Study implicates omega-3 fatty acids in prostate cancer - Is this reliable information?

I have reported on the inconsistent studies on omega-3 fatty acids and prostate cancer risk. More recently, a study has added to the confusion; the media has picked it up and scared men away from omega-3 supplements, meanwhile some experts have criticized the authors’ methodology and conclusions.

This study used data from a clinical trial on vitamin E and selenium supplementation for cancer prevention, and added on a blood test for omega-3 to determine whether there was an association between plasma levels of omega-3 fatty acids and incidence of prostate cancer.  The authors found a statistically significant difference in the average total long-chain omega-3 blood level between men who did or did not develop prostate cancer throughout the study.1

I have serious concerns about the potential risks of taking lots of fish oil capsules.  So much fish oil can have paradoxical effects, reducing immune function in later life.  Plus eating lots of fish exposes you to risky amounts of chemical pollutants, and raises IGF-1, a hormone that is causative in prostate cancer, so it is not that this relationship has no potential to be true.  However, this study does not tell us if these are valid concerns or not and we can’t make any meaningful conclusions from this new study.  This study does NOT indicate that omega-3 supplementation or eating fish are a contributory factor in the prostate cancer equation for numerous reasons.

1.       Plasma vs. erythrocyte fatty acid measurement, done only once

Although measuring omega-3 levels in the blood seems like it would be an objective and accurate indicator of fish oil intake compared to using the subjects’ reported dietary intake, this test does not  accurately reflect long-term dietary intake. There are two methods for measuring blood fatty acids; in plasma or in erythrocyte (red blood cell) membranes.  Erythrocyte omega-3 measurement has been reported to be a more accurate reflection of long-term blood levels, and to correlate more closely with dietary intake compared to plasma measurement.2   Regardless of which test was used, one blood test does not reflect one’s fish oil intake or fish exposure over a lifetime or even over a twenty year period.  Cancer is caused by what you do for many, many years, not what you do for a few weeks or months.   You would have to do multiple blood tests over many years to assure the results were indicative of a dietary pattern.  Also, since there was only one blood test at baseline in this study (and they used plasma levels), it only reflects what they consumed a few days before the test was drawn. This is very important, since cancer takes many years to develop. Some men that did have higher levels may have started taking fish oils supplements only recently, and some may have simply eaten a large piece of fish the night before the blood test.

2.       The tiny difference in blood omega-3s between the cases and controls.

The authors found a statistically significant difference in the average total omega-3 blood level between men who did or did not develop prostate cancer throughout the study. But is this a meaningful difference out in the real world?  In men diagnosed with prostate cancer, the average was 4.66% of total fatty acids; in men without cancer, the average was 4.48%. This is a very small difference, and likely reflects an insignificant difference in omega-3 intake.   

3.       No information on fish, fish oil, or other omega-3 supplement intake of subjects.

Where did the slight difference in omega-3 blood levels come from? Were the men who were diagnosed with cancer more likely to be taking fish oil capsules? Were they eating more fish overall?  More breaded and fried fish? More large, predator fish? The type of fish and how it is prepared would impact the level of environmental contaminants and dietary carcinogens.  Could the early development of prostate cancer increase blood omega-3s, rather than vice versa? 3 These unanswered questions make it very difficult to extract any useful information from this study’s results.  For it to have substantive impact they would have had to track dietary fish consumption, fish oil consumption and have confirm that was a true recall, with confirmatory blood tests taken episodically. 

4.       Rancid fish oil?

Industry experts have pointed to the potential role of rancid fish oil in the inconsistent results among omega-3 studies. Animal studies have shown that rancid fish oil could promote inflammation and even cancer, and the majority of fish oil capsules are indeed rancid. Omega-3s are highly unstable fats, very susceptible to oxidation, forming lipid peroxides and starting a chain of oxidation reactions leading to rancidity.  Exposure of EPA and DHA to light, heat and oxygen increase the likelihood of oxidation.4

(Fresh, non-rancid fish oil does not have an unpleasant taste or smell. If you take omega-3 capsules, open one up and taste the oil to test whether it has gone rancid.)  

5.       Research on omega-3s and prostate cancer remains inconsistent.

The authors state, “It is unclear why high levels of long-chain omega-3 PUFA would increase prostate cancer risk, and further study will be needed…” As discussed in my previous article, the literature on omega-3 fatty acids and prostate cancer is indeed inconsistent.

A 2010 meta-analysis of 31 studies on fish consumption and prostate cancer risk found no significant effect overall, and noted the inconsistency between studies: the risks of prostate cancer diagnosis calculated for high fish consumption ranged from a 61% decrease to a 77% increase.5  A 2013 meta-analysis of studies on blood omega-3 levels and prostate cancer also found no effect overall on prostate cancer risk, and noted significant heterogeneity (inconsistency in results) between studies. Only after removing one study from their analysis did they see an increased risk of high-grade prostate cancer.6  Interestingly, Asian populations, such as in Japan, that consume high levels of fish tend to have lower rates of prostate cancer.7-9 The 2010 meta-analysis also found a 63% decrease in risk of death from prostate cancer with high fish consumption.5  Many studies have shown that DHA and EPA decrease proliferation and increase cell death in prostate cancer cells, and that omega-3-enriched diets slow prostate tumor growth in animals.10-20  A clinical trial published in 2011 gave patients about to undergo prostatectomy either a low-fat (15% of calories) diet plus fish oil supplementation or a Western diet with no supplements for 4-5 weeks prior to surgery. The fish oil supplemented group showed a 32.2% decrease in malignant cell proliferation when prostate tissue was analyzed after surgery.21  Though many people with biases want to jump on the results of one of these studies to claim fish or fish oil are good or bad, we simply cannot do so with scientific integrity.   There are many different studies on this topic with widely varying results.

