Butylated hydroxytoluene may be beneficial …

Does Kissing Cause
Alzheimer’s Disease?

By the time Americans of all economic backgrounds reach
age 60, about 60–85 percent have become infected with HSV-1.
By Will Block

M ost individuals infected with Herpes simplex type 1 (HSV-1) in childhood usually suffer a mild feverish illness of no consequence. Some suffer recurrent infections which appear as cold sores on their lips, while others intermittently shed the virus in their oral airway secretions.

Adults uninfected in childhood may be exposed to HSV-1 later in life through kissing. Or though some other skin to skin contact (sexual or nonsexual). However, kissing is probably the principal agent of contagion in childhood; frequently from relatives, no less, who delight in smooching newcomers as a measure of their familial affability.

Adults uninfected in childhood may
be exposed to HSV-1 later in life
through kissing.

In contrast with childhood HSV-1, adults may develop acute primary herpes with fever and inflammation of the oral mucosa and gingiva, occasionally requiring hospital admission. By the time Americans of all economic backgrounds reach age 60, about 60–85 percent have become infected with HSV-1. Thus, this virus is clearly a pandemic (from the Greek words “pan,” meaning “all,” and “demos,” meaning “people”), possibly the largest in world history.

Available Treatments for Recurrent Cold Sores

After diagnosis of HSV-1, the majority of patients seen in otolaryngological (ear, nose and throat) practice are thought to need only supportive therapy, along with explanation and reassurance. Recurrent cold sores are believed to be no more than a nuisance in most patients, although occasionally they are severe and in some the cold sore may precipitate oral erythema multiforme (a skin disorder due to an allergic reaction or infection). Unfortunately, the conventional treatments available for recurrent cold sores are rather unsatisfactory. And, as we shall learn, treatments are urgently needed.

Oral Herpes: From Dormancy to Activity

Generally referred to as oral herpes, HSV-1 replicates in epithelial cells and secondarily enters local sensory neuronal processes, traveling retrograde (backward) to the neuronal nucleus where it hides from the immune system in the cell bodies of nerves and enters latency (dormancy). Upon reactivation (typically caused by stress of one kind or another), newly synthesized viral particles travel anterograde (forward) to the epithelial cells of the lip, causing the recurrent cold sore.

Unfortunately, the conventional
treatments available for recurrent
cold sores are rather unsatisfactory.

(click on thumbnail for full sized image)
The dance of HSV-1 viral particles with amyloid precursor protein (APP) eventuates breakout through the cell membrane and cleaves APP to produce Aβ in abundance.
In a new study,1 as ominous as an Edgar Allan Poe tale in its choice of title, “Herpes Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell,” coauthor Dr. Elaine Bearer—a pathology professor at the University of New Mexico School of Medicine—states that, “Herpes infects mucous membranes, such as a mouth or eye, and generates viral particles. … [which] burst out of the cells of the mucous membrane and enter sensory nerve cells where they travel inside the nerve toward the brain.”2

HSV-1 May Promote Alzheimer’s Disease

“Clinicians have seen a link between HSV-1 infection and Alzheimer’s disease in patients, so we wanted to investigate what might be going on in the body that would account for this,” adds lead author Dr. Shi-Bin Cheng, a post-doctoral associate, Department of Pathology and Laboratory Medicine, Alpert Medical School, Brown University.2 “What we were able to see in the lab strongly suggests a causal link between HSV-1 and Alzheimer’s disease.”

In the new study, HSV-1 was found together with amyloid precursor protein (APP), a cellular transmembrane glycoprotein and receptor for anterograde transport machinery that when proteolyzed (altered through the digestion of its proteins by cellular enzymes called secretases*) produces amyloid beta (Aβ), the major component of senile plaques. The researchers focused on transport inside epithelial cells of newly synthesized virus during its transit to the cell surface. They had hypothesized that HSV-1 recruits cellular APP during transport, and explored this possibility with quantitative immuno-fluorescence, immuno-microscopy, and live-cell imaging. After infection with HSV-1, viral particles in the cytoplasm occur together along with APP and travel together with APP inside living cells.

* Secretases are enzymes that “snip” pieces off proteins embedded in the cell membrane. Secretases can also act on the amyloid precursor protein (APP) to cleave the protein into three fragments. Sequential cleavage by β-secretase (BACE) and γ-secretase produces the Aβ peptide fragment that aggregates into “plaques” in the brains of those with Alzheimer’s disease. If α-secretase acts on APP first instead of BACE, no amyloid-β is formed because α-secretase recognizes a target protein sequence closer to the cell surface than BACE.

HSV-1 is Significantly Involved in Cognitive Decline

“It’s no longer a matter of determining whether HSV-1 is involved in cognitive decline, but rather how significant this involvement is,” Dr. Bearer asserts, and moreover, “We’ll need to investigate anti-viral drugs used for acute herpes treatment to determine their ability to slow or prevent cognitive decline.”2

“What we were able to see in the lab
strongly suggests a causal link
between HSV-1 and Alzheimer’s

Through the interaction between HSV-1 and APP there are functional consequences: HSV-1 infection decreases the average velocity of APP particles and results in APP maldistribution in infected cells. These in turn increase the frequency and velocity of transport proteins that decorate the outer surface of the capsid (protein) shell of HSV-1.

