Periprostatic Fat & ADT

[pjoshea13]

New study below [1].

Periprostatic fat is that which encases the prostate. As with fat stored around other internal organs, visceral fat can be excessive due to elevated triglycerides (caused by glucose spikes & insulin resistance.)

Periprostatic fat is not an innocent energy store, it is hormonally active. The secreted hormones act on the prostate in a paracrine fashion, & not in a good way.

Added to that is the fact that the prostatic stroma also has a stimulating paracrine relationship with tumor cells in the epithelium.

Removal of the prostate eliminates both of these concerns.

See past posts on periprostatic fat: [2] (2016), [3] (2018), [4] (2016).

From the new study:

"We find that the deprivation of androgen is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment."

"... the beneficial effect of therapies based on androgen deprivation may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate."

-Patrick

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

Endocr Connect. 2019 Apr 1. pii: EC-19-0029.R1. doi: 10.1530/EC-19-0029. [Epub ahead of print]

Androgen deprivation therapy promotes an obesity-like microenvironment in periprostatic fat.

Mangiola S1, Stuchbery R2, McCoy PJ3, Chow K4, Kurganovs N5, Kerger M6, Papenfuss AT7, Hovens CM8, Corcoran NM9.

Author information

Abstract

Prostate cancer is a leading cause of morbidity and cancer-related death worldwide. Androgen deprivation therapy (ADT) is the cornerstone of management for advanced disease. The use of these therapies is associated with multiple side effects, including metabolic syndrome and truncal obesity. At the same time, obesity has been associated with both prostate cancer development and disease progression, linked to its effects on chronic inflammation at a tissue level. The connection between androgen deprivation therapy, obesity, inflammation, and prostate cancer progression is well-established in clinical settings; however, an understanding of the changes in adipose tissue at the molecular level induced by castration therapies is missing. Here we investigated the transcriptional changes in periprostatic fat tissue induced by profound androgen deprivation therapy in a group of patients with high-risk tumours compared to a matching untreated cohort. We find that the deprivation of androgen is associated with a pro-inflammatory and obesity-like adipose tissue microenvironment. This study suggests that the beneficial effect of therapies based on androgen deprivation may be partially counteracted by metabolic and inflammatory side effects in the adipose tissue surrounding the prostate.

PMID: 30959474 DOI: 10.1530/EC-19-0029

[2] healthunlocked.com/advanced...

[3] healthunlocked.com/advanced....

[4] healthunlocked.com/advanced...

[Frigataflyer]

Patrick,

I have a Question. I have been taking Lupron (3 mo ) and I notice that in addition to my pectoral “muscle” gains, I feel as if my suprapubic “fat” has increased. Do you suppose that reducing this fat through diet would impact the nasty fat too?

Davis

[pjoshea13 in reply to Frigataflyer]

The problem with ADT is that symptoms of the metabolic syndrome inevitably appear.

Dietary control of glucose spikes so as to gain control over insulin sensitivity is important, IMO. The ZONE diet ratio of carbs:fat:protein would help. Nuts are a good way to get the appropriate amount of fat in meals & snacks. Fat is the key to slowing carbohydrate conversion to glucose, & release into the blood.

Another thing that is important is exercise. The reason is somewhat unexpected - exercise changes blood chemistry.

Perhaps difficult to motivate someone on Lupron to exercise, but short intense bursts of exercise are sufficient.

A more extreme approach - the ketogenic diet.

There was a study: "Ketogenic Diet in Advanced Cancer"

"clinicaltrials.gov/ct2/show...

Although the published paper was titled:

"Modified Atkins diet in advanced malignancies - final results of a safety and feasibility trial within the Veterans Affairs Pittsburgh Healthcare System"

"ncbi.nlm.nih.gov/pmc/articl...

Only one PCa patient & we know nothing about him, except: "Stable tumor size at 4 weeks, but PSA was rising".

The thrust of the study was to deprive cancer cells of glucose on the basis that those cells that are dependent on glucose would not be able to use ketones. Most PCa cells are not dependent on glucose.

My reason for suggesting a ketogenic diet is that it might result in a significant reduction of visceral fat. Another study:

"The goal of the present study was to test the hypothesis that consumption of a relatively low GL {glycemic load} diet compared to a high GL diet would result in preferential visceral fat loss and greater total fat loss following both weight maintenance and weight loss conditions."

"participants who consumed the low GL diet had 11% less intra-abdominal fat (IAAT) than those who consumed the high GL diet"

ncbi.nlm.nih.gov/pmc/articl...

-Patrick

[Frigataflyer in reply to pjoshea13]

Patrick,

Thank you for your answer. It confirms, my plan to go on a very low carb, low animal protein and high fat diet, which I know for a fact, does wonders for my lipid, inflammation, glucose/insulin numbers. I have a glucose/ketone meter and i will use feedback from it to govern how much fruit, I take on board. Mazatlan in the summer is not conducive to tennis, but I like HIIT swimming.

Again, thank you for your reply

David

[j-o-h-n in reply to Frigataflyer]

My pectoral “muscle” gains are called TITS...

Good Luck, Good Health and Good Humor.

j-o-h-n Wednesday 04/10/2019 6:32 PM EDT

[Frigataflyer in reply to j-o-h-n]

Gee, I thought it was “hanging muscle”

[j-o-h-n in reply to Frigataflyer]

No, that's down further... (and I do mean hanging)

Good Luck, Good Health and Good Humor.

j-o-h-n Wednesday 04/10/2019 7:11 PM EDT