Omega-3 supplementation: the big picture

For optimal health (including cancer protection), we require the complete composition of the nutrient-dense (Nutritarian) diet that supplies us with optimal amounts of all valuable nutrients and phytochemicals.  Avoiding deficiencies is critical, but it is important to avoid excesses too.  Omega-3 fatty acids are essential nutrients that we must get from our diets because our bodies cannot make them; they are crucial for early brain development, and there is much evidence that they promote cardiovascular health and cognitive function.22,23  Note also, that higher omega-3 blood levels have been associated with reduced risk of death from all causes.24  Avoiding supplemental omega-3s is not the appropriate response to this new study.  This is especially critical because we all convert short chain omega-3 (ALA) into long chain omega-3 (DHA) differently, and if you are one of those poor converters, the lack of DHA in your diet can turn out to be devastating to you in later life.  Many vegans are gambling with their future cognitive health to uphold a philosophical viewpoint, because once you develop a neurological or cognitive deficit in later life, it will be too late to try to fix a deficiency that could have caused it. 

Of course, too much of any potentially good thing turns it bad.  For any needed nutrient, especially fat soluble nutrients, too much can be problematic.  Since all fish oil capsules give a pretty high dose of EPA and DHA, and most of them are rancid too, they could be part of the problem. Plus, fish is an unfavorable omega-3 source, since animal protein and environmental contaminants are packaged with the DHA and EPA.   I advise most people take a low dose of algae-derived EPA-DHA, or follow your omega-3 levels episodically to assure no deficiency exists.  Maintaining adequate, but not excessively high DHA and EPA levels is the safest and most conservative and responsible strategy. 



1. Brasky TM, Darke AK, Song X, et al: Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial. J Natl Cancer Inst 2013.
2. Sun Q, Ma J, Campos H, et al: Comparison between plasma and erythrocyte fatty acid content as biomarkers of fatty acid intake in US women. Am J Clin Nutr 2007;86:74-81.
3. Liu Y: Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis 2006;9:230-234.
4. Albert BB, Cameron-Smith D, Hofman PL, et al: Oxidation of marine omega-3 supplements and human health. Biomed Res Int 2013;2013:464921.
5. Szymanski KM, Wheeler DC, Mucci LA: Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr 2010;92:1223-1233.
6. Sorongon-Legaspi MK, Chua M, Sio MC, et al: Blood level omega-3 Fatty acids as risk determinant molecular biomarker for prostate cancer. Prostate Cancer 2013;2013:875615.
7. Dewailly E, Mulvad G, Sloth Pedersen H, et al: Inuit are protected against prostate cancer. Cancer Epidemiol Biomarkers Prev 2003;12:926-927.
8. Kobayashi M, Sasaki S, Hamada GS, et al: Serum n-3 fatty acids, fish consumption and cancer mortality in six Japanese populations in Japan and Brazil. Jpn J Cancer Res 1999;90:914-921.
9. Hebert JR, Hurley TG, Olendzki BC, et al: Nutritional and socioeconomic factors in relation to prostate cancer mortality: a cross-national study. J Natl Cancer Inst 1998;90:1637-1647.
10. Cavazos DA, Price RS, Apte SS, et al: Docosahexaenoic acid selectively induces human prostate cancer cell sensitivity to oxidative stress through modulation of NF-kappaB. Prostate 2011.
11. Hu Y, Sun H, Owens RT, et al: Syndecan-1-dependent suppression of PDK1/Akt/bad signaling by docosahexaenoic acid induces apoptosis in prostate cancer. Neoplasia 2010;12:826-836.
12. Chung BH, Mitchell SH, Zhang JS, et al: Effects of docosahexaenoic acid and eicosapentaenoic acid on androgen-mediated cell growth and gene expression in LNCaP prostate cancer cells. Carcinogenesis 2001;22:1201-1206.
13. Rose DP, Connolly JM: Effects of fatty acids and eicosanoid synthesis inhibitors on the growth of two human prostate cancer cell lines. Prostate 1991;18:243-254.
14. Bureyko T, Hurdle H, Metcalfe JB, et al: Reduced growth and integrin expression of prostate cells cultured with lycopene, vitamin E and fish oil in vitro. Br J Nutr 2009;101:990-997.
15. Istfan NW, Person KS, Holick MF, et al: 1alpha,25-Dihydroxyvitamin D and fish oil synergistically inhibit G1/S-phase transition in prostate cancer cells. J Steroid Biochem Mol Biol 2007;103:726-730.
16. Yi L, Zhang QY, Mi MT: [Role of Rho GTPase in inhibiting metastatic ability of human prostate cancer cell line PC-3 by omega-3 polyunsaturated fatty acid]. Ai Zheng 2007;26:1281-1286.
17. Nakajima T, Kubota N, Tsutsumi T, et al: Eicosapentaenoic acid inhibits voltage-gated sodium channels and invasiveness in prostate cancer cells. Br J Pharmacol 2009;156:420-431.
18. Aronson WJ, Barnard RJ, Freedland SJ, et al: Growth inhibitory effect of low fat diet on prostate cancer cells: results of a prospective, randomized dietary intervention trial in men with prostate cancer. J Urol 2010;183:345-350.
19. Berquin IM, Min Y, Wu R, et al: Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest 2007;117:1866-1875.
20. Kelavkar UP, Hutzley J, Dhir R, et al: Prostate tumor growth and recurrence can be modulated by the omega-6:omega-3 ratio in diet: athymic mouse xenograft model simulating radical prostatectomy. Neoplasia 2006;8:112-124.
21. Aronson WJ, Kobayashi N, Barnard RJ, et al: Phase II prospective randomized trial of a low-fat diet with fish oil supplementation in men undergoing radical prostatectomy. Cancer Prev Res (Phila) 2011;4:2062-2071.
22. Simopoulos AP: The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med (Maywood) 2008;233:674-688.
23. Simopoulos AP: Evolutionary aspects of diet: the omega-6/omega-3 ratio and the brain. Mol Neurobiol 2011;44:203-215.
24. Mozaffarian D, Lemaitre RN, King IB, et al: Plasma Phospholipid Long-Chain omega-3 Fatty Acids and Total and Cause-Specific Mortality in Older Adults: A Cohort Study. Ann Intern Med 2013;158:515-525.

