This is a rather short version of a long story.
In 1987 I weighed about 205 lbs. I was eating all kinds of trashy foods, from doughnuts to fried fish to French fries. While I exercised regularly, I also suffered from severe eating disorders. What I ingested was a lot of sugar, and I ate very poorly One morning I woke up, and a lightning bolt smacked me in the head. I needed a change.
A gluten-free, low-carb lifestyle has been responsible for a major turn in my understanding of how what I eat affects my chances of having cognitive problems down the road. My father was a well-respected psychiatrist in the local area, and had done lots of research in neurology. Yet by the time he began his decline, while it seemed he may have caught on to the cause, it was too late. He began exercising furiously and drastically modified his eating habits, but he eventually wound up diagnosed with all three (Alzheimer’s, Parkinson’s and dementia). For so long I have eaten with zero caution. After I saw your videos, I realized what my father probably did, but while it was too late for him, I’m hoping I have time for a good turnaround.
I just got back my first A1C, which I’m using as my baseline, and while I am very concerned about it, I am also taking positive actions to correct it. Currently it is 5.6. I am now exercising aerobically between 45 and 55 minutes 6 of 7 days a week, carefully controlling my foods and supplementing based on your information. This is the first time in many attempts to lose weight that I actually believe I am going to be able to keep it off. It is SO much easier to think of this in terms of brain health and preventing cognitive decline than it ever was thinking in terms of just “losing weight”. To me that is by far and away the best motivation. It makes eating right and exercising a “no-brainer.”
Last month I had the great honor to serve as program chairman for an integrative brain symposium held in Hollywood, Florida. What was so exciting for me was the fact that I was given the opportunity to invite some of our most well-respected thought leaders in the field of brain science to lecture on their research.
One of our esteemed presenters was Dale E. Bredesen, M.D., an Alzheimer’s researcher at the Mary S. Easton Center for Alzheimer’s Disease Research at UCLA. Dr. Bredesen provided a unique assessment of the current approaches to dealing with Alzheimer’s disease. It was very clear from his presentation that the idea of focusing on a single drug or single intervention was simply not going to be appropriate if we are ever going to be able to offer up any meaningful therapy for the more than 5.4 million Americans who are afflicted with this devastating condition.
Dr. Bredesen described a “systems approach” to dealing with Alzheimer’s disease, looking at a variety of factors that seem to conspire, ultimately leading to brain degeneration that we know recognize as representing this disease. Using his approach which he termed, “systems therapeutics,” which integrates a variety of parameters, he has actually been able to reverse cognitive decline in this devastating condition. Continue reading
Studies have demonstrated that there is a direct correlation between changes in size of the brains memory center, the hippocampus, and declining memory function. So it’s obviously in our great interest to do everything we possibly can to preserve the size of hippocampus, which is to say, prevent hippocampal atrophy.
It has become clear that there is a powerful direct relationship between not only fasting blood sugar, but even average blood sugar, in terms of predicting the rate at which the hippocampus will shrink and therefore memory will decline. In a new report, recently published in the journal Neurology, researchers in Germany evaluated a group of 141 individuals, average age 63 years, with memory testing as well as a specific type of MRI scan of the brain to measure the size of the hippocampus in each participant. At the same time they looked at blood sugar levels as well as average blood sugar, by assessing a blood test called hemoglobin A1 c.