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BHT’s Use as an Antiviral

PillManA little over 25 years ago a paper was published in the journal Science showing that BHT, a common food preservative, could inactivate herpes simplex and other lipid-coated viruses in lab dishes. Two years later another paper in the same journal reported similar results, but this time in live animals – dietary BHT could prevent chickens from dying of Newcastle disease. Like herpes simplex, NDV (the virus that causes Newcastle disease) is lipid-enveloped – its nucleic acid core is sheathed in a fatty membrane. Viruses of this type require an intact membrane to be infective. BHT seems to work against such viruses by disrupting their viral membranes.

In the chicken study cited above, the amount of BHT needed to inhibit NDV turned out to be equal to the amount already present in chicken feed as an additive, i.e., 100 to 200 parts per million of total diet. Assuming a comparable result for humans and a total food intake of about 2 kilograms per day, this would mean that 200 to 400 milligrams of BHT ingested daily should be adequate to protect most people from infection by herpes and other lipid-coated viruses.

Inspired by early scientific reports on the antiviral activity of BHT, a number of people suffering from herpes began to experiment on themselves in the late 1970s. As described in several books published a few years later, the BHT experimenters discovered that a daily dose of 250 to 1000 mg resulted in rapid recovery from herpes eruptions with no recurrences.

Studies performed since then have confirmed the activity of BHT against many different human and animal viruses, including such members of the herpes family as CMV (cytomegalovirus), pseudorabies and genital herpes. BHT appears to inhibit infectivity of HIV, the AIDS virus, although contradictory results have also been reported. A protective effect of BHT against the development of influenza infection has been shown. The mechanism involved may have to do with the fact that BHT is a highly potent, membrane-active antioxidant as well as a membrane fluidizer. It’s known that reactive oxygen species (ROS) play a role in the pathogenesis of viral infections – including RNA viruses such as influenza, DNA viruses such as hepatitis B, and retroviruses such as HIV – and it’s been suggested that antioxidants may be useful as therapeutic agents in such infections.

If BHT is so effective against lipid-enveloped viruses, why don’t doctors prescribe it for their patients? The answer is that almost none of the controlled studies on the antiviral properties of BHT have been performed on humans; most of the experiments thus far have been conducted in lab dishes (in vitro) or in animals. A human clinical trial of BHT cannot be performed because the Food and Drug Administration (FDA) has approved BHT for use only as a food preservative, not as a medicine. But that hasn’t stopped some people from using BHT on their own to treat herpes or other viral conditions.

In the past, safety concerns have been sometimes raised about BHT because of its reputed toxicity when given to rats in massive doses – doses much larger than those usually consumed for their antiviral effect. On the other hand, 25 years is long enough for any adverse effects as well as positive benefits to have shown up in humans. Many individuals – including my friend Roger, whom I’ve known since high school – have been supplementing with BHT on a regular basis for years at a time. Roger looks pretty healthy to me these days, but I phoned him anyway to press him for details on his BHT experience.

Roger first began taking BHT in 1984 after reading about it in Pearson and Shaw’s groundbreaking book 3. Initially he took about 1 gram per day because he was buying BHT in bulk at the time and larger amounts were easier to measure out than smaller ones. Later he was able to obtain BHT in capsules containing 250 mg per cap, and from that point on he took 250 mg every day for 6 to 7 years. Not surprisingly, during this period he remained completely free of herpes eruptions. More surprising is that he still remains herpes-free to this day, 10 years after his last dose of BHT. Around 3 years ago Roger had a comprehensive physical exam, including blood work. His physician told him that no antibodies to the herpes simplex virus could be found in his system.

Today Roger’s health is generally excellent, with no indication that his years of supplementing with BHT have harmed him in any way. The only adverse effect he ever encountered happened early on, while he was still experimenting with the size of the dose. Roger found that taking 3 grams of BHT each day resulted in dizziness and disorientation, which quickly disappeared when he cut his dose back to 1 gram per day. No adverse effects were seen thereafter.

