On July 10, 2013, major media headlines and news stories claimed "
Too Much Fish Oil Might Boost Prostate Cancer Risk." Wow, that sure seems fishy given all of the positive health benefits linked to fish oil
intake. In examining the study, there are numerous issues that clearly
indicate that perhaps the conclusion is wrong, but really a study's
conclusion is only as good as the study itself.
Data Used was From the SELECT Study
The pedigree of the study source is impressive. It was published in the
Journal of the National Cancer Institute and was conducted by
researchers from the Fred Hutchinson Cancer Center in Seattle, WA.1 Yet,
the data they used is from the much maligned Selenium and Vitamin E
Cancer Prevention Trial (SELECT). That is the real problem.
The SELECT study was a very large clinical study that attempted to
determine whether vitamin E could prevent prostate cancer. Previous
studies had shown 50 IU of vitamin E was protective against prostate
cancer, but the SELECT study chose to use 400 IU of synthetic vitamin E
(dl-alpha-tocopherol) at a dosage of 400 IU. Results showed that the
subjects taking vitamin E alone had a 17% higher risk of prostate cancer
compared to the control group.
In the new analysis, researchers measured the levels of fats in the
blood (plasma phospholipids) and concluded that men with the highest
concentrations of EPA, DPA and DHA-three fatty acids derived from fish
and fish-oil supplements-had an increased risk of prostate cancer.
Specifically, they reported a 71 percent increased risk of high-grade
prostate cancer; a 44 percent increase in the risk of low-grade prostate
cancer and an overall 43 percent increase in risk for total prostate
cancer in a subset of patients with the highest level of these omega-3
fatty acids.
Important considerations of this data are the following:
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This study is not consistent with other studies (discussed below)
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The study did NOT include information or documentation of fish or fish
oil intake in the study group. It was NOT set up initially to evaluate
these factors, hence its relevance is not as significant as studies
designed to specifically determine the impact of omega-3 fatty acids on
prostate cancer risk.
-
There is no evidence that anybody in this study took fish oil supplements or even ate fish.
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In usual circumstances, plasma levels of EPA and DHA reflect very
recent intake and are considered a poor biomarker of long-term omega-3
intake.
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Patients with prostate cancer may have only recently increased their fish and/or fish oil consumption.
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Fish and fish oil ingestion produces a big rise in plasma omega-3 levels in about 4.5 hours and washes out around 48 hours.
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The data may reflect cancer activity rather than a causative
association. Without dietary history or documentation of fish oil use
there is no way of knowing.
Lastly, the following statement by the authors suggests that they may
have significant bias: "There is really no evidence that taking dietary
supplements is beneficial to health, and there is increasing evidence
that taking high doses is harmful." Such a statement shows a clear axe
to grind in light of a great deal of scientific evidence on the value of
dietary supplementation.
A Closer Look at the Reported Results
Let's take a closer look at the reported results to see if things add
up. The bottom line is that they do not. Let's first take a look at the
blood levels of EPA+DHA – the major forms of long-chain omega-3 fatty
acids found in fish oil supplements. As Table 1 shows the levels are
quite similar among the groups. These blood levels of EPA+DHA are
actually quite modest and do not reflect huge levels of fish or fish
supplements being consumed. The average EPA+DHA plasma level for men is
generally approximately 4%. So, the levels reported here are typical,
but a little lower than normal and the ratio of EPA to DHA is also a
little lower as well.
Table 1. Distribution of EPA and DHA among SELECT participants by prostate cancer grade (n=2273)*
That the researchers did next was divide cancer patients up by their
blood levels of fatty acids and look at the hazard ratio – the relative
risk over time – associated with different levels of the various fatty
acids (see Table 2). As it relates to EPA, statistical significance was
not achieved for total cancer or high-grade cancer (the P value has to
be less than 0.05 to be deemed anything more than random chance). For
DHA, there was statistical significance. But, again, the levels of DHA
are typical of what is found in men consuming modest amounts of fish.
However, the level of EPA was lower than that typically found and the
ratio of EPA to DHA was also lower. What this may mean is that there may
be increased conversion of EPA to DHA in prostate cancer. Though one
interesting observation is that the hazard ratio (HR) actually went down
in high-grade prostate cancer in the group with the highest level of
DHA compared to the next highest group. This suggests that it is not
that significant of a factor as one would expect if it was that the
higher the level the higher the HR. But, this finding has a P value of
0.09 so no real conclusions can be made as it was probably a random
finding.
Table 2. Associations between EPA and DHA among SELECT participants by prostate cancer grade (n=2273)
The authors conclude that men are at higher risk of aggressive prostate cancer if the total plasma level of long-chain omega-3 fatty acids
(EPA+DPA+DHA) is greater than 3.68%. If that were true, then aggressive
prostate cancer would be a major health concern and the leading cause
of death in any country with even moderate fish consumption. The facts
are that population-based studies show just the opposite effect. For
example, prostate cancer incidence and death rates are among the lowest
known in populations consuming the traditional Japanese or Mediterranean
diets, two diets with a relatively high content of EPA+DHA.
