By David Blyweiss, M.D.

May 20, 2013

• Does anyone REALLY know what causes Alzheimer’s?
• How a cold sore could rob your memory
• Quickest way to stop the downward spiral of dementia in its tracks

In the past few years I’ve noticed a big age shift when it comes to concerns about the prevention of Alzheimer’s. For many years the people worried about this memory-robbing disease were in their 60’s or 70’s.

Now I have many patients in their 50’s who are already taking proactive measures. Even some of my 40-something patients are standing up and taking notice.

Chances are good these folks have watched a parent or grandparent suffer through the memory loss and dementia that comes with Alzheimer’s. And it’s something they want to avoid at all costs.

Let’s face it. Everything about Alzheimer’s is frightening.

But the scariest part of all is our lack of knowledge about this disease. Scientists and medical experts can tell us what happens in our brains to cause the problem. But it’s been much more difficult to identify the underlying cause.

Here’s what we DO know…

Alzheimer’s disease is the result of a cascade of changes that occur in your brain. Clumps of a protein called beta amyloid begin building. These are known as amyloid plaques. At the same time, another protein called tau begins tangling around nerve cells in the brain.

It’s this combination of events that leads to the loss of brain function and cognitive ability. Some researchers believe the excess beta amyloid and tau literally choke out brain and nerve cells.

What we haven’t quite been able to pin down is why these amyloid plaques and tau filaments start accumulating in the first place.

But breaking research may be giving us some much-needed answers.

It’s common knowledge that beta amyloid plaque in the brain has a direct association with Alzheimer’s disease. So you would think the best “cure” for stopping the disease would be to get rid of the plaque.

But do you know what happened when Eli Lily created a drug to kill off this brain-altering plaque?

Instead of “curing” Alzheimer’s, killing off the amyloid plaque made the patients’ condition deteriorate much more quickly!

And now we know why.

It turns out amyloid plaques may be a part of your body’s natural immune response against infection. In other words, it’s actually trying to protect the brain from an infectious agent – such as a bacteria or virus. This is why killing off the plaque can worsen the condition instead of improving it.

But that’s only part of the equation. There’s still one more question.

What would cause this protective mechanism to race out of control?

The answer may be as simple as a virus; specifically herpes simplex type 1 (HSV-1.) This is the type of herpes that causes cold sores.

In recent years, study after study has linked HSV-1 to the accumulation of amyloid plaques and abnormal tau in the brain. One particularly eye-opening report found 90% of Alzheimer’s brains were infected with HSV-1.

Now here’s the big problem: About 57% of people in the U.S. have HSV-1. Once you acquire this virus it never leaves your body. It remains in your nerve cells until something triggers it to become active again.

It’s believed that when the virus is active, it contributes to the formation of amyloid plaques and tangles of tau. Thus, the more you can do to keep outbreaks at a minimum, the better your chances of beating Alzheimer’s.

And even though there is no medical cure for herpes, there is a natural way to prevent outbreaks and protect your brain from the downward spiral of dementia…

As far back as the 1960’s, researchers have recognized that an amino acid called arginine helps the HSV-1 virus to replicate. And that’s the last thing you want to have happen.

If you’re eating foods high in this amino acid you could inadvertently promote the growth of the herpes virus and trigger outbreaks. (Foods high in arginine include chocolate, carob, coconut, oats, wheat flour and wheat germ, peanuts and soybeans.)

Another amino acid, lysine, competes with arginine. And this is where the heart of the matter lies…

As we age, too much arginine and not enough lysine may activate dormant HSV-1. This, in turn, may lead to Alzheimer’s if you have the genetic predisposition. (You would be predisposed via the APO E 4 gene. Plus, another risk factor is being chronically inflamed from poor food choices and lack of exercise.)

So the general idea is to increase your lysine intake. I always like to get my nutrients from food sources. Fish, chicken, beef, lamb, milk, cheese, beans, brewer’s yeast, fruits and vegetables are all rich in lysine.

But sometimes food isn’t enough. To keep your arginine-lysine ratio in balance, I also recommend supplementing with 1500 mg. of lysine daily.

And before signing off I want to add one more bit of advice.

Just because you’ve never had a cold sore doesn’t mean you don’t have HSV-1. It could be lying dormant in your body. And while you may never experience an outbreak in your entire life, the virus could still affect the production of amyloid plaque and tau in your later years if your arginine-lysine intake is off-balance.

If you have any concerns at all, don’t hesitate to ask your doc to run a blood test. It’s the only way you can know for sure if herpes simplex type 1 is hiding in your body… and preparing to ravage your brain. Both the major lab companies; Quest Diagnostics and Labcorp do the HSV-1 test.

Resources:

Soscia SJ, Kirby JE, Washicosky KJ, Tucker SM, Ingelsson M, Hyman B, Burton MA, Goldstein LE, Duong S, Tanzi RE, Moir RD. The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide. PLoS One. 2010 Mar 3;5(3):e9505.

Wozniak MA, Mee AP, Itzhaki RF. Herpes simplex virus type 1 DNA is located within Alzheimer’s disease amyloid plaques. J Pathol. 2009 Jan;217(1):131-8.

Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, Berman SM, Markowitz LE. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA. 2006 Aug 23;296(8):964-73.

Rubey RN. Could lysine supplementation prevent Alzheimer’s dementia? A novel hypothesis. Neuropsychiatr Dis Treat. 2010 Oct 27;6:707-10.