Debunking the anti-soy myths

Despite the abundance of scientific evidence demonstrating the benefits of whole soy foods, many people have been scared off from healthful foods like edamame by the anti-soy propaganda (lacking responsible scientific integrity) that continues to float around the internet.

Edamame. Flickr: cl_03

It is true that the nutrient-depleted isolated soy in protein powders and processed foods is likely problematic. And of course, I recommend steering clear of genetically modified soy, as its safety, phytochemical value, and environmental impact remain questionable.

However, research has shown overwhelmingly that whole and minimally processed soy foods (like edamame, tofu and tempeh) provide meaningful health benefits. The presence of isoflavones, a class of phytoestrogen, has sparked much of the controversy around soy. There were concerns that these plant estrogens could potentially promote hormonal cancers, such as breast and prostate cancers; however, those fears were unfounded. I have previously discussed the large body of evidence that convincingly suggests that whole and minimally processed soy foods protect against breast cancer. In addition, a 2009 meta-analysis of studies on soy and prostate cancer found that higher soy intake was associated with a 26% reduction in risk.1 In addition, it appears that isoflavones have a number of anti-cancer effects that are unrelated to their ability to bind the estrogen receptor. Accordingly, soy foods are not only associated with decreased risk of hormonal cancers, but also lung, stomach, and colorectal cancers.2-4 (For further discussion of soy foods and health, see the May 2012 member teleconference.)

An article posted by John Robbins seeks to finally put the soy misinformation to rest. He provides a balanced review of the available information, addressing all the common concerns about soy, from cancer and osteoporosis risk to protein digestibility and mineral absorption.

Soy is not a magic pill or a poison; it is simply a bean.

One can’t argue with the data – the associations between minimally processed soy intake and reduced risk of cancers has been reported over and over again. There is no real controversy here.  However, one still should not eat lots of soy products, to the exclusion of other valuable foods. Variety is crucial for obtaining diversity in protective phytochemicals, and a variety of beans are health promoting, along with many other foods.  So use good judgment, avoid processed foods, GMO foods and eat a variety of whole natural plant foods including beans such as black beans, chickpeas, lentils and enjoy some edamame, tofu and tempeh as well.

 John Robbins: The truth about soy


Image credit - Flickr: cl_03


1. Hwang YW, Kim SY, Jee SH, et al: Soy food consumption and risk of prostate cancer: a meta-analysis of observational studies. Nutr Cancer 2009;61:598-606.
2. Yang WS, Va P, Wong MY, et al: Soy intake is associated with lower lung cancer risk: results from a meta-analysis of epidemiologic studies. Am J Clin Nutr 2011;94:1575-1583.
3. Kim J, Kang M, Lee JS, et al: Fermented and non-fermented soy food consumption and gastric cancer in Japanese and Korean populations: a meta-analysis of observational studies. Cancer Sci 2011;102:231-244.
4. Yan L, Spitznagel EL, Bosland MC: Soy consumption and colorectal cancer risk in humans: a meta-analysis. Cancer Epidemiol Biomarkers Prev 2010;19:148-158.

Population-wide PSA screening: no reduction in deaths

Prostate cancer is exceedingly common, especially with age. It estimated from autopsy studies that one-third of men in their forties have prostate cancer, and by age 85, that figure increases to as high as 75%.1,2 However, most of these cases of prostate cancer are not actually life-threatening. The lifetime risk of a diagnosis is 15.9%, but the lifetime risk of death from prostate cancer is only 2.8%. Even without treatment, most prostate cancers are not deadly.2 Most men with prostate cancer die from other causes, not from prostate cancer.

Because of the low risk of death from prostate cancer, there is controversy regarding population-wide PSA screening of men without symptoms suggesting prostate cancer. There is no distinction by the PSA between disease that is likely or unlikely to progress to a life-threatening disease. So should all men be screened?

The most important question is this: Does screening reduce the risk of dying from prostate cancer?
The U.S. Preventive Services Task Force, an impartial agency that assesses scientific evidence on prevention and primary care, issued a statement in 2008 saying that they had found “insufficient evidence that screening for prostate cancer improved health outcomes” in men younger than 75. In men 75 or older, the USPSTF found that “the harms of screening and treatment outweigh any potential benefits.”3

Evidence that screening does not reduce death rates
A long-term study published in January 2012 did not find any decrease in prostate cancer deaths in men undergoing annual screening compared to a control group. The Prostate, Lung, Colorectal, and Ovarian cancer screening trial (PLCO trial) of over 76,000 men had published intermediate results after 10 years of follow up, and were not updating that study, extending to 13 years of follow up. The results were similar after 13 years: about 12% more cancers were diagnosed in the screening group, but death rates were not different between the two groups, suggesting that population-wide screening does not reduce the number of prostate cancer deaths.4

This report came on the heels of a meta-analysis of PSA screening trials performed for the USPSTF in October 2011, which reported information from 5 trials (including the 10-year data from the PLCO trial). Collectively analyzing data from these trials, the authors concluded that PSA screening “results in small or no reduction in prostate cancer-specific mortality.”5

Could PSA screening be harmful?
Despite the above evidence, the idea of screening is still attractive – if you had prostate cancer, wouldn’t it be better to know it? Maybe not.

