2-4 mg 2x/day for idiopathic anaphylaxis
KETOTIFEN – ORAL TABLET side effects, medical uses, and drug interactions
Oral Ketotifen_ Some Novel Uses – CareFirst Specialty Pharmacy’s Blog
mast cell ibs citations 104 ited In for PMID_ 20650926 – Search Results – PubMed
The mast cell stabiliser ketotifen decreases visceral hypersensitivity and improves intestinal symptoms in patients with irritable bowel syndrome – PubMed
Presentation_ Ketotifen_ A Role in the Treatment of Idiopathic Anaphylaxis (2015 AAAAI Annual Meeting (February 20-24, 2015))
Calming Down Mast Cells with Ketotifen-A Potential Strategy for Multiple Sclerosis Therapy
Mast Cell Degranulation Exacerbates Skin Rejection by Enhancing Neutrophil Recruitment2018
Vitamin E occurs naturally as eight separate compounds (four tocopherols and four tocotrienols) with antioxidant activity. Most clinical research has focused on one of these compounds—alpha-tocopherol. The naturally occurring form of alpha-tocopherol is called D-alpha-tocopherol (or RRR-alpha tocopherol), and the synthetic form is called DL-alpha-tocopherol (or all-rac-alpha tocopherol). Although many studies have shown benefits from the synthetic form, the synthetic form contains isomers not normally found in the human body. Therefore, the naturally-occurring form—D-alpha-tocopherol—might be the preferred form.9
In addition, there is some evidence that supplements containing a mixture of all four vitamin E tocopherols (alpha, beta, gamma, and delta) may be safer and more effective than D-alpha-tocopherol by itself. One researcher has recommended that these mixed tocopherol supplements contain 50 to 100 mg of gamma-tocopherol per 400 IU of D-alpha-tocopherol. Also, water-miscible preparations of vitamin E may be better absorbed than fat-soluble preparations.10
The recommended dietary allowance for vitamin E is low, just 15 mg or approximately 22 International Units (IU) per day. The most commonly recommended amount of supplemental vitamin E for adults is 400 to 800 IU per day. However, some leading researchers suggest taking only 100 to 200 IU per day, since trials that have explored the long-term effects of different supplemental levels suggest no further benefit beyond that amount. In addition, research reporting positive effects with 400 to 800 IU per day has not investigated the effects of lower intakes.1 For tardive dyskinesia, the best results have been achieved from 1,600 IU per day,2 a large amount that should be supervised by a healthcare practitioner.
Wheat germ oil, nuts and seeds, whole grains, egg yolks, and leafy green vegetables all contain vitamin E. Certain vegetable oils should contain significant amounts of vitamin E. However, many of the vegetable oils sold in supermarkets have had the vitamin E removed in processing. The high amounts found in supplements, often 100 to 800 IU per day, are not obtainable from eating food.
Severe vitamin E deficiencies are rare. People with a genetic defect in a vitamin E transfer protein have severe vitamin E deficiency, characterized by low blood and tissue levels of vitamin E and progressive nerve abnormalities.3, 4
Low vitamin E status has been associated with an increased risk of rheumatoid arthritis5 and major depression.6 Women with preeclampsia have been found to have lower blood levels of vitamin E than women without the condition.7
Very old people with type 2 diabetes have shown a significant age-related decline in blood levels of vitamin E, irrespective of their dietary intake.8
2. Hashim S, Sajjad A. Vitamin E in the treatment of tardive dyskinesia: a preliminary study over 7 months at different doses. Int Clin Psychopharmacol 1988;13:147-55.
3. Traber MG. Vitamin E. In: Shils ME, Olsen JA, Shike M, Ross AC (eds). Modern Nutrition in Health and Disease. Baltimore: Williams & Wilkins, 1999, 347-62.
4. Cavalier L, Ouahchi K, Kayden HJ, et al. Ataxia with isolated vitamin E deficiency: heterogeneity of mutations and phenotypic variability in a large number of families. Am J Hum Genet 1998;62:301-10.
5. Knekt P, Heliovaara M, Aho K, et al. Serum selenium, serum alpha-tocopherol, and the risk of rheumatoid arthritis. Epidemiology 2000;11:402-5.
6. Maes M, De Vos N, Pioli R, et al. Lower serum vitamin E concentrations in major depression. Another marker of lowered antioxidant defenses in that illness. J Affect Disord 2000;58:241-6.
7. Kharb S. Total free radical trapping antioxidant potential in pre-eclampsia. Int J Gynaecol Obstet 2000;69:23-6.
8. Polidori MC, Mecocci P, Stahl W, et al. Plasma levels of lipophilic antioxidants in very old patients with type 2 diabetes. Diabetes Metab Res Rev 2000;16:15-9.
9. Gaby, AR. Nutritional Medicine. Concord, NH: Fritz Perlberg Publishing, 2011.
10. Gaby, AR. Nutritional Medicine. Concord, NH: Fritz Perlberg Publishing, 2011.
11. Roob JM, Khoschsorur G, Tiran A, et al. Vitamin E attenuates oxidative stress induced by intravenous iron in patients on hemodialysis. J Am Soc Nephrol 2000;11:539-49.
12. Panel on Dietary Antioxidants and Related Compounds, Food and Nutrition Board, Institute of Medicine, National Academy of Sciences. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press, Washington, D.C., 2000.
13. Graat JM, Schouten EG, Kok FJ. Effect of daily vitamin E and multivitamin-mineral supplementation on acute respiratory tract infections in elderly persons: a randomized controlled trial. JAMA 2002;288:715-21.
14. Skrha J, Sindelka G, Kvasnicka J, Hilgertova J. Insulin action and fibrinolysis influenced by vitamin E in obese type 2 diabetes mellitus. Diabetes Res Clin Pract 1999;44:27-33.
15. Zoler ML. Supplemental vitamin E linked to heart failure. Fam Pract News 2003 (October 1):28 [News report].
16. Miller ER III, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142:37-46.