Now Even the US Attorney General Is Slandering Supplements!

Like the flawed Frontline documentary, like New York state’s attorney general, US Attorney General Loretta Lynch is spreading gross misinformation about dietary supplements. Action Alert!

Last week, Attorney General Lynch released a video for National Consumer Protection Week about supplements. Excuse us, but since when is the US attorney general an expert on this subject? Since she obviously isn’t, she must be relying on distortions and untruths she has been fed by other agencies of the government such as the FDA and Centers for Disease Control.

For instance, Ms. Lynch warns consumers against “ingesting substances whose safety and efficacy are not guaranteed” by FDA study. As we pointed out in our response to PBS, pharmaceutical drugs are also not studied by the FDA. The agency relies on industry studies to determine if new drugs can come to market. No independent review is done to check the industry’s results, which has led to all kinds of manipulation and sometimes disastrous outcomes (see the examples of Vioxx and Avandia). And after approval is granted, the actual medicine itself is never tested, even though it may be manufactured in Chinese plants or other faraway locales.

FDA approval is certainly no guarantor of safety. Consider that pharmaceutical drugs, when properly prescribed, cause an estimated 1.9 million hospitalizations and 128,000 deaths each year. And that’s just in hospitals—deaths outside hospitals would add considerably to this total if they were recorded. In stark contrast, dietary supplements caused zero deaths in 2013, the last year reported.

Ms. Lynch also charges that supplements “endanger public health” by containing harmful ingredients. The supplement industry—like all industries—has some bad actors. But supplements that contain unsafe ingredients are already “adulterated” which means that the FDA has a responsibility to remove them and prosecute the makers. Nor does Ms. Lynch mention that supplement companies must follow stringent guidelines known as current good manufacturing practices (cGMPs) intended to ensure the safety and quality of dietary supplements. In other words, supplements are federally regulated.

Finally, Ms. Lynch says that many supplements “falsely claim to cure illness and disease.” As a student of the law, Ms. Lynch must be aware that the FTC and FDA regulate what can be said on supplement labels. By law, supplements cannot make disease claims—only drugs can. Any supplement that does make such claims is therefore breaking the law. We don’t agree with this law, but if it isn’t being followed why doesn’t the government simply enforce the law. In past years, FDA memos have indicated that sometimes the agency does not enforce the law on purpose, in the hopes that an ensuing scandal will lead to even more federal control over supplements. The cost of this would in turn drive their cost sky high and largely eliminate them as competition for drugs.

No, Ms. Lynch, supplements are regulated, are safe, and are effective. Just the opposite of what you suggested. You are not a doctor or scientist. But as the top law enforcement official of the country, you can at least get your law right.

Action Alert! Write to Attorney General Loretta Lynch and urge her to correct the misinformation she spread to consumers about dietary supplements. Please send your message immediately.


If you aren't in perfect health, then your immune system may need help.

zarkovBeta-glucan is a family of complex carbohydrates that serve as structural elements in the cell walls of plants, yeasts, and mushrooms. LifeLink’s beta-glucan comes from baker’s yeast. This supplement is now of great interest to medical researchers because of its ability to stimulate immune function, to improve cholesterol profiles, and to inhibit (or even reverse) cancer progression. Its immune effects are broad and can be directed at many health problems, including:

  • cancer
  • high cholesterol
  • hypertension
  • allergies
  • diabetes
  • wounds
  • over-eating, obesity
  • viral infections, such as hepatitis, HIV
  • bacterial infections
  • parasitic infections

Immune system modulation. The body’s first lines of defense against infections involve physical barriers and the destruction of invading microorganisms by antibodies. Pathogens that manage to evade these defenses will (one hopes) trigger further defensive processes known as ‘cell-mediated immunity’. Beta-glucan operates at both of these stages of immunity..

Beta-glucan acts in very complex ways upon the immune system. It stimulates the production of various signaling molecules, and these, in turn, activate immune cells. In this way, beta-glucan activates a wide variety of immune defenses, protecting the body against infections by viral, bacterial, fungal and protozoal pathogens, and even defending it against cancer.