PSA screening is known to produce many false-positive results - about 70% of men who have elevated PSA levels do not actually have cancer.6 Certainly, psychological harms are inherent in false-positive results, although there is insufficient research to estimate the extent of this harm.5

Healthy men who undergo annual screening may expose themselves to unnecessary and potentially harmful treatments:

  • Prostate biopsy complications include fever, infection, bleeding, pain, and urinary difficulty in some men.
  • If an abnormal PSA followed by prostate biopsy does indeed detect cancer, 90% of men will be treated with surgery, radiation, or androgen deprivation therapy.
    • Up to 0.5% of men die within 1 month of prostate cancer surgery, and 0.6-3% have cardiovascular events. One to seven percent will have serious complications. Radiation and surgery have adverse effects including urinary continence and erectile dysfunction in 20-30% of men. Radiation is also associated with bowel dysfunction.2, 3
    • Androgen deprivation therapy for localized prostate cancer is associated with erectile dysfunction in about 40% of men. Additional serious harms have been reported in patients receiving androgen deprivation therapy for advanced prostate cancers, including increased risk of heart disease, diabetes and bone fractures.2,3,7

Since most cases of prostate cancer are not life-threatening, these procedures are often unnecessary.

The U.S. Preventive Services Task Force (USPSTF) states their screening recommendations as such:

“…the USPSTF now recommends against PSA-based screening for prostate cancer in all age groups.”2

For real protection against cancer, we must focus on prevention rather than relying on early detection. A diet based on beneficial plant foods with documented anti-cancer properties is much more reliable than PSA screening, and protects against heart disease, diabetes, and all cancers, not just prostate cancer. A healthful, plant-based diet is also effective at halting the progression of prostate cancer.8-11

To learn more about protecting yourself from prostate cancer, read my 10 strategies for preventing prostate cancer. Also, in my book, Super Immunity, I discuss the latest scientific research on super foods that supercharge the immune system and fight cancer, and I explain how to put this knowledge into practice by following an anti-cancer eating style.




1. Sakr WA, Haas GP, Cassin BF, et al: The frequency of carcinoma and intraepithelial neoplasia of the prostate in young male patients. J Urol 1993;150:379-385.
2. Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement. U.S. Preventive Services Task Force; 2012.
3. Screening for Prostate Cancer: U.S. Preventive Services Task Force Recommendation Statement. 2008.
4. Andriole GL, Crawford ED, Grubb RL, 3rd, et al: Prostate Cancer Screening in the Randomized Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial: Mortality Results after 13 Years of Follow-up. J Natl Cancer Inst 2012;104:125-132.
5. Chou R, Croswell JM, Dana T, et al: Screening for prostate cancer: a review of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2011;155:762-771.
6. Esserman L, Shieh Y, Thompson I: Rethinking Screening for Breast Cancer and Prostate Cancer. JAMA: The Journal of the American Medical Association 2009;302:1685-1692.
7. Robinson D, Garmo H, Lindahl B, et al: Ischemic heart disease and stroke before and during endocrine treatment for prostate cancer in PCBaSe Sweden. Int J Cancer 2012;130:478-487.
8. Frattaroli J, Weidner G, Dnistrian AM, et al: Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology 2008;72:1319-1323.
9. Fuhrman J: Dr. Joel Fuhrman Case Study Series: Prostate Cancer.
10. Ornish D, Magbanua MJ, Weidner G, et al: Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A 2008;105:8369-8374.
11. Ornish D, Weidner G, Fair WR, et al: Intensive lifestyle changes may affect the progression of prostate cancer. J Urol 2005;174:1065-1069; discussion 1069-1070.


Omega-3 fatty acids - do they increase or decrease prostate cancer risk?

A study produced confusing results.  It found that a higher blood concentration of omega-3 fatty acids was associated with increased risk of high-grade prostate cancer, and a higher concentration of trans-fats was associated with decreased risk.1  These men were not supplementing with liquid fish oil, so it can be assumed that the blood levels represented fish intake.  So should men still take omega-3 supplements?  We know that DHA is good for the heart and the brain, but is it really bad for the prostate?  What about trans-fats – how could more of this unhealthy fat possibly be beneficial for the prostate? 

When we look more closely, we can see that this one study should not dictate major changes in our view of a cancer-preventive lifestyle. Read the entire article on

Fish oil. Flickr: D'Arcy Norman


High fish consumption/blood omega-3s increase risk in some studies, decrease risk in others


  • In a 2010 meta-analysis of 31 studies, the risks of prostate cancer diagnosis calculated for high fish consumption ranged from a 61% decrease in risk to a 77% increase in risk, and several showed no significant differences in risk at all. 
  • In the same meta-analysis, pooled data from four studies on fish consumption and death from prostate cancer (rather than diagnosis of prostate cancer) found a 63% decrease in risk for high fish consumption. 2 
  • A meta-analysis of studies on ALA intake (the omega-3 in plant foods like flax, hemp, chia, and walnuts, and small amounts in leafy greens) concluded that there was a small but significant decrease in risk (5%) for men consuming more than 1.5 grams of ALA per day.3  
  • At least 15 studies have used blood concentrations of omega-3 fatty acids as a measure of omega-3 intake.  Some studies reported increased risk, some decreased risk, and some no effect.

Remember when looking at fish intake, we are not looking at omega-3 intake alone.  

