Summary: in this study prostate size correlated with fasting blood sugar. Elevated fasting glucose is a risk factor for prostate disease.

A study recently published in the Journal of Korean Medical Science offers further evidence for the association between blood glucose regulation and prostate disease. The authors state:

“We evaluated the correlations between BMI, fasting glucose, insulin, testosterone level, insulin resistance, and prostate size in non-diabetic benign prostatic hyperplasia (BPH) patients with normal testosterone levels.”

They examined ata from 212 non-diabetic BPH patients with normal testosterone levels, excluding those with diabetes or serum testosterone levels less than 3.50 ng/mL. Their data showed that…

“Prostate size correlated positively with age, PSA , and fasting glucose level, but not with BMI, testosterone, insulin level, or HOMA-IR.Testosterone level inversely correlated with BMI, insulin level, and HOMA-IR [insulin resistance], but not with age, prostate size, PSA, or fasting glucose. HOMA-IR significantly correlated with BMI, fasting glucose, and insulin level, but not with age, PSA, or prostate size.”

There seems to be a disconnect here regarding the association of prostate size with fasting glucose but not the calculated insulin resistance that requires further investigation. The authors, however, are clear in their conclusion regarding blood sugar and prostate hypertrophy:

“In non-DM BPH patients with normal testosterone levels, fasting glucose level is an independent risk factor for prostate hyperplasia.”

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Many practitioners have used PSA velocity (the rate at which prostate-specific antigen values increase) as an important indicator to gauge the risk of aggressive prostate cancer and weigh the decision to proceed to biopsy. A study just published in the Journal of the National Cancer Institute reveals that PSA velocity is not a reliable indicator and can lead to many needless interventions. The authors state their intention to examine pre-existing assumptions about the significance of the rate of PSA change:

“The National Comprehensive Cancer Network and American Urological Association guidelines on early detection of prostate cancer recommend biopsy on the basis of high prostate-specific antigen (PSA) velocity, even in the absence of other indications such as an elevated PSA or a positive digital rectal exam (DRE)…To evaluate the current guideline, we compared the area under the curve of a multivariable model for prostate cancer including age, PSA, DRE, family history, and prior biopsy, with and without PSA velocity, in 5519 men undergoing biopsy, regardless of clinical indication, in the control arm of the Prostate Cancer Prevention Trial. We also evaluated the clinical implications of using PSA velocity cut points to determine biopsy in men with low PSA and negative DRE in terms of additional cancers found and unnecessary biopsies conducted. All statistical tests were two-sided.”

The current guideline based on an unproven assumption was clearly contradicted by their data:

“Incorporation of PSA velocity led to a very small increase in area under the curve from 0.702 to 0.709. Improvements in predictive accuracy were smaller for the endpoints of high-grade cancer (Gleason score of 7 or greater) and clinically significant cancer (Epstein criteria). Biopsying men with high PSA velocity but no other indication would lead to a large number of additional biopsies, with close to one in seven men being biopsied.”

The implication of these findings is starkly articulated in their conclusion:

“We found no evidence to support the recommendation that men with high PSA velocity should be biopsied in the absence of other indications; this measure should not be included in practice guidelines.“

The authors of an accompanying editorial thoughtfully state:

“The results…suggest that using PSA velocity may not provide more information to either physician or patient as we try to come to a decision about interpreting the results of any screening…The studies by Zeliadt et al. and Vickers et al. help us refine and focus our clinical approach, but they also remind us that the use of PSA as a screening tool still leaves much to be desired. Indeed, after more than 20 years of PSA screening, it has been estimated that approximately 1 million men may have been unnecessarily treated for clinically insignificant prostate cancer.”

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Lower urinary tract symptoms (LUTS) in men have often been blamed on increased androgens, particularly dihydrotestosterone (DHT).  A study just published in The Journal of Sexual Medicine provides more evidence for what I have noticed clinically for a long time: elevated estrogen causes more urinary tract symptoms than DHT and other androgens. The authors first observe:

“In male, lower urinary tract symptoms (LUTS) have been associated, beside benign prostatic hyperplasia, to some unexpected comorbidities (hypogonadism, obesity, metabolic syndrome), which are essentially characterized by an unbalance between circulating androgens/estrogens. Within the bladder, LUTS are linked to RhoA/Rho-kinase (ROCK) pathway overactivity.”

They conducted their investigation by testing the relative effects of estrogens, aromatase expression (aromatase converts testosterone to estrogen) and androgens (male hormones) on male genitourinary tract tissues, including cells from the bladder, prostate and urethra. What did the data show?

“Our data indicate for the first time that estrogen-more than androgen-receptors up-regulate RhoA/ROCK signaling [increases urinary tract symptoms]. Since an altered estrogen/androgen ratio characterizes conditions, such as aging, obesity and metabolic syndrome, often associated to LUTS, we speculate that a relative hyperestrogenism may induce bladder overactivity through the up-regulation of RhoA/ROCK pathway.”

This is part of the reason why I always measure free-fraction (bioactive) estrogen as part of a hormone profile for men. All too often men are given supplemental testosterone with no consideration for how much of it is being turned into estrogen by aromatase activity—with a potential increase in LUTS, not to mention cardiovascular, prostate cancer and depression risk factors.

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Here is a paper in the journal Prostate Cancer and Prostatic Diseases that is more evidence for what I have been telling Lapis Light patients for years: insulin and estrogen are both proliferating hormones that in excess promote prostatic hyperplasia (enlargement). No prostate assessment is complete without evaluating insulin regulation, free fraction steroid hormones (including estrogen in men) and Vitamin D levels.

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This interesting study from Molecular Cancer Therapeutics documents the inhibition of prostate cancer cell proliferation and the induction of apoptosis (cell death) with pomegranate extract. Of special importance is the described association with chronic inflammation driven by nuclear factor-κB (NF-κB) activity. This is involved in the transition from androgen dependence of prostate cancer cells to ones that no longer depend on male hormone stimulation. Pomegranate extract is shown to help reduce this inflammatory process.

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