Prostate
Episodes
In this clip, Drs. Bill Harris and Rhonda Patrick discuss a questionable, potentially spurious association between omega-3 and selenium supplementation and prostate cancer.
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In this clip, Drs. Bill Harris and Rhonda Patrick discuss a questionable, potentially spurious association between omega-3 and selenium supplementation and prostate cancer.
Topic Pages
News & Publications
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Prostate cancer is the most diagnosed cancer among males in the U.S., but its progression varies widely, with some cases remaining harmless and others turning deadly. In recent years, concerns have grown over a rise in advanced prostate cancer, potentially linked to changes in screening recommendations. A recent study found that in California—a racially, ethnically, and geographically diverse state—the incidence of advanced-stage prostate cancer increased by nearly 7% over the past decade, while death rates, which had been declining, leveled off.
Researchers analyzed data from nearly 388,000 prostate cancer cases diagnosed in California between 2004 and 2021. Using data from state and national cancer registries, they examined trends in incidence and death rates based on cancer stage, age, race, ethnicity, and geographic region. They used statistical models to measure how these rates changed over time, focusing on patterns before and after shifts in screening guidelines.
They found that between 2011 and 2021, cases of advanced-stage prostate cancer increased by an average of 6.7% per year, with similar trends across racial and ethnic groups and nearly all regions of California. Meanwhile, prostate cancer death rates declined by 2.6% per year from 2004 to 2012 but remained steady through 2021, marking an end to previous declines in deaths from the disease.
These findings suggest that more men in California are being diagnosed with advanced prostate cancer, and the progress in reducing deaths has stalled. The gold standard for prostate cancer screening is the prostate-specific antigen (PSA) test. The U.S. Preventive Services Task Force recommends PSA screening for prostate cancer in men aged 55 to 69, but only among those at high risk for the disease. This screening can potentially reduce death but also carries risks such as false positives and treatment complications, including incontinence and erectile dysfunction. For men 70 and older, PSA screening is not recommended due to the greater likelihood of harms outweighing benefits.
Sulforaphane, a bioactive compound derived from broccoli, may reduce the risk for some types of cancer, including prostate cancer. Learn more in this episode featuring Dr. Jed Fahey.
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Low, rather than high testosterone and hyperestrogenism may favor prostate inflammation and benign prostate hyperplasia. (2019) www.sciencedirect.com
From the publication:
Mounting evidence shows that low, rather than high, T[estosterone] levels favor prostate inflammation and that hyperestrogenism also may play a role. Considering all these data, we postulate that BPH results from the actions of multiple factors occurring together or at different time points, which can reinforce and favor their mutual detrimental effects. The initial steps in this process are likely to occur early in life with an overt or subclinical prostatitis, probably influenced by infectious agents. The resulting prostatic inflammation could be amplified and maintained by metabolic derangements occurring in such conditions as MetS [metabolic syndrome]. Low T and the relative hyperestrogenism secondary to MetS [metabolic syndrome] could further exacerbate the immune process, leading to a chronic inflammation. When prostatitis becomes chronic, a number of cytokines are produced that act in the tissue to maintain the pathological condition. On the other hand, several growth factors are secreted, and their elevated concentrations lead to prostate remodeling and enlargement. The resulting mechanical obstruction and inflammatory damage are the basis of BPH and its associated urinary symptoms.
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In addition, treating hypogonadism, which frequently accompanies MetS, not only is not detrimental for the prostate, but also could even be a therapeutic resource for relieving urinary symptoms and limiting the inflammatory process in the prostate.
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The apparent contradiction of these results with the success of 5-alpha reductase inhibitors in treating LUTS merits closer investigation. Undoubtedly, treatment with 5-alpha reductase inhibitors results in a prostate volume decrease, which in turn translates into an improvement in LUTS. Nonetheless, it should be kept in mind that studies assessing intraprostatic androgen levels have linked 5-alpha reductase inhibition with a decrease in DHT and an increase in T.
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A group of international experts takes strong stance on testosterone deficiency treatment. (2016) www.sciencedaily.com
From the article:
After examining the best available scientific evidence, Morgentaler and colleagues – who included experts with specialties in urology, endocrinology, diabetes, internal medicine, and basic science research – agreed on the following:
– TD [testosterone deficiency] is a well-established, clinically significant medical condition that negatively affects male sexuality, reproduction, general health and quality of life.
– Symptoms and signs of TD occur as a result of low levels of testosterone and may benefit from treatment regardless of whether there is an identified underlying origin.