Salmon. Flickr: Andrea Pokrzywinski

Fish are rich in omega-3s, but they also contain a significant amount of animal protein and accumulated environmental pollutants, both of which have been linked to prostate cancer. 4-7  Sufficient research has not been done on omega-3 supplements and prostate cancer to make any conclusions. 

If we were to conclude anything from all the studies available on this subject it would be that fish and omega-3 fats in general do not have a major impact on this disease, but the inconsistency and widely differing results suggest regional variation in pollutant levels in the fish consumed.

Trans-fats and blood levels; more confusion in the midst.  

Before you start eating Twinkies and French Fries fried in trans fat for their prostate cancer protection, let’s consider the possibility that after consuming trans fats (trans fats are man-made fat, already linked with cancer in multiple studies), those inflammatory fats are either burned, removed or stored in the body.  Their levels may fluctuate abnormally because of having cancer.  Therefore the high omega-3 and low trans fat blood levels in this study could be early signs of developing cancer, not the cause of it.  Also, three previous studies on either trans-fat intake or blood trans-fats have found increased risk of prostate cancer.8-10

Should men still take omega-3 supplements?  

Remember that omega-3s are essential fatty acids – the body cannot make them if we don’t get them from our diet.  A deficiency of nutrients the body requires is never favorable for health, but more than needed may not be better when it comes to omega-3 fatty acids.   I still recommend omega-3 sufficiency, which can be achieved with 100-200 mg/day of DHA plus 1 tbsp. of ground flaxseed for ALA.  Almost all nutrients can be harmful in deficiency or excess.  

Read the entire article on



1. Brasky TM, Till C, White E, et al: Serum Phospholipid Fatty Acids and Prostate Cancer Risk: Results From the Prostate Cancer Prevention Trial. Am J Epidemiol 2011.

2. Szymanski KM, Wheeler DC, Mucci LA: Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr 2010;92:1223-1233.

3. Carayol M, Grosclaude P, Delpierre C: Prospective studies of dietary alpha-linolenic acid intake and prostate cancer risk: a meta-analysis. Cancer Causes Control 2010;21:347-355.

4. 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;12:84-89.

5. Rowlands MA, Gunnell D, Harris R, et al: Circulating insulin-like growth factor peptides and prostate cancer risk: a systematic review and meta-analysis. Int J Cancer 2009;124:2416-2429.

6. Hardell L, Andersson SO, Carlberg M, et al: Adipose tissue concentrations of persistent organic pollutants and the risk of prostate cancer. J Occup Environ Med 2006;48:700-707.

7. Van Maele-Fabry G, Libotte V, Willems J, et al: Review and meta-analysis of risk estimates for prostate cancer in pesticide manufacturing workers. Cancer Causes Control 2006;17:353-373.

8. Hu J, La Vecchia C, Gibbons L, et al: Nutrients and risk of prostate cancer. Nutr Cancer 2010;62:710-718.

9. King IB, Kristal AR, Schaffer S, et al: Serum trans-fatty acids are associated with risk of prostate cancer in beta-Carotene and Retinol Efficacy Trial. Cancer Epidemiol Biomarkers Prev 2005;14:988-992.

10. Chavarro JE, Stampfer MJ, Campos H, et al: A prospective study of trans-fatty acid levels in blood and risk of prostate cancer. Cancer Epidemiol Biomarkers Prev 2008;17:95-101.


Men with recurring prostate cancer not dying from prostate cancer

       Prostate cancer is the second most common cancer in men (second to skin cancer). It is well established that the death rate from prostate cancer is quite low:

  • Men in the U.S. have a 16% lifetime chance of being diagnosed with prostate cancer, but only a 3% chance of dying from it.[1]
  • The five-year and ten-year relative survival rates for prostate cancer are over 99% and 91%, respectively. [2]
  • The primary causes of death of men with prostate cancer are cardiovascular disease and other cancers.[3]

After treatment for prostate cancer (either radiation or prostatectomy), prostate-specific antigen (PSA) levels continue to be monitored. If PSA begins to increase, this is called “biochemical recurrence” (BCR) of prostate cancer.

Biochemical recurrence and mortality

A study in U.S. veterans attempted to figure out how biochemical recurrence affected risk of dying from prostate cancer. Six hundred twenty three men were followed for 15 years after being treated for prostate cancer. In this study, 37% of men who were treated with prostatectomy and 48% of men who were treated with radiation experienced BCR.

Overall, a total of 387 men had died within 15 years – 48 of these men died of prostate cancer, representing 12% of total deaths. For men who underwent prostatectomy and experienced BCR, the total rate of death within five years was 34%, and the rate of prostate cancer death was 3%. For radiation and BCR, death rate within five years was 35%, and prostate cancer death rate was 11%.[4, 5]

In short, the researchers came to the conclusion that the probability of dying from prostate cancer, even after biochemical recurrence, is relatively small. They mention that their findings are in agreement with the often quoted phrase “most men die with prostate cancer, not of it.”

Since BCR is defined as an increase in PSA following treatment, this data also suggests that PSA levels may not be an accurate predictor of risk after treatment. Further studies will likely examine this issue.