Cancer-fighting properties. Beta-glucan’s anti-cancer effects result from its ability to modulate the immune system. And its immune effects derive from its activation of macrophage cells. Macrophages are immune cells that trap and engulf foreign cells and particles, scavenge cellular debris, and destroy infectious agents such as viruses, parasites, bacteria, and fungi.

Studies in cell culture, in lab animals, and in humans have shown that the anti-tumor activity initiated by beta-glucan can be long-lived and can occur even when beta-glucan is given orally one month prior to the presence of a tumor. Some of the cancer types that have been shown to be sensitive to beta-glucan supplementation include:

  • breast cancer
  • lymphoma
  • colon cancer
  • sarcoma
  • liver cancer
  • lung cancer

Pollen allergies. Pollen allergies are caused by a poorly regulated immune system. Beta-glucan seems to improve immune regulation. Researchers at Meiji University have shown that beta-glucan “is able to alleviate cedar pollen-induced allergic symptoms.”

Lithium Orotate targets Alzheimer's and other diseases of the brain.

And patients can’t afford to wait for clinical trials.

In 1997 a groundbreaking paper appeared in the Journal of Biological Chemistry, reporting that lithium interferes with a key process in the brain that damages nerve cells in Alzheimer’s disease. The researchers stated that “these findings could be exploited to develop a novel intervention for Alzheimer’s disease”.

More recent studies in cell culture and lab animals have added weight to this prediction and found additional ways in which lithium protects nerve cells and stimulates the repair of damaged nerve tissue. In a 2004 review of the subject, D.M. Chuang of the (U.S.) National Institutes of Health wrote: “The neuroprotective and neurotrophic actions of lithium have profound clinical implications. In addition to its present use in bipolar patients, lithium could be used to treat acute brain injuries such as stroke and chronic progressive neurodegenerative diseases.” Examples of such diseases are Alzheimer’s, Huntington’s, ALS, Parkinson’s, and other, less well-known, conditions.

Lithium salts have been used to treat manic-depression (‘bipolar disorder’) for more than 50 years, and are still considered to be among the best treatments for this ailment. ‘Bipolar’ patients usually use high doses of lithium carbonate (typically above 900 mg/day) and must receive professional guidance and testing for side effects.

At lower doses lithium has been used in recent years as a dietary supplement usually without medical supervision. Lithium Orotate is effective at less than 150 mg/day, with few or no side effects.

Although the lally-gaggers who control the world’s clinical research programs have yet to conduct a clinical trial of lithium as a prevention or treatment for Alzheimer’s or of any other neurodegenerative disorder, we needn’t wait for them to get their act together. Lithium is available as a nutritional supplement (in the U.S. at any rate). It has a very good safety profile at moderate doses – in fact, some evidence suggests that lithium may be an essential trace mineral in the human body.

Several other applications for lithium supplements have come to light recently:

  • protecting the brain from damage by alcohol
  • treating kleptomania
  • preventing symptoms of Fragile X Syndrome
  • a genetic flaw that is known to cause certain forms of autism
  • learning disabilities
  • anxiety disorders
  • mental retardation

LifeLink’s lithium product is the orotate salt of lithium, not the carbonate. This formulation was inspired by the work of Dr. Hans Nieper, the creative German physician, who used lithium orotate to treat:

  • depression
  • headaches
  • migraine
  • epilepsy
  • alcoholism

Nieper considered orotates to be superior to other anions as bioavailability enhancers for minerals like lithium. Furthermore, orotates have other useful properties:

  • protecting the heart from arrhythmias
  • reducing heart-attack damage
  • lowering mental stress
  • eliminating nerve-damaging deposits of lipofuscin and ceroid pigments.