– TD is a global public health concern.
– Testosterone therapy for men with TD is effective, rational, and evidence-based.
– There is no testosterone concentration threshold that reliably distinguishes those who will respond to treatment from those who will not.
– There is no scientific basis for any age-specific recommendations against the use of testosterone therapy in adult males.
– The evidence does not support increased risks of cardiovascular events with testosterone therapy.
– The evidence does not support increased risk of prostate cancer with testosterone therapy.
– The evidence supports a major research initiative to explore possible benefits of testosterone therapy for cardiometabolic disease, including diabetes.
“It will be surprising to those unfamiliar with the literature to learn how weak the evidence is supporting the alleged risks of cardiovascular disease and prostate cancer,” said Michael Zitzmann, MD, vice-chair of the conference and a Professor in the Centre for Reproductive Medicine and Andrology at the University of Muenster in Germany. “Indeed, there is substantial data suggesting there may actually be cardio-protective benefits of testosterone therapy.”
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High levels of free testosterone, but not total testosterone, may increase risk of prostate cancer. (2004) www.sciencedaily.com
From the article:
The researchers measured several forms of testosterone in almost 3,000 blood samples collected over a 40-year period from 759 men in the Baltimore Longitudinal Study on Aging, of whom 111 were diagnosed with prostate cancer. One form of testosterone, called free testosterone, which is biologically active and can actually be used by the prostate, was found to be associated with increased prostate cancer risk, according to J. Kellogg Parsons, M.D., instructor of urology at the Brady Urological Institute at Johns Hopkins and lead researcher of the study.
“Since testosterone replacement therapy increases the amount of free testosterone in the blood, older men considering or receiving testosterone replacement should be counseled as to the association until data from long-term clinical trials becomes available,” says Parsons.
The association between free testosterone and prostate cancer risk in older men was not affected by height, weight, percent of body fat, or muscle mass. Total testosterone levels and dehydroepiandrosterone sulfate (DHEAS), another androgenic hormone, were also unrelated to prostate cancer risk, while the protein that binds testosterone in blood, called sex hormone-binding globulin (SHBG), was associated with a slightly decreased risk for prostate cancer.
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Long-term testosterone therapy in hypogonadal men does not increase the risk of prostate cancer, study suggests. (2014) www.sciencedaily.com
From the article:
A total of 1,023 patients on T[estosterone] therapy were followed for up to 17 years with a median follow-up of approximately 5 years. Two study cohorts of 261 (cohort 1) and 340 (cohort 2) men were treated by urologists since 2004 and a third cohort of 422 men was treated at an academic andrology center since 1996. Hypogonadism was diagnosed if testosterone was ≤12 nmol/L [345.82 ng/dL] and if other symptoms were present, such as erectile dysfunction, fatigue, depression, or unfavorable changes in body composition (gaining of fat mass and waist circumference despite physical activity). If no contraindications were present, all were started on T therapy.
There were six (2.3%) diagnoses of PCa [prostate cancer] in cohort 1, there were five (1.5%) diagnoses of PCa in cohort 2, and all biopsies were negative in cohort 3. PCa incidence per 10,000 patient-years in cohorts 1 and 2 was 54.4 and 30.7, respectively, which is lower than 116 reported by the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) and 96.6 reported by the ERSPC ( European Randomized Study of Screening for Prostate Cancer).
Investigators stress that if guidelines for T therapy are properly applied, it is safe in hypogonadal men.
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From the publication
The purpose of this paper is to analyze the guidelines for TTh [testosterone therapy] from international organizations and compare their recommendations.
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All agree that TD [testosterone deficiency] is a clinical syndrome that requires a low testosterone level as well as signs and/or symptoms for a diagnosis to be made. The exact cut -off varies or is not provided, but the organizations suggest a cut -off level between 300 -350 ng/dl. All societies recommend routine laboratory monitoring within the first year and annually after. The guideline committees acknowledge limited data on cardiovascular disease and testosterone. The consensus is to withhold TTh within 3 -6 months of an MI or stroke or in patients with severe heart failure.(2, 4) Prostate cancer is another gray area. Although the consensus is that there is no data to suggest TTh causes prostate cancer.
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Patients undergoing testosterone-lowering therapy for prostate cancer had an 88% increased risk of Alzheimer's risk. (2015) www.sciencedaily.com
From the article:
Using two different methods of statistical analysis, the team showed that the ADT [androgen deprivation therapy] group, compared to the control group, had significantly more Alzheimer’s diagnoses in the years following the initiation of androgen-lowering therapy. By the most sophisticated measure, members of the ADT [androgen deprivation therapy] group were about 88 percent more likely to get Alzheimer’s during the follow-up period.
