This is our present circumstance, as described by the Alzheimer’s Association: Someone in the United States develops Alzheimer’s disease every 66 seconds.

Five and a half million people in the U.S. are living with Alzheimer’s disease today. One in 10 adults, ages 65 and older, has Alzheimer’s disease. The burden for women is great. Two-thirds of Americans with Alzheimer’s disease are women and 60 percent of Alzheimer’s caregivers are women. The rate for Alzheimer’s disease in blacks is twice that of Caucasians. Meanwhile, Hispanics are one and a half times more likely than Caucasians to develop the disease.

For South Carolina, in particular, our annual state death rate from Alzheimer’s disease is 40.1 per 100,000, the eighth highest rate in the US. Despite that high death rate, our population of Alzheimer’s patients is projected to rise by 40 percent by 2025, the seventh fastest growing state in the nation.

For these and many other reasons, I spent this past weekend in front of my computer, attending a conference called “Reversing Cognitive Decline: Advanced Clinical Training in Treating Mild Cognitive Impairment and Early Alzheimer’s Disease.” (OK, I admit I had one eye on our television during the first 30 minutes of the Clemson-Miami game, until the Saturday evening session ended at 8:30. After that, I had both eyes on the TV.)

About 500 people around the world attended. The featured speaker was Dr. Dale Bredesen, author of "The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline," and a professor at UCLA.

Dr. Bredesen began his career as a bench researcher, working in the laboratory with mouse and rat models of dementia. After years of study and work on many potential interventions for treating memory loss, he recognized that single interventions were unlikely to have much of an impact and that the disease we call Alzheimer’s was not one but at least several different diseases with a single endpoint: destruction of brain tissue.

This destruction occurs due to the body’s effort to protect itself from three main threats: inflammation (from infection, diet or other causes); decline and shortage of nutrients, hormones and other brain tissue-supporting molecules; and toxic substances such as metals and toxins produced by some molds. These threats incite the production of specific forms of amyloid, which are toxic to the brain’s synapses.

Removing amyloid has been the target of many of the drugs used in recent studies of treatment for Alzheimer’s disease. Dr. Bredesen believes that while removing amyloid may have some effect, unless the underlying threats are removed, or at least reduced, the disease will continue to progress.

The good news is that almost all of what we have discussed in previous columns on “Loving Your Brain” helps to enhance the body’s efforts to protect itself from the three main threats listed. So, if you have been doing the things we suggested to love your brain, keep doing them and attempt to do more of them.

Based on the discussions at this weekend’s conference, some items should probably be added. It appears that fasting has several benefits, particularly in the area of inflammation. We know that we tend to eat too much — witness our increasing rates of obesity — but we also eat for too many hours during the day. A 12-hour period without food is good for the digestive process, brain health and perhaps even for longevity. Fourteen hours is probably even better. Occasional day-long fasts are good for us, or relative fasts (600 calories) one day a week.

Hormone status is important. Women in menopause have been encouraged to take hormone replacement therapy for as short a duration and at as low a dose as possible. It appears that estrogen in the form of estradiol patches are brain protectors and may be continued beyond age 65 if desired (micronized topical progesterone is necessary for those who still have a uterus, to protect against uterine lining overgrowth).

Most controversially, ApoE genetic testing, should probably be recommended for those with a family history of Alzheimer’s disease and for those with cognitive decline.

Why? Persons with no ApoE 4 gene have a nine percent risk of developing Alzheimer’s. Those with one copy of the gene have a 30 percent risk and those with two copies have a 50-90 percent risk (depending on the study you believe).

Will knowing your ApoE status make any difference now? We can’t do any gene splicing to take it out, but if I knew I had two copies of the ApoE4 gene, I would do everything possible, including following as much of Dr. Bredesen’s model as was indicated by my history and laboratory values.

If you would not change your behavior based on the test results and you would rather not know, keep taking care of your brain as well as you can. 

Bert Keller and Bill Simpson write the occasional column, “Aging for Amateurs.” Simpson, a retired physician, wrote this installment. Comments, questions and suggestions are welcome at agingforamateurs@gmail.com.