Of course, a sample of one doesn’t constitute much of a survey. I needed to consult a larger database, so I turned to Steven Fowkes, resident guru at the Cognitive Enhancement Research Institute (CERI) in Menlo Park, California and co-author of Wipe Out Herpes with BHT. Steve Fowkes was unequivocal in his judgment. In the decades since BHT first arrived on the supplement scene, Steve hasn’t heard of any adverse reactions other than two minor ones. First, BHT can cause hives in some people who are sensitive to it. Second, BHT can cause a temporary decrease in blood clotting when people first begin taking it in substantial doses.

Allergic sensitivities to food additives such as dyes and preservatives have been known for some time but the role of these additives in precipitating chronic urticaria (hives) or other symptoms is still a matter of debate. Only a few cases over the years have identified low-level BHT intake as the sole cause of hives, so this reaction is not likely to be very common; however, it may well become more common if provoked by large doses of BHT. Fortunately, the condition tends to clear up after BHT use is halted.

As for the transient blood-thinning effect, Steve cautioned that people who have never taken BHT before should acclimatize themselves by starting out with small doses (less than 250 mg for the first day, if possible) and ramping up gradually over the course of a week; there is a special need for caution among those who are taking anticoagulants at the same time. In no case should the final dose exceed 1 gram per day without medical supervision. BHT’s anticlotting effect will diminish within 2 days in any event, unless extremely high doses (around 5 grams per day or higher) are being taken.

But what about liver toxicity? BHT gets metabolized in the liver, so won’t taking large amounts compromise liver function? Steve’s response was that he has spoken with literally hundreds of people who have successfully treated themselves for herpes with BHT. So long as a dose level of 1 gram per day was not exceeded, no cases of hepatic injury (as determined by pathologically high serum levels of the liver enzymes ALT and AST) have yet been reported by this group.

Unfortunately, some people taking BHT will find that not even 1 gram per day is sufficient to eradicate herpes. Rather than increasing the dose to more than a gram per day, Steve suggests maintaining the BHT level while combining it with other supplements. For example, the combination of BHT with hypericin (from St. John’s Wort) is a synergistic antiviral combination, more effective than BHT alone. To determine an appropriate dose level, hypericin intake should be ramped up gradually from 1 mg per day until an effective dose is reached, usually 10 mg per day or less. Steve also recommended pulsing the hypericin at the effective dose level, i.e., using it for about a week at a time with time off between dosing episodes. Because hypericin can cause photosensitivity of the skin, sun exposure should be limited to half the usual daily amount during and after hypericin intake. One of the nice features of BHT is that it tends to inhibit any oxidative stress induced by hypericin; for this reason, Steve feels that anyone taking hypericin should always take BHT with it.

After talking with Steve Fowkes and reviewing the scientific literature, I’ve concluded that the benefits of taking BHT seem to greatly outweigh the risks. In the process of researching this article I was reminded of a fundamental principle of toxicology first enunciated around 500 years ago by Paracelsus, the great Renaissance physician and alchemist: “All substances are poisons; there is none which is not a poison. The correct dose differentiates a poison from a remedy.” Or in the present case, “the correct dose differentiates a remedy from a food additive.”

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Herpes – Inhibition by BHT and Hypericin

by Alvin Hashimoto

BHT and hypericin, two substances available from nutritional supplement distributors, have each shown antiviral activity against herpes viruses and other viruses having lipid envelopes. The antiviral properties of both of these compounds have been investigated scientifically, but the antiviral properties of the combination of the two has so far not been studied except by individuals experimenting on themselves.

Since their mechanisms of antiviral action are different, BHT and hypericin probably act synergistically in the body – that is, their combined effects should be much greater than the effects of either one alone. Each appears to disrupt the lipid envelopes that herpes viruses must have in order to be infective, but BHT does so by dissolving in the envelope and lowering its cohesiveness, whereas hypericin damages the functionality of certain components of the envelope that are required for viral assembly.

