RECENTLY, I SPOKE on a panel for PBS TV at the American Association of Retired Persons (AARP) convention in Boston. The topic was dementia.
There was a woman with mild cognitive impairment on the panel. Her condition is sort of like pre-Alzheimer’s disease. Everyone on the panel — including the Harvard neurologist — agreed that memory loss is NOT a normal part of aging. The sad part was that the panel didn’t have much to offer people in the way of prevention. Their only solution was just a very bad and pretty ineffective selection of drugs with lots of side effects.
But there is another way to think about brain aging. The brain responds to all the same insults as the rest of the body — stress, poor diet, toxins, lack of exercise or sleep, nutritional deficiencies, and more. All we have to do is give the brain a tune-up and we can see miracles. In today’s blog I will give you nine tips that will allow you to do that. But first, let’s look a little more closely at the magnitude of this problem.
Dementia on the Rise
Dementia is a big problem and growing every day. Ten percent of 65-year olds, 25 percent of 75-year olds, and 50 percent of 85-year olds will get Alzheimer’s disease — at a cost of $60 billion a year to society. Worse, the number of people with Alzheimer’s is predicted to triple in the next few decades. It is now the seventh leading cause of death.(i)
I believe this is preventable, that we can slow this trend and even reverse it. In a moment, I will tell you how. But first I want to explain why just naming a disease — whether it is dementia or anything else — is becoming increasingly unhelpful (unless you just want to match the drug to the disease which is the only thing doctors are trained to do).
We have to think about individuals, not diseases. In medicine, our genetic differences are more important than our similarities.
Sometimes the practice of medicine lags behind the science, and sometimes the practice gets ahead of the science. Genetic testing puts us squarely in the middle of that dilemma. We are at a crossroads, where the old ideas we have about disease and diagnosis become less meaningful as we understand more and more about the importance of individual differences in determining illness. This is a time when personalized medicine will replace medicine based on diagnosis and disease.
We once thought that heart disease and artery-clogging plaques couldn’t be reversed (and now have proof that this does happen), I believe dementia can be reversed…
In fact, disease and diagnosis as we know it will soon be an obsolete concept, an artifact of medical history, like bloodletting or phrenology (the art of diagnosis based on the shape of your skull, popular in the 19th century). The reason is simply this: Naming a disease does nothing to help us identify and treat the underlying causes of the disease. We must address these causes if we have any hope of helping individuals heal.
I’d like to illustrate this through the story of one of my patients who had a diagnosis of dementia.
Treating Individuals, Not Diseases
George and his wife came to see me because he could no longer manage his business affairs, had become increasingly unable to function at home, and had to withdraw from family and social relationships. He was desperate as he felt himself slipping away.
There is no effective known treatment for dementia. But we do know a lot about what affects brain function and brain aging: our nutrition, inflammation, environmental toxins, stress, exercise, and deficiencies of hormones, vitamins, and omega-3 fats.
It is not just one gene, but the interaction between many genes and the environment that puts someone at risk for a chronic disease such as dementia. And we know that many things affect how our genes function — our diet, vitamins and minerals, toxins, allergens, stress, lack of sleep and exercise, and more.
Even though no long-term studies have been done to look at treating dementia based on genes, there are so many scientific threads that weave together a picture of how and why our brains age and what genes are involved. This leads me back to George …
For this man, whose mind and life were evaporating, I looked deeply into his genes and the biochemistry his genes controlled and found places where we could improve things.
He had a gene called apo E4, which is a high-risk gene for Alzheimer’s disease(ii) and also made it hard for him to lower his cholesterol and detoxify mercury from his brain.(iii) He also had a version of a gene for detoxification of metals and other toxins (glutathione-S-transferase, or GST)(iv) that was very inefficient, making him accumulate more toxins over his lifetime. Having the combination of a problem with GST and apo E4 puts people at even more risk for dementia.(v),(vi) In another study, people with an absent GST gene were likely to have much higher levels of mercury.(vii)
George had another gene called MTHFR(viii) that made him require very high doses of folate to lower his blood levels of homocysteine, which is a substance very toxic to the brain. Lastly, he had a gene called CETP that caused his cholesterol to be high, which contributes to dementia. Combine this gene with the apo E4 gene and your risk of dementia goes way up.(ix)
We found that George had high levels of mercury(x) and helped him detoxify with foods such as kale, watercress, and cilantro, herbs such as milk thistle, nutrients such as selenium and zinc, and medications that helped him overcome his genetic difficulties by getting rid of toxins.
We lowered his cholesterol with diet and herbs. We lowered his homocysteine with high doses of folate and vitamins B6 and B12.
What happened then was impressive …
After a year of aggressive therapy that was matched to his genes, not his diagnosis, he had a remarkable and dramatic recovery. Before I saw him, he could not manage his business, nor did his grandchildren want to be around him. After matching his treatment to his genes, he was again able to function, and his grandchildren loved being with him again.
While this area of genetic testing and nutrigenomics is new, and more research is needed to help us refine our understanding and treatment, there are ways to look through new doors into an entirely new era of medicine that no longer focuses on the disease, but on the person and their uniqueness. Here’s another example of how we can do that.
A woman named Christine was eighty and was experiencing severe memory loss and cognitive decline. Her family was obviously concerned, so she was tested with hours of neuropsychological testing and found to have dementia.
