American Fitness Professionals & Associates

From Dr. John McDonald Senior Scientist

On January 18, 1996, the National Cancer Institute (NCI) announced that it was stopping the Beta Carotene and Retinol Efficacy Trial (CARET) and reporting on the Physicians’ Health Study (PHS), two studies in which beta carotene was given to some participants. Since this announcement was in the form of a press release and press conference there is limited data available from which to make a critical analysis. The way it was handled makes it difficult for us to know exactly what the studies entailed, therefore we are forced to rely on mass media accounts of the press conference and the press release itself.

The press accounts of this news conference range from the National Enquirer’s sensational headline, “High death rate ends beta carotene study” to the Vancouver Sun’s “Studies cast doubt on beta carotene craze.” These headlines are sensational because they attract readers and sell newspapers. The mass media is a profit industry and the competition is fierce. Unfortunately, when hysteria prevails logic and objectivity suffer. Inaccurate claims and sensational stories are believed by many people who are not prepared by education or training to critically analyze the information. The lay public allows their actions to be governed by inaccurate news accounts and premature conclusions which can actually increase the risk to their health.

Two studies were the subject of the press conference. The first study, CARET, involved 17,000 participants, with smokers, former smokers and people at high risk of lung cancer due to their exposure to asbestos. The object of this study was to assess the effectiveness of an intervention using beta carotene and vitamin A on the incidence of lung cancer. The second study, the PHS study, involved 22,000 physicians (PHS) and included some smokers. This study was completed last month. The object of the PHS study was to assess the effect of beta carotene on the incidence of all cancers and heart disease.

The CARET Study

CARET included 30 mg of beta carotene and 25,000 IU of vitamin A per day for each subject. USANA does not use vitamin A. Instead, we use beta carotene because it is converted to vitamin A in the body by the action of the enzyme Beta Carotene 5,5′ dioxygenase, but at non-toxic levels.(1) With 25,000 IU of vitamin A and 30 mg of beta carotene being given on a daily basis, one would expect this chronic intake to result in some toxicity.

The investigators saw an increase in the number of lung cancer cases in the study but are careful to make the point that the increase is too small to be considered statistically significant. This study agrees closely with the 1994 study in Finland(2) also known as the Alpha Tocopherol Beta Carotene (ATBC) Study. But in the ATBC study vitamin E was used as well as beta carotene so that it is not exactly like CARET. ATBC also showed the highest cancer rates occurred in smokers who drink the most alcohol, which raises the question of whether or not the investigators factored in the alcohol consumption of the participants in CARET.

These are the only two studies that imply, but do not prove, that beta carotene may be harmful to smokers, especially in light of the fact that PHS shows that smokers were not adversely affected by beta carotene. Another incentive for smokers to quit is that CARET found a 20% reduction in the overall cancer rate for former smokers.

The NCI press release makes the point that, “In both the ATBC Study and CARET, participants with the highest levels of beta carotene in the their blood, measured before the study began, went on to have fewer lung cancers.” These facts reinforce the notion that intake of adequate levels of the carotenoids, including beta carotene, provide a measure of protection against some cancers.

Physician’s Health Study

PHS had 22,000 physicians enrolled for a period of 12 years. It found no evidence of harm in either smokers or nonsmokers from taking 50 mg of beta carotene every other day, nor any protection against cancer or heart disease. This data is in agreement with other studies that reveal no adverse effects of high doses of beta carotene. The Council for Responsible Nutrition in its press release of January 18, 1996 points out that, “Animal studies indicate that beta carotene is one of the least toxic substances known.” USANA agrees.

Analysis

Gina Kolata, the author of the America Online press account said, “Federal health officials said they hoped that this would spell the end of the beta carotene fad. The idea that a simple supplement capsule might fend off cancer and other diseases, they said, has simply been proven too good to be true.”

In my opinion, this is not the end of beta carotene but rather the beginning of another step towards better understanding of how beta carotene works. There is evidence that beta carotene:

Reduces peroxidation of Low Density Lipoprotein (LDL) in smokers. (3) Peroxidation of LDL is widely considered to be a risk factor in coronary heart disease (4);

Reduces the risk of cataracts, together with other carotenoids (5);and reduces the risk of stomach cancer. (6)

In a recent review by van Poppel and Goldbohm(7) the authors observed that of the 14 case control studies reported for lung cancer: “…these studies are remarkably consistent in indicating an association of high intakes of beta carotene with a 10-70% reduced risk.”

Further they found that:

All studies for stomach cancer show a reduced risk with high intakes of beta carotene.

