Published on: March 14, 2015
by Amy R. Beaudreault for Huffington Post:
While enjoying a family vacation in Florida, Max Lugavere’s mother, known for her ability to recall the slightest detail, couldn’t remember the current year. Her family thought she was joking, but the journey that followed was far from a laughing matter. Many years later, Lugavere continues to ask the question: Is there anything that can reduce or slow cognitive decline?
Recently, Julianne Moore’s Academy Award-winning portrayal of a Columbia University linguistics professor diagnosed with early-onset Alzheimer’s disease in Still Alice, brought the issue of dementia to life for moviegoers. In the film, Alice’s doctor recommends exercising and drinking water to slow progression of the disease. While exercise is good advice, nowhere during the movie did the role of nutrition arise. Unfortunately, the same holds true for many real-life doctor’s visits.
Despite growing evidence supporting the positive role nutrition plays in dementia prevention, nutrition is rarely employed as a prevention strategy. A new study may change that. The linkages among nutrition and brain function are made clear in the results from a first-ever randomized controlled trial of its kind led by Miia Kivipelto, MD, PhD published today in the Lancet.
The two-year research study measured the effects on brain function of an intervention — which included nutritional guidance and management of metabolic risk factors — for age-related dementia. Using the Neuropsychological Test Battery (NTB) test, intervention group scores for overall brain function were 25 percent higher. For executive functioning, intervention group scores were 83 percent higher, and processing speed was 150 percent higher.
Kivipelto will present these impressive findings for the first time during her keynote lecture at a landmark NYC scientific conference on March 26 and 27 presented by The Sackler Institute for Nutrition Science, the New York Academy of Sciences, Nestlé Nutrition Institute and Nestlé Health Science. Additional lectures will focus on research that supports nutrition as an approach to prevention of age-related diseases. Despite the growing body of literature that nutrition can positively impact brain function, debate surely will ensue between those who believe more clinical trials are necessary before clinicians should start prescribing nutritional changes, in addition to standby pharmaceutical options.
This includes studies on vitamin B12, vitamin D, omega-3 fatty acids, and phytonutrients, such as those found in cocoa, berries , and nuts, some specifically looking at populations with dementia. Furthermore, certain dietary patterns, such as the Mediterranean diet, may help prevent cognitive decline and dementia.
Let’s consider a few additional facts: The global population is undergoing an extraordinary demographic shift. By the year 2050, the population of those older than 60 is forecasted to double from 841 million to 2 billion. Today, approximately 44 million worldwide live with dementia and by2050 the estimate will reach 135 million (not to mention the costs–$640 billion USD in 2010 and increasing rapidly). I’m scared, are you?
One piece of this puzzle I know for sure: Global health needs to widen its scope to include non-pharmaceutical interventions to mitigate dementia’s startling future outlook. Instead of treating dementia, science must look at prevention and the power of environmental factors, policy, and behavior change utilizing a health systems approach. Until then, our duty is to be mindful of the long-lasting effects diet has on overall health and well-being at the micro- and macro-levels.
Our event with Dr. Wendy Suzuki explaining how higher levels of physical fitness are associated with better brain structure and higher cognitive function. Highlights video.
Our event with Dr. Wendy Suzuki explaining how higher levels of physical fitness are associated with better brain structure and higher cognitive function. Full video.
Two blood markers, phosphorylated tau 217 (p-tau217) and phosphorylated tau 181 (p-tau181), showed strong diagnostic performances for Alzheimer’s disease and discriminated Alzheimer’s from frontotemporal lobar denervation (FTLD) syndromes and normal cognition, a retrospective study...
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