Is your brain malfunctioning? Here's something that could help.

zarkovCDP-choline (Citicoline) is a form of the B-vitamin choline. The body uses it to make cell membranes and the neurotransmitter acetylcholine. CDP-choline‘s contribution is especially important for nerve cells, since nerve cell membranes are responsible for conducting signals within the nervous system. The composition of these membranes can become degraded by a number of different medical conditions, including:

  • Alzheimer’s Disease
  • stroke
  • Parkinson’s Disease
  • glaucoma
  • age-related learning and memory disorders
  • amblyopia (‘lazy eye’)
  • traumatic brain injury
  • drug addiction

CDP-choline supplementation improves the composition of nerve cell membranes by contributing a family of components called phosphatidylcholines. This contribution can rescue neurons from self-destruction and improve nerve function – in other words, they ameliorate the ailment which threatened those nerve cells.

CDP-choline has been studied extensively and has been applied clinically since the 1960s to treat brain injuries. Many thousands of human volunteers and patients have participated in clinical studies of this compound. More recently, interest in this supplement has soared because research has shown it to be neuroprotective – and even reparative – in the high-profile medical conditions listed above. Let’s look at just a few of many examples.

Glaucoma. Glaucoma results from damage to nerve cells which transmit information from the retina to the brain. Treatment of glaucoma patients with oral CDP-choline (1600 mg/day for 60 days) resulted in “improvement of retinal function”, according to a 2008 study at the G.B. Bietti Eye Foundation in Rome.

Parkinson’s. In a 1991 Spanish study, CDP-choline was administered to early-to-mid-stage Parkinson’s patients (500 mg/day for 30 days). A significant improvement in symptoms was seen.

Alzheimer’s Disease. Another Spanish study reported in 1999 that 1000 mg/day of CDP-choline “Improves cognitive performance, cerebral blood perfusion and the brain bioelectrical activity pattern in AD patients.”

Age-related learning problems. Supplementation in ‘older subjects’ with CDP-choline (500 mg/day for 6 weeks) has been shown to promote synapse formation and efficiency, and to improve performance on the California Verbal Learning Test.

The most cost-effective defense against oxygen radicals

Alpha-lipoic acid (ALA) is a substance made by cells of many kinds – bacterial, plant, and animal. It serves as a cofactor in several biochemical processes in the body, including the process by which energy is extracted from carbohydrates. ALA is also nature’s best antioxidant for neutralizing oxygen radicals that damage and age biological tissues.

ALA has been of great interest to medical biologists since it was discovered in the 1950s. Nearly 2500 scientific articles that deal with this substance have appeared since then, and numerous clinical trials have been conducted to test its effects on various medical conditions. The list of conditions for which ALA has been successfully applied is a long one, and includes:

  • Aging
  • Insulin resistance
  • Metabolic syndrome
  • Neuropathy
  • Cardiovascular disease
  • AtherosclerosisNeurological disorders
  • Burning mouth syndrome
  • Cancer
  • Hypertension
  • Chronic fatigue syndrome
  • HIV
  • Exercise-induced damage
  • Altered taste perception
  • Retinopathy
  • Down’s Syndrome
  • Pigmentation, skin bleaching
  • Cataracts
  • Diabetes
  • Multiple sclerosis
  • Lead toxicity
  • DNA damage
  • Iron depletion
  • Liver damage

Aging may be slowed by ALA.

Evidence that ALA interferes with the aging process comes from experiments showing that ALA decreases build-up of age-related lipofuscin deposits and prevents oxidative damage to mitochondria (cells’ energy extractors). In aging experiments with lab animals, ALA improves brain function, extends the lifespan, and restores age-impaired vascular function.


Treatment for 5 weeks with ALA improved neuropathic symptoms in a study of diabetic patients who received once-daily oral doses of 600 mg or more.

Other neurological disorders.

Experiments in tissue culture, lab animals, and in humans have shown that ALA counteracts the promoters (and reverses the symptoms) of neurological ailments including:

  • Alzheimer’s
  • Parkinson’s
  • Huntington’s
  • ALS
  • cognitive aging
  • various other neurological and neuromuscular diseases.

Cardiovascular conditions.

