New study below. But first, some background.
There are many PCa studies that report increased mortality in obese men. From a 2014 meta-analysis [1]:
"In total, 17 studies, which included 3,569,926 individuals overall, were selected according to predefined inclusion criteria."
"... obesity was significantly correlated with an increased risk of aggressive PCa {+14%}. Furthermore, an increased risk of PCa-associated mortality was significantly associated with obesity {+24%}"
These studies send a couple of misleading messages to men:
a) that the risk only applies to men with a BMI>30. BMI (Body-Mass Index) "is a person's weight in kilograms (kg) divided by his or her height in meters squared." Sounds complicated if one has height in feet & inches, & weight in pounds, but there are tools to quickly handle the conversion & calculation:
bcbst.com/providers/MPMTool...
It is convenient for studies to compare PCa mortality in "obese" versus "normal" BMI men, but mortality risk increases through the "overweight" range (BMI=27.8-29.9) too & doesn't only affect the obese.
b) BMI is just an approximation of what researchers would like to measure: visceral fat.
Visceral fat is the fat stored around internal organs. Although most men with a 'spare tire' may well carry significant visceral fat, some do not. And lean men might well have considerable internal fat:
theguardian.com/science/200...
Triglycerides.
Many men with PCa have insulin resistance. Chronic dietary glucose spikes ultimately leads to a loss of insulin sensitivity & increased insulin production. Insulin is a PCa growth factor.
Glucose spikes translate to elevated triglycerides, & these are preferentially stored as visceral fat. The ratio of fasting triglycerides to HDL cholesterol [TG/HDLC] is accepted as a surrogate for insulin resistance.
In a paper published in November, TG/HDLC correlated to visceral fat, as measured by a CT scan [2]:
"Although many studies have demonstrated a correlation between the TG/HDLC ratio and outcomes such as insulin resistance, an increased risk of atherosclerotic cardiovascular disease, and metabolic syndrome, to date few studies have been performed to show a direct correlation with the visceral fat area as measured by CT. In the current study, we investigated the correlation between the TG/HDLC ratio and CT-measured visceral fat as well as cardiovascular risk factors in local adult male subjects who visited the University Hospital Health Promotion Center. We also evaluated the effectiveness of the TG/HDLC ratio as an indicator of visceral fat and cardiovascular disease risk."
Triglycerides & the carbohydrate:fat ratio.
U.S. doctors seem to largely ignore the triglyceride result in a lipid panel. Too busy studying the LDL cholesterol number - LOL. The normal range typically goes to 150 mg/dL, but some experts advise having TG no higher than 2xHDLC.
The American Heart Association has some good TG info [3]. Including this: "Keep dietary fat to 25-35% of total diet."
Dean Ornish is known for promoting a low-fat (10%) vegan diet. 90% carbs! It is possible to quickly lose weight on his diet. LDL cholesterol will fall (as will HDL, typically). But the trend will be for men high in the TG=100-150 range to end up even higher. Ornish isn't concerned by this. My concern is that the Ornish diet produces thin-outside-fat-inside men who are oblivious to the risk because they feel pretty good.
Dr Myers has described the typical new patient with high CVD risk. Breakfast: Orange juice, oatmeal, wholewheat toast (no butter). The perfect carbohydrate meal. & the men tend to be proud that they are eating a healthy breakfast. Myers favors a Mediterranean diet, & he emphasizes that this is not a low-fat diet. He has spoken of liking the carb/fat/protein proportions specified by Barry Sears in his Zone Diet books.
Fatty Prostates.
Some researchers have finessed the visceral fat issue by looking at the fat around removed prostates (periprostatic adipose tissue) or in prostate scans, e.g. [4].
"The Gleason score was significantly correlated with ... periprostatic fat thickness ..."
Finley (2009) [5] reported that periprostatic fat secreted factors that acted in a paracrine way on the prostate:
"these findings suggest that periprostatic adipose tissue may have a role in modulating prostate cancer aggressiveness by serving as a source of interleukin-6. Also, we found low numbers of inflammatory cells in the fat, suggesting that adipocytes are the major secretors of interleukin-6."
Yes - fat acts as though it were a gland in the endocrine system. Visceral fat is not merely excess weight.
New study [6].
"Why is visceral fat worse than subcutaneous fat?" April 25, 2016 University of Illinois at Chicago.
"Researchers have long-known that visceral fat -- the kind that wraps around the internal organs -- is more dangerous than subcutaneous fat that lies just under the skin around the belly, thighs and rear. But how visceral fat contributes to insulin resistance and inflammation has remained unknown.
A study led by researchers at the University of Illinois at Chicago points blame at a regulatory molecule in cells called TRIP-Br2 that is produced in response to overeating's stress on the machinery cells use to produce proteins.
The findings are published in the journal Nature Communications.
All body fat is not created equal in terms of associated health risks. Visceral fat is strongly linked to metabolic disease and insulin resistance, and an increased risk of death, even for people who have a normal body mass index. Subcutaneous fat doesn't carry the same risks -- some subcutaneous fat may even be protective.
In previous studies, Chong Wee Liew, assistant professor of physiology and biophysics in the UIC College of Medicine, and his colleagues found that in obese humans TRIP-Br2 was turned-up in visceral fat but not in subcutaneous fat. When the researchers knocked out TRIP-Br2 in mice and fed them a high-calorie, high-fat diet that would make the average rodent pack on the grams, the knockout mice stayed relatively lean and free from insulin resistance and inflammation.
"TRIP-Br2 appears to block or prevent normal lipolysis," Liew explained. Lipolysis is the breakdown of fat in fat cells, for use as fuel, and ongoing lipolysis can prevent the buildup of excess fat in those cells, Liew said.
"Without TRIP-Br2, lipolysis and oxidative metabolism take place at an increased rate, so fat is broken down and quickly used as energy and does not have a chance to build up in organs like the liver," he said.
But Liew and his colleagues still didn't know why TRIP-Br2 was found in higher amounts in visceral fat than in subcutaneous fat.
Their search for answers led them to a cellular structure called the endoplasmic reticulum, or ER, which is responsible for producing all the proteins in the cell. Nutrients from a meal enter the ER, but an excess due to overeating can significantly stress it. In obesity, a stressed ER in visceral fat cells leads to production of inflammatory molecules called cytokines -- but exactly how was unclear.
Liew and coworkers found that in the absence of TRIP-Br2, ER stress could no longer trigger cytokine production and inflammation in obesity. They also found that the up-regulation of TRIP-Br2 in visceral fat depends on an intermediary factor called GATA 3 that turns on TRIP-Br2.
"Together, our findings indicate that these molecular regulators, TRIP-Br2 and GATA3, could be viable targets for small drug molecules that could serve as potential therapeutic agents against obesity," Liew said.
sciencedaily.com/releases/2...
-Patrick
[1] ncbi.nlm.nih.gov/pmc/articl...
[2] ncbi.nlm.nih.gov/pmc/articl...
[3] heart.org/idc/groups/ahamah...
[4] ncbi.nlm.nih.gov/pubmed/255...
Prostate cancer uses fat to spread and resist medications
250 mg dose of Abiraterone with low fat meal
The human microbiome and its link in prostate cancer risk and pathogenesis
Reducing saturated fat intake may delay progression in men with MYC amplification
