herbsandinfluenza.com Blog

Recently, the news reported that lavender and tea tree oil may cause gynecomastia (breast growth) in young boys.

The underlying study described three young boys. One was exposed to lavender essential oil in a “compounded healing balm” “starting shortly before the visit to the doctor for gynecomastia. The condition resolved within 4 months of discontinuing use of the balm. The second boy used a styling gel on his hair and scalp every morning and regularly used a shampoo. Both the gel & the shampoo listed lavender oil and tea tree oil as ingredients. Nine months after discontinuing use, his gynecomastia was substantially reduced but still present. The third used a “lavender-scented soap” and intermittently a lavender-scented skin lotion. His gynecomastia resolved completely after discontinuing the products. His fraternal twin brother used the lotion but not the soap without any problems.

Based on the researchers’ in vitro studies showing that lavender oil and tea tree oil “possess weak estrogenic and antiandrogenic activities” they “suspect” that these essential oils caused these cases of gynecomastia.

The problems with the study are obvious: There is no convincing correlation between the products and the resolution of gynecomastia, and a rechallenge was not done. The study completely ignored the other ingredients in the various products used. Many body care products, for instance, contain parabens that are strongly estrogenic. And some of the products may not have contained either lavender or tea tree oil. “Lavender scent” usually refers to a synthetic compound, not lavender oil. The news this little “study” generated shows a disturbing bias against natural products.

Henley DV, Lipson N, Korach KS, Bloch CA. Prepubertal gynecomastia linked to lavender and tea tree oils. New England Journal of Medicine 2007; 356:479-485.

We have all heard of colicky babies but I had no idea how much those babies can cry. It turns out that 15-30% of infants in the Western world have colic which means that they cry for more than 3 hours a day and more than 3 days a week for more than 3 weeks. To be defined as severely colicky, these babies have a history of persistant, full-force crying for no apparent reason several times a day for a duration of more than 4 hours a day for more than 4 days a week. That is a lot of crying. And the solution is so simple:

In a study of healthy, breast fed babies, an herbal tea consisting of chamomile (Matriacaria recutita), fennel (Foeniculum vulgare), and lemon balm (Melissa officinalis) did the trick. They were given small doses of tea (so as not to interfere with their desire to breast feed) twice a day. For the first three days, placebo and herbal tea worked about equally as well. But then: The herbal babies began by crying about 201.2 min/day [The parents must have been counting every second, praying for peace and quiet]. By day 7, the herbal babies were crying about 76.9 min/day. The placebo babies cried 198.7 min/day initially and were crying 169.9 min/day on day 7. Moreover, a reduction in crying was seen in 85.4% of the herbal babies.

The babies were given 2 ml/kg/day of tea in two doses. One at 5 PM and another at 8 PM shortly before feeding. Each dose contained 164 mg fennel, 177 mg chamomile, and 96 mg lemon balm. The effect of the tea lasted for 15 days after treatment.

Of course, you do not need to run out and buy a gram scale to make up the tea but the point made that the babies should not be given a large volume of tea makes good sense. Nor can I see any reason to stop giving the baby a tea that makes them stop crying. Imagine: Those old midwives and wise women were right when they suggested soothing herbal teas for fussy kids.

Savino F, Cresi F, Castagno E, et al. A randomized double-blind placebo-controlled trial of a standardized extract of Matricariae recutita, Foeniculum vulgare and Melissa officinalis (ColiMil) in the treatment of breastfed colicky infants. Phytotherapy Research 2005; 19(4):335-340.

The Bush administration just put into effect a new law that frees manufacturers from product liability suits for damages caused by vaccines or drugs produced for use in avian flu.

The law, enacted in 2005, gives the Secretary of Health and Human Services the power to grant immunity to companies based on an assessment of risk to public health.  HHS has just invoked that clause “based on a credible risk that an avian virus spreads and evolves into a strain capable of causing a pandemic of human influenza.”

Of course, if the government and manufacturers knew that these products were beneficial and unlikely to cause harm, these measures would be unnecessary.  And of course, if they knew that there was a likelihood of harm, they would make every effort to shield themselves and their profits far in advance of any real threat of a pandemic.  Draw your own conclusions about the benefits and detriments of the treatments they are proposing.

Cats used to be considered immune to influenza. Even crafty researchers could not infect them with the virus. Then zoo cats in Asia were fed birds that died of avian influenza. They contracted fatal cases of the flu and, moreover, were able to transmit the disease to other cats. In the laboratory, cats could be infected with avian flu either by inhaling or eating the virus and could then transmit it to other cats. It had a fairly high mortality rate.

Today, I learned that avian flu is wide spread among cats in Indonesia. In a survey of cats in areas of the country where humans had contracted the flu, about 20% of the 500 stray cats tested had antibodies to the virus. These were the cats that had contracted influenza and survived. It is likely that many more cats had caught the flu and died from it.