The analyses also suggested a “dose-response effect.” The longer individuals underwent ADT the greater their risk of Alzheimer’s disease, they found. The longer-duration ADT patients also had more than double the Alzheimer’s risk of non-ADT controls.
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How low testosterone would lead to increased Alzheimer’s risk isn’t precisely known, but there is some evidence that testosterone has a general protective effect on brain cells, so that lowering testosterone would leave the brain less able to resist the processes leading to Alzheimer’s dementia. Studies in mice and in humans also have suggested that lower testosterone levels may allow greater production of the Alzheimer’s protein amyloid beta. Moreover, low testosterone may increase Alzheimer’s risk indirectly, by promoting conditions such as diabetes and atherosclerosis that are known to predispose to Alzheimer’s.
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High-dose testosterone therapy may help some men with advanced prostate cancer. (2015) www.sciencedaily.com
From the article:
Previous studies, he adds, have shown that taking testosterone at the wrong time – particularly by men with symptoms of active cancer progression who have not yet received testosterone-blocking therapy – can make the disease worse.
In men whose prostate cancer spreads, doctors typically prescribe drugs that block testosterone production, but cancer cells eventually become resistant to this means of reducing the hormone, says Denmeade, a professor of oncology at the Johns Hopkins University School of Medicine. At that point, physicians switch to other drugs, such as enzalutamide, which block testosterone’s ability to bind to receptors within prostate cancer cells.
Denmeade says the combination of drugs that block testosterone production and receptors, called androgen deprivation therapy, may make prostate cancer more aggressive over time by enabling prostate cancer cells to subvert attempts to block testosterone receptors. And many men on these drugs experience harsh side effects, including impotence, weight gain, muscle loss and intense fatigue.
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With this context, the new study tested an approach based on the idea that if prostate cancer cells were flooded with testosterone, the cells might be killed by the hormone shock. The cells also might react by making fewer receptors, which may make the prostate tumor cells vulnerable once more to androgen deprivation therapy.
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The men were given three 28-day cycles of an intramuscular injection of testosterone and two weeks of a chemotherapy drug called etoposide. Men who showed decreases in PSA levels after three cycles were continued on testosterone injections alone.
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Of the 14 remaining in the trial, seven experienced a dip in their PSA levels of between 30 and 99 percent, an indication their cancers were stable or lessening in severity. Seven of the men showed no decrease in PSA.
In addition, four of the seven men stayed on testosterone therapy for 12 to 24 months with continued low PSA levels. Of 10 men whose metastatic cancers could be measured with imaging scans, five experienced tumor shrinkage by more than half, including one man whose cancer completely disappeared.
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Testosterone therapy over a five-year period may not be associated with an increased risk of aggressive prostate cancer. (2015) www.sciencedaily.com
From the article:
A new population-based study from The University of Texas Medical Branch at Galveston showed for the first time that exposure to testosterone therapy over a five-year period was not associated with an increased risk of aggressive prostate cancer. Further, risk of high-grade prostate cancer did not increase according to the total number of testosterone injections.
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Although several longitudinal studies have shown no increased risk of prostate cancer incidence associated with testosterone use, no population-based studies have examined the association of high-grade prostate cancer with testosterone exposure beyond one year.
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Testosterone administration to deficient older men did not affect atherosclerosis rates, sexual function, or health-related quality of life. (2015) www.sciencedaily.com
From the article:
Shalender Bhasin, M.B.B.S., of Brigham and Women’s Hospital, Harvard Medical School, Boston, and colleagues randomly assigned 308 men 60 years or older with low or low-normal testosterone levels to receive 7.5 g of 1 percent testosterone (n = 156) or placebo (n = 152) gel packets daily for 3 years. The dose was adjusted to achieve testosterone levels between 500 and 900 ng/dL. Characteristics were similar between groups at study entry: patients were an average age of 68 years; 42 percent had hypertension; 15 percent, diabetes; 15 percent, cardiovascular disease; and 27 percent, obesity.
The researchers found that the rates of subclinical atherosclerosis progression, as measured by changes in common carotid artery intima-media thickness or coronary artery calcium, did not differ significantly between men assigned to the testosterone or placebo groups. Changes in intima-media thickness or calcium scores were not associated with change in testosterone levels among individuals assigned to receive testosterone.
