Thought provoking to say the least. Effectively we are understanding
that obesity generates an imbalance at the genetic level that
plausibly accelerates the onset of active cancers.
At least it adds one clear additional reason to limit obesity itself.
This does not cure the risk but it promises to somewhat postpone
things.
In the event obesity is damaging enough anyway and applying the
arclein diet clearly works. In my own case I have watched 45 pounds
drift away. Google this blog for information.
ScienceDaily (Sep. 25,
2012) — Prostate cancer is one of the most common cancers in
men and early treatment is usually very successful. However, like
other cancers, obesity increases the risk of aggressive prostate
disease. New research, published in BioMed Central's open access
journalBMC Medicine, finds that the fat surrounding the prostate of
overweight or obese men with prostate cancer provides a favorable
environment to promote cancer growth.
Fat is a generally
underrated organ. Not only is it an energy store but it secretes a
wide range of growth factors, cytokines and hormones, including
leptin and adiponectin, and is a major player in the immune system,
which protects the body from infection and disease. But too much fat
can cause these systems to go haywire and can increase risk of
diabetes, cardiovascular disease and cancer.
An international team
led by Prof Gema Frühbeck and Dr Ricardo Ribeiro analyzed fat, from
around the prostate, taken from patients undergoing surgery for
prostate disease. Samples were included from men with benign
prostatic hyperplasia (BPH), prostate cancer (PC), and from men where
their cancer was no longer confined to the prostate. The men were
also classified as being either lean (BMI<25 obese="obese" or="or" overweight="overweight">25).
Regardless of type
of prostate disease the overweight men had different levels of gene
activity in the fat surrounding their prostates compared to the lean
men. This included genes which encode proteins involved in
immunity and inflammation (such as LEP, which encodes the protein
leptin), and cell growth and proliferation (including ANGPT1 which
encodes angiopoietin 1), fat metabolism and programmed cell death.
Additionally the
activity of more genes was altered between hyperplasia and prostate
cancer, and between cancer and non-confined cancer, suggesting a
gradual increase in dysregulation during cancer progression.
Prof Frühbeck
explained, "Both LEP and ANGPT1 encode proteins which are
thought to have roles beyond adipose tissue itself, especially
because prostate cancer cells have receptors for leptin, and
angiopoietin 1. Taken together with the abnormal activity levels of
other genes they will ultimately foster fat mass growth, reduce
immune surveillance, and promote the formation of new blood vessels,
so producing a favorable environment for prostate cancer
progression."
Dr Ribeiro continued,
"In an increasingly obese population, understanding how fat,
especially the fat surrounding the prostate, can influence the growth
and severity of prostate cancer may provide an opportunity for
implementing personalized lifestyle and therapeutic strategies."
This article is part
of the thematic series Metabolism, Diet and Disease from BMC
Biology and BMC Medicine.
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