© 2005 Oxford University Press
CORRESPONDENCE |
RESPONSE: Re: Cancer as a Risk Factor for Long-Term Cognitive Deficits and Dementia
Affiliations of authors: Department of Psychology, University of Southern California, Los Angeles, CA (LHH, BEM, NLP, MG); Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden (PH, PL, NLP, MG); Department of Psychology, Goteborg University, Goteborg, Sweden (BJ)
Correspondence to: Beth E. Meyerowitz, PhD, Department of Psychology, University of Southern California, Los Angeles, CA 90089-1061 (e-mail: meyerow{at}usc.edu).
Grant points out that cancer and dementia share several dietary and lifestyle risk factors. Although the analyses reported in our recent article (1) did not control for possible shared risk factors such as high-fat diets because we used a co-twin control design and twins tend to be similar in their eating and other habits, there was considerable control for diet and other lifestyle factors built into the design itself. Further, there is reason to believe that diet alone cannot account for the association between cancer and cognitive dysfunction. The most convincing studies in this respect are those that randomly assigned patients to receive different cancer treatments and found poorer cognitive performance among those randomized to some treatments than that found with other treatments; for example, to high-dose versus standard-dose chemotherapy (2) or to chemotherapy versus radiation (3). It seems unlikely that dietary and lifestyle covariates could be fully responsible for the adverse cognitive effects that were observed in these studies. It also seems improbable that the experience of "chemobrain" that patients report following their cancer treatment (4) is an effect of diet rather than a side effect of chemotherapy. In short, it seems likely that a major explanation for cognitive sequelae of cancer is cancer treatment.
We agree that there is provocative overlap in some of the potentially protective dietary factors that have been recommended in relation to cancer and to dementia, e.g., low fat (except for omega-3 fatty acids) and high intake of dark-skinned fruits and vegetables (5). We also note that in a recent survival analysis, Roe et al. (6) report that people with Alzheimer disease have a slower rate of subsequently developing cancer than a nondemented group; this finding raises more unresolved questions. Clearly, research is needed to understand the multiple mechanisms that are likely to play a role in the link between cancer and its treatments and later cognitive dysfunction, as we have noted previously (1).
REFERENCES
(1) Heflin LH, Meyerowitz BE, Hall P, Lichtenstein P, Johansson B, Pedersen NL, et al. Cancer as a risk factor for long-term cognitive deficits and dementia. J Natl Cancer Inst 2005;97:854–6.
(2) van Dam FS, Schagen SB, Muller MJ, Boogerd W, vd Wall E, Droogleever Fortuyn ME, et al. Impairment of cognitive function in women receiving adjuvant treatment for high-risk breast cancer: high-dose versus standard-dose chemotherapy. J Natl Cancer Inst 1998;90:210–8.
(3) Kaasa S, Olsnes BT, Mastekaasa A. Neuropsychological evaluation of patients with inoperable non-small cell lung cancer treated with combination chemotherapy or radiotherapy. Acta Oncol 1988;27:241–6.[Medline]
(4) Huff C. Chemobrain: the hunt for answers. Monitor Psychol 2005;36:28.
(5) Alzheimer's Association. Adopt a brain-healthy diet. Available at: http://www.alz.org/maintainyourbrain/healthydiet.asp.
(6) Roe CM, Behrens MI, Xiong C, Miller JP, Morris JC. Alzheimer disease and cancer. Neurology 2005;64:895–8.
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J Natl Cancer Inst 2005 97: 1549.
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