Routine PSA screening

Routine PSA screening is known by the scientific community not to be as accurate or valuable as the public is led to believe. About 70% of men with elevated PSA do not actually have cancer, and PSA screening is not thought by scientists to reduce prostate cancer-related deaths.[6-8] Richard J. Ablin, who originally discovered PSA in 1970, called PSA screening a “hugely expensive public health disaster” in a New York Times editorial. Dr. Ablin supports his assertion with these facts:

  • FDA approval of PSA tests occurred largely in response to a study that found that PSA screening was only able to detect 3.8% of cancers, and that blood PSA levels may be elevated due to a number of factors, such as drug use, infections, and benign prostatic hyperplasia (BPH).
  • The U.S. Preventive Services Task Force, the American College of Preventive Medicine, and the American Cancer Society do not recommend routine PSA screening. However, PSA screening is still routinely used.[1]

Men should not rely on PSA screening as a method of “early detection” to prevent prostate cancer. Rather they should avoid the cause of prostate cancer. Diets high in vegetables (especially cruciferous vegetables and tomato products) and fruit, and low in dairy products, meat, and processed foods, are known to be protective.[9-11] Living and eating healthfully protects against prostate cancer, as well as the other chronic diseases common to Americans (such as heart disease, strokes, and colon cancer) – the same diseases that kill most men with prostate cancer. For those who already have prostate cancer, a healthy, plant-based diet is effective at halting progression of the disease.[12-15]



1. Ablin, R.J., The Great Prostate Mistake, in New York Times. 2010. p. 27.
2. American Cancer Society. What are the key statistics about prostate cancer? 06/30/2010 09/02/2010]; Available from:
3. Ketchandji, M., et al., Cause of death in older men after the diagnosis of prostate cancer. J Am Geriatr Soc, 2009. 57(1): p. 24-30.
4. Uchio, E.M., et al., Impact of biochemical recurrence in prostate cancer among US veterans. Arch Intern Med, 2010. 170(15): p. 1390-5.
5. Harding, A. Even when prostate cancer returns, most survive. Reuters Health 08/25/10; Available from:
6. Esserman, L., Y. Shieh, and I. Thompson, Rethinking Screening for Breast Cancer and Prostate Cancer. JAMA: The Journal of the American Medical Association, 2009. 302(15): p. 1685-1692.
7. Coldman, A.J., N. Phillips, and T.A. Pickles, Trends in prostate cancer incidence and mortality: an analysis of mortality change by screening intensity. CMAJ, 2003. 168(1): p. 31-5.
8. Andriole, G.L., et al., Mortality results from a randomized prostate-cancer screening trial. N Engl J Med, 2009. 360(13): p. 1310-9.
9. Steinbrecher, A., et al., Dietary glucosinolate intake and risk of prostate cancer in the EPIC-Heidelberg cohort study. Int J Cancer, 2009. 125(9): p. 2179-86.
10. van Breemen, R.B. and N. Pajkovic, Multitargeted therapy of cancer by lycopene. Cancer Lett, 2008. 269(2): p. 339-51.
11. Ma, R.W. and K. Chapman, A systematic review of the effect of diet in prostate cancer prevention and treatment. J Hum Nutr Diet, 2009. 22(3): p. 187-99; quiz 200-2.
12. Frattaroli, J., et al., Clinical events in prostate cancer lifestyle trial: results from two years of follow-up. Urology, 2008. 72(6): p. 1319-23.
13. Ornish, D., et al., Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A, 2008. 105(24): p. 8369-74.
14. Ornish, D., et al., Intensive lifestyle changes may affect the progression of prostate cancer. J Urol, 2005. 174(3): p. 1065-9; discussion 1069-70.
15. Fuhrman, J., Dr. Joel Fuhrman Case Study Series: Prostate Cancer.







Zinc, omega-3 fatty acids, and prostate cancer survival

A study in Sweden examined the effects of zinc and the omega-3 fatty acid DHA on mortality in prostate cancer patients. Five-hundred twenty-five men with prostate cancer were followed for twenty years after being diagnosed with prostate cancer.  Baseline dietary habits, stage of cancer at diagnosis, and deaths over the twenty years were recorded and analyzed.1

The authors chose to investigate these two nutrients because zinc and omega-3s share the common action of attenuating the inflammatory response, and chronic systemic inflammation may fuel prostate cancer progression. Importantly, zinc and DHA are both difficult to obtain on a plant-based diet.

Zinc is especially concentrated in the prostate, but zinc levels become depleted in cancerous cells. Addition of zinc to cultured prostate cancer cells leads to cell death, possibly by suppressing the activity of inflammatory molecules. A previous study found that long-term zinc supplementation was associated with reduced risk of advanced prostate cancer.2

The researchers organized the study participants into quartiles according to their intakes of zinc and DHA. In men who were diagnosed with early stage cancers, the highest quartile of zinc intake (15.7 mg zinc daily or more) was associated with a 74% reduction in risk of death from prostate cancer compared to the lowest quartile (12.8 mg zinc daily or less). Absorption of zinc tends to be low on a vegan diet – beans, whole grains, nuts, and seeds have high zinc content, however these foods also contain substances that inhibit the aborption of zinc.3 A 2009 study of vegetarians found a high prevalence of zinc deficiency.4 To correct for bioavailability, the zinc requirement for vegans may be as much as 50% higher than that of omnivores.5

I recommend zinc supplementation with a multivitamin and mineral to ensure sufficient zinc intake in vegans or those who minimize animal foods.

The connection between omega-3 intake and prostate cancer is somewhat complex. For example, flaxseed oil was found to increase prostate cancer risk, whereas whole flaxseed, EPA, and DHA were found to be protective.6,7,8 EPA and DHA are known to have anti-cancer and anti-inflammatory properties.9 In this study, the highest quartile of DHA intake was associated with 30% reduced risk of overall prostate cancer mortality, and a 45% risk reduction in men diagnosed at early stages, supporting the idea that DHA is protective against prostate cancer. Plant foods contain ALA, which can be elongated to DHA, but the major food source of DHA is fish, which often contains pollutants and is not acceptable for vegetarians and vegans. For these reasons, I recommend a laboratory cultivated DHA supplement made from micro-algae, which is also a more environmentally sustainable option than fish or fish oil.

