Updated December, 2014
On his page called:
Dr. Oz: How Much Vitamin E Is Too Much?
...Dr. Oz said, "...recently it was found that high doses of vitamin E actually can cause lung cancer. At low doses, vitamin E is an anti-oxidant, but at high doses vitamin E becomes an anti-anti-oxidant, damages DNA and can lead to cancer.... He also said, "...if you get Vitamin E naturally through food, it is the safest way to go. For example, by eating 2 handfuls of pistachio nuts everyday you will get all the Vitamin E that you need. You do not want over 150 IU of Vitamin E..."
Michael Mooney's Comment:
I've watched Dr. Oz a number of times and was at first surprised to find that he provided enlightening information about foods and herbs, including some things I didn't know.
On the other side he shows a surprising lack of understanding of basic vitamins and minerals, for instance, his take on vitamin E is greatly lacking in depth.
Several studies confirm that vitamin E delivers its optimal effects at 400 IU and above. [See: Fuller CJ et al. Effects of increasing doses of alpha tocopherol in providing protection of low-density lipoprotein from oxidation. American Journal of Cardiology 1998 Jan 15;81(2):232-3.]
And vitamin E is very safe, even when dosing is higher than 800 IU, according to the US Goverment's National Academy of Sciences' Institute of Medicine, which assigns a Lowest Observed Adverse Effect Level (LOAEL) of 1,200 IU to vitamin E. The LOAEL is a dose where toxicity may occur when taken over a period of time "rarely, but for some sensitive sub-groups it does occur."
Further, Professor Maret Traber, at Oregon State University College of Public Health and Human Sciences and true vitamin E expert scientist, that has published over 150 studies on vitamin E, found that "Toxic levels of vitamin E in the body simply do not occur."
The study that gave Dr. Oz the conclusion that vitamin E caused cancer was seriously flawed.
Rather than use natural form d-alpha tocopherol vitamin E, which is the only type sold in natural food stores, such as Whole Foods Market, the study used synthetic dl-alpha tocopherol, which is known to be about half as effective as an antioxidant as d-alpha tocopherol vitamin E, with some scientists saying that it might block cellular uptake of natural vitamin E gleaned from foods or reduce the potential anti-cancer effects of gamma tocopherol, another one of the natural vitamin E tocopherols.
Below I give you studies that say that vitamin E (alpha tocopherol), especially higher amounts of vitamin E, such as 400 IU and 800 IU, reduced the risk of the development or the effects of several types of cancers.
As an aside, Dr. Oz was torn apart in an article in the press at: http://www.consumeraffairs.com/news/study-less-than-half-of-dr-ozs-recommendations-are-actually-supported-by-evidence-121914.html
I do believe that Dr. Oz is more credible than the article said. However, the article did point out some of his flaws.
Watters JL, et al. Associations between alpha-tocopherol, beta-carotene, and retinol and prostate cancer survival. Cancer Res. 2009 May 1;69(9):3833-41.
Previous studies suggest that carotenoids and tocopherols (vitamin E compounds) may be inversely associated with prostate cancer risk, yet little is known about how they affect prostate cancer progression and survival. We investigated whether serum alpha-tocopherol, beta-carotene, and retinol concentrations, or the alpha-tocopherol and beta-carotene trial supplementation, affected survival of men diagnosed with prostate cancer during the alpha-Tocopherol, beta-Carotene Cancer Prevention Study, a randomized, double-blind, placebo-controlled primary prevention trial testing the effects of beta-carotene and alpha-tocopherol supplements on cancer incidence in adult male smokers in southwestern Finland (n = 29,133). Prostate cancer survival was examined using the Kaplan-Meier method with deaths from other causes treated as censoring, and using Cox proportional hazards regression models with hazard ratios (HR) and 95% confidence intervals (CI) adjusted for family history of prostate cancer, age at randomization, benign prostatic hyperplasia, age and stage at diagnosis, height, body mass index, and serum cholesterol. As of April 2005, 1,891 men were diagnosed with prostate cancer and 395 died of their disease. Higher serum alpha-tocopherol at baseline was associated with improved prostate cancer survival (HR, 0.67; 95% CI, 0.45-1.00), especially among cases who had received the alpha-tocopherol intervention of the trial and who were in the highest quintile of alpha-tocopherol at baseline (HR, 0.51; 95% CI, 0.20-0.90) or at the 3-year follow-up measurement (HR, 0.26; 95% CI, 0.09-0.71). Serum beta-carotene, serum retinol, and supplemental beta-carotene had no apparent effects on survival. These findings suggest that higher alpha-tocopherol (and not beta-carotene or retinol) status increases overall prostate cancer survival. Further investigations, possibly including randomized studies, are needed to confirm this observation.
Prasad KN, et al. Alpha-tocopheryl succinate, the most effective form of vitamin E for adjuvant cancer treatment: a review. J Am Coll Nutr. 2003 Apr;22(2):108-17.
