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Adopting a brain-healthy diet is a powerful tool in maximizing cognitive health and helping prevent dementia and Alzheimer's disease, says neuroscientist and nutritionist Lisa Mosconi. What's more, it may even ward off common ailments that affect many women, from slow metabolism to insomnia and depression. Here are 8 steps to take. Read more »
Benefits independent of the Mediterranean diet, researchers say
by Nicole Lou, Staff Writer, MedPage Today
Eating more chili peppers is linked to lower risk of dying, researchers found in a Mediterranean cohort study.
People who ate chili peppers regularly had less mortality over a median 8.2 years compared to peers who didn't eat them or only rarely did so. This was observed after adjustment for age, sex, and caloric intake:
Food for Thought periodically reports on nutrition research aimed at improving health and well-being.
The science behind food’s effects on human health is discovering some tasty benefits.
Berries and Grapes Linked With Memory Boost
As the world’s elderly population races toward an estimated 2 billion by 2050, memory loss is expected to take a substantial toll. But recent research shows that polyphenols from grapes and blueberries combined may help boost declining memory among some older adults.
The study by investigators in France and Canada built not only on their own work in mice, but also on other preclinical and clinical studies showing that blueberries and grapes or their extracts may offer benefits for age-related cognitive decline. Their previous animal research also showed a synergistic effect—grape extract enhanced the absorption of polyphenols in the blueberry extract.
Itseems like every other week a new study comes out questioning long-held wisdom about food and nutrition. First fat was vilified; now it’s considered a part of a healthy diet. Eggs used to be off-limits for people with heart problems due to the high amount of cholesterol, but that’s no longer the case.
***************************** Many people are confused about healthy eating. What’s your advice on how to eat healthy?
I advocate a “low glycemic load” diet — one that controls the surge in blood glucose and insulin after the meal. The way to achieve this is by cutting back on processed carbohydrates (refined grains, potato products, and sugar); increasing healthy fats, like nuts and nut butters, avocado, olive oil, and even dark chocolate; and having an adequate amount of protein, which can come from animal or plant-based sources. This approach involves a moderate reduction in total carbohydrates but still offers lots of flexibility in food choice. For people with diabetes, more severe restriction of carbohydrates may have additional benefits.
Not all researchers or clinicians, of course, will agree with this recommendation. That’s why we need the definitive research.
Improving the quality of nutrition research will be critical to public health and the international economic competitiveness of the U.S. in years to come. The default mode — relying on the pharmaceutical industry to devise ever more powerful drugs to treat diseases caused by diet — doesn’t make sense. It’s an ounce of prevention for a pound of cure.
JAMA Intern Med. Published online July 15, 2019. doi:10.1001/jamainternmed.2019.2633
The ketogenic diet has recently received much attention for its promise of treating obesity and type 2 diabetes. However, the enthusiasm for its potential benefits exceeds the current evidence supporting its use for these conditions. Although the temptation is great to recommend a potentially novel approach for otherwise difficult-to-treat diseases, it is important to remain grounded in our appraisal of the risks, benefits, and applicability of the diet to avoid unnecessary harm and costs to patients.
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Although the ketogenic diet has garnered much attention for the dietary treatment of chronic diseases such as obesity and type 2 diabetes, the evidence supporting its use is currently limited and the diet’s potential risks are real. Physicians and patients should continue to judiciously appraise the benefits and risks of the ketogenic diet in accordance with the evidence, not the hype.
Artgo sugerido pelo AMICOR Moacyr Saffer Dietary patterns during adulthood and cognitive performance in midlife The CARDIA study Claire T. McEvoy, PhD, Tina Hoang, MSPH, Stephen Sidney, MD, Lyn M. Steffen, PhD, David R. Jacobs, Jr., PhD, James M. Shikany, DrPH, John T. Wilkins, MD, and Kristine Yaffe, MD Neurology® 2019;92:e1589-e1599. doi:10.1212/WNL.0000000000007243
Abstract Objective To investigate whether dietary patterns (Mediterranean diet [MedDiet], Dietary Approaches to Stop Hypertension [DASH], and A Priori Diet Quality Score [APDQS]) during adulthood are associated with midlife cognitive performance.
Carnitine and choline are major nutrient precursors for gut microbiota-dependent generation of the atherogenic metabolite, trimethylamine N-oxide (TMAO). We performed randomized-controlled dietary intervention studies to explore the impact of chronic dietary patterns on TMAO levels, metabolism and renal excretion.
Methods and results
Volunteers (N = 113) were enrolled in a randomized 2-arm (high- or low-saturated fat) crossover design study. Within each arm, three 4-week isocaloric diets (with washout period between each) were evaluated (all meals prepared in metabolic kitchen with 25% calories from protein) to examine the effects of red meat, white meat, or non-meat protein on TMAO metabolism. Trimethylamine N-oxide and other trimethylamine (TMA) related metabolites were quantified at the end of each diet period. A random subset (N = 13) of subjects also participated in heavy isotope tracer studies. Chronic red meat, but not white meat or non-meat ingestion, increased plasma and urine TMAO (each >two-fold; P < 0.0001). Red meat ingestion also significantly reduced fractional renal excretion of TMAO (P < 0.05), but conversely, increased fractional renal excretion of carnitine, and two alternative gut microbiota-generated metabolites of carnitine, γ-butyrobetaine, and crotonobetaine (P < 0.05). Oral isotope challenge revealed red meat or white meat (vs. non-meat) increased TMA and TMAO production from carnitine (P < 0.05 each) but not choline. Dietary-saturated fat failed to impact TMAO or its metabolites.
Conclusion
Chronic dietary red meat increases systemic TMAO levels through: (i) enhanced dietary precursors; (ii) increased microbial TMA/TMAO production from carnitine, but not choline; and (iii) reduced renal TMAO excretion. Discontinuation of dietary red meat reduces plasma TMAO within 4 weeks.