Sexual desire, erectile function, overall sexual function scores, partner intimacy, and health-related quality of life did not differ significantly between groups. Hematocrit (a measure of red blood cells) and prostate-specific antigen levels increased more in testosterone group.
The authors write that this trial was not designed to determine the effects of testosterone on CVD events, and that a substantially larger trial would be needed to determine this.
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Testosterone raised the risk of prostate cancer and exacerbated the effects of carcinogenic chemical exposure in rats. (2014) www.sciencedaily.com
From the article:
Two dose-response studies examined the incidence of prostate cancer in rats. The rats were given testosterone through slow-release implant devices. Before the rats were dosed with testosterone, some of the animals were given injections of the carcinogenic chemical N-nitroso-N-methylurea (MNU). These rats were compared to a control group that received MNU but had empty slow-release devices implanted.
Among the rats that received testosterone without the carcinogenic chemical, 10 to 18 percent developed prostate carcinomas. Testosterone treatment alone did not induce specific tumors at other sites, but compared with control rats, it caused a significant increase in the number of rats with malignant tumors at any site. When rats were exposed to testosterone and the carcinogen, the treatment caused prostate cancer in 50 to 71 percent of the rats. Even when the hormone dose was too low to elevate testosterone levels in the bloodstream, half of the rats developed prostate tumors. Animals that were exposed to the carcinogenic chemical but not testosterone did not develop prostate cancer.
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Prostate cancer is a leading cause of cancer death among men in the United States. While some prostate cancers respond well to local treatment, many cases require systemic treatments, such as chemotherapy or hormone therapies, which can have many side effects. Because having overweight or obesity increases the risk of death from prostate cancer](https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.22443), newer and alternative therapies that slow cancer growth and help patients lose weight are needed. Findings of a new report show that a low carb diet generates ketones and other metabolic compounds associated with slower prostate cancer growth.
Low carbohydrate and ketogenic diets are popular with adults looking to lose weight, but they also have therapeutic power for a growing list of diseases such as epilepsy, [diabetes](https://www.magonlinelibrary.com/doi/full/10.12968/pnur.2020.31.4.176), Parkinson’s disease, and some cancers. In addition to the metabolic benefits of weight loss, many anticancer compounds are produced during ketosis such as beta-hydroxybutyrate, a short-chain fatty acid with documented antioxidant and anti-inflammatory effects. Additional research is needed to characterize the wide range of molecules generated on a low carb diet and explore their relationship to prostate cancer growth.
The investigators recruited participants who had recurrent prostate cancer and a BMI in the overweight or obese range (greater than 24). They assigned participants to consume a low carbohydrate diet (less than 20 grams of carbohydrates per day) for six months or continue their habitual diet. Participants provided a blood sample to measure metabolic and cancer biomarkers at multiple time points.
The investigators found increased concentrations of multiple ketone bodies in the blood and increased expression of genes for ketone production, indicating participants succeeded in maintaining ketosis. A low carbohydrate diet altered serum concentrations of multiple amino acids, such as glycine, alanine, and asymmetric dimethylarginine, and increased the expression of genes involved in the synthesis of malate, citrate, and branched-chain amino acids. The researchers found a relationship between increased concentrations of ketosis-related compounds and prostate specific antigen (PSA) double time (a marker of prostate cancer growth rate), indicating that cancer growth was reduced as ketosis intensified.
These results show that metabolites produced in response to a ketogenic diet may contribute to the beneficial effects of a low carb diet for patients with prostate cancer.
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Sulforaphane reduces biochemical recurrence in men who have had prostate cancer. pubmed.ncbi.nlm.nih.gov
Prostate cancer is the second most common cancer among men, affecting more than 1.3 million men worldwide. Many men undergo radical prostatectomy to treat their cancer. Findings from a 2015 study demonstrated that sulforaphane reduces biochemical recurrence in men who have had prostate cancer.
Biochemical recurrence is a phenomenon in which serum levels of prostate specific antigen (PSA) levels increase. It is an indicator of localized or metastatic disease. As many as 40 percent of men treated with radical prostatectomy experience biochemical recurrence; 34 percent of these will develop metastatic disease.
The double-blind, randomized, placebo-controlled study involved 75 men (average age, 69 years) who had undergone radical prostatectomy and were experiencing increased PSA levels. Roughly half of the men took a supplement providing 60 milligrams of sulforaphane for six months; the other half took a placebo. The authors of the study measured the men’s PSA levels before and two months after the treatment ended.
