Qualified Health Claim That Tea May Reduce Risk of Cardiovascular Disease Rejected by FDA

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 9 No. 4 • December 2006

Qualified Health Claim That
Tea May Reduce Risk of Cardiovascular Disease
Rejected by FDA

The FDA rejected a petition by the Japanese company Ito En Ltd. and its US subsidiary Ito En, Inc., which produce and market green tea, for a qualified health claim that daily consumption of at least 5 fluid ounces of green tea may reduce a number of risks associated with cardiovascular disease. Though the consumption of a mere 5 ounces of tea seems a bit small on which to base a claim, the FDA’s “review” of the data on the potential beneficial effects of tea on cardiovascular disease was ludicrous: the FDA claimed “that there is no credible evidence to support a relationship between consumption of green tea or green tea extract and a reduced risk of CVD [cardiovascular disease].” [Emphasis added]

We do not intend to do a review of the literature here, nor a complete analysis of the FDA’s methodology. We would simply like to note that the agency first threw out all data derived from cell-culture, mechanistic, and animal-model studies. They also threw out meta-analyses and government reports. (!) The agency winnowed down the body of data to only four human observational studies and four human intervention studies. The claim that there is “no credible evidence” is simply a lie, as the agency conveniently ignored most of the scientific literature on tea.

There was, for example, credible evidence in one very large epidemiological (observational) study published in the Journal of the American Medical Association.1 In the Ohsaki National Health Insurance Cohort Study, a study of 40,530 Japanese adults aged 40 to 79 years, without a history of stroke, coronary heart disease, or cancer at baseline, subjects were followed for up to 11 years for all-cause mortality and for up to 7 years for cause-specific mortality.

Green tea consumption was inversely associated with mortality due to all causes and due to cardiovascular disease. The strongest inverse association was found for stroke mortality. Cancer mortality was not significantly different from 1.00 (that is, from no tea consumption) in all green tea categories.

A few other examples include: habitual tea consumption for a year or more significantly reduced the risk of developing hypertension in 1507 Chinese men and women;2 green and black teas inhibited atherosclerosis in a hamster model by improving levels of LDL, lipid peroxides, and fibrinogen;3 there was reversal of endothelial dysfunction in patients with coronary artery disease or risk factors;4,5 and green tea EGCG induced programmed cell death in proliferating bovine aortic vascular smooth muscle cells (a mechanism for the development of atherosclerotic plaques).6 The search for mechanisms has resulted, as is often the case, in contradictory results. For example, a recent paper did not find changes in plasma antioxidant capacity or reductions in 8-hydroxy-2'-deoxyguanosine or urinary 8-isoprostane levels of human consumers of black tea.7 However, in the latter paper, the authors concluded that tea consumption has a strong beneficial effect on endothelial function and “we must consider the possibility that noncatechin components of tea may account for the observed benefit.” They suggest looking further at the polymeric polyphenols found in black (and also green) tea, as they may more potently increase endothelial nitric oxide synthesis compared to polyphenol monomers.

The FDA is holding foods and dietary supplements to the same standards as prescription drugs, despite their lack of statutory authority to do so. An editorial in a recent American Journal of Clinical Nutrition8 included this enlightening analysis of the difficulty with the FDA’s approach to judging nutrients by drug standards:

The randomized controlled trial (RCT), which has become the gold standard for establishing the efficacy of pharmacologic agents, is poorly suited to the evaluation of nutritional effects, a fact that I believe many have been reluctant to acknowledge. Several important differences between nutrients and drugs lead to this conclusion. In addition to long latency and multifactorial causation for the diseases concerned, nutrients and drugs differ in three crucial respects. First, whereas a drug-free state exists that can be contrasted with a drug-added state, with respect to nutrients, the only contrast can be between different intakes, both usually well above zero. [Comment: Even if you drink no tea, you will still be ingesting catechins and other constituents of tea from other foods.] Second, most nutrients have what is known as threshold behavior, i.e., some physiologic measure improves as intake rises up to a level of sufficiency, above which higher intakes produce no additional benefit. Third, most nutrients have beneficial effects on multiple tissues and organ systems, and thus a focus on a single or ‘primary’ outcome measure, which is favored by RCTs, is often procrustean. As a consequence of the second point, investigators using the RCT design must contrast two groups of subjects, at least one of which has a distinctly inadequate intake of the nutrient concerned. Failure to do that, as occurred in the calcium arm of the Women’s Health Initiative (WHI), constitutes an invalid test of the corresponding hypothesis. However, the assignment of subjects to an intake that is inadequate by current standards, for the span of time required to produce the necessary difference in serious outcomes, raises significant and probably insurmountable ethical problems.

From the FDA’s point of view, however, the RCT can be used as a convenient and stealthy way to discount nearly all studies of likely beneficial effects of nutrients until some hypothetical future certainty, a certainty that will never arrive; hence, this allows the FDA to reject all nutrient health claims other than those few by favored “clients” or as forced by very expensive lawsuits in a legal climate where courts are likely to defer to agencies.


  1. Kuriyama et al. Green tea consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: the Ohsaki Study. JAMA 296(10):1255-65 (2006).
  2. Yang et al. The protective effect of habitual tea consumption on hypertension. Arch Intern Med 164:1534-40 (2004).
  3. Vinson et al. Green and black teas inhibit atherosclerosis by lipid, antioxidant, and fibrinolytic mechanisms. J Agric Food Chem 52:3661-5 (2004).
  4. Duffy et al. Short and long term black tea consumption reverses endothelial dysfunction in patients with coronary artery disease. Circulation 104:151-6 (2001).
  5. Hodgson et al. Regular ingestion of black tea improves brachial artery vasodilator function. Clin Sci 102:195-201 (2002).
  6. Hofmann and Sonenshein. Green tea polyphenol epigallocatechin-3-gallate induces apoptosis of proliferating vascular smooth muscle cells via activation of p53. FASEB J Feb 5 2003.
  7. Widlansky, Duffy, et al. Effects of black tea consumption on plasma catechins and markers of oxidative stress and inflammation in patients with coronary artery disease. Free Rad Biol Med 38:499-506 (2005).
  8. Heaney. Nutrition, chronic disease, and the problem of proof. Am J Clin Nutr 84:471-2 (2006).

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