The new research results indicate that most intracellular HSV-1 particles undergo frequent dynamic interplay with APP in a manner that facilitates viral transport and interferes with normal APP transport and distribution. The result is an accumulation of Aβ, a defining characteristic of Alzheimer’s disease. Such dynamic interactions between APP and HSV-1 suggest a mechanistic basis for the observed clinical relationship between the identification of HSV-1 in serum, along with the risk of Alzheimer’s disease.

Not the First to Demonstrate HSV-1/Alzheimer’s Relationship

As early as 1980, a letter to the editors of The Lancet suggested a possible link between HSV-1 and Alzheimer’s.3 Then, in a 2007 paper, other researchers proposed that HSV-1 is a strong risk factor for Alzheimer’s, especially when it is present in the brains of people who possess the type 4 allele of the apolipoprotein E gene (APOE-epsilon4).4 These researchers found that when cultured neuronal and glial cells are infected with HSV-1, the result is a dramatic increase in the intracellular levels of Aβ, of the 1-40 and 1-42 varieties (the types most associated with disease states), while levels of APP in cells were found to decrease. The data showed that HSV-1 can directly contribute to the development of senile plaques.

In further work, the same researchers discovered a striking localization of HSV-1 DNA within plaques.5 In fact, in Alzheimer’s disease brains, 90% of the plaques contained the viral DNA and 72% of the DNA was associated with plaques compared to normal aged brains, which contain amyloid plaques at a lower frequency. In normal brains, 80% of plaques contain HSV-1 DNA, but only 24% of the viral DNA are plaque-associated. This suggests that in normal aged individuals, there is a lesser production and/or greater removal of Aβ, so that less of the viral DNA is seen to be associated with Aβ in the brain.

This data, together with the finding of Aβ accumulation in HSV-1-infected cells and mouse brain, suggest that this virus is a major cause of amyloid plaques and hence probably a significant etiological (causal) factor in Alzheimer’s disease. The researchers point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it.

The Drug Acyclovir Is Not Sufficient

Of the conventional drugs used to treat HSV-1, acyclovir (chemical name, acycloguanosine) is the most touted of the antivirals. It is primarily used for the treatment of herpes simplex virus infections, as well as in the treatment of varicella zoster (chickenpox) and herpes zoster (shingles).

Acyclovir was believed to be the start of a new era in antiviral therapy when first introduced, due to its extreme selectivity and low cytotoxicity. If fact, pharmacologist Gertrude B. Elion was awarded the 1988 Nobel Prize in Medicine, in part for the development of acyclovir. Dr. Richard Whitley, a University of Alabama at Birmingham researcher and pioneer in antiviral therapy, was the first to successfully use the drug in humans.

Nevertheless, acyclovir has poor oral bioavailability (15–30%), hence intravenous administration is necessary if high concentrations are required. Furthermore, HIV-1 progression can only be slightly delayed by using acyclovir, so that Aβ production is only slightly reduced. At the same time, adverse effects include: nausea, vomiting, diarrhea and/or headache. In high doses, hallucinations have been reported.

Another Approach

On the other hand is butylated hydroxytoluene (BHT), a synthetic antioxidant and a phenolic compound that acts as a preservative and is commonly added to foods such as cooking and salad oils, as well as other fats. Surprisingly, BHT may be naturally produced in the sea.* Regardless, it works to preserve fats by preventing the rancidity of fats that occurs because of reactions between fat molecules and oxygen molecules. Besides food, BHT is used as a preservative in cosmetics and pharmaceuticals. Moreover, there is some scientific speculation about the role of BHT in extending lifespan via its antioxidant effect, and some intriguing research in this regard has been done with animals. Biogerontologist Denham Harman, M.D., Ph.D., widely known as the father of the Free Radical Theory of Aging found that BHT could reduce amyloidosis in mice back in 1976!6

* See the article “BHT Found to Be Naturally Produced in Phytoplankton” in the November 2009 issue.

BHT works at least as well as, or
better, than any of the anti-viral
drugs, and it is much easier and more
comfortable to take.

The use of BHT as a treatment for herpes began in the 1970s in response to scientific reports that BHT had anti-viral activity. Some of these results were reported in the prestigious journal, Science.7 Other studies in live animals followed, showing that BHT seems to work by disrupting the lipid membrane of viruses. However, controlled clinical trials involving human patients with herpes are lacking for the simple reason that the FDA won’t allow them. The FDA approves BHT only for use as a food preservative. It has been reported that government grants or facilities cannot be used to study the antiviral effects of BHT, and strong sanctions are threatened against those who would sponsor such research privately. And because BHT could stand to benefit by paying for expensive research.