Increases in the average PSA levels were much lower among the men who took the sulforaphane. The PSA doubling time among men who took sulforaphane was ~29 months; doubling time among the men who took the placebo was ~16 months – an 86 percent difference. The effects of sulforaphane remained up to three months after the intervention.
These findings suggest that sulforaphane shows promise as a strategy to prevent biochemical recurrence among men who have had radical prostatectomy for prostate cancer. Additional studies are needed to confirm these findings.
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Prostate cancer was completely eliminated in 80 percent of men treated with MRI-guided ultrasound. newatlas.com
Prostate cancer is the second most common cancer among men worldwide. Nearly 165,000 men in the United States will be diagnosed with prostate cancer this year. Findings from a recent study presented at the annual meeting of the Radiological Society of North America indicate that a new ultrasound technique may be a promising treatment for this disease.
Current prostate cancer treatments often involve surgery to remove malignant tissue. Many men who undergo surgery develop urinary incontinence, and as many as 85 percent experience erectile dysfunction. The new treatment technique, called transurethral ultrasound ablation, or TULSA, is a minimally invasive treatment that uses MRI-guided ultrasound to heat and destroy tumors while sparing normal tissue.
The multi-center study involved 115 men between the ages of 59 and 69 years old who had been diagnosed with localized prostate cancer. Each of the men received TULSA treatment (average time, 51 minutes) and then were reassessed 12 months later.
At the 12-month follow-up, 80 percent of the men displayed no evidence of clinically significant cancer; 65 percent of the men had no evidence of cancer in biopsied tissue; and 96 percent of the men had significantly reduced prostate-specific antigen levels, a biomarker for prostate cancer. Only 1 percent of the men were incontinent after the treatment, and 25 percent experienced erectile dysfunction.
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Sulforaphane Ameliorates Bladder Dysfunction through Activation of the Nrf2-ARE Pathway in a Rat Model of Partial Bladder Outlet Obstruction www.hindawi.com
Study used a silk thread to create an animal model of “bladder outlet obstruction (BOO),” which is a condition affecting nearly 30% of men over the age of 60 and usually caused by benign prostatic hyperplasia (BPH).
FTA:
The bladder pressure was significantly increased in obstructed rats relative to sham rats. However, the peak voiding pressure of bladders in obstructed rats treated by SFN is lower than obstructed rats at the 4-week time point. Bladder capacity was significantly higher in BOO rats compared to sham rats. Rats of the BOO+SFN group showed the highest bladder capacity among all groups. Bladder compliance decreased significantly at the 4-week time point after BOO. However, SFN treatment rescued the compliance increase in bladder capacity. Moreover, we found that the interval of micturition was shorter in BOO rats than in sham rats. The micturition interval in BOO+SFN rats was significantly increased compared to BOO rats (Table 2).
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Lifestyle And Diet May Stop Or Reverse Prostate Cancer Progression (Dean Ornish Study) www.sciencedaily.com
FTA:
The research team studied 93 men with biopsy-proven prostate cancer who had elected not to undergo conventional treatment for reasons unrelated to this study. The participants were randomly divided into either a group who were asked to make comprehensive changes in diet and lifestyle or a comparison group who were not asked to do so.
[…] After one year, the researchers found that PSA levels (a protein marker for prostate cancer) decreased in men in the group who made comprehensive lifestyle changes but increased in the comparison group. There was a direct correlation between the degree of lifestyle change and the changes in PSA. Also, they found that serum from the participants inhibited prostate tumor growth in vitro by 70 percent in the lifestyle-change group but only 9 percent in the comparison group. Again, there was a direct correlation between the degree of lifestyle change and the inhibition of prostate tumor growth.
Participants in the lifestyle-change group were placed on a vegan diet consisting primarily of fruits, vegetables, whole grains, and legumes supplemented with soy, vitamins and minerals. They participated in moderate aerobic exercise, yoga/meditation, and a weekly support group session.
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Lower LDL Cholesterol Leads To Lower PSA & Lower Prostate Cancer Risk, Study Suggests www.sciencedaily.com
FTA:
In 2007, a retrospective study showed that men taking statins to lower their cholesterol also experienced a proportional decline in their PSA levels. This new study confirms that evidence and highlights the fact that cholesterol may play a role in prostate cancer development and progression. […] It remains to be seen whether or not lowering your PSA through statin medications could potentially mask the presence of prostate disease.
It would be nice if it talked about particle size! To understand why particle size matters (in the context of atherogenic dyslipidemia and heart disease), watch this video featuring @rhonda and Dr. Ronald Krauss.