Visceral Fat.

[pjoshea13]

New German study below [1].

I doubt that The European Journal of Obesity is required reading for most of our doctors.

I have posted before how visceral fat secretes hormones that can affect PCa. In effect, the fat operates as though it were a gland in the endocrine system. Studies that associate obesity with a poorer outcome in PCa, generally use BMI (body mass index) as a (usually unstated) surrogate for the more metabolically active visceral fat.

The danger of visceral fat is most clear in studies of fat around the prostate, where periprostatic fat density is associated with more aggressive disease. BMI is not a perfect predictor of periprostatic fat. One can lose weight on a low-fat Dean Ornish diet, but elevated triglycerides from high carbs are preferentially stored around internal organs.

The new paper is not prostate-specific.

"Adipose tissue secretes factors with hormone-like functions, the adipokines, and is therefore categorized as an endocrine organ. Current research demonstrates the ability of adipose tissue to alter DNA methylation and gene expression in peripheral tissues, probably affecting microRNA (miR) expression."

"The three selected and analyzed adipokines, adiponectin, leptin, and resistin, induce more strongly oncogenic miRs and simultaneously reduce anti-tumoral miRs than vice versa."

"The link of obesity and cancer is analyzed under the aspect of adipokine-regulated miRs. At the same time the impact of miR abundance is considered as a regulatory variable. This context offers new strategies for tumor therapy and diagnostics."

***

Unfortunately, in advanced PCa, where ADT is a common treatment, it can be very difficult to control fat accumulation.

***

I wonder how periprostatic fat might affect the risk of progression during active surveillance?

& how periprostatic fat affects the outcome in men who still have intact prostates.

-Patrick

[1] ncbi.nlm.nih.gov/pubmed/309...

Obes Facts. 2019 Apr 18;12(2):211-225. doi: 10.1159/000496625. [Epub ahead of print]

Adipokines Regulate the Expression of Tumor-Relevant MicroRNAs.

Jasinski-Bergner S1, Kielstein H2.

Author information

1

Department of Anatomy and Cell Biology, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany, [e-mail].

2

Department of Anatomy and Cell Biology, Faculty of Medicine, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany.

Abstract

BACKGROUND:

Increasing prevalence of obesity requires the investigation of respective comorbidities, including tumor diseases like colorectal, renal, post-menopausal breast, prostate cancer, and leukemia. To date, molecular mechanisms of the malignant transformation of these peripheral tissues induced by obesity remain unclear. Adipose tissue secretes factors with hormone-like functions, the adipokines, and is therefore categorized as an endocrine organ. Current research demonstrates the ability of adipose tissue to alter DNA methylation and gene expression in peripheral tissues, probably affecting microRNA (miR) expression.

METHODS:

Literature was analyzed for adipokine-regulated miRs. Many of these adipokine upregulated or downregulated miRs exert either oncogenic or anti-tumoral potential.

RESULTS:

The three selected and analyzed adipokines, adiponectin, leptin, and resistin, induce more strongly oncogenic miRs and simultaneously reduce anti-tumoral miRs than vice versa. This effect is not only true for the pure number of regulated miRs, it is also the case by consideration of the abundance of the respective miR expression based on actual data sets derived from next-generation sequencing.

CONCLUSION:

The link of obesity and cancer is analyzed under the aspect of adipokine-regulated miRs. At the same time the impact of miR abundance is considered as a regulatory variable. This context offers new strategies for tumor therapy and diagnostics.

© 2019 The Author(s) Published by S. Karger AG, Basel.

KEYWORDS:

Adipokines; Cancer; MicroRNA; Obesity

PMID: 30999294 DOI: 10.1159/000496625

[Frigataflyer]

Thank you Patrick. This is another low cost tool for those of us w/o insurance.

