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From The January 1999 Issue of Nutrition Science News

Nutrition Q&A

Question:
Pediatricians often recommend topical steroids to relieve childhood eczema. Can you suggest alternatives?

Answer:
First of all, allergy causes eczema. The onset generally coincides with the introduction of allergenic foods such as cow's milk, wheat or eggs. Low-allergen diets often alleviate it.

Eczema sufferers often have fatty acid imbalances—too much omega-6 and not enough omega-3 fatty acids. Good sources of omega-3 fatty acids, which generally decrease inflammation, include flaxseed and cold-water fish. However, research on the effect of gamma-linolenic supplements in children with eczema have produced varying results.1,2

Several herbs may help. Licorice (Glycyrrhiza glabra) contains potent anti-inflammatory properties. In one study, topical use of the licorice constituent glycyrrhetinic acid improved eczema even more than topical cortisone.3 In another study, when 38 children with eczema drank a decoction of 10 Chinese herbs containing predominantly licorice for four weeks, their improvement surpassed that of the placebo group. Half the children showed a 90 percent reduction in symptoms.4

Long-term ingestion can result in sodium and water retention, potassium loss and estrogenic effects, so patients taking licorice for more than a few weeks should be monitored by a doctor. Topical use of licorice or a salve containing glycyrrhetinic acid may be a better way to start.

Other herbs traditionally used to decrease inflammation and promote skin healing include gotu kola (Centella asiatica), echinacea (particularly Echinacea purpurea) and burdock (Arctium lappa), which can be taken both internally and externally. Comfrey (Symphytum officinale) also works but should be used only externally.

Question:
Do women with cervical dysplasia have treatment options other than surgery?

Answer:
Yes, if the condition is mild. Abnormal cervical cell growth is triggered primarily by the human papillomavirus (HPV), but other risk factors include early age at first intercourse, multiple sexual partners, cigarette smoking and poor nutrition.

A host of studies demonstrate a relationship between low levels of antioxidant nutrients and HPV infection, cervical dysplasia and cancer.

A study of 123 women found that blood levels of vitamin E and carotenoids such as beta-carotene, cryptoxanthin and lutein were on average 24 percent lower among women who had active HPV cervical infection, compared with women who had no infection or whose infection cleared. Furthermore, those with the lowest vitamin levels tended to have the most severe dysplasia.5

Blood tests from 147 women with cervical dysplasia and 191 control women showed those with the highest levels of cryptoxanthin and vitamin E reduced their risk of cervical dysplasia by about two-thirds. Other carotenoids and vitamin C offered weaker protection.6

A study of 206 women found a correlation between high plasma levels of vitamin A and regression of cervical dysplasia. It also uncovered a protective effect from high zinc levels.7 Preliminary trials of the prescription vitamin A derivative retinoic acid (Retin-A®) applied topically to the cervix show complete regression in about 45 percent of patients treated with higher concentrations (0.1583 to 0.484 percent) of retinoic acid.8

Low folic acid levels appear to play a role in the initiation of cervical dysplasia. Although this vitamin probably helps prevent dysplasia, it is not clear whether supplements can reverse it. A study of 47 women with mild to moderate dysplasia found that taking 10 mg of folic acid daily for three months produced significant improvement compared with placebo.9 A subsequent trial of 235 women taking the same dose of folic acid for six months failed to find a significant change.10 To avoid masking a B12 deficiency, most practitioners suggest folic acid be taken with 400­1,000 mcg of B12.

Holistic practitioners generally recommend reducing risk factors including smoking, unsafe sex and poor diet, as well as taking daily supplements of 10 mg folic acid, 25,000­50,000 IU beta-carotene, 1­3 g vitamin C, and 200­400 IU vitamin E. Herbs such as echinacea (E. purpurea), astragalus (Astragalus membranaceus), and shiitake (Lentinus edodes) and reishi (Ganoderma lucidum) mushrooms can also boost immune function to help fight HPV infection.

Question:
Can nutritional therapies successfully treat obsessive-compulsive disorder?

Answer:
What few studies there are indicate yes. Obsessive-compulsive disorder (OCD) involves unwanted, recurrent thoughts that drive a person to repeatedly perform behaviors such as hand washing or counting objects. The cause may be a brain chemical imbalance, most likely a serotonin deficit.

Although St. John's wort (Hypericum perforatum) may diminish depression by raising serotonin levels, I know of no trials on people with OCD.

However, two recent studies suggest that the B-vitamin relative, inositol, may help. In both studies, 13 OCD patients took placebo, then inositol (18 g/day) for six weeks each. In each case, the inositol group's symptoms were significantly reduced compared with placebo—an improvement on par with Prozac® treatment.11,12

Natural products stores stock powdered inositol preparations that typically contain 3 g per teaspoon. The amount used in studies is equivalent to 6 teaspoons daily, dissolved in water.

Linda White, M.D., is a freelance writer and editor.

References

1. Biagi PL, et al. Drugs Exp Clin Res 1994;20:77-94.

2. Hederos C, Berg A. Arch Dis Child 1996;75:494-7.

3. Evans FQ. Brit J Clin Pract 1958;12:269-79.

4. Sheehan MP, Atherton DJ. Brit J Dermatol 1992;126:179-84.

5. Giulianao AR, et al. Cancer Epidemiol Biomarkers Prev 1997;6:917-23.

6. Goodman MT, et al. Cancer Epidemiol Biomarkers Prev 1998;7(6):537-44.

7. Liu T, et al. Cancer Epidemiol Biomarkers Prev 1995;4(4):373-80.

8. Meyskens FL Jr, Surwit ES. J Am Acad Dermatol 1986 Oct;15:826-9.

9. Butterworth CE Jr, et al. Am J Clin Nutr 1982;35:73-82.

10. Butterworth CE Jr, et al. Am J Obstet Gynecol 1992;166:803-9.

11. Fux M, et al. Am J Psychiatry 1996;153:1219-21.

12. Levine J. Eur Neuropsychopharmacol 1997;7:147-55.



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