OK, a slightly vainglorious title. But my subscribers know by now, if you want to learn something new, I’m always on top of it before the herd. Every once in a while I yell, “I told ‘em!”
For a number of years now I’ve been writing that Alzheimer’s Disease (AD) is most likely an infection. As with any function of the immune system, poor nutrition will have an impact, so some evidence will suggest that certain supplements are beneficial, even if AD turns out to be the result of an infectious pathogen.
But the infectious origin of AD is gaining a lot of traction lately. You probably read a week or two back that gum infections have been found to be statistically significant. The finger has been pointed at a toxic oral microbe called Porphyromonas gingivalis. I doubt it will be the only contender.
In 2017, Dr. Leslie Norins launched Alzheimer’s Germ Quest Inc., a public benefit corporation he hopes will drive interest to the germ theory of Alzheimer’s, and through which a prize of $1million will be distributed. A white paper he penned for the site reads: “From a two-year review of the scientific literature, I believe it’s now clear that just one germ—identity not yet specified, and possibly not yet discovered—causes most AD. I’m calling it the ‘Alzheimer’s Germ.'”
Now he’s gone further and Norins says he is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer disease, the most common form of dementia worldwide, caused by a germ?
By “germ,” he means microbes like bacteria, viruses, fungi, and parasites. In other words, Norins, a physician-turned-publisher, wants to know whether Alzheimer’s is caused by an infectious agent.
It’s not a new idea. Far from it. Even early 20th century Czech physician Oskar Fischer—who, along with his German contemporary Dr Alois Alzheimer, was integral in first describing the condition—noted a possible connection between the newly identified dementia and tuberculosis.
The evidence that AD is microbe-related has always been there. A 2010 study published in the Journal of Neurosurgery showed that neurosurgeons die from Alzheimer’s at a rate nearly 2.5 times higher than that of the general population.1
How can that be?
Another study from 2010, published in the Journal of the American Geriatric Society, found that people whose spouses have dementia are at a 1.6 times greater risk for the condition themselves.2
It certainly suggests they are “catching” AD.
Yet another study published in Neuron in July suggests that viral infection can influence the progression of Alzheimer’s. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with those affected by dementia.3
But something kept getting in the way: herpes.
Dudley’s team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).
Now this is where American scientists try to pretend everything is their idea. The article I was reading in Medscape made no mention whatever of other researchers. Yet in 2016 I published a newsletter on the British work on this topic, notably the research of Ruth Itzhaki, professor emeritus of molecular neurobiology at Britain’s University of Manchester (where I qualified in medicine!)
Ruth’s research goes back to 1991 (long before Norrins started to get a bee in his bonnet). In fact Dr Itzhaki has probably already earned his million dollars!
In 1997, she came out strongly in favor of the hypothesis that microbes may play a much bigger role in AD than suspected. She and her team named herpes simplex virus Type 1 (HSV-1), Chlamydia pneumoniae and spirochetes. The spirochetes are the spiraling ones that include those bacteria responsible for syphilis (Treponema pallidum) and Lyme disease (Borrelia bugdorferi).
Herpes The Lead Contender
But for Alzheimer’s, HSV-1 could be especially significant. Itzhaki has found that elderly people who carried both HSV-1 in the brain and the e-4 subtype of the APOE gene (responsible for creating a protein that helps transport cholesterol throughout the body) were 12 times more likely to develop Alzheimer’s than people without either. In a 1997 paper in The Lancet, Itzhaki’s group concluded that HSV-1 infection, in conjunction with APOE-e4, could account for about 60 percent of the Alzheimer’s cases they studied. Due to limited funds, however, her group was able to study only a relatively low number of cases.4
Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as shingles, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.
But having the herpes viruses alone doesn’t spell inevitable brain decline. After all, up to 75% of us may harbor HHV-6.5
The current obsession of doctors and Big Pharma for AD is the characteristic accumulation of a protein called amyloid in the brain. It’s supposed to be the “cause” of Alzheimer’s but that such “yesterday’s science”, no intelligent scientists would accept it as causative, or even crucial. People can have amyloid and no AD and people can have AD and no amyloid plaques! Go figure.
Maybe the amyloid is just a reaction to the infection that is the real cause of AD? Harvard neuroscientist Rudolph Tanzi suggests that it might be so.6 Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube and also in mice. He now believes that the protein is part of our ancient immune system that, like antibodies, ramps up its activity to help fend off unwanted bugs.
On this model, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease process, amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, tau, to form tangles, which further harm brain cells.
But as Tanzi explains, the ultimate neurologic insult in Alzheimer’s is the body’s reaction to this neurotoxic mess. All of the excess protein revs up the immune system, causing inflammation and it’s this that does the most damage to the brain in AD.
So, as I have been telling you for years, you need your immune-enhancers and anti-inflammatories to fight AD: omega-3s, beta-glucans, curcumin, eupatorium and vitamin D.
And don’t forget homeopathy. As I said in a 2016 piece, one of the most devastating outbreaks of disease in history was the 1918 “Spanish Flu” Pandemic. Over a billion people were affected. Nobody knows the exact death toll but estimates put it around 40 – 50 million (perhaps as high as 100 million).
While the mortality rate of people treated with traditional medicine and drugs was 28%, those treated by homeopathic physicians had mortality rate of 1%.
Make no mistake: homeopathy works, despite the derisive bleatings of the ignorant mob. But it is not a simple skill. You need a GOOD homeopath.
Meanwhile, Big Pharma is on a stampede to find any scientific justification for drug treatments of AD. The money they will make for them is a wet dream.
At the very least, antimicrobials are just around the corner.
Look after your little grey cells!
Original source article: https://www.medscape.com/viewarticle/904650_1
- Lollis SS, Valdes PA, Li Z, et al. Cause-specific mortality among neurosurgeons. J Neurosurg. 2010;113:474-478
- Norton MC, Smith KR, Østbye T. Greater risk of dementia when spouse has dementia? The Cache County study. J Am Geriatr Soc. 2010;58:895-900
- Readhead B, Haure-Mirande JV, Funk CC. Multiscale analysis of independent Alzheimer’s cohorts finds disruption of molecular, genetic, and clinical networks by human herpesvirus. Neuron. 2018;99:64-82.e7
- The Lancet, Volume 349, No. 9047, p241–244, 25 January 1997
- Chan PK, Ng HK, Hui M, Cheng AF. Prevalence and distribution of human herpesvirus 6 variants A and B in adult human brain. J Med Virol. 2001;64:42-46
- Elmer WA, Kumar DK, Shanmugam NK, et al. Alzheimer’s disease-associated ?-amyloid is rapidly seeded by herpesviridae to protect against brain infection. Neuron. 2018;99:56-63.e3