Her neurologist offered her words of comfort, but told her and her family there is no treatment truly effective to stop or reverse the progression of dementia. That’s when her daughter brought her to see me.
We discovered many subtle changes in her health that on their own wouldn’t explain dementia, but when added all together put a strain on her brain function. All we did was correct those problems — low thyroid function, mercury toxicity, inflammation, and deficiencies in vitamins B6 and D, folate, coenzyme Q10, and omega-3 fats — and improved her diet overall. I encouraged her to exercise, because exercise can help improve cognitive function and prevent dementia.
Six months later, she had the extensive memory tests repeated. Her psychologist was surprised to report that her scores got BETTER!
To put this in perspective, mental decline happens progressively, sometimes quickly, sometimes slowly, but NEVER gets better — according to our traditional medical thinking.
But just like we once thought that heart disease and artery-clogging plaques couldn’t be reversed (and now have proof that this does happen), I believe dementia can be reversed (if caught early enough) by attending to all the factors that affect brain function – diet, exercise, stress, nutritional deficiencies, toxins, hormonal imbalances, inflammation, and more.
It is really quite simple. Like everything I describe in UltraWellness, you get rid of the bad stuff, put in the good stuff, and the body heals. It’s common sense, but we are so far from that in the way we treat chronic illness with conventional medicine.
So if you know someone with memory loss, look at all the keys to UltraWellness extremely aggressively to find what imbalances are present and how to fix them. Remember, there will be no one treatment that works for everyone, because everyone is different. But here are some things to think about if you or a loved one are experiencing memory loss or dementia.
9 Steps to Reversing Dementia
Start by looking hard for correctable causes of memory loss. They include:
- Pre-diabetes or metabolic syndrome
- Low thyroid function
- Deficiencies in B vitamins, especially vitamin B12
- Omega-3 fat deficiencies
- Mercury or other heavy metal toxicity
- Vitamin D deficiency
- High cholesterol
- Unique genes that predispose you to nutritional or detoxification problems
Doctors who practice Functional Medicine and follow the principles I talk about in UltraWellness can help you find these problems.
Once you identify the underlying causes of the imbalance, here are a few things that can help your mind get a tune-up:
- Balance your blood sugar with a whole foods, low glycemic diet
- Exercise daily — even a 30-minute walk can help
- Deeply relax daily with yoga, meditation, biofeedback, or just deep breathing
- Take a multivitamin and mineral supplement
- Take an omega-3 fat supplement
- Take extra vitamin B6, B12, and folate
- Take vitamin D
- Treat thyroid or low sex hormones
- Get rid of mercury through a medical detoxification program
This is just a start, but it can go a long way to giving your brain the chance to heal and recover if you have memory problems. Even if you aren’t suffering from cognitive decline, you should take these steps because they can help you prevent the aging of your brain and obtain lifelong health.
Now I’d like to hear from you…
Have you noticed memory loss as you’ve gotten older?
What have you done about the problem so far?
Which of these steps do you plan to follow?
Do you have any other recommendations?
Please leave your thoughts by adding a comment below — but remember, we can’t offer personal medical advice online, so be sure to limit your comments to those about taking back our health!
To your good health,
Mark Hyman, MD
(ii) Tsai, M.S., Tangalos, E.G., Petersen, R.C., et al. (1994). Apolipoprotein : Risk factor for Alzheimer’s disease. American Journal of Human Genetics. 54 (4):643-649.
(iii) Godfrey, M.E., Wojcik, D.P., and C.A. Krone. (2003). Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. Journal of Alzheimer’s Disease. 5 (3):189-195.
(iv) Stroombergen, M.C., and R.H. Warring. (1999). Determination of glutathione S-transferase me and theta polymorphisms in neurological disease. Human and Experimental Toxicology. 18 (3):141-145.
(v) Bernardini, S., Bellincampi, L., Ballerini, S., et al. (2005). Glutathione S-transferase P1 *C allelic variant increases susceptibility for late-onset Alzheimer’s disease: Association study and relationship with Apolipoprotein E4 allele. Clinical Chemistry. 51(6):944-951.
(vi) Spalletta, G., Bernardini, S., Bellincampi, L., et al. (2007). Glutathione S-transferase P1 and T1 gene polymorphisms predict longitudinal course and age at onset of Alzheimer’s disease. The American Journal of Geriatric Psychiatry. 15 (10):879-887.
(vii) Gundacker, C., Komarnicki, G., Jagiello, P., et al. (2007). Glutathione s-transferase polymorphism, metallothionein expression, and mercury levels among students in Austria. Science of the Total Environment. 385 (1-3):37-47.
(viii) Dorszewska, J., Florczak, J., Rozycka, A., et al. (2007). Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer’s and Parkinson’s disease. Acta Neurobiologiae Experimentals. 67 (2):119-129.
(ix) Rodriguez, E., Mateo, I., Infante, J., et al. (2005). Cholesteryl ester transfer protein (CETP) polymorphism modifies the Alzheimer’s disease risk associated with APOE 4 allele. Journal of Neurology. 253 (2):181-185.
(x) Mutter, J., Naumann, J., Schneider, R., et al. (2007). Mercury and Alzheimer’s disease. Fortschritte der Neurologie-Psychiatrie 75 (9):528-538.