754

Correspondence

Dietary Strategies for Cancer Prevention

I have just read the supplement reporting the proceedings of the September 1992 American Cancer Society National Con- ference on Cancer Prevention and Early Detection. This is a timely and valuable addition to the literature.

I am concerned, however, about the content of the con- clusion of Bal and Foerster's article.' They state that, with resources dedicated to dietary modification in the general pop- ulation, there would be potential savings of 300,000 new cancer cases, 160,000 deaths, and $25 billion in associated costs.

Current scientific evidence simply does not support this clearly inflated and overoptimistic estimate of the capability of dietary modification to influence cancer risk. Promulgation of unrealistic expectations from any intervention results in skepticism in the populations being approached and loss of confidence in the "authorities" who make the intervention recommendations. 1 would hope that the American Cancer Society will not base diet recommendations on uncritical esti- mates of risk reduction or on current policy statements, but will define sound advice based solely on hard, scientifically reliable clinical data. This may result in very soft recommenda- tions. If so, perhaps strengthening the links between groups working with dietary change to affect other risks such as car- diovascular disease would be valuable. I remember an apho- rism from my teacher and colleague Kenneth B. Olson, M.D. "To be positive is to be wrong in a loud voice!" Let's be more careful and conservative about what we say about diet and cancer prevention.

Reference

1. Bal DG, Foerster SB. Dietary strategies for cancer prevention. Cancer 1993: 72(Suppl):1005-10.

John Horton, M.B., Ch.B., F.A.C.P. Division of Medical Oncology and Hematology Department of Internal Medicine University of South Florida H. Lee Moffitt Cancer Center and Research Institute Tampa, Florida

This is in response to Dr. Horton's letter about our article in the August 1, 1993, Cancer supplement.' We are indebted to Dr. Horton on several counts.

First, we do appreciate his caution that hyperbole de- tracts from any intellectual position. We will explain below how we derived our numbers.

Second, he illustrates with his letter the very essence of our opening gambit, that is "The history of cancer prevention and control has been characterized by decades of delay be- tween the acquisition of new knowledge and its widespread application." With a sense of deja vu we hearken back to whence we were in tobacco control a couple of decades ago, due to the need for us to be careful and conservative about what we say about tobacco and prevention. Having initially listened to the naysayers at that time, we set the tobacco use prevention and cessation movement back considerably, at the cost of innumerable lives and billions of dollars. Ironically, the tobacco industry and their academic apologists in the To- bacco Institute still staunchly defend tobacco's innocence in the causation of disease.

Third, we agree with Dr. Horton that using some of the better documented dietary data linking this risk factor with other diseases such as cardiovascular disease would be valu- able. In fact, the federal government did just that in their 1990 dietary guidance policy, which synthesized optimum dietary change for reducing one's risk to multiple chronic diseases. Again, there is ample precedence for this in that the American Cancer Society, American Lung Association, and American Heart Association work together on tobacco issues.

Finally, concerning the derivation of our numbers: Our numbers were premised on several presumptions. Firstly, we used Doll and Peto's much-quoted statistic that 35% of cancers are related to diet.' As the citation on this was the journal of the National Cancer Institute, we were gratified at having Dr. Pet0 himself verify its validity at the very meeting, the proceedings of which are summarized in this special sup- plement to Cancer. Furthermore, the base numbers to which we conservatively chose to apply this percentage are statistics from the Surgeon General's Report on Nutrition and He.alth.3 Taking this 35% and applying it to the total costs of cancer ($72 billion), new cases (900,000), and deaths (475,000) illus- trates our quoted numbers, that is, $25 billion, 315,000 fewer new cases, and 166,000 fewer deaths.

Had we elected to use the equivalent Cancer Facts and Figures 1992 estimates, that is, $104 billion, 1,130,000 new cases, and 520,000 deaths, the corresponding figures using the 35% statistic would be $36 billion in savings, 395,000 fewer new cases, and 182,000 fewer death^.^ Thus, if any- thing, we could equally be accused of erring on the side of being cautious and conservative.

In closing, we respectfully submit that in view of the in- creasing medical and financial burden of cancer, taken in con- cert with the marked differences in cancer incidence and mor- tality rates among racial minorities (some of which has been attributed to dietary differences), to refrain from making strong cancer prevention dietary recommendations (coinci-

Correspondence 755

dentally identical to those for cardiovascular disease) would indeed justify the skepticism and even the scorn of the special populations whom we are assiduously attempting to court and affect. The parallel to the debate about the tobacco “pseudo issue” decades ago is both uncanny and troubling.

References

1.

2.

Bal DG, Foerster SB. Dietary strategies for cancer prevention. Cancer 1993; 72(SuppI):1005-10. Doll R, Peto R. The causes of cancer: quantitative estimates of avoidable risk in the United States today. / N a f I Cancer Irisf 1981; 66: 1191-308. C.S. Department of Health and Human Services. The Surgeon General’s report on nutrition and health. DHHS (PHS) pub. no. 88.520210. Washington, DC: US. Government Printing Office, 1988.