Hypericin‘s antiviral effects require that the compound be exposed to light while in the body. Visible light, especially in the orange-to-green wavelengths, appears to be the most effective. UV light also activates hypericin, but carries a higher risk of side effects. Exposure to too much sunlight while using hypericin can cause severe rashes, blistering, and skin damage.

It has been suggested that the antiviral action of hypericin (which involves the generation of free radicals) might be reduced by BHT (which is a quencher of free radicals). Would such a reduction in antiviral activity be large or small compared with the synergistic action of the two compounds? It would probably be quite small, because the compounds would be present in the body in low concentrations. This means that their interactions with each other would be rare events as compared with their interactions with cellular and viral components.

What would a regimen of BHT and hypericin for herpes infections consist of? A reasonable way to start would be to use the two compounds in the same way they are used individually. BHT would be started at 250 mg/day (or less, if possible), and ramped up over a period of a week to no more than 1000 mg/day. Meanwhile, hypericin would be started at 1 mg/day, and ramped up to no more than 10 mg/day. Doses in excess of these amounts should be supervised by a physician. In addition, the parts of the body affected by herpes should be exposed to a bright fluorescent light to activate the hypercin.

Some people have had severe reactions to light when using hypericin. To prevent this, the initial exposure should be only for a few minutes, and then increased gradually over a period of a week or two. In addition, exposure to sunlight should be kept to an absolute minimum.

The reader should bear in mind that these suggestions and precautions are based only on common-sense, and that no actual data is available to support them. As appealing as this combination regimen seems, it does carry unknown risks.

U.S. herpes rates remain high – CDC

1 in 6 Americans infected with herpes

Highest rates found among blacks, women

WASHINGTON, March 9 (Reuters) – About 16 percent of Americans between the ages of 14 and 49 are infected with genital herpes, making it one of the most common sexually transmitted diseases, U.S. health officials said on Tuesday.

Black women had the highest rate of infection at 48 percent and women were nearly twice likely as men to be infected, according to an analysis by the U.S. Centers for Disease Control and Prevention.

About 21 percent of women were infected with genital herpes, compared to only 11.5 percent of men, while 39 percent of blacks were infected compared to about 12 percent for whites, the CDC said.

There is no cure for genital herpes, or herpes simplex virus type 2 (HSV-2), which can cause recurrent and painful genital sores and also increases the likelihood of acquiring and transmitting the AIDS virus. It is related to herpes simplex virus 1, or oral herpes, which causes cold sores.

Several drugs are available to treat herpes symptoms and outbreaks, including acyclovir, which is available generically or under the Zovirax brand name, and valacyclovir, known generically as Valtrex — both made by GlaxoSmithKline PLC (GSK.L). Ganciclovir, sold as Zirgan, is made by privately-held Sirion Therapeutics, Inc.

The CDC estimates that more than 80 percent of people with genital herpes do not know they are infected.

“The message is herpes is quite common. The symptoms can be often very innocuous,” Dr. John Douglas of the CDC said in a teleconference.

“Because herpes is so prevalent it becomes … a really important reason to use condoms on a consistent and correct basis with all of your partners,” Douglas said.

Douglas said the increased rate of infection in blacks is not do to increased risk behavior but likely due to biological factors that make women more susceptible as well as the higher rate of infection within black communities.

The CDC estimates that there are 19 million new sexually transmitted disease infections every year in the United States, costing the health care system about $16 billion annually.

Source: Reuters By JoAnne Allen

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'Broad Spectrum' Antiviral Fights Multitude of Viruses

Comment: A little over 25 years ago a paper was published in the journal Science showing that BHT (Butylated hydroxytoluene), a common food preservative, could inactivate herpes simplex and other lipid-coated viruses in lab dishes. Two years later another paper in the same journal reported similar results, but this time in live animals—dietary BHT could prevent chickens from dying of Newcastle disease. Like herpes simplex, NDV (the virus that causes Newcastle disease) is lipid-enveloped, i.e., its nucleic acid core is sheathed in a fatty membrane. Viruses of this type require an intact membrane to be infective. BHT seems to work against such viruses by disrupting (“fluidizing”) their viral membranes. BHT is so effective against lipid-enveloped viruses, why don’t doctors prescribe it for their patients? The answer is that almost none of the controlled studies on the antiviral properties of BHT have been performed on humans; most of the experiments thus far have been conducted in lab dishes (in vitro) or in animals. A human clinical trial of BHT cannot be performed because the Food and Drug Administration (FDA) has approved BHT for use only as a food preservative, not as a medicine. But that hasn’t stopped some people from using BHT on their own to treat herpes or other viral conditions.