Other animals, pigs and dogs, have also gotten avian flu. Should we be concerned? I think yes. The 1918 flu was a bird virus that adapted to mammals through an intermediate host, probably the pig. One expert now suggests that “Maybe for H5N1, the intermediate host is cats.” The more opportunities cats and humans have to eat infected animals, the more opportunity the virus has to mutate to a transmissible form.

And to make matters worse, in Jakarta authorities are slaughtering large numbers of chickens that are then provided as free food to people in the area. It is possible for chickens to have mild cases of avian flu and not appear symptomatic. They could still infect the person or cat eating them, creating more opportunities for the virus to adapt and mutate. Obviously, the potential for avian flu to turn into a more transmissible form still looms on the horizon.

Two of the avian flu patients in Egypt had a strain resistant to Tamiflu.  This means that in only a few hundred cases, three humans have had resistant strains.  Logically, this means that in a pandemic, resistance will be established quickly.  In turn this means that all of the money we have spent stockpiling the drug and relying on it as a primary treatment is likely misplaced.

Robyn Klein sent me a fascinating article Tamiflu® (oseltamivir phosphate) resistance and suggested that it would make an interesting blog. It was indeed an interesting article. The active antiviral metabolite of Tamiflu passes through us unchanged, is not altered by our water treatments, and ultimately will be picked up by the bird population in their drinking water. This will give avian viruses an excellent opportunity to build resistance to Tamiflu.

Frankly, the influenza virus does not seem to need this latest advantage. Even in the relatively small population of human avian flu victims treated with Tamiflu, one has already had a resistant strain. And resistance was seen early on in the test tube and test animals. When the next epidemic/pandemic influenza rages across the world, there is no doubt that resistance will build rapidly. This means that the drug would be virtually ineffective. Although, I do not think it was all that effective to begin with. Certainly, avian flu victims are not surviving very well, even though they get Tamiflu. This is blamed on the length of time that often passes between the onset of symptoms and treatment. Still.

Worst of all, though, is that there is virtually no discussion of the side effects of Tamiflu. Its ability to cause psychosis and suicide received a flurry of attention and led to some additional warning labels on the drug. But a deafening silence reigns when it comes to its potential ability to cause birth defects. In the approval process, Tamiflu in pregnancy did cause birth defects. “There were a variety of defects detected in developing [rabbit] fetuses. Most of the observations were an increased incidence of minor skeletal abnormalities and variants. The sponsor has argued that most of the incidence values were within normal range and were not considered real. However,… coupled with the ossification problem in rats and mortalities associated with bone problem in marmosets it is suggested that [Tamiflu] may have effects on bone.” This dilemma was fixed by language on the label saying that pregnant women should not take Tamiflu – unless the benefits outweigh the risks. Whatever that means.

I have not found any additional research on Tamiflu and birth defects. I did read, however, that the drug was being dispensed to pregnant women in South East Asia, so perhaps we will learn more eventually.

There are indications that Tamiflu may cause bone problems in adult animals but, in testing, these were attributed to genetic defects in the lab animals. The government did not require additional testing. And Tamiflu is much more toxic to newborns and is passed through breast milk. Again that problem was solved by labeling: The drug should not be taken by women who are nursing children – unless the benefits outweigh the risks. Whatever that means.

My advice: Forget Tamiflu and stockpile the herbal remedies the Eclectic physicians used in the 1918 pandemic instead.

About the spread of Tamiflu into our water ways: http://www.ehponline.org/realfiles/docs/2007/115-1/ss.html

Documents submitted in support of FDA approval of Tamiflu

http://www.fda.gov/cder/foi/nda99/21087_Tamiflu-pharmr.P1.pdf

http://www.fda.gov/cder/foi/nda99/21087_Tamiflu-pharmr.P2.pdf

A recent small study suggests that Hypericum spp. (St. John’s wort) may help people quit smoking. The study was based on research showing that some prescription antidepressants can help people quit smoking, and hypothesized that St. John’s wort might have a similar effect but with fewer side effects. The participants took 450 mg of standardized (0.3% hypericin and a minimum of 4% hyperforin) twice daily. Almost 38% were not smoking 12 weeks later. This study did not have a control group but other studies suggest that maybe 17% of those determined to quit are able to do so cold turkey. The study is well reasoned and admits that it is preliminary, cautioning us not to “over interpret the results.”

They also note that Zyban (buprion, an antidepressant studied in smoking cessation) yielded about the same results but was only available by prescription, cost $120/month plus the cost of a doctor visit, and up to 48% of those taking it experienced side effects such as dry mouth, seizures, insomnia, and headaches. They even calculated that patients with good insurance coverage actually might only spend $20 on the drug. In contrast, St. John’s wort is readily available at a cost of about $11/month and at most 7.5% suffered side effects of GI disturbances and photosensitivity.

Anyone who has smoked knows that quitting smoking involves much more than overcoming nicotine addiction. Smoking, like drug use and overeating, is a form of self-medication. I have found that adaptogens are useful in helping people maintain their resolve to quit smoking. I will now be advising people to take St. John’s wort as well to provide some more focused emotional relief.