Oxidative stress is implicated as a major causative factor in atherosclerosis and hypertension. ALA‘s antioxidant activity has been shown to reduce arterial plaques, decrease lipid concentrations in the blood, and to improve the function of heart arteries. In experiments with mice, “the development of hypertension could be either totally prevented or markedly attenuated by chronic treatment with potent antioxidative therapies such as alpha lipoic acid.”

» For a more detailed discussion of alpha-lipoic acid and R-alpha-lipoic acid the medical studies that support its use, see the article on our website at:

Hypericin: the active ingredient in Saint John's Wort

by A.Y. Oubre

Hypericin, a photochemical extracted from St. Johns Wort (Hypericum perforatum) and related species, has been shown to have potent, broad spectrum antimicrobial activity. This compound is an aromatic polycyclic anthrone, a class of colored or pigmented chemical substances which have photosensitizing activity. In both in vitro (laboratory) and in vivo (animal) studies, low, non-toxic doses of hypericin significantly inhibited the replication of several viruses, including HIV, influenza A, cytomegalovirus (CMV), Herpes simplex 1 and 2 (HSV-1 and HSV-2), and Epstein-Barr virus (EBV). Hypericin and its chemical relative, pseudohypericin, produce antiviral activity through a different mechanism of action than do AZT and other nucleoside antiviral agents. Hypericin does not appear to directly alter the activity of reverse transcriptase although it does block the formation of HIV synctium. Recent findings have shown that the antiretroviral action of this compound disrupts uncoating of the lipid envelope of both DNA and RNA viruses, thus preventing infected cells from releasing HIV copies. Theoretically, hypericin and AZT, in combination, may have synergistic antiviral effects against HIV. On the other hand, hypericin actually may increase the toxicity of antiretroviral nucleosides such as AZT, ddI, or ddC.

Traditionally, extracts of St. Johns Wort (which contain hypericin) have been used as an antidepressant, possibly by acting as a MAO inhibitor. The psychotropic effects attributed to hypericin in St. Johns Wort extract suggest that the pigment compound can cross the blood brain barrier (possibly treating neuropsychological symptoms such as dementia). Laboratory investigations indicate that hypericin may be beneficial as an HIV therapy. However, its administration should be carefully monitored by a physician. The levels of hypericin found in most commercially available extracts of St. Johns Wort generally are not sufficient to be therapeutically effective against viral infections.

Liver function should be tested periodically in persons taking hypericin. Also, extreme photosensitivity has been observed in a few cases of people taking this high doses (in excess of 10 mg per day) of this compound. Finally, there is a very small possibility that adverse reactions could occur on occasion between hypericin and other foods or drugs which interfere with MAO inhibitors.

Active principles in St. Johns Wort

The quantity and quality of active principles in Hypericin species vary according to geographical locale, climate, time of day, and time of year. St. Johns Wort contains dianthrone derivatives, mainly in the form of hypericin and pseudo-hypericin as well as flavonoids. Small amounts of coumarins, phenolic carboxylic compounds, phloroglucinol derivatives, monoterpenes, sesquiterpenes, n-alkanes, n-alkanols, carotenoids, and beta-sitosterol are present. The roots contain zanthones. Practitioners and consumers should note that St. Johns Wort extracts, whether standardized or not, consist of other active ingredients in addition to hypericin and pseudohypericin.

Pre-clinical studies

Both in-vitro (test tube) and in-vivo (animal) pre-clinical studies suggest that hypericin (and, to a lesser extent, pseudo-hypericin) may have therapeutic benefits for HIV infection and other retroviral diseases. Certain compounds other than hypericin extracted from Hypericum species have antibiotic activity. marked antiretroviral effects, however, have been reported primarily for hypericin which is isolated mainly from Hypericum perforatum. However, synthetic hypericin has been used in recent studies.

