Ethan's Portal

Prostate Cancer and diet - Part I and II

Thu, 08 Nov 2018 02:52:00 GMT

How to boost your immune system

Tue, 10 Apr 2018 20:02:00 GMT

How do I boost my immune system? It is one of the most frequently asked questions at CANCERactive. People who want to prevent disease know that a strong immune system will give them better protection. People who have an illness understand that their immune system has failed them and they want to rebuild it.

But there´s a third group of people. Those who have cancer and have taken the chemotherapy - they need a quick fix.

1. EAT a high SOLUBLE FIBRE, high BIOACTIVE FOODS DIET

The University of Illinois Medical School has shown conclusively that a high intake of soluble fibre boosts the immune system. Indeed, people with the highest intake of soluble fibre have the best immune systems - oats, nuts and seeds and pulses would be a start.

The Rainbow Diet is the CANCERactive diet of choice because there is so much quality and clear research to support it (See Here). It advocates eating whole foods with lots of natural fibre (think lentils, nuts, seeds, fresh vegetables), low but ´whole´ carbs, high good fat levels and serious amounts of foods with vibrant colours.

A growing number of research studies has now shown that the Rainbow Diet is actually a better diet for all manner of chronic diseases like heart, diabetes, stress reduction and cancer than that recommended by Health Authorities! Research even shows it will help you live longer!

It provides great levels of essential minerals (fundamental to controling your body´s alkalinity and pH) while giving the body bioactive natural compounds like phenols, carotenoids, anthocyanins and sulforaphanes. Garlic, selenium, fish oils, carotenoids, salvestrols like resveratrol, the dark red anthocyanins of beetroot and cherries are all important. There is plenty of reference to what is in the Corrective and Protective Rainbow Diet on this website. You can also look at our review on Epigenetics - See here - 60 or more natural compounds have corrective benefits in cancer.

Importantly, the diet also involves no ´empty´ sugar, processed or refined foods. There are two big benefits. Firstly, a glucose-rich food or meal temporarily flattens the immune system. Secondly, reducing glucose and High Fructose Corn Syrup consumption greatly, also reduces your insulin levels and thus inflammation in the body - really important when fighting cancer.

Go to: 20 links between glucose and cancer

You can buy the Rainbow Diet book (and also Rainbow Recipes) by clicking this link.

2. CLEAN UP YOUR LIVER; lower your LDL

The liver is the largest organ in the body and is your organ of detoxification but few people understand it is crucial to your immune system. Furthermore, cancer cells produce lactate which poisons the liver resulting in fat building up in the liver and ´backwashing´ into the lymph and blood systems. People with the highest levels of LDL in their blood stream get more metastases and survive least. It is essential that you tackle this.

Go to: Simple ways to defat your liver and reduce LDL

3. TAKE EXERCISE where you get out of breath

Exercise produces hormones called endorphins, and these are powerful positive drugs inside your body. Exercise massively improves the immune system. It moves the lymph and dissolves visceral fat, both taking toxins away from cells. It oxygenates the blood, and endorphins neutralise the harmful hormones like Cortisol, the stress hormone, and Human Growth Hormone. Research now clearly shows that LIGHT TO MODERATE DAILY EXERCISE is the aim - about 40 to 60 minutes a day, ideally early morning and, ideally, you need to get puffed/out of breath. If you can manage it. It improves survival rates of some cancer patients by 50 per cent. It does not have to be strenuous. But you have to do it. Movement is essential as you have no ´heart´ to pump the immune system for you. You have to do this for yourself. You don´t need to go for the ´burn´ or wear lycra; Tai Chi, Qi Gong, Yoga are a good place to start. You need to move your thoracic duct in your chest - so press ups and swimming breast stroke are great if you feel more energetic.

4. HEAL Ur GUT

Have you ever known a small child who seemed to get a cold every week? It wasn´t a cold. They´d touched the cat, then put their fingers in their mouth. They´d put a new bacterium in their gut. Their white immune cells had come out to attack. The immune system had developed some new cell structures to deal with the invader. Your gut is responsible for 85 per cent of your immune system - and your immune memory, until you take drugs, Proton Pump Inhibitors and antibiotics. But you can also damage it with stress, smoking, pickles (vinegar) and alcohol and parasites, amongst other things.

Research has now shown your gut ´microbiome´ gets ill first, then you get ill. And you cannot get better until it gets better. But then it doesn´t just control your immune system; it MAKES certain compounds like short-chain esters which can reduce chronic inflammation throughout the body. Without them, your body takes another battering. It it is imperative that you give yourself a HUG -

Go to: Heal Ur Gut, and so Heal Ur Body

5. TAKE SUPPLEMENTS

OK. So they are the long-term fixes. What can you do in the short-term?

You have approximately 20 different types of white cell. You are unlikely to boost all the different types with just one supplement. We suggest a spectrum - for example, curcumin, grape seed extract/pine bark extract, herbs such as echinacea or astragalus or cat´s claw, beta-glucans, and melatonin. That should cover pretty well everything.

Curcumin - take with olive oil and black pepper (piperine) - is an antioxidant, anti-inflammatory and immune booster of some note.

Melatonin is the largest antioxidant we make as animals and is very calming. It´s why sleep is so healing.

Beta-glucans - naturally occurring polysaccharides from pathogenic bacteria and fungi (like ´medicinal´ mushrooms´). They have a strong effect on the immune system (1) by causing a positive reaction, and enhancing natural killer and macrophage action. You can eat mushrooms, and buy extracts. Immiflex, PSP and PSK are the ´in´ ones at the moment.

There are other ´polysaccharide´ immune boosters - like extracts from seaweed, and the Chinese herb astragalus.

And astragalus has a double benefit - it boosts the immune system and helps the white cells see the bad guys. On the subject of herbs, you could consider echinacea and cat´s claw.

Vitamin E (all 8 forms) is good, as is vitamin A.

We prefer natural chlorella, to vitamin A as it lets your body make the amount of A it needs. Then there´s vitamin C, but this is poorly absorbed if consumed in pill or powder form (more expensive, but better is liposomal vitamin C.

Finally, there is MGN-3 Biobran, which has a great deal of research to support it. It is expensive and total white cell count goes impressively high. But I´d like to see more information on the width of the white cells enhanced.

" If you are thinking of supplementing with any of the above products you may like to see what NATURAL SELECTIONhas to offer. Please CLICK HERE "

6. ACTIVATE YOUR IMMUNE SYSTEM WITH VITAMIN D

It seems that boosting the volume of the white cells AND getting them to recognise a rogue cell still isn´t enough. 2011 research showed that the first thing your T-cells do before they attack a rogue cell is pick up a vitamin D molecule to ´activate´ themselves. Without the vitamin D, they cannot attack. This is one reason why vitamin D is so important. If you cannot get 2 to 4 hours in the sunshine a day, take Boston Medical School´s recommendation. Supplement with 5,000IUs a day.

Vitamin K plays some part in this binding process but this is not perfectly clear as yet.

So, Vitamin D is crucial to a strong immune system. It is important to note however that taking drugs greatly reduces your plasma vitamin D levels and so you should increase you intake of sunshine or supplement.

7. CUT OUT TRANS FATS AND GLUCOSE FROM YOUR DIET

I have told you that cholesterol and fat can ´clog up´ (it´s a biochemical term!) your liver, pancreas and lymph. Trans fats are the worst - they come on fast food and junk food, and also in some packaged foods and processed foods. But saturated fats are not helpful either, causing not just a build up of fat in your liver and lymph, they are the building blocks for certain hormones like oestrogen.

Sugar (glucose and high fructose corn syrup) is awful. 2015 research in the American Journal of Public Health showed that a daily glucose rich fizzy soft drink damages your immune system AS MUCH AS SMOKING!!