1. Meyer MS, Kasperzyk JL, Andren O, et al. Anti-inflammatory nutrients and prostate cancer survival in the Örebro Prostate Cancer Survivors Cohort. [Abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; 2010. Abstract nr 5747

MedPageToday. AACR: Zinc Linked to Prostate Cancer Survival.

2. Gonzalez A, Peters U, Lampe JW, White E. Zinc intake from supplements and diet and prostate cancer. Nutr Cancer. 2009;61(2):206-15.

3. Hunt JR. Bioavailability of iron, zinc, and other trace minerals from vegetarian diets. Am J Clin Nutr 2003;78(suppl):633S–9S.

4. de Bortoli MC, Cozzolino SM. Zinc and selenium nutritional status in vegetarians. Biol Trace Elem Res. 2009 Mar;127(3):228-33.

5. Frassinetti S, Bronzetti G, Caltavuturo L, et al. The role of zinc in life: a review. J Environ Pathol Toxicol Oncol. 2006;25(3):597-610.

6. Brouwer IA, Katan MB, Zock PL. Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis. J Nutr 2004 Apr;134(4):919-22

7. Demark-Wahnefried W, Polascik TJ, George SL, et al. Flaxseed supplementation (not dietary fat restriction) reduces prostate cancer proliferation rates in men presurgery. Cancer Epidemiol Biomarkers Prev. 2008 Dec;17(12):3577-87.

8. Leitzmann MF, Stampfer MJ, Michaud DS, et al. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. Am J Clin Nutr. 2004 Jul;80(1):204-16.

9. Spencer L, Mann C, Metcalfe M, et al. The effect of omega-3 FAs on tumour angiogenesis and their therapeutic potential. Eur J Cancer. 2009 Aug;45(12):2077-86. 

Eggs and poultry with skin double prostate cancer recurrence risk

Approximately 1300 men who had been diagnosed with prostate cancer were followed for two years to document their dietary patterns and recurrence or progression of their disease. In this study, two specific animal foods were found to be risky - the men that ate the most eggs or poultry with skin were twice as likely to have their disease recur or progress.1

This study makes three important points.

  1. Diet does matter, even after a prostate cancer diagnosis.
  2. There is something in chicken, specifically in the crispy outer portion and skin that is powerfully cancer-inducing. Heterocyclic amines, carcinogenic compounds that are formed when meat is cooked at high temperatures, are a probable culprit. A November 2009 study of 175,000 men showed an increase in prostate cancer risk with consumption of barbequed and grilled meat.2
  3. Consumption of eggs and egg whites is not without risk. Eggs are high in animal protein, which has been linked to cancers. Our populations’ idea that more protein is favorable and that egg (whites) are the perfect food does not hold up to scrutiny. Eggs also could affect prostate cancer due to their high choline content – egg consumption increases the amount of choline in the plasma, and high plasma choline increases prostate cancer risk.3 

Four previous studies implementing a plant-based diet and exercise following prostate cancer diagnosis found a decrease in prostate cancer progression rates.4 

Dietary strategy for prostate health 



1. Richman EL et al. Intakes of meat, fish, poultry, and eggs and risk of prostate cancer progression. Am J Clin Nutr. 2009 Dec 30. [Epub ahead of print]

2. Sinha R et al. Meat and meat-related compounds and risk of prostate cancer in a large prospective cohort study in the United States. Am J Epidemiol. 2009 Nov 1;170(9):1165-77. Epub 2009 Oct 6.


4. R. W.-L. Ma, K. Chapman. A systematic review of the effect of diet in prostate cancer prevention and treatment. J Hum Nutr Diet, 22, pp. 187–199 

Dr. Fuhrman warns: DO NOT take multivitamins or prenatal vitamins that contain folic acid

Folic acid supplementation is dangerous – especially for pregnant women

In a 10-year study,1,2 scientists found that women who take multivitamins containing folic acid increase their breast cancer risk by 20-30%.

Even more alarming are the associations between supplemental folic acid during pregnancy and death from breast cancer,8 and asthma and respiratory tract infections in children.5-6

Read full article


Folic acid is the synthetic form of folate, a B vitamin, which is abundant in green vegetables. Folate protects against birth defects known as neural tube defects (NTDs). Pregnant women could safely increase their folate status and prevent NTDs by eating green vegetables, but instead they are instructed to take folic acid supplements, putting them and their children at risk. Folic acid supplements are not a substitute for folate-containing green vegetables – there are inverse associations between maternal vegetable intake and childhood cancers.12-13

Unlike synthetic folic acid, folate obtained from food sources – especially green vegetables – protects against breast and prostate cancer.

There is inverse relationship between dietary folate intake and breast and prostate cancer.14,3 Chemical differences between folate and folic acid translate into differences in uptake and processing of these two substances by the cells in the intestinal wall – excess folic acid in the circulation can occur. Luckily, folate from food comes naturally packaged in balance with other micronutrients and the body regulates its absorption.9

Rich sources of food folate

As a reference point, the U.S. RDA for folate is 400μg. Below is the approximate folate content for a 100-calorie serving.8

Spinach, raw

843 μg

Romaine lettuce

800 μg

Asparagus, cooked

750 μg

Mustard greens, raw

700 μg

Collards, raw

550 μg

Broccoli, cooked

300 μg


225 μg


150 μg


90 μg


70 μg


55 μg


50 μg

Sunflower seeds

40 μg

Quinoa, cooked

35 μg

Additional foods listed in full article

Clearly, we do not need synthetic folic acid supplements to meet our daily folate requirements.

