New review below [1].
Details are in the full text, but it's a reminder that visceral fat secretes hormones that can spur PCa growth.
A number of studies have measured periprostatic fat thickness & found that it has prognostic value. Which implies that it has an active role in progression.
"... several recent studies have identified secreted factors from both the {peri-prostatic adipose tissue} and PCa that potentially mediate the two-way communication between these intimately-linked tissues."
There are now many studies that link obesity to poorer PCa survival. Two things that I don't like about the studies:
1] Most of us do not have a BMI of 30 or over, so might feel safe. However, there is danger too for overweight men (BMI = 20-29.9).
2] BMI is easy to measure and acts as a surrogate for visceral fat, which can only be measured via a scan. Some men have high BMIs but little visceral fat, while others are slim but with a lot of visceral fat.
For men who have insulin resistance (triglycerides > twice HDL-cholesterol is a decent surrogate), excess triglycerides from a high-carb diet are preferentially dumped from the circulation into visceral fat stores. Slim men on a Dean Ornish-type low-fat diet will be unaware that their internal organs may be loaded with fat - the TOFI phenomenon [2].
For men who have had the prostate removed, periprostatic fat is no longer a concern, but fat around the other organs act as an uncontrolled gland in the endocrine system, with a growth effect on PCa cells.
-Patrick
[1] ncbi.nlm.nih.gov/pubmed/294...
BJU Int. 2018 Feb 20. doi: 10.1111/bju.14173. [Epub ahead of print]
Peri-Prostatic Adipose Tissue: The metabolic microenvironment of prostate cancer.
Nassar ZD1,2,3, Aref AT1,2,3, Miladinovic D4, Mah CY1,2,3, Raj GV5, Hoy AJ4, Butler LM1,2.
Author information
Abstract
Emerging data has linked certain features of clinical prostate cancer (PCa) to obesity and, more specifically, increased adiposity. Whereas the large number of clinical studies and meta-analyses that have explored the associations between PCa and obesity have shown considerable variability, particularly in relation to prostate cancer risk, there is an accumulating weight of evidence consistently linking obesity to greater aggressiveness of disease. In probing this association mechanistically, it has been posited that the peri-prostatic adipose tissue (PPAT), a significant component of the prostate microenvironment, may be a critical source of fatty acids and other mitogens and thereby influences PCa pathogenesis and progression. Notably, several recent studies have identified secreted factors from both the PPAT and PCa that potentially mediate the two-way communication between these intimately-linked tissues. In this review, we summarise the available literature regarding the relationship between PPAT and PCa, including the potential biological mediators of that relationship, and explore emerging areas of interest for future research endeavours. This article is protected by copyright. All rights reserved.
KEYWORDS:
Prostate cancer; adipocytes; obesity; peri-prostatic adipose tissue; tumour microenvironment
PMID: 29460324 DOI: 10.1111/bju.14173
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