People reach for a fruit smoothie on their supermarket shelf and do not realise how the glucose ´hit´ hammers their immune system about 30 minutes after drinking it. Cut out all added glucose (and HFCS) from your life (Fizzy soft drinks, puddings, ice cream, chocolate cake, smoothies and bought fruit juice, biscuits, refined foods, refined honey etc).

Sugar damages your immune system and cancer cells love it. People with the highest levels of blood glucose develop more cancers and survive least. Glucose has even been shown to cause cancer.

8. HAVE UNINTERRUPTED SLEEP IN A DARKENED, EMF-free ROOM

Always sleep in a fully darkened room with no EMFs around you - Elctromagnetic Fields include WiFi, computers, cell phones, masts and aerials and more. About 1 hour after you fall asleep your pineal gland makes Melatonin and it pushes you into a deeper sleep. People who have disturbed sleep develop more hormonally-driven cancers.

What few people seem to know is that melatonin is the biggest antioxidant we animals make. It is also anti-inflammatory and why sleep is so healing. It also regulates oestrogen and growth hormone in the body. We make less and less of it as we pass the age of 50 years.

You can supplement about 30 minutes before going to bed. It is thought that supplements above 10 mgs can cause hallucinations but there is clear research on the benefits of 20 mg supplements of melatonin to fight cancer. You will have to buy it on-line. Available in supermarkets in the USA, you can only obtain it on prescription in Europe.

9. LAUGH, BE HAPPY

Remember what you enjoyed doing a decade ago? Playing Tennis, watching comedy shows? People who laugh a lot have stronger immune systems; so go and buy some old funny videos. People who have good sex lives have stronger immune systems - no comment. People who meditate have stronger immune systems - find a meditation class to go with the yoga. UCLA have produced several studies showing those who meditate survive significantly longer! People who and in awe of a wonderful view - they have a boost in their immune system too.

Be Happy - Conversely, cut out the things (and people) who make you feel inadequate, worthless, guilty, cause you stress.

10. AVOID ´CHEMICALS OF CONCERN´

Go toxin-free. A UK Royal Commission stated that there were over 4,000 chemicals in common use in your own homes, two-thirds were probably toxic and one-third probably carcinogenic. The EuroMPs voted to ban over 1,000 chemicals of concern in 2005. Nothing happened. The average woman comes in to contact with approximately 680 ´chemicals of concern´ in her own home every month. These chemicals damage your immune system and worse.

It is not hard to go ´Toxin-free´.

Go to: Live Clean - build a clean home

11. DON´T SMOKE

Hardly a surprise really. The main reason is that it reduces blood oxygen levels, increases the acidity in the blood and the gut. The first directly down-grades the immune system; the second stops your commensal gut bacteria doing their immune boosting job.

12. DON´T DRINK TOO MUCH ALCOHOL

Latest Government advice is for a maximum of 15 units a week. Alcohol reduces your magnesium and B vitamin levels, poisons your liver and depresses the immune system.

MRI before biopsy better than TRUS

Mon, 26 Mar 2018 21:03:00 GMT

COPENHAGEN, Denmark — The standard of care for diagnosing prostate cancer is set to change because of results now published from a head-to-head comparison of two different approaches.

The study, known as Prostate Evaluation for Clinically Important Disease: Sampling Using Image-Guidance or Not? (PRECISION), was conducted in 500 men for whom there was suspicion of prostate cancer, based on elevations in the levels of prostate-specific antigen (PSA) and/or abnormal results on digital rectal examination (DRE).

The results show that multiparametric MRI followed by targeted biopsy performed only on patients whose scans were positive detected more clinically significant prostate cancer and less clinically insignificant prostate cancer than the standard approach of 10- to 12-core transrectal ultrasonography-guided biopsy (TRUS), and it did so with fewer biopsy cores.

The findings were presented here during the European Association of Urology (EAU) 2018 Congress and were simultaneously published online March 19 in the New England Journal of Medicine.

"In 2012, we set out to try and design a study in which we compared the standard of care to a pathway involving MRI so that we could change that standard of care," lead author Veeru Kasivisvanathan, MD, University College London, United Kingdom, told delegates here.

"And we found that in biopsy-naive men with a clinical suspicion of prostate cancer, a diagnostic pathway involving prebiopsy MRI risk stratification with MRI-targeted biopsy is superior to 10- to 12-core TRUS biopsy," he emphasized.

"In men who need to have investigation for prostate cancer for the first time, PRECISION shows that using an MRI to identify suspected cancer in the prostate and performing a prostate biopsy targeted to the MRI information leads to more cancers being diagnosed than the standard way that we have been performing prostate biopsy for the last 25 years," he added in a statement.

"While I still think there is a role for systematic biopsy in some men in whom we still have some concerns, this is an incredibly important, practice-changing study, and we need to fast-forward MRI to the diagnostic pathway prior to biopsy," commented Declan Murphy, MB BCh, director of genitourinary oncology, Peter MacCallum Cancer Center, Melbourne, Australia, who acted as discussant for the study at the meeting.

It has been estimated that if high-quality MRIs can be introduced across Europe, more than a quarter of the one million men who currently undergo a biopsy could safely avoid it.

The PRECISION trial involved 500 men who had not previously undergone a biopsy of the prostate. The patients were referred because either their PSA level was abnormal (≤20 ng/mL), or they had an abnormal result on digital rectal examination, or both

The Prostate Imaging-Reporting and Data system, version 2 (PI-Rads v2) was used to categorize areas suggestive of prostate cancer. A score of 1 or 2 designated a negative MRI; a score of 3 was considered equivocal with respect to the likelihood of the area being cancerous; a score of 4 indicated that prostate cancer was likely; and a score of 5 indicated that prostate cancer was highly likely.

If the MRI was negative, men could avoid undergoing a biopsy. "This is the first trial in which men who have a negative MRI have had a chance to avoid biopsy altogether," Kasivisvanathan noted.

If the biopsy was positive, men underwent a targeted biopsy only, thereby avoiding systematic biopsy, he added.

"The primary outcome was the proportion of men with clinically significant cancer, defined as a Gleason 3+4 or greater," Kasivisvanathan observed, "while important secondary outcomes included the proportion of men with clinically insignificant cancer, Gleason grade 3+3."

Results showed that for 28% of men who were randomly assigned to the MRI arm, MRI scanning was negative (PI-RADS v2 score ≤2 ). These patients did not undergo biopsy.

"Among the participants who underwent biopsy, a median of 4 biopsy cores were obtained...compared with a median of 12 cores in the standard-biopsy group," the team reported.

Clinically significant cancer was detected in 38% of the MRI-targeted biopsy group compared with 26% of the TRUS group, a difference between the groups that was significant (P = .005).

Furthermore, fewer men in the MRI-targeted group had clinically insignificant cancer, at only 9%, compared to 22% in the TRUS group, a difference between the two groups that was again significant (P < .001).

Kasivisvanathan pointed out that the proportion of cores that were positive for cancer was also much greater in the MRI arm, at 44% for the group that underwent MRI-targeted biopsies vs 18% for the standard-biopsy group.

At 30 days, patients who underwent an MRI-targeted biopsy reported fewer complications than the TRUS group. Complications included blood in the urine (30% for the MRI-targeted biopsy group vs 63% for the TRUS group); blood in the semen (32% vs 60%); pain at the procedural site (13% vs 23%); rectal bleeding (14% vs 22%), and erectile dysfunction (11% vs 16%).

ivisvanathan observed that the more favorable complication profile seen in the MRI arm reflected the fact that fewer men had to undergo biopsy at all, and for those who did, fewer cores were required for the diagnosis of prostate cancer.

Senior author Carole Moore, MD, University College London, the United Kingdom, commented that not having to undergo a biopsy and not receiving a diagnosis for insignificant cancer are both "huge advantages" in favor of the MRI risk-stratification approach.

"First of all, men miss out on the discomfort and the worry associated with biopsy," she told Medscape Medical News.

The other bonus of not receiving a diagnosis of cancer, even if it is "insignificant," is that it is better psychologically overall for patients.

