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Up | Skin Cancer | Why Diet? | Step One | Step Two | Step Three | Step Four | Sources | Acknowledgements | About The Authors | Appendix I | Appendix II | Appendix III | Appendix IV | Appendix V | Appendix VI

 

Low Fat Dietary Guide To Aid In The Management Of Skin Cancer

Why Diet?

The first indication that dietary fat could influence the development of UV-induced skin cancer came in 1939. The researchers reported  that  when  experimental  animals  were  fed  a  diet  that  contained  a  high  fat  level,  the  time for cancer development after exposure to  UV rays was significantly shortened. Although there was some interest in this area of investigation in the early 1940’s, this research lead was not actively pursued for another 45 years.  In  the  1980’s  American  and  Australian  researchers  confirmed,  in  closely-controlled  nutritional  studies,  that  the  level  and  nature  of  dietary  fat  could  exert  profound  influence  on  the  course  of  experimental  UV-induced  skin  cancer.

Subsequently, this influence of dietary  fat was shown to occur principally after a cancer  causing  dose  of  UV  had  already  been  administered. Further, by switching from a high- fat to a low-fat diet shortly after administration  of the cancer causing dose of UV, the influence  of high-fat intake in provoking the appearance  of  skin  cancers  could  be  significantly  diminished.  It  is  known  that  among  persons  who  have  had  at  least  one  skin  cancer,  28%  are  at  risk  to  have  another  within  the  following  two  years.  Thus, the experimental findings suggested that by adopting a low-fat diet, skin cancer patients might reduce their risk for developing new skin cancers and provided the basis for undertaking a clinical trial to test this hypothesis. 

Skin  cancer  patients  were  assigned  to  one  of  two  groups  in  the  study. In  the  first  group  no  changes  in  eating  habits  were  introduced,  allowing  patients  to  continue  to  consume  about  36-40% of their total calorie intake as fat.  Patients  in  the  other  group  were  instructed  in  adopting  low-fat  eating  habits  with    the    goal   of  reducing  the  percent  of  calories from  fat to around 20%. The potential benefit for this low-fat intervention became apparent early in the clinical study. A clear and significant difference  in  the  number  of  actinic  keratoses  (pre-malignant  skin  lesions  that  result  from  excessive  sun  exposure  and  that  sometimes  develop  directly  into  skin  cancer)  occurred  between  patients  who  continued  to  consume  diets high in fat and those who adopted low- fat  eating  habits.  Patients  consuming  high  levels of fat were found to be at nearly five- times greater risk of developing one or more  actinic  keratosis  during  the  2-year  period  of  the   study than   patients   in   the   low-fat  “intervention”  group.  Further,  after  115  patients had completed the study, a similar, dramatic  effect  on  non-melanoma  skin  cancer  (both  basal  and  squamous  cell  carcinoma)  occurrence was observed.

Overall,  the  methods  for  controlling  fat  intake permitted considerable flexibility in food  choices since foods with little or no fat were  emphasized,  although  higher-fat  foods  could  be included as long as one did not go beyond  the  recommended  fat gram  goal (the grams  of  fat  a patient  could  consume  which  would  not exceed 20% of his or her total daily calorie intake from fat). Thus, a singular strategy  of reducing fat intake, with the goal of 20%  of calories from fat, could be an effective aid  in  the  management  and  prevention  of  non- melanoma  skin  cancer  and  pre-malignant  actinic  keratosis.  The question now remains, “How do I follow such a diet?”


Copyright 2005.  All rights reserved.  Homer S. Black, PhD, Department of Dermatology, Baylor College of Medicine, One Baylor Plaza, Houston, TX  77030
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