In in-vitro and in-vivo studies, both hypericin and pseudohypericin (extracted from Hypericum triquetifolium) had antiviral activity against several retroviruses. In one experiment, mice were simultaneously injected with low doses of the compounds and with Friend leukemia virus (FV). This aggressive retrovirus normally causes rapid splenomegaly (swelling of the spleen) and acute erythroleukemia in mice. However, these symptoms were effectively suppressed by the addition of hypericin. Splenomegaly had not occurred ten days after infection at the close of the study. No infectious virus could be recovered from the spleen. Also, viremia normally associated with FV was absent. Mice treated with hypericin and pseudohypericin survived a much longer time than mice treated with a toxic antiviral (N3dthd). Unlike most antiretroviral drugs, hypericin (given in a single dose of low concentration) was effective without being cytotoxic. Even when it was administered after viral infection had already started, it still inhibited the onset of disease.

In in-vitro studies, mouse cell lines were infected with radiation leukemia virus (Rad LV) and then incubated with hypericin. The activity of reverse transcriptase in these cells was suppressed through indirect mechanisms. In contrast to nucleoside analogues, polycyclic diones such as hypericin interfere directly with the viral replication cycle during stages in which virions are assembled or intact virions are shedded from immature cores. Alternatively, these aromatic compounds may directly inactivate mature retrovirus that contains normal, assembled cores. Other findings indicate that hypericin is able to inactivate virions and block viral release from infected cells by interacting with the cell membrane.

Unpublished data show that hypericin disrupts the formation of synctia in HIV disease as well as in de novo infection of cells. In in-vitro studies, hypericin showed selective activity against HIV and modest inhibition of reverse transcriptase. In vitro research also revealed that hypericin lowered viral activity in whole human blood taken from HIV infected persons. “Wild” strains of HIV taken directly from infected patients are sometimes more resistant to antiviral agents than are viral strains bred in the laboratory.

Other investigations indicate that the antiviral effects of hypericin on murine cytomegalovirus (MCMV), Sindbus virus (SV), and HIV are enhanced by exposure to fluorescent light. Hypericin and to some degree, pseudohypericin, were effective against FV and HSV-1 when the viruses were first incubated with the compounds for one hour at 37 degrees C before mice were infected. Pre-incubation for one hour at 4 degrees C, however, produced no antiviral effects. The authors of this study (who are scientists at Lilly Research Laboratories) reported that hypericin and pseudohypericin were effective in vitro against enveloped viruses such as HSV and influenza when the cultures were pre-incubated with these agents at 37 degrees C. They also correctly showed that hypericin and its analogue inhibit DNA and RNA viruses, but not viruses which lack a lipid envelope. The Lilly researchers, who call AZT a preferred therapy for HIV, however, claim that single dose administration of hypericin is not efficacious. Human clinical trials are needed to evaluate the appropriate dose ranges at which hypericin is therapeutic but nontoxic, and to assess the differences, if any, between natural and synthetic hypericins. In animal studies, natural sources of hypericin (in combination with its analogue, pseudohypericin), showed greater antiviral activity that did synthetic hypericin. Preliminary findings thus far strongly indicate that the wide spectrum antiviral properties of hypericin, its experimental effectiveness at low concentrations, and its unconventional mechanisms of antiviral action make it a promising candidate for a new class of HIV therapies.

Mechanisms of action

Hypericin and pseudohypericin had no effect on purified reverse transcriptase alone. They did not alter levels of intracellular viral mRNA. Instead, hypericin lowers the number of mature viral particles without suppressing intracellular levels of viral mRNA. The concentrations of viral antigens on the cell surface were also unaffected by hypericin. These findings, as a whole, imply that the compounds interfere with viral assembly, budding, shedding or stability at the level of the cell membrane When hypericin was added to viral-infected cell cultures, red fluorescence appeared at localized areas on the lipid surface membrane.

Unlike nucleoside analogues, polycyclic diones such as hypericin have no effects on transcription, translation, or transport of viral proteins to the cell membrane. They are not directly active against reverse transcriptase even though reverse transcriptase activity was reduced in infected cells that had first been incubated with hypericin. Cells treated with hypericin form immature or abnormally assembled cores. This indicates that hypericin may block the processing of gag-encoded precursor polypeptides. Hypericin, whether in the intracellular medium or bounded to the membrane, is thought to lower the activity of reverse transcriptase by interfering with protein synthesis. (It is noteworthy that the antiviral effects of harmine, a photoactive alkaloid, involve disrupted kinase activity in enveloped RNA viruses.)