"We know these indolent cancers are never going to cause trouble, but we also know that some people are nervous about hearing they have cancer and choose treatment anyway, which can be impactful in terms of erections and urine leakage and so on," Moore elaborated.

"So to test negative is a huge advantage, and the rate of indolent cancer was less than half in the MRI arm in the study than in the TRUS arm, which is a big advantage," she emphasized.

Practice-Changing Study

In his formal discussion of the study, Murphy said that PRECISION is "a truly-practice changing study" that will fundamentally transform the standard TRUS biopsy approach to the early detection of prostate cancer.

"I would also propose to you that this is very good news for our patients," Murphy added.

Not only are a significant proportion of men able to avoid biopsy altogether, but when they do require a biopsy, "there is much less core involvement, therefore fewer complications [while at the same time], more significant cancer — and less insignificant cancer — is diagnosed," he emphasized.

Murphy did point out that all men whose MRI results are negative prior to undergoing a biopsy may not be at uniformly low risk. Such patients have a 1 in 4 chance of having Gleason pattern 4 cancer on biopsy, and a Gleason pattern 4 signifies a higher-grade component to the tumor.

"The take-home message is, I think we have heard a new paradigm today, and we should embrace it," Murphy said.

"So I would agree that everyone should have an MRI if possible, and I now believe that in those patients with visible lesions, we can afford to only target the lesion as well," he added.

Commenting on the new results, Prof Hein Van Poppel, EAU adjunct secretary general, University Hospitals of the Leuven, Belgium, said in a statment: "This is a significant study. Prostate cancer can only really be confirmed by a biopsy, which is invasive and, like almost all medical procedures, carries some risk of side effects. Of course, in the majority of men who have a biopsy, no cancer is found. This work shows that using MRI to decide whether or not to perform a biopsy has the potential to save around a quarter of a million European men each year from going through the biopsy procedure, and so may be cost-effective in the long run. MRI use also shows up small, aggressive cancers at a curable stage and allows us to delay or simply not perform biopsies for some cancers which will not turn out to be dangerous. We need time to digest the study, but at first reading, it looks like it has the potential to change clinical practice."

The study was funded by the National Institute for Health Research and the European Association of Urology Research Foundation. The investigators and Dr Murphy have disclosed no relevant financial relationships.

European Association of Urology (EAU) 2018 Congress. Presented March 19, 2018.

Radiation and Surgery among High Risk Cancer Patients

Tue, 13 Mar 2018 16:08:00 GMT

Prostate Cancer News, Reviews Views

Brachy boost therapy and surgery extend survival about the same in high risk patients, but brachy boost does more

Posted: 08 Mar 2018 09:04 AM PST

Two retrospective studies were published in the last week, and they had some similar findings, but some dissimilar things to say about which treatment is best for high risk prostate cancer. The three therapies they looked at were the combination of brachytherapy and external beam radiation (brachy boost therapy - BBT), external beam therapy alone (EBRT), and surgery (RP).

Kishan et al. reported on 1,809 men with Gleason score of 9 or 10 who were treated between 2000 and 2013 at 12 tertiary cancer care institutions (UCLA, Los Angeles VA, California Endocurie Therapy Center, Fox Chase, Mt. Sinai, Cleveland Clinic, Wheeling Jesuit University, University of Michigan, Johns Hopkins, Oslo University, William Beaumont Hospital, and Dana-Farber).

Patient characteristics:

639 were treated with radical prostatectomy (RP).
734 were treated with EBRT only.
436 were treated with BBT (BT was either low dose rate in 62% or high dose rate in 38%).
All patients were Gleason 9 or 10 on biopsy.
Pelvic LN involvement was discovered in 17% of RP patients ; 40% had positive surgical margins.
RP patients were younger (61 years of age) compared to EBRT or BBT patients (68 years of age)
RP patients were lower stage ( 87% clinical stage T1/T2) compared to EBRT (70% clinical stage T1/T2 ) or BBT patients (79% clinical stage T1/T2)
RP patients had lower pre-therapy PSA (7 ng/ml) compared to EBRT or BBT patients (10 ng/ml)
RP patients had lower percentage of Gleason score 10 (4%) compared to EBRT (6%) or BBT patients (9%)

Treatment specs

Among the RP patients, 43% had adjuvant or salvage radiation therapy (68 Gy).
Among radiation patients, about 90% had adjuvant ADT
Median dose of EBRT was 74 Gy.

adjuvant ADT continued for 22 months, median.

Median equivalent dose of EBRT+BT was 92 Gy

adjuvant ADT continued for 12 months.

Oncological outcomes

After a median follow-up of 4.2, 5.1 and 6.3 years for RP, EBRT, and BBT, respectively, the oncological outcomes (adjusted for age and disease characteristics) were as follows:

The 10-year rates of distant metastases were

46% for RP
44% for EBRT
13% for BBT
Differences between BBT and the two others were statistically significant.

The 10-year rates of prostate cancer-specific mortality (PCSM) were

23% for RP
26% for EBRT
13% for EBRT + BT
Differences between BBT and the two others were statistically significant.

The 10-year rates of all-cause mortality (ACM) were

32% for RP
39% for EBRT
31% for BBT
None of the differences were statistically significant.
There was a difference at 7.5 years in favor of BBT that vanished by 10 years.

In additional analyses, the authors looked at outcomes by duration of androgen deprivation for those receiving any kind of radiation. They found that ADT duration made no significant difference in detected metastases or PCSM within EBRT or BBT, and did not account for the difference between them. They also looked at radiation doses. EBRT patients who received <70 Gy had PCSM significantly worse than those who received ≥ 78 Gy. The rates of metastases did not differ. Notably, very few (11%) of the EBRT patients had both ≥ 78 Gy and ≥2 years of ADT, a combination that is now considered standard of care. Those that did had superior outcomes compared to RP. The use of LDR-BT or HDR-BT as part of BBT made no difference.

The authors conclude:

Among patients with Gleason score 9-10 prostate cancer, treatment with EBRT+BT with androgen deprivation therapy was associated with significantly better prostate cancer–specific mortality and longer time to distant metastasis compared with EBRT with androgen deprivation therapy or with RP.

In an analysis of the National Cancer Database, Ennis et al. reported on the overall survival of patients who were treated with RP, EBRT, and BBT for high-risk PC from 2004 to 2013. The database covers about 70% of all new prostate cancer patients treated in the US. The patient profile was:

24,688 patients treated with RP, at least at first
15,435 patients treated with EBRT
2,642 patients treated with BBT.
All EBRT patients also had adjuvant ADT
BBT patients may or may not have had ADT
All were high risk by the NCCN definition: Either Gleason score 8-10, stage T3/4, or PSA≥20 ng/ml
RP patients were younger (62 years of age) compared to EBRT (70 years of age) or BBT patients (67 years of age)
RP patients were lower stage ( 89% clinical stage T1/T2) compared to EBRT (84% clinical stage T1/T2 ) or BBT patients (85% clinical stage T1/T2)
RP patients had lower pre-therapy mean PSA (19 ng/ml) compared to EBRT (23 ng/ml) but the same as BBT patients (19 ng/ml)
RP patients had lower percentage of Gleason score 8-10 (70%) compared to EBRT (78%) or BBT patients (73%)
Comorbidities were similar among groups.
The above risk factors as well as socioeconomic factors and year of diagnosis were used to adjust the raw data.
It is unknown what percent of RP patients had adjuvant or salvage radiation.
There was no data available on post-reatment metastases or prostate cancer-specific survival

Because surgery is sometimes aborted when pelvic LN cancer is discovered, they estimated the probability that patients had positive nodes, and included it as a risk factor. This would seem to double count those risk factors, but the authors say it had little effect. Based on their model, they estimated that the percent who had positive nodes was 10% of RP patients, 34% of EBRT patients, and 23% of BBT patients.

