For decades, mainstream medicine has been chasing down all kinds of cockamamie theories about what causes Alzheimer’s disease (AD) and dementia. Most recently, they’ve set their sights on amyloid plaques and tau tangles.
Of course, that explanation never made any sense to me. (I’ll explain more about why in a moment.)
But now, scientists on the front lines of research are developing an intriguing theory about what really causes these debilitating brain diseases.
So, let’s take a look…
Researchers slowly unravel the bacteria-AD connection
In the mid-19th century, Western medicine began to understand that bacteria (or “germs”) can cause disease. And within a generation, that new understanding completely transformed the practice of medicine…
For one, doctors began using antiseptics to prevent infections during and after medical and surgical procedures, which saved countless lives.
Then in 1907, German researchers began to think that dementia might be linked to infection and inflammation. But by the mid-20th century, the mainstream dropped this line of research.
Instead, they began to blame AD and dementia (as well as cancer, diabetes, and heart disease) on diet, lack of exercise, and lifestyle habits. This approach cleared them of any responsibility, and placed it on the individual to manage their own risk factors.
Thankfully, a few decades later, American physician and medical researcher Carleton Gajdusek picked up the trail. In fact, in 1976, he shared the Nobel Prize for discovering that a “slow virus” causes a rare form of contagious dementia among the Fore Highlanders of Papua New Guinea.
By the early 1980s, researchers began looking at infectious causes of Jakob-Creutzfeldt Disease—another form of dementia. I even remember sending autopsy specimens from the Hospital of the University of Pennsylvania, where I was working at the time, to Gajdusek’s lab at the National Institutes of Health (NIH) for analysis.
(As a side note, in 1989, Michael Bishop and Harold Varmus won the Nobel for discovering that some viruses cause cancer. And in 2005, another Nobel prize was awarded for the discovery that the Helicobacter pylori bacteria—not a spicy diet—causes chronic gastritis and peptic ulcers.)
Finally, in 1997, researchers in the U.K. learned that 60 percent of people with AD also test positive for the herpes simplex virus.
Of course, the herpes virus is present in the brains of most people over 70. But those who develop AD typically also carry a gene that makes them more susceptible to the virus.
Plus, it’s possible that the body forms amyloid in response to infection by a virus or bacterium. In fact, recent studies show that amyloid beta reduces growth of the E. Coli bacteria by 200-fold in vitro. It’s also active against the yeast Candida albicans.
Amyloid may even have protective, antimicrobial effects, as it seems to destroy the cell membranes of pathogenic microbes. And by forming into “plaques,” these proteins actually trap the microbes. (No wonder older adults have more amyloid plaques. They’ve spent a lifetime trapping microbes!)
So, when it comes down to it, AD may be the body’s natural response to infection, particularly in those who carry certain genes.
Rethinking the failed amyloid and tau theory
So, here we are halfway through 2019. And this rather “old” idea about AD and dementia is finally starting to catch on…once again.
Of course, accepting these findings will require scientists to rethink—or even abandon—the failed theory of amyloid plaques and tau tangles.
But that shift is already starting to happen…
In fact, in a recent interview in Medscape, Jorgen Rungby, M.D., Ph.D., of the University of Copenhagen, said, “I believe the amyloid theory is more or less on the way out, that amyloid is a byproduct.”
That’s exactly what I’ve been saying for years! In fact, pathologists and medical examiners like myself have long-known that amyloid isn’t the cause of AD, as forensic studies show it appears throughout the body as a “byproduct.”
In the end, it’s just more evidence that blaming AD on amyloid and tau is incorrect. And it explains why the treatments to prevent the formation of amyloid and tau proteins don’t work.
In fact, trying to treat AD and dementia by going after amyloid and tau in the brain is like trying to put out the fire by killing the firemen who’ve been called to the scene.
As a physician, I find it incredibly frustrating that we have an abundance of new science on what really contributes to AD. But the mainstream would rather continue to waste billions of dollars chasing down failed theories.
That’s why three years ago, I released a simple, step-by-step guide to target—and reverse—every stage of cognitive decline. It’s called my Complete Alzheimer’s Cure. People who are following my protocol are already making tremendous strides against this devastating condition.
P.S. Tune back in tomorrow to learn about how similar infectious mechanisms can contribute to Type II diabetes and heart disease.
“Rethinking the most common causes of death.” Medscape, 2/27/2019. (medscape.com/viewarticle/909445#vp_2)