Obesity can improve overall survival in men with late-stage, castration-resistant prostate cancer, a study showed. However, obesity does not seem to change the risk of death due to prostate cancer nor the likelihood of the cancer’s spread.
The study, “Obese patients with castration‐resistant prostate cancer may be at a lower risk of all‐cause mortality: results from the Shared Equal Access Regional Cancer Hospital (SEARCH) database,” was published in the journal BJU International.
Several studies support obesity being a risk factor for aggressive prostate cancer at diagnosis, and of increasing the chances of cancer recurrence and mortality after radical prostatectomy – surgery to remove the prostate gland and surrounding tissues. (Overall survival refers to a patient’s death from any cause, not just cancer-related causes.)
But very few studies have analyzed the influence of obesity on the outcomes of men undergoing hormone therapy, also called androgen deprivation therapy (ADT) — a treatment to lower the levels of male sex hormones, such as testosterone, with the goal of halting tumor growth.
ADT is particularly indicated for patients whose cancer has spread too far to be treated with surgery or radiation; those that cannot undergo surgery or radiation; or patients whose cancer is resistant to, or returns after, previous treatments.
It can also be used in combination with radiation, or before radiation therapy, to increase the probability of success.
Although ADT is the mainstay of advanced prostate cancer treatment, in most cases patients eventually progress to a castration-resistant prostate cancer — a cancer that can grow even with low levels of androgens in the body.
Surprisingly, a few studies found that a higher body mass index is associated with lower mortality risk among men with metastatic castration-resistant prostate cancer. But results of other studies differ.
To better understand the link between obesity and prostate cancer, researchers investigated clinical outcomes in men with non-metastatic castration-resistant prostate cancer. They analyzed the association between body mass index and the development of metastasis, mortality rates due to prostate cancer, and overall mortality.
Clinical data on 1,192 patients in the SEARCH database – obtained from eight U.S. Veterans Affairs hospitals — were analyzed.
Body mass index was determined at the time of diagnosis of castration-resistant prostate cancer, and used to categorize patients as underweight (below 21), normal weight (21 to 24.9), overweight (25 to 29.9), and obese ( equal to or over 30).
The initial hypothesis was that obesity would worsen long-term outcomes, similar to what was observed in patients with localized prostate cancer who underwent surgery. But results proved somewhat different.
In total, 51 (4%) men were underweight, 239 (25%) were normal weight, 464 (39%) were overweight, and 438 (37%) were obese.
Interestingly, the higher the body mass index of a patient, the lower his risk of all-cause mortality. In agreement, obese patients showed a significant reduction in overall mortality, or better overall survival, compared to normal weight patients.
But obese men were at equal risk of prostate cancer-specific mortality and of metastasis.
In other words, obesity is associated with better overall survival but did not impact prostate cancer-related outcomes.
A possible explanation for the better overall survival in obese patients could be that a higher body mass helps these men avoid the strains of marked weight loss due to the cancer, a phenomenon called cachexia.
Although non-metastatic patients normally are at low risk of weight loss, patients may have cachexia from other causes such as heart disease, chronic obstructive pulmonary disease, or other types of cancer.
“Thus, greater BMI [body mass index] may demonstrate a current lack of cachexia but also perhaps provide some protection from future cachexia allowing patients to live longer,” the researchers wrote.
The finding that obesity did not change prostate cancer outcomes can also result from competing biological factors related with obesity; these can both drive and inhibit prostate cancer, the researchers said.
“Finally, our results require validation in other datasets and if validated, then future studies are needed to explain why obesity is associated with more aggressive cancers at diagnosis, but better outcomes in late stage disease,” they concluded.