After a median follow-up of 36 months, the relative oncological outcomes (adjusted for age and other patient and disease characteristics), expressed as hazard ratios were as follows:

RP: 1.0
EBRT: 1.53 (i.e., 53% worse survival vs. RP)

EBRT with < 79.2 Gy: 1.68
EBRT with ≥79.2 Gy: 1.33

BBT: 1.17 (not significantly different from RP)

not different if ADT included
no interaction between comorbidities and treatment effects

The authors conclude:

This analysis showed no statistical difference in survival between patients treated with RP versus EBRT plus brachytherapy with or without AD. EBRT plus AD was associated with lower survival.

- with thanks to Amar Kishan for allowing me to see the full text.

Imaging Agent Can Change Plans for Recurrent Prostate Cancer

Wed, 14 Feb 2018 03:23:00 GMT

SAN FRANCISCO — When men with prostate cancer experience biochemical recurrence, the rise in levels of prostate-specific antigen (PSA) suggests that the disease may have spread.

This is distressing both for clinicians and patients, because it suggests that curative-intent primary therapy has not succeeded.

It also prompts immediate questions: What is the extent of local recurrence and of metastases? And what should be done next therapeutically?

At present, there is uncertainty as to how to address these issues, because when patients experience biochemical recurrence, the PSA level rises, but there is no visual evidence of disease on conventional scans.

A new study shows that adding an imaging agent to the scans provides more information, and this has a "substantial impact" on clinical decisions for such patients.

The imaging agent, 18F-fluciclovine, was used in conjunction with positron-emission tomography (PET)/CT scanning.

The results from the new study, known as FALCON (Fluciclovine [18F] PET/CT in Biochemical Recurrence of Prostate Cancer), were presented here at the Genitourinary Cancers Symposium (GUCS) 2018.

For 52 of 85 men enrolled in the study (61%), clinical management was changed after 18F-fluciclovine PET/CT imaging, reported Eugene Jueren Teoh, MBBS, an oncologist at Oxford University Hospital in the United Kingdom.

For some patients, management was changed to "provide a better chance at cure or to avoid possibly futile salvage therapy," Teoh told the meeting audience.

He also pointed out that 18F-fluciclovine is a synthetic amino acid that is taken up by amino acid transporters that are "massively" upregulated in many cancers, including prostate cancer.

It is already approved in the United States and the European Union for PET/CT imaging in cases of biochemical recurrence of prostate cancer. In the United States, costs are reimbursed by insurance through the Centers for Medicare & Medicaid Services, Teoh said.

Sumanta Pal, MD, a urologic oncologist from the City of Hope Cancer Center in Duarte, California, said the rate of management change in the study was thought provoking: "I think 60% is awfully impressive.

"If I had any other diagnostic test that changed my management more than half of the time, I would definitely implement it," said Pal, who was asked for comment.

He also placed the results in the context of currently used technology.

"We realize that many patients with localized disease [and rising PSA levels] may actually have brewing metastasis. But we just don't have the technology with current modalities, such as CT scans and technetium bone scans, to detect these areas of disease spread," said Pal.

Study Details

In the FALCON study, the investigators recorded the intended management plan for patients being considered for radical salvage treatment after the patients experienced initial biochemical recurrence; the investigators subsequently recorded newly recommended plans following scanning with 18F-fluciclovine.

The primary objective was assessment of the clinical impact of the scanning agent on patient management.

Postscan changes to treatment modality, such as a change from salvage radiotherapy (RT) to systemic therapy, were classed as "major"; changes within a modality (eg, a modification of RT fields) were classed as "other," said Teoh.

Of the 52 men for whom changes in management were made, 31 underwent a major change (for 18 patients, planned salvage treatment was changed to systemic noncurative therapy; for 13 patients, planned salvage treatment was changed to watchful waiting). For 21 patients, changes in management were classified as "other" (planned RT was modified to include a boost to a positive lesion or a widening of the field to include the whole pelvis).

For the 85 enrolled patients, the mean period following initial diagnosis was 4.8 years; the patients' median age was 67 years. Most (56; 65.9%) had previously undergone radical prostatectomy (RP), and 27 had received RT (± other therapy). For 12 men (14.1%), the Gleason score was ≤6; for 60 (70.6%), the score was 7; and for 13 (15.3%), the score was ≥8.

Notably, the median PSA level among the men was 0.63 ng/mL.

That median PSA level worried a clinician in the GUCS audience.

Daniel Lin, MD, an urologist at of the University of Washington in Seattle, said, "I would put someone forward for salvage radiotherapy much before PSA got to 0.6."

Lin wondered whether waiting for disease spread to show up on a scan, even with highly sensitive 18F-fluciclovine PET/CT imaging, might result in "missing the window for cure."

Toeh responded that, in the study, not all the scans were positive. Among men who had already undergone prostatectomy and whose PSA level was <.5, there was a 25% detection rate upon scanning. That would have triggered salvage RT at Toeh's institution at Oxford, he said.

Furthermore, the study was multicenter, and "hypersensitive" PSA tests were used "heterogeneously" in the study, he noted in explaining the relatively high trigger point for progressing to salvage RT.

There is a need for "robust" criteria for employing 18F-fluciclovine scanning, Toeh admitted. "It's not for everyone," he commented. "But I do believe there will be a subset [of patients], particularly post prostatectomy, who will benefit."

Teoh also said there is no cutoff PSA value with regard to not performing the scan. "I would scan patients with a fast doubling time" whose PSA level was ≥0.1, he said.

The inclusion criteria for the study was a PSA level >0.1 and a doubling time <15 months or a PSA >1, regardless of doubling time.

Enrollment in the UK trial was stopped after this interim analysis with 85 patients, said Teoh, because of "overwhelming efficacy."

Toeh said more research is needed. Currently, follow-up is underway to assess whether patients in the current study experienced clinically related outcomes — PSA dropping/stabilizing or increasing — after 18F-fluciclovine scanning. Long-term studies are needed to determine the impact of this tool on disease outcomes, he added.

Teoh said 18F-fluciclovine is "well established" as a diagnostic tool for detecting sites of recurrent prostate cancer. However, a member of the Dana Farber Cancer Institute in Boston, Massachusetts, who attended GUCS, told Medscape Medical News that the cutting-edge center had added 18F-fluciclovine scanning only in the past 6 months.

Pal said it was his impression that the technology was still mostly limited to use in major academic centers. "If we continue to see compelling trends like these — namely, fluciclovine changing patient management upwards of 60% of the time — we may see greater clinical implementation," he added.

"This modality can be used in the confines of most existing radiology practices," Pal also observed.

The new study is an important step for this imaging agent, he suggested. "Assessing the rate of change in management is really key, as opposed to simply identifying the additional sites of metastases that you can pick up with fluciclovine above and beyond standard modalities."

The study was jointly funded by Innovate UK and Blue Earth Diagnostics. Dr Toeh has received research funding from Blue Earth Diagnostics. The study authors included company employees. Dr Pal has financial ties to Eisai, Ipsen, Astellas, Medivation, Bristol-Myers Squibb, Exelixis, Genentech, Myriad Pharmaceuticals, Aveo, Novartis, and Pfizer.

Genitourinary Cancers Symposium (GUCS) 2018. Abstract 165, presented February 8, 2018.

Follow Medscape senior journalist Nick Mulcahy on Twitter: @MulcahyNick

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Gadolinium Based Contrast Agents - the Side Effect Risks

Thu, 07 Dec 2017 15:52:00 GMT

Gadolinium Based Contrast Agents: Benefits and Risks

Recent stories in the media (http://www.newsweek.com/what-gadolinium-chuck-norris-claims-it-poisoned-his-wife-704647) have highlighted an existing but not well-known concern: that MRI is not a risk-free procedure. This has to do with one of the MRI imaging techniques that is based on the injection of a contrast agent. The most widely used contrast agent for prostate cancer detection is gadolinium, or more precisely, chelated gadolinium that is marketed in various forms under numerous brand names, but known collectively as gadolinium based contrast agents (GBCA’s).