Viral particles are not formed when gag-related polyproteins fail to be cleaved or synthesized. Gag-related polyproteins, therefore, may play a decisive role in the virucidal actions of hypericin. Reverse transcriptase within the core of the assembled virus probably takes the form of an inactive enzyme or proenzyme. Mechanisms involving viral-encoded proteases or kinases might be required to activate reverse transcriptase. These mechanisms could transform the enzyme from a nonfunctional to a functional state. Both hypericin and pseudohypericin are thought to influence protease activity. In turn, altered protease activity could disrupt the cleavage or synthesis of gag-related polyproteins. As a result, immature viral cores would be formed. Alternatively, by selectively binding to viral polyproteins, hypericin could interfere with the gag and gag-pol polyproteins needed for viral assembly. Thus, hypericin could block the process whereby RNA packages encapsulated viral particles.

Some investigators, however, propose that hypericin lyses infectious virion by interacting directly with the viral envelope instead of disrupting gag-encoded precursor polyproteins or modifying other proteins. In any case, the antiviral properties of hypericin appear to involve its interactions with the cell membrane or cell surface recognition sites. Molecular modifications at or near the surface provide a model for rationally designing a new class of anti-HIV agents. Such therapies may be able to block HIV-encoded protease located in the gag-pol region. Importantly, drugs of this type would not be toxic like AZT and other agents whose pharmacological actions are based on direct inhibition of reverse transcriptase.

The aromatic, ringed structure encircled by six phenolic hydroxy groups seems critical to the antiviral activity of the hypericin molecule. Quinone groups, which often have antiviral properties, also exert photodynamic effects. Hypericin is thought to generate singlet oxygen. However, free radical quenchers can interfere with singlet oxygen reactions involving hypericin thereby reducing its antiviral properties.

Hypericin has a unique molecular structure in which one-half of the molecule is hydrophilic (water loving) while the other half is hydrophobic (water repelling). The top, bottom and side (non-polar) of the hypericin molecule which contains the methyl groups are hydrophobic. It is thought that the molecule might bond to the outer surface of the cell membrane. Presumably, the hydrophobic side would be immersed in fat Singlet oxygen, though less reactive than triplet oxygen, binds with two-electron targets, including, for example, the double bonds found in polyunsaturated fatty acids. The hydrophilic sides, in contrast, could hydrogen-bond to the aqueous media.

Discrepancies between in vivo findings from different studies on the antiretroviral effects of hypericin and pseudo-hypericin may be due partly to variations in light. However, differences in hypericin isolation methods and in the strains of mice used also could account for variable findings in several investigations. The antiviral effects of hypericin are largely but not completely, attributed to its photodynamic properties. In the presence of light, hypericin completely inhibited infection of cell cultures of equine infectious anemia virus (EIAV). On exposure to fluorescent light, hypericin inactivated MCMV, Sindbis virus (SV), and HIV-1. Both membrane virions and virus-infected cells were more strongly inactivated by visible light. (Polyacetylene phenylheptatriyine (PHY), a substance purified from the plant, Bidens pilosa, also shows antiviral activity against membrane-bound viruses such as MCMV. The antiviral effects, which involved interactions between PHY and membrane, occurred in the presence of long wave ultraviolet light). Significant advances in photobiological research have been made in recent years. New findings demonstrate clearly that photodynamic action accounts for the antiviral properties of several natural product derivatives, including hypericin.

Light is required for the photosensitization of hypericin. The compound absorbs light quanta and generates it in the form of singlet oxygen. In so doing, hypericin triggers the photo-oxidation of cellular components, including, for example, the photohemolysis of red blood cells. The underlying mechanism of photodynamic reactions is not fully understood. It is thought to involve interactions between oxygen and light as well as sensitizing pigment which binds to the cell membrane.

