Last week I explained the current thinking about cognitive decline, whose worst manifestation, Alzheimer’s disease, occurs because a protein called amyloid accumulates in the brain, destroying delicate brain cells. Focusing on clearing out amyloid as a treatment of Alzheimer’s has been unsuccessful. The answer is prevention.
In his important book The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline, Dale Bredesen, MD, a UCLA-trained research neurologist, shows that amyloid appears as a reaction to any of several threats to our brain. He divides these threats into three groups.
Three main threats to the brain
The first, and most important, is chronic inflammation. You’ve probably read a lot about inflammation. We eat more fish for its anti-inflammatory omega-3s and we take baby aspirin or turmeric for their anti-inflammatory effects.
There are two forms of inflammation, one that helps us and one that harms. Brief episodes of inflammation are described as acute. These include your body’s elegant, normal response to any attack, whether by a bacterial or viral infection or to a foreign body, such as a splinter in your thumb. In medical vocabulary, adding “-itis” to a body part indicates an inflammation is taking place. Think appendicitis or dermatitis.
Chronic inflammation is the harmful version, now known to be the villain behind heart disease, autoimmune disease, and some cancers. Last week I mentioned that individuals carrying a specific gene–APOe4–are especially susceptible to brain inflammation and subsequently to Alzheimer’s. But susceptibility isn’t the same as inevitability. Certainly not all APOe4 carriers get Alzheimer’s (or any form of cognitive decline) and plenty of Alzheimer patients do not carry the APOe4 gene.
Dr. Bredesen has compiled an extensive list of triggers that create the chronic inflammatory state capable of igniting the smoldering fire of cognitive decline and Alzheimer’s. These include chronic infections like chronic Borrelia (Lyme disease), Herpes simplex (cold sores), chronic sinusitis, and even gingivitis (gum disease).
Equally risky triggers for inflammation in susceptible people are dietary (gluten grains, trans fats, sugars, dairy). Gluten, for example, can inflame the lining of your intestine, rendering it more permeable to a variety of other inflammatory foods, a condition called leaky gut. Too much sugar or too many simple carbohydrates (such as white bread), which convert to sugar, can cause your body to become resistant to the sugar-lowering effect of insulin. This is insulin resistance, which we now know can increase amyloid deposition.
How much inflammation you have in your body and discovering what’s triggering it can be established with lab tests, part of a diagnostic protocol Dr. Bredesen dubs a cognoscopy, sort of a colonoscopy of your brain.
Atrophic threats. Keeping in mind that amyloid appears as a reaction to any of several threats to our brains, Dr. Bredesen describes this second risk group using the medical word atrophic, meaning gradual decline in function due to neglect or underuse. This, too, occurs more often among APOe4 carriers.
The neglect list can be pretty long, but it’s manageable. Neglect includes an unhealthful diet; vitamin deficiencies such as low B-12, vitamin D, and vitamin E; smoking; homocysteine levels; and lower-than-normal levels of virtually every hormone our bodies manufacture (thyroid, adrenal, estrogen, progesterone, testosterone, pregnenolone).
The underuse list can pretty much be summed up by the phrase “use it or lose it.” Challenging your brain constantly keeps it vital and healthy. Sitting slack-jawed in your recliner binge watching and binge eating is risking trouble. Dr. Bredesen recommends a variety of brain exercise websites, such as BrainHQ, and let me also remind readers that uncorrected hearing loss has been associated with early dementia.
Toxic threats. Bredesen’s third Alzheimer’s threat occurs more frequently in carriers of the fairly common APOe3 gene rather than APOe4. This type of Alzheimer’s is less common and usually begins earlier, in the late 40s and 50s. It often starts after a period of physical or emotional stress. The initial symptoms may be difficulty with spelling, reading, word-finding, or simple arithmetic. Significantly, people in this group have blood-test abnormalities in tests not normally performed as part of a dementia diagnostic work-up.
Among these are low levels of zinc, high levels of copper, adrenal gland abnormalities, and a history of excessive exposure to toxins like mercury or black mold (mycotoxins). Here’s a page that shows good food sources of zinc.
Do I need a cognoscopy?
You might reasonably ask who really should get tested for all this. Who really needs Dr. Bredesen’s cognoscopy?
First, if there’s dementia in your family start with APOe testing. Obviously you’ll not be thrilled if you learn you’re carrying the APOe4/4 gene, but knowing you’re at risk means you can start taking preventive steps immediately. If you have a positive test result for APOe4/4 or APOe4/3, further tests can be individualized according to your age, gender, and lifestyle.
Second, if you’re experiencing cognitive decline, either the subjective form (you sense it but others don’t notice) or the mild type (noticed by you and others), step right up and get a thorough battery of tests (Bredesen’s cognoscopy).
Next week, I’ll discuss the specific tests in a cognoscopy and the steps you can take to normalize them. When members of our WholeHealth Chicago staff read Dr. Bredesen’s book, the general consensus was “Hey, this is us. This is what we do!” So we’re here if you need help.
David Edelberg, MD
For Part 3, click here.