Gadolinium is a rare earth metal whose paramagnetic properties are the reason for its use as a contrast agent. Since it is toxic to the body, it is chelated with an organic compound that allows it to be rapidly excreted from the body through the kidneys. Other materials have also been used for enhancing con-trast – all have known toxicities.

To understand the importance of GBCA’s in cancer detection (and hence the tension that exists between their benefits and risks) requires a basic understanding of how MRI works. A reader already familiar with this subject or perhaps time limited can skip over the next few paragraphs to the section titled “GBCA Risks”.

How MRI Works

The following description is taken from https://en.wikipedia.org/wiki/Magnetic_resonance_imaging. In MRI, the person is positioned within an MRI scanner and an oscillating magnetic field is temporarily ap-plied at the appropriate resonance frequency. The excited hydrogen nuclei (protons) in various tissues within the magnetic field emit a radio frequency signal which is measured by a receiving coil. The radio signal may be made to encode position information by varying the main magnetic field using gradient coils. As these coils are rapidly switched on and off they create the characteristic repetitive noise of an MRI scan. The contrast between different tissues is determined by the rate at which excited atoms re-turn to the equilibrium state. This is called relaxation. Exogenous contrast agents may be given to the person to make the image clearer. That’s where GBCA’s come into play.

The technique that makes use of GBCA is called dynamic contrast enhancement (DCE). But before get-ting into that, the reader should know that the two commonly used imaging techniques – T1 weighted imaging and T2-weighted imaging, have limitations, because the contrast between types of tissue (the basis for reading the images) is not tissue-specific. T1-weighted imaging results in bright signals for fat tissue and low signals for what could be tumor but also might be edema, inflammation, infection, he-morrhage or calcification. T2-weighted imaging results in bright signals for tumor but also for inflamma-tion or infection and low signals for fat, air or calcification. Thus the radiologist reading either image is seeing contrasting tissue but not knowing precisely what is tumor and what is other kinds of benign tissue.

DCE helps him make a more informed decision. The spin polarization used to form the T1 image decays with a characteristic time constant known as the T1 relaxation time. The hydrogen protons in different tissues have different T1 values, which is the main source of contrast in MR images. GBCA’s shorten the T1 relaxation time of nearby hydrogen protons thereby enhancing the contrast in the image. One of the important ways DCE helps to guide the radiologist is by enhancing vascularity. The injected GBCA tends to concentrate more in blood vessels and in the intrastitial space between the blood vessels. Since tu-mors are characterized by increased vascularity, areas of enhanced signal immediately after injection could be tumor sites. An area that projects a bright signal on a T2 weighted image, which could be a tu-mor, but does not enhance on a T1-weighted image with DCE may not be a tumor. The radiologist has another tool that helps him make the final decision – diffusion weighted imaging.

The use of all the tools of MPMRI (including DCE) is especially warranted when scanning a prostate that has been treated, either by radiation or by any of the focal therapies, because scarring and inflammation can make reading the scans tricky. Unfortunately, some post-treatment protocols and most forms of ac-tive surveillance require MRI at regular intervals forever, thus the concerns about gadolinium are of spe-cial importance for those men for whom the probability of toxicity is greatly increased by repeated MRIs.

GBCA Risks

The following is taken in part from https://en.wikipedia.org/wiki/Gadolinium#Safety

As a free ion, gadolinium is highly toxic due to interference with a number of calcium-ion channel de-pendent processes. The influx of calcium ions into the cell can initiate a myriad of calcium-dependent processes including muscle contraction, gene expression, and secretion. Thus gadolinium should not be allowed in the body in its free state. GBCA’s are chelated compounds considered safe enough to be used in most persons. However, it is known that gadolinium can dissociate from its chelate before being eli-minated from the body.

There are two main types of GBCA, linear and macrocyclic. They differ in the way gadolinium is bound to the chelate. The macrocyclic chelates bind the gadolinium much more strongly, which minimizes the possibility of dissociation. On March 10, 2017, the committee of the European Medicines Agency (EMA) recommended the suspension of marketing authorizations for four linear GBCAs used for MRI scans be-cause of concerns about small amounts of gadolinium from administered GBCAs being deposited in the brain. At the completion of its year-long review of GBCAs, the EMA’s Pharmacovigilance and Risk Assess-ment Committee (PRAC) “found convincing evidence of accumulation of gadolinium in the brain from studies directly measuring gadolinium in brain tissues and areas of increased signal intensity seen on MRI scan images many months after the last injection of a gadolinium contrast agent”. Linear agents recommended for suspension by the PRAC are:

Gadobenic acid, marketed as MultiHance by Bracco Diagnostics Inc.

Gadodiamide, marketed as Omniscan by GE Healthcare

Gadopentetic acid, marketed as Magnevist by Bayer HealthCare Pharmaceuticals

Gadoversetamide, marketed as OptiMARK by Mallinckrodt Inc.

Dr. Barentsz, who is considered by many to be the leader in the field of clinical MRI, uses a macrocyclic GBCA, called Gadovist, which is considered the safest agent.

Unfortunately, in the USA radiologists are still using the banned linear GBCA's. Among them is my radio-logist, Dr. Busch in Chattanooga, TN. He uses MultiHance which, though not the worst, is still a linear agent on the banned list. I understand that using the most effective agent is important, especially when scanning a prostate that has been treated, however, as post-treatment protocol demands repeated MRIs, there is a significant risk of incurring toxicities for which at present there are no known cures. MPMRI is becoming standard of care for initial diagnosis and for follow-up, therefore the number of men being scanned is rising, so that the probability of gadolinium toxicity is rising too.

What to Discuss with your Radiologist before an MRI

Based on recent findings, it makes sense to discuss the need for contrast with the radiologist. Ask if it is really necessary. There is growing awareness of the toxicity problem among the radiological community, and as a result contrast is being used less frequently, especially in men who have not been treated. BTW, multiple biopsies may be one reason for using contrast, as scar tissue makes reading the scans more difficult… another reason to get an MRI first, before biopsy.

Before an MRI with contrast, be confident that your kidney function is normal (GFR > 60 ml/min) At a minimum, ask him/her to use a macrocyclic GBCA.

Exercise Reduces PCa Mortality - New Data

Mon, 09 Oct 2017 20:20:00 GMT

A recent article in European Urology (http://www.europeanurology.com/article/S0302-2838(17)30537-7/fulltext) reconfirms the theory that exercise significantly reduces the risk of death from PCa whether low, intermediate or high risk. Since most PCa is low risk, this may indicate the importance of exercise for men with high risk PCa.

2017 PCRI Conference Summary

Tue, 03 Oct 2017 02:37:00 GMT

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Vitamin D and Prostate Cancer

Wed, 24 Aug 2016 18:49:52 GMT

Much has been written lately about the role of vitamin D in the prevention of many cancers, including prostate cancer (PCa) and also in potentially slowing cancer progression. However, before discussing this further, it should be noted that there are countervailing studies that cast doubt on the efficacy of vitamin D and at least one study that claims it can actually be harmful.

Before going further, let's define what vitamin D is. From the Wiki article ():

Vitamin D and Prostate Cancer

Tue, 19 Apr 2016 23:18:00 GMT

Before going further, let's define what vitamin D is. From the Wiki article (https://en.wikipedia.org/wiki/Vitamin_D):

Vitamin D refers to a group of fat-soluble secosteroids responsible for enhancing intestinal absorption of calcium, iron, magnesium, phosphate, and zinc. In humans, the most important compounds in this group are vitamin D3 (also known as cholecalciferol) and vitamin D2 (ergocalciferol).[1] Cholecalciferol and ergocalciferol can be ingested from the diet and from supplements.[1][2][3] Very few foods contain vitamin D; synthesis of vitamin D (specifically cholecalciferol) in the skin is the major natural source of the vitamin. Dermal synthesis of vitamin D from cholesterol is dependent on sun exposure (specifically UVB radiation).