What do other Studies Show?
In addition to population-based studies, several studies have been
conducted that were actually designed to determine the effects of fish
and fish oil consumption in prostate cancer. In a detailed meta-analysis
conducted in 2010, while fish consumption did not affect prostate
cancer incidence, it was associated with a 63% reduced mortality due to
prostate cancer.2 A meta-analysis examines all previously conducted
studies. Here are some of the results from some of these studies:
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Researchers investigated the effect of dietary fatty fish intake
among 6,272 Swedish men who were followed for 30 years. Results showed
that men who ate no fish had a two- to three-fold increase in the risk
of developing prostate cancer compared with those who consumed large
amounts of fish in their diet.3
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Data from the Physician's Health Study, a study spanning 22 years,
found that fish consumption (≥5 times per week) reduced the risk of
dying from prostate cancer by 36%.4 -specific death.
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A study conducted by the Harvard School of Public Health that
involved 47,882 men over twelve years found that eating fish more than
three times a week reduced the risk of prostate cancer but had an even
greater impact on the risk of metastatic prostate cancer. For each
additional 500 mg of marine fat consumed, the risk of metastatic disease
decreased by 24%.5
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In one of the best-designed studies, researchers in New Zealand
examined the relationship between prostate cancer risk and EPA+ DHA in
red blood cells (a more reflective marker for long-term omega-3 fatty
acid intake). Higher levels of EPA+DHA were associated with a 40%
reduced risk of prostate cancer.6
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In a study of 47,866 US men aged 40-75 years with no cancer history
in 1986 who were followed for 14 years EPA+DHA intake at the highest
levels was associated with a 26% reduced risk of developing prostate
cancer.7
While some studies make an important distinction, others do not.
When ascertaining the benefits of fish consumption it is important to
find out how the fish is being prepared. For example, regular ingestion
of fried fish was associated with a 32% increased risk for prostate
cancer.8 In addition, many studies do not control for the quality of
fish or fish oil. Some fish (and fish oil supplements) can contain
environmental chemicals that can contribute to prostate cancer such as
PCBs, heavy metals, and other toxic chemicals.9, 10 These are important
considerations.
Final Comments
The best thing about this study is that it will stimulate more
research into the role of omega-3 fatty acids in prostate health. The
worst thing about this study is that it may lead to many men abandoning
the use of fish oil supplements. Based upon a large amount of clinical
data it makes sense for men to be consuming 1,000 mg of EPA+DHA daily
for general health. And, if they are suffering from one of the over 60
different health conditions shown to be benefitted by fish oil
supplementation the dosage should be increased to 3,000 mg of EPA+DHA
daily.
References:
1. Brasky TM, Darke AK, Song X, et al.
Plasma phospholipid fatty acids and prostate cancer risk in the SELECT Trial. J National Cancer Inst Online. July 10, 2013 doi: 10.1093/jnci/djt174
2. Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and
prostate cancer risk: a review and meta-analysis. Am J Clin Nutr. 2010
Nov;92(5):1223-33.
3. Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A.
Fatty fish consumption and risk of prostate cancer. Lancet 2001; 357:
1764-6
4. Chavarro JE et al. A 22-y prospective study of fish
intake in relation to prostate cancer incidence and mortality. Am J Clin
Nutr 2008; 88: 1297-303.
5. Augustsson, K., et al., A prospective study of intake of
fish and marine fatty acids and prostate cancer. Cancer Epidemiol
Biomarkers Prev, 12(1): p. 64-7, 2003.
6. Norrish AE, Skeaff CM, Arribas GL, Sharpe SJ, Jackson RT.
Prostate cancer risk and consumption of fish oils: a dietary
biomarker-based case-control study. Br J Cancer 1999;81:1238-42.
7. 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.
8. Stott-Miller M, Neuhouser ML, Stanford JL. Consumption of
deep-fried foods and risk of prostate cancer. Prostate. 2013
Jun;73(9):960-9.
9. Ritchie JM, Vial SL, Fuortes LJ, Robertson LW, Guo H,
Reedy VE, Smith EM.Comparison of proposed frameworks for grouping
polychlorinated biphenyl congener data applied to a case-control pilot
study of prostate cancer. Environ Res. 2005;98(1):104-13.
10. Mullins JK, Loeb S. Environmental exposures and prostate cancer. Urol Oncol. 2012 Mar-Apr;30(2):216-9.
: This article is not intended to provide medical advice, diagnosis or treatment.
When wheat was genetically modified to address world hunger, it was
fattened up and made into a short, stubby dwarf species, which is vastly
different from the ancient einkorn wheat mentioned in the Bible. Fattened up
wheat kernels are not just carbohydrates but super carbs that our bodies never
evolved to work with.