[cujoe]

That is a pretty good list of the principal ingredients of the large majority of processed foods. Eat Well to Be Well - cujoe

[3putt]

Spot on article. I follow Dr. Steven Gundry’s The Plant Paradox regiment that addresses good bugs versus bad bugs in our guts. I was never over weight to point of obese but the PC meds helped create a beer gut I didn’t want at this stage of life. While I’m not a big fan of living on nuts & berries, the loss of gut weight has been impressive. Not only am I losing the mid sectional baggage, I’m rarely hungry and have zero sugar or bread cravings, I will no longer allow food, or for that matter, PC to define my golden years! Good luck and God bless to all.

PS- his cook book arrived today and my wife just left for the market. Hopefully that’ll add a little more variety to the food intake mix.

[monte1111 in reply to 3putt]

Glad to see Zytiga is working well for you. Nuts and berries? Even Yogi Bear was on the constant lookout for a pic-i-nic basket. Wonder if your wife stops at Taco Bell on way to market. Don't eat the cook book. Good luck, and enjoy, sir.

[Hidden]

I'm 6'4" and I've managed to get my weight just under 200 lbs. 10 or 15 more pounds to go. I've got the exercise thing going but the diet part is a challenge. Thanks for this post. It is a reminder to not slack off.

[j-o-h-n]

youtube.com/watch?v=rSU3bza...(Not working as expected?)

Good luck, Good Health and Good Humor.

j-o-h-n Sunday 04/21/2019 2:17 PM DST

[JimVanHorn]

I was fat in 2007 when I started PCa therapy. On Christmas Eve my doctor called and told me I no longer have PCa. I am still fat.

[tallguy2]

Thanks for posting this. As a 6'7" tall fellow with a BMI of close to 25 I think I will continue to enjoy my food and drink, continue to swim laps, and have a bit of belly fat thanks to the ADT. We all just need to reduce the amount of processed stuff. Need to stick to the "outer aisle" at the grocery store.

[Bjry]

A recent Australian study has uncovered a weakness in prostate cancer cells. The researchers studied the energy needs of prostate cancer cells grown in the laboratory and in mice. Their results indicate that blocking fatty acid uptake may slow the progression of prostate cancer.

"Suppressing fatty acid uptake has therapeutic effects in preclinical models of prostate cancer. "

Abstract

Metabolism alterations are hallmarks of cancer, but the involvement of lipid metabolism in disease progression is unclear. We investigated the role of lipid metabolism in prostate cancer using tissue from patients with prostate cancer and patient-derived xenograft mouse models. We showed that fatty acid uptake was increased in human prostate cancer and that these fatty acids were directed toward biomass production. These changes were mediated, at least partly, by the fatty acid transporter CD36, which was associated with aggressive disease. Deleting Cd36 in the prostate of cancer-susceptible Pten-/- mice reduced fatty acid uptake and the abundance of oncogenic signaling lipids and slowed cancer progression. Moreover, CD36 antibody therapy reduced cancer severity in patient-derived xenografts. We further demonstrated cross-talk between fatty acid uptake and de novo lipogenesis and found that dual targeting of these pathways more potently inhibited proliferation of human cancer-derived organoids compared to the single treatments. These findings identify a critical role for CD36-mediated fatty acid uptake in prostate cancer and suggest that targeting fatty acid uptake might be an effective strategy for treating prostate cancer.

ncbi.nlm.nih.gov/pubmed/307...

[pjoshea13 in reply to Bjry]

"Suppressing fatty acid uptake" should not be confused with "Suppressing fatty acid intake". The body is factory for making fat. We could, with difficulty avoid fat altogether, but excess carbs are turned into palmitic acid - the preferred fuel of prostate cells.

The problems identified in the paper are:

i) "de novo lipogenesis". It is well-established that advanced PCa cells have elevated FAS (fatty acid synthase), the enzyme required for lipogenesis

ii) "the fatty acid transporter CD36, which was associated with aggressive disease"

These are PCa-related problems & cannot be solved via diet.

-Patrick