Vitamin D from the diet or dermal synthesis from sunlight is biologically inactive; activation requires enzymatic conversion (hydroxylation) in the liver and kidney. In the liver, cholecalciferol (vitamin D3) is converted to calcidiol, which is also known as calcifediol (INN), 25-hydroxycholecalciferol (aka 25-hydroxyvitamin D3 — abbreviated 25(OH)D3). Ergocalciferol (vitamin D2) is converted in the liver to 25-hydroxyergocalciferol (aka 25-hydroxyvitamin D2 — abbreviated 25(OH)D2). These two specific vitamin D metabolites are measured in serum to determine a person's vitamin D status.

The possible relationship between vitamin D and PCa was highlighted in a recently published study conducted at Northwestern University (http://jco.ascopubs.org/content/early/2016/02/17/JCO.2015.65.1463.abstract) and summarized in their press release (http://www.news-medical.net/news/20160302/New-study-finds-link-between-vitamin-D-deficiency-and-aggressive-prostate-cancer.aspx):

A new study provides a major link between low levels of vitamin D and aggressive prostate cancer. Northwestern Medicine research showed deficient vitamin D blood levels in men can predict aggressive prostate cancer identified at the time of surgery.

The finding is important because it can offer guidance to men and their doctors who may be considering active surveillance, in which they monitor the cancer rather than remove the prostate.

"Vitamin D deficiency may predict aggressive prostate cancer as a biomarker," said lead investigator Dr. Adam Murphy, an assistant professor of urology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine urologist. "Men with dark skin, low vitamin D intake or low sun exposure should be tested for vitamin D deficiency when they are diagnosed with an elevated PSA or prostate cancer. Then a deficiency should be corrected with supplements."

Previous studies showing an association between vitamin D levels and aggressive prostate cancer were based on blood drawn well before treatment. The new Northwestern study provides a more direct correlation because it measured D levels within a couple of months before the tumor was visually identified as aggressive during surgery to remove the prostate (radical prostatectomy).

The relationship between vitamin D and prostate cancer may explain some disparities seen in prostate cancer, especially among African American men. Prior research by Murphy and colleagues showed African American men who live in low sunlight locations are up to 1½ times more likely to have vitamin D deficiency than Caucasian men.

But because vitamin D is a biomarker for bone health and aggressiveness of other diseases, all men should check their levels, Murphy said.

A big promoter of vitamin D as a cancer preventer is Dr. Bruce W. Hollis, PhD, a professor at the Medical University of South Carolina. In this Youtube vid he shares the results of a recent trial including identifying the vitamin D level needed to protect the prostate gland: https://www.youtube.com/watch?v=QrU1yrmNIqc. In a nutshell, Dr. Hollis believes our vit. D levels should be above 60 ng/ml.

On the other hand, the Wiki article states the following: "It is unclear, however, if taking additional vitamin D in the diet or as supplements affects the risk of cancer. Reviews have described the evidence as being "inconsistent, inconclusive as to causality, and insufficient to inform nutritional requirements"[59] and "not sufficiently robust to draw conclusions".[77]

Snce there is so much recent evidence in favor of Vitamin D, we should pay attention at a minimum.

Nutrition and Prostate Cancer

Mon, 28 Mar 2016 14:32:00 GMT

The following was extracted from the website of the Academy of Nutrition and Dietetics, http://www.oncologynutrition.org/erfc/eating-well-when-unwell/prostate-cancer-and-diet/

Health experts have noted that prostate cancer rates vary greatly from country to country, and from region to region, across the globe. There are many reasons for these differences, such as how much exercise people get, differences in obesity rates, and genetics. However, one of the biggest differences between countries with low vs. high rates of prostate cancer is diet.

Many prostate cancer specialists believe these differences in diet are one of the biggest reasons why prostate cancer rates vary so much among the different areas of the world. In other words, some ways of eating seem to protect against prostate cancer, while other dietary patterns may increase prostate cancer risk.

In general, following a plant-based diet is associated with lower risk of prostate cancer. A plant-based diet does not have to be completely vegetarian or vegan. Plant-based simply means that the majority of the foods you eat are minimally processed, whole plant foods. This includes vegetables, fruit, legumes, nuts, seeds, and whole grains. Lean protein from healthful sources, such as fatty fish (salmon, sardines, and others), also can be part of a diet plan designed to reduce prostate cancer risk, or risk of recurrence.

According to the American Institute for Cancer Research (AICR), a plant-based, cancer prevention diet should start with your plate:

Approximately ½ of the surface should be covered with vegetables, fruits and/or legumes (beans).
Approximately ¼ of the surface should be covered by starches, such as whole grains or potatoes.
The remaining ¼ of the surface is covered by lean protein sources, such as fish, chicken, or other lean meats. If you want to follow a vegetarian or vegan diet, lean protein can come from legumes, and soy products, such as tofu or tempeh.

Research supports that this type of eating pattern reduces prostate cancer risk. As well, plant-based diets may reduce the risk of recurrence and progression of disease in men who already have prostate cancer. Dr. Dean Ornish, who has been studying the positive benefits of plant-based or vegetarian/vegan diets to reverse heart disease, also has used this approach with men with prostate cancer.

Dr. Ornish’s studies suggest that following a low-fat, plant-based diet, as part of a comprehensive lifestyle program that includes exercise and stress reduction, may improve outcomes in men with prostate cancer. This approach may slow the increase of prostate specific antigen (PSA)—an increasing level suggests the tumor is growing and possibly spreading—and decrease the need for more aggressive treatment in men with low-risk prostate cancer.

Some men opt to “watch and wait,” meaning they don’t get treatment for prostate cancer right away, because their particular type of cancer is slow growing and less likely to spread. Dr. Ornish’s program was tested in a group of men who were following the “watch and wait” approach for managing lower risk prostate cancers.

As well, the healthy lifestyle intervention increased relative telomere length after five years of follow-up, compared with men not following the program (controls). This is a good thing, because longer telomeres protect DNA, our genetic material, from damage. This, in turn, may be protective against chronic diseases, including cancer.

According to the Prostate Cancer Foundation, poor diet is the major risk factor for prostate cancer, and the group offers the following nutritional guidelines to prevent or delay the onset of prostate cancer. These guidelines also stress a healthy, plant-based diet as an important part of a prostate cancer risk reduction plan.

Eat fewer calories or exercise more so that you maintain a healthy weight.
Try to keep the amount of fat you get from red meat and dairy products to a minimum.
Watch your calcium intake. Do not take supplemental doses far above the recommended daily allowance. Some calcium is OK, but avoid taking more than 1,500 mg of calcium a day.
Eat more fish – evidence from several studies suggest that fish can help protect against prostate cancer because they have "good fat" particularly omega-3 fatty acids.
Avoid trans fatty acids (found in margarine).
Try to incorporate cooked tomatoes that are cooked with olive oil, which has also been shown to be beneficial, and cruciferous vegetables (like broccoli and cauliflower) into many of your weekly meals. Soy and green tea are also potential dietary components that may be helpful.
Avoid smoking for many reasons. Drink alcohol in moderation, if at all.
Seek medical treatment for stress, high blood pressure, high cholesterol, and depression. Treating these conditions may save your life and will improve your survivorship with prostate cancer.
What about supplements? Avoid over-supplementation with megavitamins. Too many vitamins, especially folate, may “fuel the cancer”, and while a multivitamin is not likely to be harmful, if you follow a healthy diet with lots of fruits, vegetables, whole grains, fish, and healthy oils you likely do not even need a multivitamin.

Specific nutrients

In addition to focusing on a healthy, plant-based diet, specific foods and nutrients may help men reduce risk of prostate cancer or its recurrence.

Isoflavones

Compounds called isoflavones are found mainly in soybeans, and these nutrients seem to protect against prostate cancer. Good sources of isoflavones include tofu, soymilk, soy nuts, tempeh, and edamame (steamed soybeans in the pod).

