Fasting diets boost brain power

Intermittent fasting may provide brain with more energy, improves memory and learning capabilities. When mice were fed every other day, they grew more neurons and synaptic connections, improving their cognitive functions. During intermittent fasting, the body switches energy sources from glucose, made in the liver, to fat cells, which stimulate activity and cell growth in the brain.

The body runs off of the liver's energy stores for about 10 to 14 hours in humans, when those stores are out, human, as well as animal bodies switch to fat stores, which are converted into compounds called ketones in the blood. Ketones act directly on the nerve cells to stimulate production of BDNF'- a key protein to neuron growth-and may help optimize cognition, learning and memory building.

Simply eating less will not have the same effects, eating three meals a day and having an overall relatively low calorie intake - between 1,800 and 2,000 every time-replenish their liver energy stores. The mice in the study were more alert and showed more activity in the areas of their brains responsible for learning and memory during the fasting period. Every-other-day fasting his team used for the mice wouldn't work in human, two days of fasting each week can help in human.
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Ketogenic diet prevents inflammation

The high-fat, low-carbohydrate regimen of ketogenic diets changes the way the body uses energy. In response to the shortage of carb-derived sugars such as glucose, the body begins breaking down fat into ketones and ketoacids, which it uses as alternative fuels.

In rodents, ketogenic diets and caloric restriction reduce inflammation, improve outcomes after brain injury, and extend lifespan. These benefits have not been confirmed in human.
Ketogenic diets can modulate the inflammatory response in rodents.
Researchers used a small molecule known as 2-deoxyglucose, 2DG, to block glucose metabolism and produce a ketogenic state in rats and controlled laboratory cell lines.

The team found that 2DG could bring inflammation to control levels. Reduced glucose metabolism lowered a key barometer of energy metabolism – the NADH/NAD+ ratio which in turn activated a protein called CtBP that acts to suppress activity of inflammatory genes. Researchers designed a drug-like peptide molecule that blocks the ability of CtBP to enter its inactive state – essentially forcing the protein to constantly block inflammatory gene activity and mimicking the effect of a ketogenic state.

Peptides, which are small proteins, don't work well themselves as drugs because they are unstable and people make antibodies against them. But other molecules that act the same way as the peptide could provide ketogenic benefits without extreme dietary changes. Excess glucose in people with diabetes, is associated with a pro-inflammatory state that often leads to atherosclerosis; the buildup of fatty plaques that can block key arteries.
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