Overeating and Memory Loss

A recent study shows that overeating more than 2,100 calories a day nearly doubled the risk of memory loss or mild cognitive impairment (MCI). The study concerned those over 70 years old and will be presented at the American Academy of Neurology’s 64th Annual Meeting in New Orleans April 21 to April 28, 2012. According to study author Yonas E. Geda, MD, MSc, with the Mayo Clinic in Scottsdale, Arizona and a member of the American Academy of Neurology, “We observed a dose-response pattern which simply means the higher the amount of calories consumed each day, the higher the risk of MCI.”

According to Wikipedia, MCI is a brain-function syndrome involving the onset and evolution of cognitive impairments beyond those expected based on the age and education of the individual, but which are not significant enough to interfere with their daily activities. It is often found to be a transitional stage between normal aging and dementia.

For this investigation, they turned to the Mayo Clinic Study on Aging, an ongoing, population-based cohort study in Olmsted County, Minnesota. The analysis involved 1233 nondemented participants aged from 70 to 89 years; 1070 patients were cognitively normal, and 163 had MCI.

The subjects noted the amount of calories they ate or drank in a food questionnaire. They were divided into three equal groups based on their daily caloric consumption.

  • One-third consumed between 600 and 1,526 calories per day.
  • One-third consumed between 1,526 and 2,143 calories per day.
  • One-third consumed between 2,143 and 6,000 calories per day.

The analyses were adjusted for history of stroke, diabetes, amount of education, and other factors that can affect risk of memory loss. The risk for the highest calorie group was nearly double that of the lower calorie group. There was no noticeable difference in risk for the middle group.

According to Geda, the findings should be considered preliminary. However, consuming in moderation is a good idea for other medical reasons as well.

The co-authors of the study include Ronald C. Petersen, MD, Fellow of the American Academy of Neurology, and other investigators of the Mayo Clinic Study of Aging in Rochester, Minn.

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Scientists are looking at a biomaker that may possibly aid in the identification of individuals with mild memory problems who will eventually develop Alzheimer’s disease. The finding, which was published in the online version of Neurology, the journal of the American Academy of Neurology. It is believed that the new biomarker may prove to be more accurate compared to already established biomarkers.

According to the study author Robert Perneczky, MD, of the Technical University Munich in Germany, identifying individuals who will have Alzheimer’s disease earlier will be an important development. Once treatments that can be used for the prevention of the disease are available, it will become easier to treat and even prevent memory loss.

Fifty eight people with mild cognitive impairment (MCI) participated in the study. It is estimated that as many as 15% of the people who have MCI will develop Alzheimer’s every year.

Cerebrospinal fluid was taken from each participant and tested for certain proteins. Participants were then studied for about three years. Of the participants, 21 developed Alzheimer’s, 27 remained with MCI while 8 people regained normal cognitive skills. Researchers discovered that participants who later developed Alzheimer’s had significantly high levels of sAPPβ or soluble amyloid precursor protein beta in their cerebrospinal fluid.

Based on their findings, the researchers discovered that the person’s age, a protein called tau, and sAPPβ were excellent predictors of future cases of Alzheimer’s. Using these factors as a basis, it was easier to predict if an individual ran the risk of developing the disease. The accuracy for this prediction is pegged at about 80%.

A protein amyloid known as Aβ1-42 or amyloid beta1-42 was once considered one of the biomarkers significant to Alzheimer’s disease. However, it was not used as one of the predictive factors in the study.

The results, Perneczky said, suggest that sAPPβ could be useful as a biomarker and that it may even be better than Aβ1-42 for use in diagnosing Alzheimer’s earlier. The reason for this may be that Aβ1-42 can only indicate events at a later stage – events that already point to the accumulation of amyloid plaques in the brain. Since sAPPβ can be used as a critical initial step in determining if the disease will develop, it is likely to provide a more accurate indication on important pathological events.

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Misdiagnosis of Alzheimer’s Disease

Having grown up in Hawaii and having a father who was diagnosed with Alzheimer’s disease (AD), this article published in MedicalNewsToday.com caught my attention. Furthermore, this study was done on 426 Japanese American men who were residents of Hawaii and who had passed away at an average age of 87. My father who died at 85 was a Japanese American man living in Hawaii. Of the 426 men, 211 had been diagnosed with dementia (mostly AD) while they were living. However, the study found that about half of the 211 “did not have sufficient numbers of the brain lesions characterizing that condition to support the diagnosis.”

The brain autopsies that were performed showed that some of the cases of severe dementia and Alzheimer’s disease were misdiagnosed before death. Misdiagnoses increase with aging and also the manifestations of dementia are non-specific.
The article goes on to say that brain lesions are areas of the brain which have been damaged by disease, congenital malformation, trauma, or other causes. Lesions, such as abnormal protein plaques and tangled fibers, proliferate in the brains of people with Alzheimer’s disease, which affects more than five million Americans. Dementia, a condition marked by cognitive decline that interferes with daily life, is most often caused by Alzheimer’s.

According to author Lon White, MD, MPH, with the Kuakini Medical System in Honolulu:

Diagnosing specific dementias in people who are very old is complex, but with the large increase in dementia cases expected within the next 10 years in the United States, it will be increasingly important to correctly recognize, diagnose, prevent and treat age-related cognitive decline. Larger studies are needed to confirm these findings and provide insight as to how we may more accurately diagnose and prevent Alzheimer’s disease and other principal dementing disease processes in the elderly.

The research was released February 24 and will be presented as part of a plenary session at the American Academy of Neurology’s  63rd Annual Meeting in Honolulu April 9 to April 16, 2011. The study was supported by the National Institute on Aging and the Department of Veterans Affairs.

For a discussion on the stages of Alzheimer’s disease, see a previous post.

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