Dr. Fuhrman’s Gentle Care Formula Multivitamin does not contain folic acid

Supplemental folic acid has also been linked to prostate cancer3, colorectal cancer4, and overall cancer mortality.7 Because folate is abundant in the nutritarian diet, and synthetic folic acid is so potentially dangerous, folic acid is not included in Dr. Fuhrman’s Gentle Care multivitamin.

Dr. Fuhrman does not recommend prenatal vitamins because of the potentially harmful ingredients, such as folic acid.

Dr. Fuhrman’s special recommendations for pregnant women:

(See full article for references)


Breast cancer and prostate cancer: Early detection saves lives?

If breast and prostate cancer were detected early, via mammograms and PSA tests, treatment could begin earlier, and lives would be saved – right?

Wrong, according to an article in the Journal of the American Medical Association that examined incidence and mortality rates for breast and prostate cancer over the past 20 years.1

Why? The authors think that we are in a state of “overdiagnosis” – that many slow-growing, non-threatening tumors are being detected and treated; at the same time, the more dangerous and aggressive cancers may be missed because they can grow and become lethal in the time interval between screenings, and by then treatment will not work. Overall, the mortality rates of breast and prostate cancer have not decreased significantly in the past 20 years.

Still, are there sound reasons to skip these screenings altogether? You decide…

Mammograms: Following detection of a tumor, 80% of biopsies are negative, and the risk of false positives is very high in women under 50.2 This equates to thousands and thousands of unnecessary surgical procedures performed on women after they have had a suspicious mammogram result. In a review, it was estimated that for every 2000 women screened, one will benefit, more than 200 will have a false positive result, and 10 healthy women will be treated unnecessarily.3 And those women who are treated for cancers earn many chemotherapy-related deaths counterbalancing any life-span enhancements in those treated.4 PSA tests: About 70% of men who have elevated PSA levels do not actually have cancer.1 And the side effects of the associated treatments include bowel, urinary, and sexual dysfunction.5 Additionally, a 9-year study in Sweden showed that men who had undergone endocrine treatment for prostate cancer were at a 20-30% increased risk of cardiovascular diseases and death from myocardial infarction.6 

With both of these tests, detection of low-risk cancers also causes much undue emotional trauma to patients and their families.


(image credit: Samat Jain @Flickr)

The American Cancer Society now advises:

“There are some cancers for which we don’t currently recommend screening, such as prostate cancer, because the benefits are unclear or unproven.”7 

The authors of the JAMA article offer strategies for the scientific and medical communities: to find specific biomarkers that can differentiate high-risk from low-risk cancers, and to target high-risk individuals with preventive treatments.

I offer a strategy to you: Be proactive – reduce your risk of breast and prostate cancer. Practice prevention by maintaining a healthy weight and eating an anti-cancer diet - a high-nutrient diet rich in protective phytochemicals from cruciferous vegetables, leafy greens, and berries, and minimizing or eliminating browned foods, animal products, and refined flour and sugar. Taking sufficient Vitamin D is also important. You can read more about the strong connections between diet and cancer in my article “Eat for Health – the Anti-Cancer Diet."



1. Esserman L, Shieh Y, Thompson I. JAMA. 2009 Oct 21;302(15):1685-92. Rethinking screening for breast cancer and prostate cancer.

2. Wright CJ, Mueller CB. Screening mammography and public health policy: the need for perspective. Lancet 1995;346(8966(:29-32.

3. Gøtzsche PC, Nielsen M. Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2009 Oct 7;(4):CD001877.

4. Rock E, De Michele. A Nutritional approaches to late toxicities of adjuvant chemotherapy in breast cancer survivors. J Nutr 2003 Nov;133(11 Suppl 1):3785S-3793S.  

5. Albertsen PC, Hanley JA, Fine J. 20-year outcomes following conservative management of clinically localized prostate cancer. JAMA 2005;293 (17):2095-2101

6. M. Van Hemelrijck et al. 1BA Increased cardiovascular morbidity and mortality following endocrine treatment for prostate cancer: an analysis in 30,642 men in PCBaSe Sweden. EJC Supplements - September 2009 (Vol. 7, Issue 3, Page 1, DOI: 10.1016/S1359-6349(09)72024-5)



Prostate Cancer Over-Diagnosed - Lots of Money to Be Made

People are getting unnecessary medicals test that cost a ton of money? No, you don’t say! A new study in the Journal of the National Cancer Institute reveals large-scale screening for prostate cancer using the prostate-specific antigen, or PSA, test has resulted in mass over-diagnosis and over-treatment:

The death rate from prostate cancer has fallen in the United States, but not necessarily because of mass screening, study co-author Dr. H. Gilbert Welch, a professor of medicine at the Dartmouth Medical School's Institute for Health Policy and Clinical Practice contended. "There are a number of reasons why mortality might fall, but the most obvious is that we have better treatment," he said. "Even without early detection, I expect mortality would fall."

Results of a European study reported earlier this year indicated that "to save the life of one man, 50 must be over-diagnosed," he said.

Guidelines for screening for blood levels of PSA -- a protein produced by the prostate gland -- differ widely. The American Cancer Society does not recommend PSA screening. But, the society says a PSA test can be offered to men, starting at age 50, during a discussion with their physician. That discussion should also include an explanation of the potential benefits and limitations of such screening.

It all comes down to money! I asked Dr. Fuhrman about it and he said, “It’s true. Prostate cancer screening in general is flawed, but it is big business and the business of medicine trumps science because of the money to be made.” And Dr. Fuhrman insists the PSA test does not accurately detect cancer anyway.

An important thing to remember is prevention, prevention, prevention! Reports come out all the time highlighting the benefits of plant foods on prostate cancer prevention:

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