In 1982, it was established that alpha-tocopheryl succinate (alpha-TS) was the most effective form of vitamin E in comparison to alpha-tocopherol, alpha-tocopheryl acetate and alpha-tocopheryl nicotinate in inducing differentiation, inhibition of proliferation and apoptosis in cancer cells, depending upon its concentration. During the last two decades, several studies have confirmed this observation in rodent and human cancer cells in culture and in vivo (animal model). The most exciting aspect of this alpha-TS effect is that it does not affect the proliferation of most normal cells. In spite of several studies published on the anti-cancer properties of alpha-TS, the value of this form of vitamin E has not drawn significant attention from researchers and clinicians. Therefore, a critical review on the potential role of alpha-TS in the management of cancer is needed. In addition, such a review can also provide in-depth analysis of existing literature on this subject. alpha-TS treatment causes extensive alterations in gene expression; however, only some can be attributed to differentiation, inhibition of proliferation and apoptosis. alpha-TS also enhances the growth-inhibitory effect of ionizing radiation, hyperthermia, some chemotherapeutic agents and biological response modifiers on tumor cells, while protecting normal cells against some of their adverse effects. Thus, alpha-TS alone or in combination with dietary micronutrients can be useful as an adjunct to standard cancer therapy by increasing tumor response and possibly decreasing some of the toxicities to normal cells.
Chan JM, et al. Supplemental vitamin E intake and prostate cancer risk in a large cohort of men in the United States. Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):893-9.
A clinical trial of vitamin E and beta-carotene supplementation for lung cancer prevention among male smokers in Finland recently reported an unexpected, strong protective effect of vitamin E against prostate cancer incidence and mortality. Our objective was to prospectively examine supplemental vitamin E intake and prostate cancer risk in a distinct U.S. population. In 1986, we identified 47,780 U.S. male health professionals, free from diagnosed cancer, who completed a dietary and lifestyle questionnaire; supplemental vitamin E and prostate cancer incidence were updated biennially through 1996. We estimated relative risks (RRs) from multivariate pooled logistic regression models. There were 1896 total (non-stage A1), 522 extraprostatic, and 232 metastatic or fatal incident prostate cancer cases diagnosed between 1986-1996. Men consuming at least 100 IU of supplemental vitamin E daily had multivariate RRs of 1.07 (95% confidence interval [CI], 0.95-1.20) for total and 1.14 (95% CI, 0.82-1.59) for metastatic or fatal prostate cancer compared with those consuming none. Current use, dosage, and total duration of use of specific vitamin E supplements or multivitamins were not associated with risk. However, among current smokers and recent quitters, those who consumed at least 100 IU of supplemental vitamin E per day had a RR of 0.44 (95% CI, 0.18-1.07) for metastatic or fatal prostate cancer compared with nonusers. Thus, supplemental vitamin E was not associated with prostate cancer risk generally, but a suggestive inverse association between supplemental vitamin E and risk of metastatic or fatal prostate cancer among current smokers and recent quitters was consistent with the Finnish trial among smokers and warrants further investigation.
Michael's Comment: Even with a relatively low dose of vitamin E - 100 IU or more, a beneficial effect was noted.
Mahabir S, et al. Dietary alpha-, beta-, gamma- and delta-tocopherols in lung cancer risk. International Journal of Cancer. 2008 Sep 1;123(5):1173-80.
Studies of vitamin E and cancer have focused on the alpha-tocopherol form of the vitamin. However, other forms of vitamin E, in particular gamma-tocopherol may have unique mechanistic characteristics relevant to lung cancer prevention. In an ongoing study of 1,088 incident lung cancer cases and 1,414 healthy matched controls, we studied the associations between 4 tocopherols (alpha-, beta-, gamma-, and delta-tocopherol) in the diet and lung cancer risk. Using multiple logistic regression analysis, the adjusted odds ratios (OR) and 95% confidence intervals (CI) of lung cancer for increasing quartiles of dietary alpha-tocopherol intake were 1.0, 0.63 (0.50-0.79), 0.58 (0.44-0.76) and 0.39 (0.28-0.53), respectively (p-trend < 0.0001). For dietary intake of beta-tocopherol, the OR and 95% CI for all subjects were: 1.0, 0.79 (0.63-0.98), 0.59 (0.45-0.78) and 0.56 (0.42-0.74), respectively (p-trend < 0.0001). Similar results for dietary gamma-tocopherol intake were observed: 1.0, 0.84 (0.67-1.06), 0.76 (0.59-0.97) and 0.56 (0.42-0.75), respectively (p- trend = 0.0002). No significant association between delta-tocopherol intake and lung cancer risk was detected. When the 4 tocopherols were summed as total tocopherol intake, a monotonic risk reduction was also observed. When we entered the other tocopherols in our model, only the association with dietary alpha-tocopherol intake remained significant; i.e., increasing intake of dietary alpha-tocopherol accounted for 34-53% reductions in lung cancer risk. To the best of our knowledge, this is the first report of the independent associations of the 4 forms of dietary tocopherol (alpha-, beta-, gamma- and delta-tocohperol) on lung cancer risk. Given the limitations with case-control studies, these findings need to be confirmed in further investigations.
