PCa Commentary
 

Currently in the United States about 1.8 million men are survivors of prostate cancer treatment. Obesity in the US is on a steep increase. If the above thesis is correct, then there may be a useful counseling message for clinicians to pass on to obese PC survivors. Two studies regarding this thesis appear in the JCO, February 1, accompanied by a thoughtful editorial (www.jco.org/cgi/content/full/22/3/395?etoc).

Although no consistent relationship as yet has been found between obesity and prostate cancer incidence, these two studies demonstrate that obesity, expressed in terms of body mass index (BMI > 35 Kg/m2 in Freedland, and > 30 Kg/m2 in Amling), is associated with an increase in prostate cancer mortality. Obese men present with higher Gleason scores at diagnosis and have a shortened PSA recurrence-free survival post radical prostatectomy.

Freedland et al. studied the clinicopathological and biochemical outcome post radical prostatectomy of 1106 men and found that a BMI > 35 kg/m2 "significantly predicted biochemical failure [median follow-up 33 months] after RP (P = .012). "Obese patients had higher biopsy and pathological grade tumors (P < .001)." In their study, PSA, Gleason score, and BMI were each independent predictors of time to PSA recurrence. They noted that obesity doubled in their RP patients in the past 10 years.

mling et al. studied 3162 men post prostatectomy and compared the 19% obese men (> 30 kg/m2) with those having a lower BMI and also found that "obesity is associated with higher grade cancer [P < .001] and higher recurrence rates after RP [P = .003]". They argue that their data supports the hypothesis that "obesity is associated with the progression of latent to clinically significant prostate cancer". Both studies found that "black men have higher recurrence rates and greater BMI than white men".

The accompanying editorial cites the Cancer Prevention Study II finding that "men with BMI > 30 kg/m2 had a 20% to 34% increased risk of prostate cancer death compared with men with BMI 18.5 to 24.9 kg/m2." They further conjecture that basic science gives the JCO study findings plausible theoretical basis by pointing out that obesity is associated with higher insulin and insulin-like growth factor 1 levels (both are mitogens); and that the lower testosterone levels in obese men may be a cause of higher grade prostate cancer.

How should we clinicians use this information? To date no human studies have shown that weight reduction post diagnosis and treatment slows the rate of prostate cancer progression. (A recent study of mice reported in Cancer Research, Feb 2004, however, did find evidence that a low fat diet prolonged tumor latency to 18 vs. 9 weeks and prolonged survival compared to a standard diet.) Until, and if, human studies find that weight reduction after diagnosis improves outcome, advice to our prostate cancer patients to lose weight is an expression of faith. But many life style decisions are based on speculations less convincing than may be inferred from these studies. Since maintaining a proper body weight promotes good overall health, it seems there is little to loose and possibly something to gain in the control over prostate cancer progression from reducing obesity.

[ An easy to use table for calculating BMI can be found at http://www.consumer.gov/weightloss/bmi.htm ]

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