Science says probably yes.
We are beginning to understand that many chronic health problems are, in truth, caused by hidden infections. This renders some of the old “explanations” obsolete and defective.
For example, it is now known that a great deal of arthritic trouble comes from bacterial infections in the troubled joints. It is NOT a wear-and-tear effect, as the scientific pseuds like to claim. They keep saying this often enough to have begun to believe their own baloney, without any evidence whatever.
Look, people reach the age of 100 years or more without any measurable trace of arthritis or joint discomfort. Yet some people in there 30s and 40s are badly handicapped by it. Are they trying to tell us that these younger cases have incredibly soft, fast-wearing joints? It doesn’t make sense; but an infective cause for arthritis would fit this observation.
What’s new is that hidden infections with viruses, parasites, bacteria and other pathogens can lie hidden in the body for decades, all the while slowly damaging our brains, and can be the cause of dementia, depression and schizophrenia.
We call this effect stealth pathogens. They can be very hard to detect. Cytomegalovirus for example infects more than 50% of adults in the US. Stealth pathogens are hard to get rid of. Be afraid; be very afraid, as the movie trailers say… moo-ha-ha-ha-ha!
It’s not a crazy idea, with Toxoplasmosis (a single-celled parasite) now known to infect and inflame the human brain, producing strange, even psychotic behaviors; prion diseases like Creutzfeldt-Jakob causing terminal cognitive decline; Chlamydia causing widespread systemic inflammation; and Herpes simplex causing Herpes simplex encephalitis (HSE) with psychiatric symptoms in 71% of cases, one can say with certainty that the understanding of chronic infectious psychiatry is only just beginning. This goes way beyond the stage of tertiary syphilis, the scourge of three generations ago.2
In January 2016, a team led by Shawn Gale, an associate professor in psychology at Brigham Young University, looked at the infection history of 5,662 young to middle-aged adults alongside the results of tests intended to measure cognition. The team tested for the burden of chronic infections, specifically immunoglobulin G antibodies for toxocariasis (cat or dog toxocara roundworm, sometimes known as visceral larva migrans (VLM)), toxoplasmosis, hepatitis A, hepatitis B, hepatitis C, cytomegalovirus, and herpes 1 and 2.
The team created an index of infectious burden and the higher that score, the worse the person performed on cognitive function testing (worse learning and memory skills, as well as slower information-processing speed than those with a lower score, even after controlling for other factors, like age, sex and financial status).
The important point about this study is that it was the first to quantify multiple infections and connect them to markers of early dementia. The result was not striking but it was definite.1
Other researchers, like Ruth Itzhaki, professor emeritus of molecular neurobiology at Britain’s University of Manchester (where I qualified in medicine!), believes microbes may play a much bigger role than suspected in one of the most devastating neurodegenerative disorders around: Alzheimer’s disease, which affected 47 million people worldwide in 2015.
Last March, Itzhaki and a world-wide group of researchers wrote an editorial in the Journal of Alzheimer’s Disease, asking the scientific community to consider a proposed link between Alzheimer’s and certain microbes, notably 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).
Treponem pallidum, the cause of syphilis, caused a terrible insanity known as general paresis of the insane (GPI) in the late stages. Neurosyphilis has virtually vanished today but syphilis has not.
Science is Held Back By Ignorance
Despite the known history of diseases like GPI, unfortunately, as Itzhaki complains, “There’s great hostility to the microbial concept of cognitive decline amongst certain influential people in the field, and they are the ones who usually determine whether or not one’s research grant application is successful.” True to form, the powers that be reject her reasoning but without ever providing scientific objections – they just reject unfamiliar ideas out of hand. Itzhaki is, of course, bitterly frustrated at what seems to her a perfectly sound hypothesis that demands credible investigation being blocked by the old stagers, who are just plain ignorant.
Plus we all know the corrupting influence of Big Pharma dollars. They do not want dementia to become an infectious disease. They make too much money “treating” Alzheimer’s, instead of trying to cure or fix it.
So although Itzhaki and her lab published their first paper in 1991 finding a clear HSV-1 link to Alzheimer’s. Since then, according to Itzhaki, over 100 published studies, from her lab and elsewhere, have been supportive of the same link.
Nevertheless, Itzhaki says, the work has received only a cursory nod from the greater research world and little funding. Out of the $589 million allocated to Alzheimer’s research by the National Institutes of Health in 2015, exactly zero appeared to be spent on studying the proposed HSV-1 connection.
So they can go on saying “there’s no scientific proof” because there isn’t any; they are making sure of that.
Nearly all of us carry the Herpes simplex virus 1 or HSV-1 (the one that causes cold sores), our peripheral nervous system serves as its dormant nesting ground. From there, HSV-1 can reactivate and occasionally cause mild flare-ups of disease, typically when our immune system is overwhelmed due to stress or other infections.
Itzhaki’s lab, however, found that by the time we reach our golden years, the virus often migrates to the brain, where it remains capable of resurrecting itself and wreaking a new sort of havoc when opportunity presents, such as when our immune system wavers in old age.
Another group found both HSV-1 and HSV-2 may produce a more subacute (long-term) encephalitis, leading to apparent psychiatric syndromes, and benign recurrent meningitis.3
Infection and Alzheimer’s
Izzhaki’s team has discovered the presence of HSV-1 in the telltale plaques—clumps of proteins in the nerve cells of the brain—used to diagnose Alzheimer’s.
So I think she’s onto something here…
Plaques and neurofibrillary tangles, while sometimes found in normal aging brains, have been found to overflow in the brains of deceased Alzheimer’s sufferers; neuroscientists believe these protein accumulations can cause neuron death and tissue loss. Itzhaki speculates that herpes-infected cells may produce the proteins in an attempt to fend off HSV-1.
In other words, the plaques are a defense mechanisms and NOT the cause of Alzheimer’s. Alternatively, the virus itself may be commanding neurones to produce the inflammatory proteins somehow needed to jump-start the virus’s replication.
Itzhaki, Gale and their colleagues emphasize that rather than being the sole cause of memory loss, slower reaction time or depression, viral and bacterial infections are likely just one ingredient in a soup of risk factors. 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
“If more funding had been available, more information would probably have been obtained, providing even more supportive data,” she says.
As things stand, though, she believes there is enough evidence to go ahead with treatment trials; for instance, giving Alzheimer’s patients HSV-1-targeted antivirals in hopes of slowing down or stopping the progression of the disease. She and a team of clinicians are trying to obtain a grant for just such a pilot clinical trial to do just that.
It’s an exciting future, even if we have to just wait for the old stagers to die or get out of the way.
Meantime, what can you do for yourself or a loved one that would help combat stealth pathogens of all kinds? As usual, there is a lot I can recommend that will stimulate better immune function and help through off these deeply buried raiders.
1. Shawn D Gale, Lance David Erickson, Andrew Berrett, Bruce L Brown, Dawson W Hedges (2016). Infectious disease burden and cognitive function in young to middle-aged adults. Brain Behavior and Immunity. 2016 Feb;52:161-8
2. Whitley RJ, Soong SJ, Linneman C Jr, Liu C, Pazin G, Alford CA. Herpes simplex encephalitis. Clinical Assessment. JAMA. 1982 Jan 15. 247(3):317-20
3. Whitley RJ, Soong SJ, Linneman C Jr, Liu C, Pazin G, Alford CA. Herpes simplex encephalitis. Clinical Assessment. JAMA. 1982 Jan 15. 247(3):317-20
4. The Lancet, Volume 349, No. 9047, p241–244, 25 January 1997