodegenerative disorders such as Alzheimer's or Parkinson's disease. The link appears to be insulin de-sensitisation in the brain. Insulin is an important neuroprotective growth factor. GLP-1 and GIP are growth factors that re-sensitise insulin and GLP-1 mimetics are used in the clinic to treat diabetes. GLP-1 and GIP mimetics initially designed to treat diabetes show good protective effects in animal models of Alzheimer's and Parkinson's disease. Based on these results, several clinical trials have shown first encouraging effects in patients with Alzheimer's or Parkinson’ disease. Novel dual GLP-1/GIP receptor agonists have been developed to treat diabetes, and they also show good neuroprotective effects that are superior to single GLP-1 analogues. Several newer dual analogues have been tested that have been engineered to cross the blood –brain barrier. They show clear neuroprotective effects by reducing inflammation and oxidative stress and apoptotic signalling and protecting memory formation, synaptic numbers and synaptic activity, motor activity, dopaminergic neurons, cortical activity and energy utilisation in the brain. These results demonstrate the potential of developing disease-modifying treatments for Alzheimer's and Parkinson's disease that are superior to current single GLP-1 mimetics.

This article is part of the Special Issue entitled ‘Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.’