4 . American Cancer Society. Facts and figures-1992. Atlanta: American Cancer Society, 1992.

3.

Dileep G. Bal, M.D., M.S., M.l’.i-I. Cancer Control Branch Susan B. Foerster, M.P.H., R.D. Nutrition and Cancer Prevention Program State of California -Health and Welfare Agency Department of Health Services Sacramento, California

Prognostic Factors of Malignant Mesothelioma of the Pleura

I read with interest the study and review of prognostic factors of malignant mesothioma of the pleura by Dr. Manzini and colleagues.' In this context, 1 would like to draw your atten- tion to some recent data relevant to the subject.

Dejmek and associates studied DNA ploidy patterns in 37 cases of malignant pleural mesothelioma.’ The prognosis was found to be much better in the 4196 of patients with a near-diploid/polyploid pattern than in the remaining 59% with highly aneuploid tumors. Another group of investigators examined 5-phase fraction in 51 patients with malignant me- sotheliomas and found that 5-phase fraction significantly correlated with prognosis (P = 0.039).3 Patients with a low S-phase fraction had almost double the survival duration as those with a high 5-phase fraction.

One study determined the effect of chromosome num- bers (determined by cytogenetic analysis) on survival in 34 patients with diffuse malignant pleural mes~thelioma.~ Me- dian survival with mean chromosome number (ME) greater than 46 was 13 months, ME less than 46 was 26 months and ME equal to 46 (the normal number) was 31 months (p =

0.0007). The investigators concluded that the additional chro- mosomal material may be a marker of enhanced gene expres- sion and more aggressive tumor behavior. Finally, pleural fluid characteristics were determined in 26 patients with ma- lignant me~othelioma.~ Patients with pleural fluid pH less than 7.30 had decreased mean survival. Survival from time of initial thoracentesis also directly correlated with reduced pleural fluid/serum glucose ratios, but not to protein or lactic dehydrogenase levels.

The above data, in conjunction with Manzini et al.’s study and review, helps better define the prognostic variables of malignant pleural mesothelioma.

References

1. Manzini VDP, Brollo A, Franceschi S, De Matthaeis M, Talamini R, Bianchi C. Prognostic factors of malignant mesothelioma of the pleura. Cancer 1993; 72:410-7.

2. Dejmek A, Stromberg C, Wikstrom B, IIjerpe A. Prognostic im- portance of the DNA ploidy pattern in malignant mesothelioma of the pleura. Anal Quarit Cytol Hisfol 1992; 14:217-21.

3. Pyrhonen S, Laasonen A, Tammilehto L, Rautonen J , Anttila S, Mattson K, et al. Diploid predominance and prognostic signifi- cance of S-phase cells in malignant mesothelioma. Eur / Cancer

4. Tiainen M, Rautonen J , Pyrhonen S, Tammilehto L, Mattson K, Knuutila S. Chromosome number correlates with survival in pa- tients with malignant pleural mesothelioma. / Genrt i rs and Cylo- genefics 1992; 62:21-4.

5. Gottehrer A, Taryle DA, Reed CE, Sahn SA. I’leural fluid analysis in malignant mesothelioma: prognostic implications. Clirsf

1991; 27: 197-200.

1991; 100:1003-6.

Ajay Anand, M.D. New England Deaconess tlospital Division of Hematology and Oncology Boston, Massachusetts

Nausea Induced by Mental Images of Chemotherapy

The article by Dr. Redd and colleagues regarding the role of classical conditioning in chemotherapy-induced anticipatory nausea made interesting and informative reading.’ The au- thors stated that although nausea may be secondary to anxi- ety, nausea and anxiety may not always be related phenom- ena. In this context, I would like to draw their attention to a recent study that evaluated the role of classical conditioning on chemotherapy-related psychologic d is t res2 Sixty-six pa- tients given adjuvant chemotherapy for breast cancer were assessed in the clinic on the first day of every chemotherapy cycle and at home 3-5 days before their final cycle. Consider- able psychologic distress was found during the course of che- motherapy, especially before the first infusion. In the setting before the last chemotherapy cycle, psychological distress was much higher in the clinic than in patients’ homes. The investigators found that, in keeping with classical condition- ing, psychological distress did not increase over the days be- fore therapy but increased abruptly on return to the clinic. This finding, in conjunction with the authors’ study, may indi- cate that nausea and psychological distress both result from classical conditioning and may be epiphenomena. This would explain the data that anticipatory nausea does not always di- rectly result from high levels of anticipatory anxiety alone.

Another group evaluated the role of low-dose alprazo- lam (0.5-2 mg/day) in addition to a psychological support program in the prevention of anticipatory nausea in the che- motherapy setting3 In a double-masked, placebo-controlled study of 56 women undergoing adjuvant chemotherapy for