Since it is not considered a natural product, the U.S. Food and Drug Administration has prohibited its sale as a supplement (although approving its use in food as a preservative).  BHT is therefore sold as a food preservative… To use this product in a government-approved manner, “add BHT to cooking oils or salad dressings to retain their freshness.”

ScienceDaily (Feb. 2, 2010)

The development of antibiotics gave physicians seemingly miraculous weapons against infectious disease. Effective cures for terrible afflictions like pneumonia, syphilis and tuberculosis were suddenly at hand. Moreover, many of the drugs that made them possible were versatile enough to knock out a wide range of deadly bacterial threats.

Unfortunately, antibiotics have a fundamental limitation: They’re useless against viruses, which cause most infectious diseases. Antiviral drugs have proven far more difficult to create, and almost all are specifically directed at a few particular pathogens — namely HIV, herpes viruses and influenza viruses. The two “broad-spectrum” antivirals in use, ribavirin and interferon-alpha, both cause debilitating side effects.

Now, researchers from the University of Texas Medical Branch at Galveston, UCLA, Harvard University, the U.S. Army Medical Research Institute of Infectious Diseases and Cornell University have teamed up to develop and test a broad-spectrum antiviral compound capable of stopping a wide range of highly dangerous viruses, including Ebola, HIV, hepatitis C virus, West Nile virus, Rift Valley fever virus and yellow fever virus, among others.

UCLA researchers led by Dr. Benhur Lee — corresponding author on a paper on the work appearing in the Proceedings of the National Academy of Science — identified the compound (which they call LJ001), after screening a “library” of about 30,000 molecules to find a one that blocked the host cell entry of deadly Nipah virus. Subsequent experiments revealed that LJ001 blocked other viruses that, like Nipah, were surrounded by fatty capsules known as lipid envelopes. It had no effect on nonenveloped viruses.

“Once we started testing more and more, we realized that it was only targeting enveloped viruses,” said Alexander Freiberg, director of UTMB’s Robert E. Shope, M.D. Laboratory, the Biosafety Level 4 lab where much of the cell-culture work was done, as well as mouse studies with Ebola and Rift Valley fever viruses. “We followed up and determined that it was somehow changing the lipid envelope to prevent the fusion of the virus particle with the host cell.”

Additional experiments indicated that while LJ001 also interacted with cell membranes, whose composition is nearly identical with that of virus envelopes, it caused them no ill effects. The reason, according to the researchers: Cells can rapidly repair their membranes, but viruses can’t fix their envelopes.

“At antiviral concentrations, any damage it does to the cell’s membrane can be repaired, while damage done to static viral envelopes, which have no inherent regenerative capacity, is permanent and irreversible,” said Lee.

UTMB authors of the PNAS paper include graduate student Sara Woodson and adjunct associate professor Michael Holbrook, former director of the Shope BSL4 lab and principal investigator on the UTMB portion of the project. UCLA contributors are Mike Wolf, Tinghu Zhang, Zeynep Akyol-Ataman, Andrew Grock, Patrick Hong, Natalya Watson, Angela Fang, Hector Aguilar, Robert Damaoiseaux, John Miller, Steven Chantasirivisal, Vanessa Fontanes, Oscar Negrete, Paul Krogstad, Asim Dasgupta, Kym Faull and Michael Jung. Other authors are Jianrong Li and Sean Whelan of Harvard; Matteo Porotto and Anne Moscona of Cornell; and Anna Honko and Lisa Hensley of USAMRIID.