Green tea

Green tea contains compounds called flavonoids, which act as antioxidant and may have anticancer activities. Studies suggest several cups of green tea per day are needed to maximize the potential cancer-preventive effects of the beverage. And early trials have found that green tea extract may prevent pre-cancerous prostate growths from becoming cancerous tumors.

Steep for about 4 minutes, because this maximizes the flavonoid content. According to Dr. Douglas Balentine of the Lipton Tea company, if green tea is steeped for only one minute, the average flavonoid content is 208 mg. If it is steeped for four minutes, the flavonoid content increases to 300 mg. If a bitter taste bothers you, try using water that is just slightly less than boiling when you brew up a cup.

Red fruits and vegetables

Lycopene is one of a group of compounds called carotenes, which are known for their antioxidant properties, and which may have cancer preventive properties as well. Cooked tomato products, such as tomato juice and soup, and tomato sauce have the most lycopene. Watermelon and pink grapefruit also contain some lycopene, though not as much as cooked tomatoes.

Some studies suggest lycopene may decrease prostate cancer risk. Other research doesn’t show a large cancer preventive effect of lycopene. However, given that eating lycopene-rich foods is unlikely to cause harm, it makes sense to include these foods in a healthy diet.

Cruciferous vegetables

Cruciferous vegetables include broccoli, cauliflower, cabbage, and Brussels sprouts, kale, collard greens, and several other pungent and bitter vegetables. These foods seem to be particularly good at protecting against cancer, and this includes prostate cancer. Eating these foods raw or lightly cooked—steam, sauté, or stir fry—seems to maximize the body’s ability to absorb important nutrients.

Dairy and calcium

Dozens of research studies have looked at potential connections between calcium, dairy foods, and prostate cancer risk. These studies present a mixed picture, but some do suggest that high intakes of calcium and/or dairy foods may increase prostate cancer risk.

When studies have found an increased risk of prostate cancer associated with dairy foods or dietary calcium (food sources), the results suggest that more than three to five servings of dairy per day may be a problem. This suggests that moderate dairy intake—up to three servings per day, but no more—is not associated with increased prostate cancer risk.

But remember that calcium is important to health. Not getting enough calcium can increase the risk of osteoporosis, even among men. Further, for men with prostate cancer, some treatments can increase the risk of bone loss and fractures, so trying to completely avoid calcium is not a good idea.

Talk to a registered dietitian for advice on how best to meet your calcium needs.

Look at the big picture

No one food or supplement can protect against prostate cancer. However, a diet that is lower in fat, contains at least five servings of fruits and vegetables per day (more is better), and whole soy foods, will go a long way in protecting your prostate.

The original question and answer were generously donated by Diana Dyer, MS, RD a cancer survivor, registered dietitian, organic garlic farmer, and the author of "A Dietitian's Cancer Story: Information & Inspiration for Recovery & Healing from a 3-time Cancer Survivor.

Question and Answer updated by Suzanne Dixon, MPH, MS, RD on behalf of the ON DPG

References

Dyer D. A Dietitian’s Cancer Story: Information & Inspiration for Recovery & Healing from a Three-Time Cancer Survivor. Available at: American Institute for Cancer Research.
Ornish D, Lin J, Chan JM, Epel E, Kemp C, Weidner G,... , Blackburn EH. Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study. Lancet Oncol. 2013;14(11):1112-20.
Frattaroli J, Weidner G, Dnistrian AM, Kemp C, Daubenmier JJ, Marlin RO,..., Ornish D. Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology. 2008;72(6):1319-23.
Ornish D, Weidner G, Fair WR, Marlin R, Pettengill EB, Raisin CJ,..., Carroll PR. Intensive lifestyle changes may affect the progression of prostate cancer. J Urol. 2005;174:1065-9; discussion 1069-70.
Prostate Cancer Foundation. Understanding Prostate Cancer Prevention. Accessed January 2, 2014.
Mahmoud AM, Yang W, Bosland MC. Soy isoflavones and prostate cancer: A review of molecular mechanisms. J Steroid Biochem Mol Biol. 2013 Dec 25. pii: S0960-0760(13)00283-5. doi: 10.1016/j.jsbmb.2013.12.010.
Yuan JM. Cancer prevention by green tea: evidence from epidemiologic studies.Am J Clin Nutr. 2013;98(6):1676S-81S.
Vance TM, Su J, Fontham ET, Koo SI, Chun OK. Dietary antioxidants and prostate cancer: a review. Nutr Cancer. 2013;65(6):793-801.
Holzapfel NP, Holzapfel BM, Champ S, Feldthusen J, Clements J, Hutmacher DW. The potential role of lycopene for the prevention and therapy of prostate cancer: from molecular mechanisms to clinical evidence. Int J Mol Sci. 2013;14(7):14620-46.
W Watson G, M Beaver L, E Williams D, H Dashwood R, Ho E. Phytochemicals from cruciferous vegetables, epigenetics, and prostate cancer prevention. AAPS J. 2013;15(4):951-61.
Abdull Razis AF, Noor NM. Cruciferous vegetables: dietary phytochemicals for cancer prevention. Asian Pac J Cancer Prev. 2013;14(3):1565-70.

Page updated: January 2014

Effect of Lifestyle on Prostate Cancer

Mon, 07 Mar 2016 12:21:00 GMT

There have been several recent articles on the impact of lifestyle changes on prostate cancer in the medical literature that have attracted wider notice and been amplified in the lay media. One example is this recently published study in the Journal of the National Cancer Institute (Volume 108, Issue 3, 10.1093/jnci/djv329) by researchers working at highly regarded institutions:

Development and Application of a Lifestyle Score for Prevention of Lethal Prostate Cancer

Authors: Stacey A. Kenfield*, Julie L. Batista*, Jaquelyn L. Jahn, Mary Kathryn Downer, Erin L. Van Blarigan, Howard D. Sesso, Edward L. Giovannucci, Meir J. Stampfer and June M. Chan

I have asked for permission to reproduce the article here. In the meantime I will summarize the key findings.

The most important finding is the conclusion: relatively simple lifestyle changes can have a significant impact on reducing the chance of mortality due to aggressive PCa.

Here are the details.

The authors studied the combined effect of several lifestyle factors known to have association with risk of lethal prostate cancer. They developed what they call a lifestyle score for prevention of lethal prostate cancer based on a statistical analysis of the habits of two large cohorts of men. Each man was rated with a score of 1 to 6 based on adherence to the following lifestyle factors:

non-smoking
body mass index normal
vigorous physical activity (min. 3 hrs/week)
high intake of tomatoes
high intake of fatty fish
low intake of processed meat.

Bottom line: men who scored the highest had a reduced chance of dying from aggressive PCa vs. those who scored lowest.

The single most important factor was vigorous physical activity. Other articles have hypothesized that vigorous activity is linked to another thought to be beneficial factor - improved insulin sensitivity.

Not only does this help reduce serum glucose levels ("starving the tumor"), but also reduces the amount of insulin in the blood. High insulin levels are particularly associated with risk of aggressive prostatic tumours (http://www.ncbi.nlm.nih.gov/pubmed/20126849).

A very good article on exercise to reduce lethal PCa risk (that also links to the JNCI article) is: http://drgeo.com/lifestyle-exercise-prevents-deadly-prostate-cancer-a-new-study/.

Fat Consumption and Prostate Cancer

Mon, 07 Mar 2016 12:19:00 GMT

Low-Fat Diet

Eating a low-fat diet has many benefits. Here are some points to keep in mind.

The increased cancer risk observed in developed countries may be, in part, due to the fact that a high-fat diet stimulates increased testosterone levels, which is known to be associated with prostate cancer growth.
A comprehensive review reported that 24 of 32 studies found positive, although not all statistically significant, associations between dietary fat intake and prostate cancer risk.
Prospective studies to date, however, have failed to find a consistent association between prostate cancer and overall fat intake.

