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Is Diabetes Related to Artificial Sweeteners?

Artificial sweeteners in mice changed the gut microbiome altering glucose absorption.

Mice given non-caloric sweeteners developed glucose intolerance more quickly than those given sucrose or glucose. In these animals the artificial sweeteners quickly altered the mouse microbiome in favor of pathways that enhance absorption of calorie rich glucose and short-chain fatty acids. Authors suggest this may help explain the diabetes epidemic, although this needs to be reproduced in humans.

PositiveTip: Emphasizing healthy food choices, cutting back on "junk" food, and physical activity is better than depending on non-caloric sweeteners to control weight.

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Sugar Counteracts the Anti-inflamatory Effects of Essential Oils

Sugar can negate the beneficial effects of omega 3 fats in mice.

Among the many benefits of the polyunsaturated n-3 fatty acids (omega-3 fats) is that they protect against high-fat diet induced obesity and the inflammation of fat cells  Researchers have found that excess table sugar (sucrose) added to the diets of mice significantly reduced the anti-inflammatory properties of these beneficial fats, and increased obesity.

PositiveTip: How much sugar are you using? Too much may counteract the good fats found in nuts, plant oils and some fish.

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Obesity Increases Risk of H1N1 Virus

Obesity increases susceptible and mortality to H1N1 virus.

In the 2009 H1N1 pandemic medical science recognized that obesity increased the risk of contracting the virus. Tests on vaccinated obese individuals showed immunecell function at only 70% compared to normal weight individuals. Death rates in obese and morbidly obese H1N1 patients were 3 and 7.6 times the rate of normal weight patients. Research in obese mice showed a 25% mortality rate compared to zero in lean mice with similar immune deficiencies as found in humans.

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Reversing Age-Related Memory Loss (In Mice)

Scientists have discovered a way to reverse age-related memory loss in mice.

Geneticists in Germany trained mice of different ages to solve a variety of cognitive tests. The oldest mice had the hardest time learning these tasks, and failed to activate genes that are important for memory.

Treating these older mice with a specific molecule that repaired a specific histone modification defect in the mouse DNA resulted in significant improvement in the animals' ability to learn. Of course, this is mouse research, but it is encouraging to know that human age-related memory loss may be reversible in the future.