Put down the bread and pick up the…bacon?

      Two independent studies published in Cell Metabolism found that a ketogenic diet- high fat, low protein and extremely low carbohydrates- significantly improved memory performance and reduced early mortality in aging mice.  These studies are one of the first to examine long term effects of ketogenic diets on the longevity and health span of normal mice.  The goal of ketogenic diets is to force the body to burn fats, rather than carbohydrates.  Typically, our bodies convert carbohydrates into glucose, which is then used for energy.  However, if very few carbohydrates are consumed, the body will be in a state of ketosis, and the liver will convert fat into ketone bodies.  These ketone bodies replace glucose as the body’s energy source.

      The UC Davis study found that aged mice fed a ketogenic diet had a 13% increase in median lifespan versus mice fed the control diet.  In addition, mice receiving the ketogenic diet displayed improved memory, motor function, and muscle mass.  The Buck Institute study found that aged mice given a ketogenic diet, alternated with a control, non-ketogenic diet, also had reduced early mortality, and improvements in memory tasks.  Interestingly, the improvements in memory where observed when the aging mice were on the control diet, suggesting that a cyclic ketogenic diet may have long lasting effects.  While the exact mechanism of how a ketogenic diet improves memory and health in aged mice is unknown, the authors hypothesize that the elevation of the ketone beta-hydroxybutryrate (BHB) may alter the expression of genes involved in aging and insulin regulation.

      But don’t abandon your plate of spaghetti just yet.  Most health professionals caution against individuals starting a ketogenic diet without consulting a doctor, and research has even found that a continuous ketogenic diet leads to obesity. Future studies need to examine these ketogenic diets in different strains of mice, as well as determine if the timing of the diets produces similar effects.  However, these findings get researchers one step closer to better understanding dietary interventions that impact aging.  So while there’s no need to avoid spaghetti, maybe spoon an extra helping of meatballs on top.

A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice

Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice

Both articles published September 5, 2017 in Cell Metabolism

Could our eyes be the window to detecting Alzheimer’s?

We use our eyes to scan the menu and watch our favorite show, but could they also help doctors determine if we are at risk for developing Alzheimer’s?  We may be one step closer to this reality, thanks to researchers at Cedars-Sinai Medical Center.  They showed that non-invasive retinal imaging could detect and quantify beta-amyloid deposits in the eyes of patients with Alzheimer’s disease.

Looking at the eyes for Alzheimer biomarkers is somewhat novel, as researchers have largely focused on the role of beta-amyloid deposits in the brain.  Beta-amyloid deposits are formed by fragments of the amyloid precursor protein, which is found in the tissue surrounding brain cells.  In Alzheimer’s, these fragments will aggregate together, and form plaques that surround healthy brain cells.  These plaques can disrupt cell communication and can trigger inflammatory processes.  The accumulation of these plaques can occur years before a clinical diagnosis of dementia (often referred to as prodromal Alzheimer’s disease) can be given.

In order to image the retina, subjects were orally administered curcumin, a component of the spice turmeric.  Curcumin labels amyloid plaques, and emits a fluorescence signal, which allows researchers to identify and quantify amyloid-beta plaques using their imaging software.  After scanning the eyes of 10 Alzheimer’s disease (AD) patients, and 10 healthy controls, they found that those with AD had a 4.7 fold increase in the number of retinal amyloid-plaques.  Researchers also found similar results when analyzing the retinas of 23 deceased AD patients and 14 controls, reporting an increase in amyloid-plaques in AD patients.

Importantly, a strong correlation was observed between the number of retinal and brain plaques in patients with AD.  Future studies will look to determine when the accumulation of retinal plaques begin, as well as testing the imaging on a larger sample size.  Taken together, these findings provide a promising non-invasive, cost-effective, diagnostic for a disease that will cost the nation $259 billion dollars in 2017.

Published August 17, 2017 in JCI Insight

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