What to Do: Most researchers agree to aim for 20 percent of your total calories from fat, with less than 10 percent of total calories from saturated fat.

Ethan's comment: The above comment is controversial. Other experts claim that more calories should be obtained from fat because calories obtained from carbs increase insulin-like growth factor. The IGF pathway is known not only to be integral in the progression of prostate cancer but also well known to be highly controlled through dietary intake (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959866/). Many similar articles have been published on the benefits of a ketogenic diet and high intensity exercise (which also affects IGF-1). See references at bottom of this article for partial list.

The type of fat is significant.

Saturated Fat

Several studies indicate a positive association between saturated fat intake from meat and dairy products and prostate cancer. Intakes of red meat and dairy products appear also to be related to increased risk of metastatic prostate cancer. Therefore, it is wise to reduce or eliminate consumption of red meat, milk and other dairy products.

What to Do: Reduce or eliminate consumption of red meat, milk and other dairy products. Limit use of butter, mayonnaise, baked goods and regular salad dressing due to their high saturated fat and total fat content. Consider rice vinegar, balsamic vinegar, lemon juice or salsa as alternative salad dressings. Limit cheese consumption. Cheese is typically between 60 to 80 percent fat, much of which is saturated fat.

Trans Fat

Trans fatty acids are known to be atherogenic, or heart disease causing. They also may cause an imbalance in hormonal systems that regulate healing, lead to the construction of defective membranes and encourage the development of cancer.

What to Do: Limit use of hydrogenated fats found in products such as margarine, fried foods and processed foods, which are high in harmful trans fatty acids. When you read that a product contains "hydrogenated" or "partially-hydrogenated" oils, you may want to consider putting it back on the shelf. Trans fatty acid labeling went into effect in 2006, so nutritional labels should spell out the amount of trans fatty acids in the product.

Omega-6 Fatty Acids

Omega-6 fatty acids, which is linoleic acid that can be converted to arachidonic acid, may stimulate growth of prostate cancer cells. These fatty acids are found in corn oil, safflower oil, sunflower oil, cottonseed oil, soybean oil and other polyunsaturated oils.

What to Do: Substitute olive oil for your current cooking oil, but remember to use in moderation. These oils are rich in monounsaturated fats, which have not been shown to increase cancer risk.

Omega-3 Fatty Acids

Omega-3 fatty acids may reduce your risks for prostate cancer and cancer progression. They induce apoptosis (cell death), suppress cancer cell initiation and compete with arachidonic acid, which limits harm from arachidonic acid. One study indicated that men who consumed cold-water fish three to four times per week had a reduced risk of prostate cancer. A more recent study found similar results. Men who consumed fish three or more times per week also had a lower risk of prostate cancer, especially for metastatic prostate cancer where the effect was even greater.

Researchers in New Zealand reported that men with high levels of EPA and DHA, the omega-3 fats found in fish, had a 40 percent lower risk of prostate cancer than those with low blood levels. A 30-year follow-up study found that men who ate no fish had a two to three times higher frequency of prostate cancer than those who ate moderate or high amounts of fish. The mechanism of cancer reduction may occur through the inhibition of arachidonic acid-derived eicosanoid biosynthesis.

Dietary sources of omega-3 fatty acids include cold-water fish — such as salmon, trout, herring and sardines — flaxseeds, walnuts, soybeans and canola oil.

What to Do: It may be wise to consume fish at least twice weekly to obtain an adequate amount of omega-3 fatty acids.

Fish and plant-based foods contain different types of omega-3 fatty acids. Fish contains EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), two specific fatty acids that have shown promising results in research. The plant-based omega-3 fatty acid sources, such as flaxseed and others listed above, contain ALA (alpha-linolenic acid). In an ideal environment, ALA is converted to EPA and DHA, however, in 10 percent to 20 percent of the population, this conversion process is dysfunctional. On the positive side, the conversion process is enhanced by following a diet that is low in saturated fats and low in omega-6 fatty acids.

20. Barnard RJ, Ngo TH, Leung PS, Aronson WJ, Golding LA. A low-fat diet and/or strenuous exercise alters the IGF axis in vivo and reduces prostate tumor cell growth in vitro. Prostate.2003;56:201–6.[PubMed]

21. Dewell A, Weidner G, Sumner MD, et al. Relationship of dietary protein and soy isoflavones to serum IGF-1 and IGF binding proteins in the Prostate Cancer Lifestyle Trial. Nutr Cancer.2007;58:35–42.[PubMed]

22. Giovannucci E, Pollak M, Liu Y, et al. Nutritional predictors of insulin-like growth factor I and their relationships to cancer in men. Cancer Epidemiol Biomarkers Prev. 2003;12:84–9. [PubMed]

23. Gunnell D, Oliver SE, Peters TJ, et al. Are diet-prostate cancer associations mediated by the IGF axis? A cross-sectional analysis of diet, IGF-1 and IGFBP-3 in healthy middle-aged men. Br J Cancer.2003;88:1682–6. [PMC free article] [PubMed]

24. Ngo TH, Barnard RJ, Tymchuk CN, Cohen P, Aronson WJ. Effect of diet and exercise on serum insulin, IGF-1, and IGFBP-1 levels and growth of LNCaP cells in vitro. Cancer Causes Control.2002;13:929–35. [PubMed]

25. Powolny AA, Wang S, Carlton PS, Hoot DR, Clinton SK. Interrelationships between dietary restriction, the IGF-1 axis, and expression of vascular endothelial growth factor by prostate adenocarcinoma in rats. Mol Carcinog. 2008;47:458–65. [PubMed]

26. Saxton JM. Diet, physical activity and energy balance and their impact on breast and prostate cancers.Nutr Res Rev. 2006;19:197–215. [PubMed]

27. Mavropoulos JC, Buschmeyer WC, III, Tewari AK, et al. The effects of varying dietary carbohydrate and fat content on survival in a murine LNCaP prostate cancer xenograft model.Cancer Prev Res.2009;2:557–65. [PMC free article] [PubMed]

28. Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low- carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359:229–41. [PubMed]

29. Vekateswaran V, Haddad AQ, Fleshner NE, et al. Association of diet-induced hyperinsulinemia with accelerated growth of prostate cancer (LNCaP) xenografts. J Natl Cancer Inst.2007;99:1793–800.[PubMed]

Asprin and Prostate Cancer

Mon, 07 Mar 2016 12:17:00 GMT

In men with prostate cancer, regular aspirin use is associated with a slower rate of disease progression and a reduced risk of dying from the disease, according to a new study.

The findings come from an analysis of data from the large prospective Physicians' Health Study, in which 3193 men developed prostate cancer over a 27-year period. Of these cancers, 403 were lethal, defined as metastatic disease or death from prostate cancer.

But the risk developing lethal prostate cancer was 24% lower in men who took aspirin on a regular basis, explained lead investigator Christopher Brian Allard, MD, a urologic oncology fellow at Brigham and Women's Hospital and Massachusetts General Hospital in Boston.

Dr Allard was speaking at a press briefing held in advance of the Genitourinary Cancers Symposium 2016 in San Francisco.

"Men with prostate cancer who took aspirin regularly had a 39% lower risk of dying from prostate cancer," said Dr Allard.

However, aspirin use did not measurably reduce the overall incidence of prostate cancer. It also did not prevent high-grade cancers or locally advanced prostate cancers, Dr Allard noted.

"We found that aspirin intake before prostate cancer diagnosis was not beneficial," he reported.

Several observational studies that have looked at the association between aspirin use and prostate cancer outcomes have produced mixed results. For example, a large population-based study conducted last year in the United Kingdom showed that aspirin use after newly diagnosed nonmetastatic prostate cancer does not lower disease-specific or overall mortality.

However, an earlier study showed that anticoagulants reduced the risk of dying from the disease from 10% to 4% at 10 years, and that the benefit was greatest with aspirin use