In the study, the participants began taking St. John’s wort for a week before their “quit date.” The study also suggested that it might be better to take it for a while longer before that date as studies suggest that the effect of the herb builds slowly in most people. The same is true of adaptogens, so it probably makes sense to have people take both for 3-4 weeks before trying to quit.

Lawvere S, Mahoney MC, Michael Cummings K, et al. A phase II study of St. John’s wort for smoking cessation. Comp Ther Med 2006; 14:175-184.

As one person commented on a previous blog, it can be tricky to distinguish colds from flu. In reviewing an article on just that topic, I was surprised to read that the color of mucus (aka nasal discharge, sputum, plegm, snot) did not accurately reflect whether an infection was viral or bacterial. I, like many herbalists, was taught that nasal discharge turning from clear to yellow or green shades indicated that a bacterial infection was settling in. It turns out that doctors also share this view. They are most likely to prescribe antibiotics in patients who have a cough and colored nasal discharge. In fact, one study found that patients were seven more times to be prescribed antibiotics if their nasal discharge was “discolored.”

Bad idea, said the article as they may be dispensing antibiotics for viral infections, an unnecessary and inappropriate use of antibiotics. “[T]he appearance of these secretions alone is not predictive of bacterial infection or the effectiveness of antimicrobial therapy.” Overall, the view is that changes in mucus to yellow, thick, or green occur naturally in the course of viral respiratory infection and do not support the use of antibiotics. Antibiotics are only appropriate where there is a persistent daytime cough or rhinorrhea lasting more than 10-14 days or there are severe symptoms of acute sinus infection (fever with purulent nasal discharge).

Herbalists tend to begin prescribing goldenseal (Hydrastis canadensis) when the color of the mucus changes, often explaining that this shows that the infection is now bacterial. Perhaps, however, what we are really doing is using an excellent mucus membrane tonic to reduce inflammation rather than using the herb as an antibacterial. Paul Bergner suggests this is the appropriate use of goldenseal in one of his excellent articles: “It is my opinion that goldenseal acts as an “antibiotic” to the mucous membranes not by killing germs directly, but by increasing the flow of healthy mucous, which contains it’s own innate antibiotic factors — IgA antibodies. This effect is unnecessary in the early stages of a cold or flu, when mucous is already flowing freely.”

That said, even Paul shares the hard to shake view that the color of the discharge indicates the nature of the infection: “a client with a chronic dry bronchitis had been coughing up only slight amounts of clear phlegm for several weeks. Then the discharges turned to yellow and green — a sign of the onset of bacterial infection and the threat of pneumonia.” What we should be saying is that the change in the color of the discharges indicates inflamed mucus membranes in need of a mucus membrane tonic (goldenseal being one of, if not the best) to prevent a condition from developing that will favor a secondary bacterial infection from taking hold.

Paul Bergner on goldenseal: http://www.medherb.com/84.HTM

Mainous, AG III, Hueson WJ, Eberlein C. Color of respiratory discharge and antibiotic use. Lancet 1997; 350:1077-1079.

Eccles. Understanding the symptoms of the common cold and influenza. Lancet 2005; 5:718-725.

Careful antibiotic use. http://www.cdc.gov/drugresistance/community/files/ads/rhini_vs_sinus.pdf

In general, most of us use Latin plant names to minimize confusion as to which plant we are talking about. This, however, does not always work.

One of my favorite articles begins by noting that there is a fair amount of research on the use of Sanguinaria canadensis as a treatment for gingivitis. It then explains that there is “a high gingival index” in Mexico as well as a Mexican plant known as sanguinaria (Polygonum aviculare). Given this information, the logical next step was to sign on 60 male dental students with gingivitis to test a Mexican sanguinaria mouthwash.

These students agreed not to brush their teeth for two weeks and instead rinse their mouths twice daily with a Mexican sanguinaria extract. [I found it amazing that they could find 60 dental students who would offer to go without brushing their teeth for 2 weeks. In fact, 9 did not complete the study]

The mouthwash was made of triturated (dried & ground) Mexican sanguinaria (aka Polygonum aviculare) roots, stems or leaves & flowers dissolved in ethanol and diluted in water. In the end, it actually significantly reduced gingivitis. The dental students suffered an increase in plaque [need that mechanical brushing to fight plaque] but its composition did not seem to aggravate the gums and was easily removed.

The study explained that Mexican sanguinaria is astringent and has flavonoid components that may decrease capillary fragility but also merrily noted that their results agree “with those reported elsewhere in which a decrease in gingivitis with the utilization of Sanguinaria canadensis alone was demonstrated”. They also note that sanguinarine (an alkaloid from Sanguinaria) appears to prevent plaque and gingivitis.

I am tickled by this study because it shows that confusion can lead to insight. I suspect that the Mexican sanguinaria may be a better long term treatment for the gums than its harsher, completely unrelated friend, Sanguinaria canadensis.

Gonzalez Begne M, Yslas N, Reyes E, et al. Clinical effect of Mexican sanguinaria extract (Polygonum aviculare L.) on gingivitis. J Ethnopharmacol 2001; 74(1):45-51