In photodynamic reactions mediated by hypericin, singlet oxygen serves as the main oxidant. Singlet oxygen has a strong affinity for pi electron-systems found in compounds such as polycyclic diones. The pi electrons, responsible for the photoactive properties of hypericin, absorb visible and ultraviolet light and then reemit it within the range of green and red light. The two hydroxy groups and the two methyl groups flanking each side of hypericin’s eight ringed structure do not lie within the same plane. Instead, they repel each other, placing strain on the benzenoid structure. This causes the hypericin molecule to twist and become unstable. Hypothetically, the steric strain could increase the energy state of the pi electrons. This would allow them to form temporary bonds with singlet oxygen which, at a later point, could be released to disrupt mechanisms of viral replication. Pi electrons therefore, seem to play a major role in the antiviral activity of hypericin.

The “impressive light-mediated antiviral activities” of hypericin have been shown in several studies. Sindbus virus (SV), for example, was 99% inhibited in the presence of light. In the dark, however, the antiviral effects of hypericin were reduced by more than two orders of magnitude. On exposure to light (650-700nm.), hypericin undergoes type II photosensitization in which singlet oxygen and other reactive molecular species are produced. Though not as destructive as free radicals (which are generated in Type I photosensitization, singlet oxygen could damage viral membranes, thereby interfering with proteins and nucleic acids. Nonetheless, hypericin also has some degree of virucidal activity in the dark, though much less so than in light. It is thought that the antiviral effects produced in the absence of light take place through a different mode of action than light-mediated virucidal activity. Protein kinase C, for example, may represent an alternative target for hypericin’s antiviral action in the absence of light.

One of the therapeutic advantages of hypericin is that it works by multiple steps. Hypericin is probably able to interrupt various phases in the replication of enveloped retroviruses. These stages include polyprotein cleavage and protein alterations as well as assembly, budding and shedding of viral components. The compound’s disadvantages as an anti-HIV agent involve its potential toxicity when patients are exposed to sunlight. Also, it has been reported that in humans, hypericin is more effective in suppressing HSV-1 and HSV-2 than HIV. Future research is required to elucidate the mechanisms through which hypericin generates and reacts with singlet oxygen in triggering antiviral effects.


Clinical trials that were being conducted in early 1990’s by Dr. Bihari in New York City recommend the following regimen. For the first two weeks, patients were given 10 mg of hypericin once a day for two weeks. During the second two weeks, the dosage alternates between 10 mg per day on the first day, 20 mg on the second day, 10 mg on the third day, and so forth. The ultimate dosage was given during the fifth and sixth weeks when patients were given 20 mg per day.

It has been proposed that beta-carotene, a known free radical quencher, be administered in combination with hypericin. Theoretically, this might reduce any toxic side-effects associated with hypericin’s generation of free radicals. Some investigators, however, have warned that quenchers also may lessen the anti-viral properties of hypericin. The role of beta-carotene and other free-radical scavengers in hypericin therapy deserves further clarification.


Hypericin, a pigment molecule with photodynamic activity, has dramatic antiviral activity, especially in the presence of light. Like several other plant derived substances, hypericin only inhibits viruses with membranes. It has antiviral effects against a wide range of retroviruses, including HSV-1, HSV-2, (murine) CMV, and HIV-1. In contrast to nucleoside agents such as AZT, hypericin and its chemical relative, pseudohypericin, do not directly affect the activity of reverse transcriptase. Rather, these agents seem to disrupt various stages of viral replication, including assembly, budding, shedding and possibly protein synthesis, all of which depend on the integrity of the viral membrane.

Hypericin and related compounds, with their alternative targets for virucidal activity, comprise a new class of potential anti-HIV drugs. It is not yet known how effective hypericin will be in human AIDS. Preliminary findings, however, strongly suggest that this compound is one of the most promising, new anti-HIV prototype molecules currently under investigation.