Carman S, et al. Vitamin E intake and risk of esophageal and gastric cancers in the NIH-AARP Diet and Health Study. Int J Cancer. 2009 Jul 1;125(1):165-70.
We investigated the association of dietary alpha-tocopherol, gamma-tocopherol and supplemental vitamin E intake with the risk of esophageal squamous cell carcinoma (n = 158), esophageal adenocarcinoma (n = 382), gastric cardia adenocarcinoma (n = 320) and gastric noncardia adenocarcinoma (GNCA; n = 327) in the NIH-AARP Diet and Health Study, a cohort of approximately 500,000 people. Data on dietary and supplemental vitamin E intake were collected using a validated questionnaire at baseline and were analyzed using Cox regression models. Intakes were analyzed as continuous variables and as quartiles. For dietary alpha-tocopherol, we found some evidence of association with decreased esophageal squamous cell carcinoma and increased esophageal adenocarcinoma risk in the continuous analyses, with adjusted hazard ratios and 95% confidence intervals of 0.90 (0.81-0.99) and 1.05 (1.00-1.11), respectively, per 1.17 mg (half the interquartile range) increased intake. However, in quartile analyses, the p value for trend was nonsignificant for both these cancers. There was no association between dietary alpha-tocopherol and gastric cardia adenocarcinoma or GNCA. We observed no statistically significant associations with gamma-tocopherol. For supplemental vitamin E, the results were mainly null, except for a significantly lower risk of GNCA with higher doses of supplemental vitamin E, which were 400 and 800 IU. An increase of 71 mg/day (half the interquartile range) in supplemental vitamin E had an hazard ratio (95% confidence interval) of 0.92 (0.85-1.00) and the p value for trend in the quartile analysis was 0.015.
Goodman GE, et al. The association between lung and prostate cancer risk, and serum micronutrients: results and lessons learned from beta-carotene and retinol efficacy trial. Cancer Epidemiol Biomarkers Prev. 2003 Jun;12(6):518-26.
beta-Carotene and Retinol Efficacy Trial is a nationwide chemoprevention trial that recruited 18,314 high-risk individuals to test the effect of supplemental beta-carotene and retinol on lung cancer incidence. In this report, we conducted a prospective nested case-control study of the association between serum carotenoids, retinoids, and tocopherols on both lung and prostate cancer incidence. Prerandomization serum samples were selected from 278 lung cancer cases and 205 prostate cancer cases, and 483 controls matched by high-risk population, study center location, age, sex (lung cancer only), smoking status, and year of randomization. Carotenoids, retinoids, and tocopherols were analyzed by high-performance liquid chromatography. Endpoints were confirmed by pathology review (lung cancer) or review of the pathology report (prostate cancer). In the control-only population, there was a significant association between tobacco use and serum micronutrient concentration. Current smokers compared with former smokers had lower mean levels of all of the micronutrients tested with zeaxanthin, beta-cryptoxanthin, alpha-carotene, alpha-tocopherol, retinol, and retinyl palmitate reaching statistical significance at P = 0.05. In the overall population, the mean serum concentrations of all of the micronutrients except gamma-tocopherol were lower for lung cancer cases than controls. Statistically significant trends across quartiles were observed in lutein (P = 0.02), zeaxanthin (P = 0.02), and alpha-tocopherol (P = 0.03). The carotenoid findings in the overall population were because of the strong inverse association between serum micronutrients and lung cancer in females. Statistically significant odds ratios (ORs) comparing 4(th) to 1st quartiles in the female population were seen in lutein [OR, 0.31; confidence interval (CI), 0.13-0.75], zeaxanthin (OR, 0.31; CI, 0.12-0.77), and beta-cryptoxanthin (OR, 0.34; CI, 0.14-0.81). For prostate cancer, mean serum concentrations were lower in cases for all of the nutrients except alpha-carotene. Only for alpha-tocopherol (P(trend) = 0.04) were the findings statistically significant. There was no statistically significant association between serum carotenoids and prostate cancer. Our findings provide additional support for the association between physiological levels of dietary micronutrients and cancer incidence.
See also: http://orthomolecular.org/resources/omns/v07n11.shtml
One of the takeways you might get from looking at what I've presented is that the most important factor in optimizing the effects of nutrients is the dose that is used. Higher doses generally work better.
That's why every day I take 800 IU of vitamin E, as d-alpha tocopherol, plus 300 mg of gamma tocopherol, which is just as important as the d-alpha tocopherol form of vitamin E.
For an in-depth look at vitamin and mineral doses, their safety and effective ranges, see: http://www.michaelmooney.net/safety.pdf