Nutrition and Dementia

The Role of Nutrition in Dementia Prevention and Management

Sponsored by the Sackler Institute for Nutrition Science

Hosted by the New York Academy of Sciences
26-27-March-2015
& World Trade Center, New York, NY
#NutrDementia

Day 1 of the New York Academy of Sciences Symposium on Nutrition and Dementia left me bursting at the seams with a newfound understanding of how nutrient status dictates cognitive health. First, I’d like to begin this summary by expressing my appreciation to the Sackler Institute and Nestlé Health Science center for their commitment to identifying Nutrient gaps that affect early childhood development and aging. 

Dr. Irwin Rosenberg, from Tufts University, was the first speaker to point out the inverse relationship between homocysteine levels, which are regulated by B vitamins, and cerebrovascular disease.  This introductory presentation laid the groundwork for the presentations by David Smith and Helga Refsum who showed that B vitamin supplementation (folate, B6 and B12) reduce the rate of brain atrophy by lowering total homocysteine levels.  Although B12 and folate rely on one another for metabolism this effect is largely driven by B12 levels.  The reason why media outlets reported that a large-scale clinical trial showed that B vitamins do not prevent dementia was due to a gross misinterpretation of the data.  In order for the data to be significant baseline levels of B vitamins need to be measured because those who have normal levels will not show any brain changes if treated with B vitamins.  Also, the study was conducted with an inappropriate patient population that did not meet suitable inclusion criteria. Finally, Dementia was not an assessment outcome for the study, only cognitive function.

I must admit that I was unmoved by Gary Gibson’s discussion of how reduction of the mitochondrial alpha-ketoglutarate- dehydrogenase complex (KGDHC) correlates with diminished mental performance, but was very intrigued by the correlation between thiamine (vitamin B1) levels and Alzheimer’s disease (AD).  Thiamine deficiency, which leads to impaired glucose metabolism, can be treated with Benfotiamine, a synthetic S-acyl derivative of thiamine (vitamin B1).  This theme was further elaborated by Dr. Stephen Cunnane who reported that glucose hypometabolism may be abrogated by following a ketogenic diet where ketone bodies may be used as a source of energy for the brain.

Given my own personal interest in the Microbiome I was quite intrigued by Kirsten Tillisch’s assertion that decreased Microbiota diversity correlates with aging.  As such, it may be possible to reverse cognitive decline by increasing Microbiota diversity.  The observation that anxiety and depression decrease when given probiotics supports this hypothesis.

Richard Wurtman was not a speaker at the symposium but certainly piqued my interest by calling the audience’s attention to a product called Souvenaid®, an elemental product, largely consisting of uridine, choline and Omega-3 fatty acids, that has been shown to promote synaptogenesis, thus reversing the synapse loss seen in AD.  This product is currently available in Europe but not in the US.

The data presented by Cédric Annweiler to support the role of vitamin D in cognitive function were rather weak but were supported by Katherine Tucker who shared a list of published studies to show vitamin D levels correlate with reduced incidence of dementia, AD and stroke.  Dr. Tucker cited the outcome of a Boston-Puerto Rican Health Study that provided support for the roles of vitamin B6, Omega-3 fatty acids and vitamin D in improving cognitive abilities.  High sugar consumption and reduced fruit and vegetable consumption correlate with cognitive impairment.

The final presentation of the day, presented by Dr. Martha Clare Morris, was reviewed in the Health Section of the a number of media outlets.  Based on the unique nutritional needs of those at risk for cognitive decline, Dr. Morris compared the benefits of a “Mind” diet, designed to improve cognitive function, with a Mediterranean diet and the DASH (Dietary Approaches to Stop Hypertension) diet.  While all three diets improved cognitive function, the Mind diet was significantly better than the other two.  The Mind diet consists of the following foods:

·         Three servings of whole grains every day

·         A salad and one other vegetable every day

·         A single glass of wine every day

·         Mostly nuts as snacks

·         Beans every other day

·         Poultry twice a week

·         Berries twice a week

·         Fish once a week

·         Olive oil as the primary oil used in meal preparation

The following foods should be avoided:

·         Red meats

·         No more than one tablespoon of butter or margarine per day

·         Less than a serving a week of cheese, fried or fast food

·         No fruits beyond blueberries and perhaps strawberries

·         No pastries or sweets, may be replaced with a teaspoon of jam per week

A subsequent blog will be posted shortly to review Day 2 of the Symposium.