Calorie Restriction Better than Exercise in Slowing the Age-Related Onset of Inflammation in the Brain

All age-related neurodegenerative conditions appear in conjunction with rising levels of chronic inflammation. The immune system runs awry with age, and while the immune cells of the central nervous system are significantly different in type and character from those of the rest of the body, inflammation is still a major consequence of age-related immune failure. In turn, that inflammation accelerates other ongoing degenerative processes. Calorie restriction is the most reliable and well-studied way of modestly slowing aging, and here researchers demonstrate that it is more effective than exercise when it comes to postponing the rise of inflammation in the brain.

Practicing both calorie restriction and regular exercise is a great idea, but only because these options are free. Calorie restriction results in sizable health benefits in humans, and even though it doesn't extend human life spans by anywhere near the same proportion as is observed in mice, it is still something for nothing. But should be we supportive of research efforts that expend billions and decades on attempts to recreate slices of the calorie restriction response? Probably not, when that is a poor alternative to building rejuvenation therapies after the SENS model of damage repair. Why spend large amounts of time and funding on trying to slightly slow aging rather than trying to halt and reverse aging? Both are equally plausible goals at the present time. Why pick the worse option?

Microglia are brain cells that help maintain the integrity and normal functioning of brain tissue. Dysfunction of these cells, as may occur in disease, is linked to neurodevelopmental disorders and neurodegenerative conditions. Aging is also associated with inflammation driven by microglia in specific regions of the brain, but it is unclear whether diet or lifestyle can influence this process.

Researchers investigated the impact of high- and low-fat diets on inflammation and microglial markers in a specific brain region - the hypothalamus - of 6-month-old mice. They further looked at the effect of low- or high-fat diets on the microglia of 2-year-old mice, which were also given a lifelong exercise regime (voluntary running wheel) or lifelong restricted diets (a 40% reduction in calories). "Aging-induced inflammatory activation of microglia could only be prevented when mice were fed a low-fat diet in combination with limited caloric intake. A low-fat diet per se was not sufficient to prevent these changes."

The researchers also found that exercise was significantly less effective than caloric restriction at preventing these changes, although work by others has shown that exercise is associated with reducing the risk of other diseases. There is still much more work needed to understand the meaning of these findings. In the study, mice were only given one type of diet throughout their lives. It remains unclear how changing between diets would alter these results - for example whether switching to a low-fat diet could undo the negative consequences of a high-fat, unrestricted diet. Further studies are also needed to determine how these changes correspond to the cognitive performance of the mice.



Hi ! Just a 2 cent.

''The researchers also found that exercise was significantly less effective than caloric restriction at preventing these changes, although work by others has shown that exercise is associated with reducing the risk of other diseases.''

I believe this has to do with conversion of calories to liver glycogen and glucose/carbohydrates intake which are tied to Diabetes and Alzheimer's (Diabetes Type III); since hyperglycemia is causal to overactivation of IGF/mTOR/Insulin production/activation which means mTOR/NF-Kb/IL-6 inflammation (and blocking of epigenetic SIR/DAF genes in nucleus that help redox through antioxidation) and production of AGEs/Hba1c; in the brain it means protein aggregation and amyloid formation by excess carb/glucose intake; brain inflammation which is more Damaging and Weighting than the activation of BDNF production by exercise (exercise was found to create neurogenesis through BDNF (Brain-Derived Neutrophic Factor) and by activating telomerase (exercise increase hormone leves which activate estradiol receptors -> telomerase and on avergage exercised people are thinner/less Free Fatty Acids in plasma (means leans oxidation going on/less visceral found aroud the organs (like diabetes has liver fat excess for overconsumption of Calories/Glucose/Carb intake which, by Insulin from pancréas ebta cells signal of mTOR, transforms as Triglycerides and body fat increase if overindulging on the sweet candies carb/sugar full). You don't need excess carbs/calories, as many studies showed in the past about the calorie intake vs survival of specie/need vs energy kJ/calorie intake/Burning each day (if you have slow metabolism you can't burn those extra calories/carbs and it's end up mostly on your waist as belly vsiscral fat; with age metabolism slows thus can't burn as much as when you were a kid and could a box full of MayWest and eat 2 Big Macs like it's Nothing; and your burn it all in the next hour). Plus it was showm that certain sugars are far more Dangerous, namely, the worse one - Fructose (think High Fructose Corn Syrup), fructose was shown to produce 10-times more AGEs glycation crosslink formation in ECM than any other sugar (sucrose is far weaker, so it dextrose, lactose, xylittose, maltose, maltitose, and whatever other ose). This contributes to diabetes and HbA1c formation; and thus brain degenerensce by Amyloid formation (protein aggregation); it's why Alzheimer's Disease is Diabetes Type III. Calorie is more powerful than exercise because the body is an energy fuelling machine, and what you feed it; just like a car/fuel; it can haev dramatic impact on its performance than simply making your 'car run' (exercise). Thus, if feeding bad stuff in, in excess; it accelerates the diabetes axis through mTOR/Hyperinsulinemia (which activâtes said mTOR/inflammatory cytokines like TNF-a/IL-6)).
The brain is not immune to those effects and it is why; you see ischemia and anerysm by microlesion in brain vasculature from excess calorie intake. Exercising Nullifyies a little bit this excess of calorie intake but does not stop anything; the damage is long lasting and exercise curbs it somewhat; My uncle died of Alzheimer's at 74 years old, his brain was gone from filled amyloid, he was biker very athlete like and thus all this exercise was almost nill in effect (think people who exercise quite often and drop dead at like 41 yaer old). He did not do 'true' CR but was in fact doing it since from overt exercise; yet it did not stop onset of Alzheimer's disease coming (genetic factor (inherited), environment and epigenome failing through mass demethylation); this tells you that if someone is very careful and does 'sort of' CR and still dies anyway; it means both CR and exercise/weight loss only midly slow onset of predispositions. There this whole other genetic aspect/SNPs etc that is why no single person responds same to CR/exercise (and why you must due diligently/carefully to not provoke induced starvation/malnourishment which be worse and acelerate frailty/an already frail body (I was thin and I nearly died of Atherosclerosis; thin people die of tons of stuff and show that CR/exericse is not even half the story)..I guess the moral is moderation is key; overindulging or even in specific cases (if unhealthy) you need a new diet and it safe to say; it has More Good to being done than bad as long as you control it carefully and measure/see how your body responds; Your Body.

Just a 2c.

Posted by: CANanonymity at March 13th, 2018 6:38 AM

to CANanonymity
Ketogenic diet seems to check a lot of boxes then. A decrease of mTor and IL-6 (shown in children epilepsy treatment study), increase in BDNF, mitochondrial mass and overall protective brain environment(I believe its shown on TBI models)

Posted by: Andey at March 13th, 2018 11:14 AM

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