Q: I know that chromium may help control diabetes, but will it work if I use it just to control my blood sugar?
A: This is an interesting question. You seem to be aware there is significant evidence showing that long-term chromium supplementation may be beneficial in type 2 diabetes.1 It seems this is because chromium affects the action of insulin and, therefore, improves insulin sensitivity. This was assumed to be a long-term effect. But does it also have an immediate effect?
Anecdotally, short-term use of chromium has been said to help control blood-sugar swings, and I have used it clinically this way. Now, a recent study seems to support the concept that chromium has an immediate effect. Researchers tested if chromium influenced the glycemic index of a meal. The GI is the effect equal amounts of different types of carbohydrates have on blood-sugar elevation. The lower the GI of a food or meal, the less insulin you need to control blood-sugar fluctuations. The researchers had 13 healthy, nonsmoking, young men of normal weight perform three trials, each separated by one week. During these trials, the men consumed a meal without chromium or with 400 or 800 mcg of chromium picolinate. When compared, chromium supplementation resulted in a trend to lower the meal GI.
The researchers further analyzed the data and noticed that when they divided the group into those that responded to supplementation (10 participants) and those who did not (three participants), the dose of chromium picolinate made no difference, suggesting that 400 mcg might be enough to achieve this effect. Why was that? It's not certain, but it may be that some of those volunteers were deficient in chromium, and they were the ones who were the "responders." So the bottom line is that chromium may help to lower the GI of a meal in those who are low in chromium.
Q: I was recently diagnosed with macular degeneration. Can fish oil help?
A: Age-related macular degeneration is the leading cause of irreversible blindness in adults. ARMD is caused by hardening of the arteries that nourish retina cells. This deprives sensitive retinal tissue of the oxygen and nutrients it needs to function. Macular degeneration may be caused by a variety of factors, including diet, especially the amount and type of fats consumed.
Animal studies suggest diets rich in omega-3 fatty acids may enhance certain enzyme reactions in the eye that, in turn, may reduce oxidative damage to the cells of the retina and thus prevent ARMD.2 Human epidemiological studies have shown that after adjusting for other risk factors, diets higher in omega-3 fatty acids and fish were inversely associated with ARMD risk—particularly when intake of linoleic acid (omega-6 fatty acids) was low.3,4
I have not seen any studies that have tried fish oils in the treatment of ARMD, only those that show you can decrease your risk of developing ARMD. However, there was a recent 12-month study that looked at a combination of acetyl-L-carnitine, omega-3 fatty acids and coenzyme Q10 (supplement amounts were not given) for ARMD. The researchers reported that in this double-blind, placebo-controlled trial, the treated group showed significant improvement.5 So taking fish oils may be helpful in combination, although I think it's a bit too early to make a strong recommendation.
Q: I've heard that broccoli may be helpful in healing stomach ulcers. Is this true?
A: You may be referring to research on the effects sulforaphane glucosinolate, a constituent of broccoli, has on Helicobacter pylori—a bacterium that infects the stomach and is now widely understood to be a primary cause of stomach (peptic) and duodenal ulcers. H. pylori also dramatically enhances the risk of gastric cancer.6
Sulforaphane is a phytonutrient that is derived from broccoli or broccoli sprouts after they have been eaten. Both in vitro and in vivo studies show it to have potent antibacterial activity against H. pylori.7,8 This is helpful, as eradication of this bacteria is often complicated by the development of resistance to conventional antibiotics and by the persistence, even post-antibiotic treatment, of a low-level reservoir of H. pylori within gastric epithelial cells.9
H. pylori infection also induces oxidative stress on gastric mucosa, thereby causing mucosal damage and retarding mucosal repair. Because cells can survive such chronic oxidative stress by enhancing their antioxidant enzyme activities, sulforaphane may also work by stimulating antioxidant enzymes in the cells lining the stomach.10
Recently, researchers sought to determine whether orally consumed broccoli sprouts could eradicate H. pylori in infected human volunteers. H. pylori-positive patients consumed broccoli sprouts (14, 28 or 56 g) twice daily for seven days. Nine patients completed the course of treatment. Using various laboratory analyses, researchers concluded that consumption of the sprouts was temporarily associated with eradication of H. pylori infection in three of the patients.11
Another study reported that after more than two months on a diet rich in broccoli sprouts—100 g of broccoli sprouts per day, which contained 250 mg of sulforaphane glucosinolate—there was a significant reduction in H. pylori infection in a group of 20 volunteers compared to 20 infected volunteers given alfalfa sprouts in their diets.12
1. Frauchiger MT, et al. Effects of acute chromium supplementation on postprandial metabolism in healthy young men. J Am Coll Nutr 2004;23(4):351-7.
2. Elner VM. Retinal pigment epithelial acid lipase activity and lipoprotein receptors: effects of dietary omega-3 fatty acids. Trans Am Ophthalmol Soc 2002;100:301-38.
3. Seddon JM, et al. Dietary fat and risk for advanced age-related macular degeneration. Arch Ophthalmol 2001;119(8):1191-9.
4. Cho E, et al. Prospective study of dietary fat and the risk of age-related macular degeneration. Am J Clin Nutr 2001;73(2):209-18.
5. Feher J, et al. Improvement of visual functions and fundus alterations in early age-related macular degeneration treated with a combination of acetyl-L-carnitine, n-3 fatty acids, and coenzyme Q10. Ophthalmologica 2005;219(3):154-66.
6. Huang JQ and Hunt RH. The evolving epidemiology of Helicobacter pylori infection and gastric cancer. Can J Gastroenterol 2003;17 Suppl B:18B-20B.
7. Haristoy X, et al. Efficacy of sulforaphane in eradicating Helicobacter pylori in human gastric xenograft implanted in nude mice. Antimicrob Agents Chemother 2003;47(12):3982-4.
8. Haristoy X, et al. Evaluation of the antimicrobial effects of several isothiocyanates on Helicobacter pylori. Planta Med 2005;71(4):326-30.
9. Fahey JW, et al. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. Proc Natl Acad Sci USA 2002;99(11):7610-5.
10. Yanaka A, et al. Role of the nrf-2 gene in protection and repair of gastric mucosa against oxidative stress. Inflammopharmacology 2005;13(1-3):83-90.
11. Galan MV, et al. Oral broccoli sprouts for the treatment of Helicobacter pylori infection: a preliminary report. Dig Dis Sci 2004;49(7-8):1088-90.
12. Yanaka A. Dietary intake of sulforaphane-rich broccoli sprouts improves gastritis in H. pylori-infected human subjects. Abstract 3442, presented at the American Association for Cancer Research Meeting Baltimore, Md., Nov. 2, 2005.
Natural Foods Merchandiser volume XXVII/number 10/p. 110, 112