For esophageal cancer all case-control studies reported decreased risk with higher intakes of beta carotene with a statistically significant difference in four of the eight studies.

Other cancer sites show inconsistent results with virtually no effect in breast cancer.

The favorable results reported in this review article are supported by other studies showing the benefits of beta carotene including the large Chinese study on stomach cancer. (8)

Even though the studies covered by the NCI press conference do not support the position that beta carotene can, by itself, reduce the risk of cancer, they do not rule out the probability that it is one vital component among others found in nutritional supplements that reduce the risk of cancer. Both epidemiologic and animal studies suggest that carotenoid intakes, that result in increased blood levels, are protective against a variety of chronic degenerative diseases, including heart disease, cancers at certain sites and cataracts. Animal studies using beta carotene (and other antioxidant nutrients) indicate that the protective effects occur in the early stages of cancer development.

Cancer scientists agree that the development of lung cancer is a 20- to 25-year process. Therefore, in a 12-year clinical trial, such as the PHS effort, the research subjects who developed diagnosed lung cancer must have been in the development process before the study began. This research indicates that beta carotene has no beneficial effect when given in the mid to late stages of cancer development. The current CARET and PHS studies similarly show that there is no beneficial effect of beta carotene when given in the mid to late stages of cancer development. However, no responsible scientist has ever suggested that beta carotene can cure lung cancer after its initiation. Furthermore, these studies do not rule out an effect in preventing cancer before it starts. The overall beneficial properties of antioxidants (including beta carotene) are well documented by more than 200 scientifically valid studies.

Here are some interesting quotations from the NCI news conference along with my comments.

NCI Director Richard Klausner said, “There is one very clear message: the only way to reduce your (cancer) risk is to stop smoking.”

USANA could not agree more since smoking is a major source of free radicals and damages the skin, eyes and lungs.

Charles Hennekens of Harvard who led the PHS study said, “A beta carotene supplement neither substitutes for a good diet nor compensates for a bad one.”

USANA agrees since there is no supplement that will take the place of a good diet, which is why they are called supplements - they supplement the diet.

Dr. Gilbert Omenn, Dean of Public Health at the University of Washington said, ” ..its results were not definite proof that beta carotene is harmful. But the reason it was halted, he said, is that its findings were reminiscent of those in the Finnish study.”

The researchers must know that the lag period is 20-25 years between the initiation of lung cancer and its diagnosis so one would not expect to see any difference between the placebo and test groups for another 12 to 15 years.

Conclusion

The current studies do not present enough evidence that anyone should give up the benefits of beta carotene. Smokers should be aware of the non-statistically significant rise in cancer cases when beta carotene was used together with 25,000 IU of vitamin A. If it turns out that the group taking the beta carotene and vitamin A, and that’s a big IF, did in fact have a biologically significant increase in cancer cases then the question is, was it the:

A.Beta carotene B.Vitamin A or C.A combination of the two that was responsible for the rise?

We question the validity of the studies and whether the conclusions are valid and think that smokers have nothing to fear from taking beta carotene. Our advice to smokers who are worried about the effects of beta carotene and vitamin A, is to take a supplement that does not contain high doses of beta carotene and has a maximum of 10,000 IU of vitamin A.

The USANA Essentials provide about one third of the amount of beta carotene used in the CARET, although the dose is still more than the minimum RDA requirement, it is not a mega dose.

USANA is continuing to research the reported findings of CARET and PHS. Updates will be provided as the scientific data becomes available.

References

1.Rothman, K. J., Moore, L. L., Singer, M. R., Nguyen, USANA.-S. D. T., Salvatore, M., and Milunsky, A. (1995)  The New England Journal of Medicine 333 (November (21)), 1369-73
2.Group, A.-T. B. (1994) New England J Med 330(15), 1029-1081
3.Allard, J. P., Royall, D., Kurian, R., Muggli, R., and Jeejeebhoy, K. N. (1994) Am J Clin Nutr 59, 884-90 4.Nyyssonen, K., Porkkala, E., Salonen, R., Korpela, H., and Salonen, J. T. (1994) European Journal of Clinical Nutrition 48, 633-642
5.Taylor, A., Jacques, P. F., and Epstein, E. M. (1995) Am J Clin Nutr 62, 1439S-47S
6.Hansson, L., Nyren, O., and Bergstrom, R. (1994) Int J Cancer 57, 638-44
7.Van Poppel, G., and Goldbohm, A. R. (1995) Am J Clin Nutr 62(suppl), 1393-1402S
8.Blot, W. J. (1993) Journal of the National Cancer Institute 85(18), 1483-92