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.

Enhanced by Zemanta

One of the distinguishing characteristics of Alzheimer’s disease (AD) is the destruction of brain cells that lead to diminished brain function. Scientists from the University of California at Santa Barbara have discovered what actually happens to these cells in patients with Alzheimer’s and other types of dementia. The findings of the study have been published in The Journal of Biological Chemistry online version.

According to senior author Stuart Feinstein, Ph.D, co-director of UCSB’s Neuroscience Research Institute, brain cells (also known as neurons) stop working properly. Neurons are essential for an individual to perform cognitive skills. The loss of neuronal capacity signals the onset of dementia.

Feinstein, a Molecular, Cellular and Developmental Biology professor, had spent 30 years studying the ‘tau’ protein utilizing cultured cells and test tube bio-chemistry models. Tau is present in long axons which are responsible for connecting neurons and their specific targets. Tau proteins also stabilize microtubules, a component of the cells’ cytoskeleton which is critical to the function and structure of neuronal cells.

For years, it was known that amyloid beta, a type of peptide, can cause the death of neuronal cells and lead to Alzheimer’s disease. The only problem is that it has never been understood how the mechanism that triggers it works. Recent research has shown that amyloid beta requires tau in order to destroy neurons. What is not clear is how it does the action. Most researchers believe that it triggers the excessive chemical modification of tau proteins. For Feinstein, the important goal was to discover the exact details involved in the process of abnormal phosphorylation. By determining what exactly happens, drug companies would have sufficient clues to make the right decisions and pharmaceutical solutions for the problem.

But there is a glitch. The initial hypothesis regarding the effect of amyloid beta on tau phosphorylation was incorrect. What the team discovered was that taking neuronal cells and adding amyloid beta did not result in massively phosphorylated tau proteins. Instead, it resulted in the fragmentation of the proteins within one to two hours and the death of the cells within 24 hours.

According to Feinstein, tau performs multiple jobs, the most widely understood of which is the regulation of cellular cytoskeleton. Cell skeletons, unlike human skeletons, do not undergo abrupt change in its shape. Cell skeletons constantly move, grow and shorten to allow the cell to perform its many functions. The length of cytoskeleton is essential to neurons due to its length.

After the findings, Feinstein’s argument is that the death of neurons that occur in Alzheimer’s is due to a malfunctioning cytoskeleton and that destroying tau proteins can lead to cell death. Feinstein hypothesized the same action that destroys the cytoskeleton in cells treated with cancer drugs could be the same action that was triggered in the neuronal cells.

University of Pittsburgh Heinz Chapel

A study done at the University of Pittsburgh Alzheimer Disease Research Center, The impact of physical activity on neurocognitive function in adults with cognitive impairment, led by Kirk Erickson, PhD, found that greater amounts of walking are associated with greater gray matter volume, which in turn is associated with a reduced risk of cognitive impairment. The study, published in Neurology, showed that walking 72 blocks was necessary to detect increased gray matter volume, but walking more than 72 blocks did not spare additional volume.

According to Medscape Medical News, Dr. Erickson stated, “These findings are really quite astonishing.  Other studies have previously shown that exercise is related to brain function, but the fact that we found that walking as little as 1 mile a day is related to brain volume 9 years later, and dementia 13 years later, is truly novel and really quite impressive.”

Furthermore, BBC quotes Dr. Erickson, “If regular exercise in midlife could improve brain health and improve thinking and memory in later life, it would be one more reason to make regular exercise in people of all ages a public health imperative.”

If you have not yet started moving, what’s hold you back? Let’s start walking.

Phosphatidylserine Memory Booster

Last month a friend gave me an issue of  Woman’s World magazine. In it was a tiny article, Ward off Alzheimer’s with the new “Memory” Pill! As the author of this Alzheimer’s disease blog, that certainly caught my attention. It’s called phosphatidyl serine (PS) or more commonly spelled as one word in the scientific community, phosphatidylserine. It says, “it’s a supplement proven to prevent age-related memory loss and help your brain function as if it were 12 years younger!” Now, wouldn’t that catch your attention, too? Could we all use a memory booster?

Since it’s such a short article, let me share the rest of it.

PS helps restore the brain’s supply of acetycholine, a neurotransmitter that’s crucial for memory, reports Thom Lobe, M.D., of Beneveda Medical Group in Beverly Hills, California. In one study, folks who took 100 mg., three times a day, scored 30% higher on memory tests after just 12 weeks! Your Rx: 200 mg. to 300 mg. daily in supplement form (find it in health-food stores). Important: Ask your doctor before taking this or any supplement, especially if you also take an anticoagulant drug.

If phosphatidylserine is such an impressive supplement, shouldn’t all Alzheimer’s patients be on it? According to the Mayo Clinic, “Several studies involving phosphatidylserine indicate a benefit — improved cognitive abilities and behaviors. However, improvements in memory lasted only a few months and were seen in people with the least severe symptoms.” They go on to say that earlier studies were based on brain cells of cows. However, because of concerns about mad cow disease, most manufacturers now produce phosphatidylserine supplements from soy or cabbage derivatives. So it’s not really known if the plant-based supplements are equally effective.

WebMD adds that phosphatidylserine is a chemical that the body can make, but it gets most of what it needs from foods. Side effects include insomnia and upset stomach for doses over 300 mg. They warn that there could be drug interactions. Click here for more information and click on Interactions.

So the old adage, if it’s too good to be true, it probably is, appears to be in effect here. Have you ever taken phosphatidylserine? What is your opinion?