Wide Availability Has Encouraged Personal Trials

Yet, since BHT was (and is) available for purchase by anyone as a food preservative, people have bought BHT and used it as they wished, even to treat herpes. And since the 1970s, there have been thousands of anecdotal reports of people taking BHT in daily doses of 250 to 1000 mg and successfully suppressing the herpes virus and the resultant outbreaks.

The book that put BHT on the map was Wipe Out Herpes with BHT by John A. Mann and Steven Fowkes, which came out in 1983. Fowkes is the head of the Cognitive Enhancement Research Institute (CERI) in Menlo Park, California, and besides documenting numerous successful cases of treating herpes with BHT, Mr. Fowkes reports that side effects and problems have been few, minor, and very much dose-related.

Side Effects of BHT

What are the side effects of BHT? Over-dosing with BHT can cause hives in a few people—but only temporarily. It goes away when you stop the BHT or reduce the dosage. Taking too much BHT (multi-gram doses daily) has also caused dizziness and disorientation in some people, but again, with no permanent harm. However, based on his experience, both personal and clinical, Steve Fowkes recommends limiting BHT consumption to 1 gram daily and never exceeding it. That measure alone should prevent adverse effects in virtually everyone who takes BHT.

Others report that 1 gram daily is too much to start with. Some claim that it makes sense to start with a lower dose, such as 350 mg and keep it there for a while, perhaps 6 weeks. For one thing, that much may be enough to achieve viral suppression. If not, then the dose can be doubled to 700 mg daily, and even that dose can be safely taken indefinitely. Higher doses, such as 1000 mg daily should be the ceiling for most individuals.

It is well known that BHT slows down the body’s ability to metabolize alcohol, therefore those taking BHT should limit their alcohol consumption. Also, BHT has somewhat of a blood-thinning effect, so those taking blood thinners and those who have blood clotting problems should consult with their doctors before using BHT. The vast majority of people who take BHT daily to treat herpes experience no side effects at all.

How long do you have to take BHT to treat herpes? Suppressing herpes outbreaks is the most important objective, whether you are taking anti-viral drugs or BHT. And in both cases, the improvement is gradual, marked by a gradual reduction in the number and severity of outbreaks, usually over a course of months, until eventually the outbreaks stop completely. Taking BHT, it may take a few months to notice a significant reduction in outbreaks, and the full benefit may take a year. However, BHT works better than any of the anti-viral drugs, and it is much easier and more comfortable to take. It is also much less expensive and has other benefits, including an anticarcinogenic value.

In answer to the question, “Have people experienced a reversal in their herpes blood antibody test going from positive (bad) to negative (good) from taking BHT?” the answer is yes. Yet reports are anecdotal; there have been no formal studies, nor are there likely to be, because BHT is not patentable.

Is There Any Toxicity from Taking BHT?

Another book authored by Steven Wm. Fowkes (and continuously updated) is The BHT Book, A Practical Guide to Resolving Viral Disease (available online at http://www.ceri.com/BHTbook-StevenWmFowkes-100903.pdf). This free book is a masterwork on the subject, and puts to rest the question of toxicity. Fowkes also advocates supplementation with adequate amounts of vitamins, minerals, amino acids, and other nutrients to compliment BHT use. Donations are appreciated.

No Need to Avoid Kissing

The question remains: Should one give up kissing? Of course not! Kissing is duly celebrated as one of the great social customs of our culture, and it would be a sad day if we dismissed the pleasure of the kiss. However, in the meantime, acquire the above book and then do whatever you deem necessary to reduce the herpes activity that may help to preserve your memory.


  1. Cheng SB, Ferland P, Webster P, Bearer EL. Herpes Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell. PLoS One 2011 Mar 31;6(3):e17966.
  2. Brown University (2011, April 4). Herpes linked to Alzheimer’s disease: ‘Cold sores’ connected to cognitive decline. ScienceDaily. Retrieved May 19, 2011, from http://www.sciencedaily.com/releases/2011/04/110404122203.htm
  3. Middleton PJ, Petric M, Kozak M, Rewcastle NB, McLachlan DR.Herpes-simplex viral genome and senile and presenile dementias of Alzheimer and Pick. Lancet 1980 May 10;1(8176):1038.
  4. Wozniak MA, Itzhaki RF, Shipley SJ, Dobson CB. Herpes simplex virus infection causes cellular beta-amyloid accumulation and secretase upregulation. Neurosci Lett 2007 Dec 18;429(2-3):95-100.
  5. 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.
  6. Harman D, Eddy DE, Noffsinger J.Free radical theory of aging: inhibition of amyloidosis in mice by antioxidants; possible mechanism. J Am Geriatr Soc 1976 May;24(5):203-10.
  7. Snipes W, Person S, Keith A, Cupp J. Butylated hydroxytoluene inactivated lipid-containing viruses. Science 1975 Apr 4;188(4183):64-6.

Will Block is the publisher and editorial director of Life Enhancement magazine.

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