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All,

 

Anyone who has been following discussions around here will realize that I've been criticizing salmon as a healthy food, and Saul has been vehemently defending it, which has lead to some amusing exchanges, e.g. here, here and especially here, where Saul wrote:

 

Bullshit, Dean!

You're quoting the biased statements of Dr. Gregor (however you spell his name [its Greger, for at least the 10th time... --Dean]).  Fish is no more (and no less) contaminated than vegetables, fruit or beef -- it depends on the quality of what you're eating.

 

Well, the evidence just keeps piling up against Saul's sacred cow, er, fish.

 

Background

 

Summary: PCBs are bad sh*t.

 

PCBs (or polychlorinated biphenyls) are man-made organic chemicals widely manufactured and used in a variety of industries, but mostly for cooling and insulating fluid for electrical devices, all over the world up until 1979 when they were banned. Unfortunately, PCBs are very persistent, remaining in the water and soil for many years, and bioaccumulating the in flesh (mostly fat) of animals. Fish, especially fatty fish, seems to be the food in the human diet where the most PCBs bioaccumulate, as illustrated by this graph (data from [2]) of PCB content in 12,000+ food samples from around Europe:

 

kY6mfCp.png

 

Notice that fish oil is off the chart, but people typically only consume a gram or two of FO per day, and this graph represents micrograms per kilograms.  Fish itself (all types) was about 5x higher than any other animal products.  Fruit, vegetables and cereals had close to zero PCBs.

 

Interestingly though, most exposure in North America comes from beef, dairy and other animal flesh rather than fish, since we eat so much more of them than fish:

 

dioxin_chart.png

 

So how bad are PCBs? Pretty bad across the board, including causing cancer, endocrine disruption, reproductive and neurological effects. See here for more details about all the bad effects PCBs have on human health. 

 

With that background, this new study [1] posted by Al (thanks Al!) looked at dietary PCBs levels based on self-reported food-frequency questionnaires from ~36,000 elderly Swedish women, and then followed them for an average of 12 years to see how heart attack risk related to dietary PCB exposure.

 

First, off a helpful chart of demographics of study participants by quartile of dietary PCB intake:

 

IXpIRa7.png

 

As you can see from my highlights, the dietary PCB (and mercury) levels in these women was strongly correlated with fish and long-chain omega-3 intake. Women who ate the most fish had almost 3x the level of PCBs of those who ate the least.

 

So what about heart attacks? Here is what the authors' found:

 

Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of
myocardial infarction of 1.21 (95% confidence interval [CI], 1.01–1.45) compared to the lowest quartile (median
101 ng/day) before, and 1.58 (95% CI, 1.10–2.25) after adjusting for EPA-DHA. Stratification by low and high EPADHA
intake, resulted in RRs 2.20 (95% CI, 1.18–4.12) and 1.73 (95% CI, 0.81–3.69), respectively comparing highest
PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction
after but not before adjusting for dietary PCB.

 

In other words, having the highest intake of PCBs (mostly from fish) was associated with a 21% increase in the risk of heart attack relative to being in the lowest PCB intake group. But it was only a 21% increase because EPA/DHA was pulling the other way, helping to prevent heart attacks. If you statistically factor out the EPA/DHA benefits, PCBs alone would raise heart attack risk by 58% in the top vs. bottom quartile group.

 

Analyzed the other way, EPA/DHA intake wasn't associated with fewer heart attacks, largely because of the PCBs that typically accompany them, it would appear. In fact, those in the highest quartile of DHA/EPA intake had a (non-significant) 11% increase in risk of heart attack. But when they statistically factored out the PCBs, DHA/EPA was (weakly and non-significantly) associated with a 26% reduction in heart attack risk. The relevant data is summarized in this table with my highlights, for anyone who wants to see the details:

 

Li4vgg8.png

 

To summarize, it looks like if you can get DHA/EPA without the accompanying PCBs, it may be a slight win for heart attack risk. But when the DHA/EPA comes as a package deal with PCBs (would you like fries with that?), as it did for these fish-eating Swedish women, it's bad news. And its looks it might be even worse for us skinny folks, since they found:

 

In a stratified analysis, we observed a higher RR [of high dietary PCBs]
(2.39; 95% CI, 1.15–4.96) among lean women (waist circumference
b80 cm) than among those with abdominal adiposity, however the
interaction was not statistically significant (p value = 0.18) and the
confidence interval was wide.
...
Our results indicate a stronger association between PCB and risk of
myocardial infarction among lean women meanwhile no association
among women with abdominal adiposity. One likely explanation behind
the observation is the higher concentrations of circulating PCBs
in blood and lower dilution of PCBs in adipose tissue of lean than of
obese woman [22].

 

Fortunately, it is possible to ensure one gets DHA/EPA without the PCBs, by choosing an algae source of DHA/EPA, like this one, rather than taking one's chances eating fish what one hopes is low in contaminants like PCBs, but which can often be mislabelled.

 

--Dean

 

------------

[1] Int J Cardiol. 2015 Mar 15;183:242-8. doi: 10.1016/j.ijcard.2015.01.055. Epub

2015 Jan 27.
 
Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction -
a population-based prospective cohort study.
 
Bergkvist C(1), Berglund M(2), Glynn A(3), Wolk A(1), Åkesson A(4).
 
 
BACKGROUND: Fish consumption may promote cardiovascular health. The role of major
food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish,
is unclear. We assessed the association between dietary PCB exposure and risk of 
myocardial infarction taking into account the intake of long-chain omega-3 fish
fatty acids.
METHODS: In the prospective population-based Swedish Mammography Cohort, 33,446
middle-aged and elderly women, free from cardiovascular disease, cancer and
diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of
dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and
docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire
at baseline.
RESULTS: During follow-up 1386 incident cases of myocardial infarction were
ascertained through register-linkage. Women in the highest quartile of dietary
PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial
infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the
lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after
adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in
RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing
highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely
associated with risk of myocardial infarction after but not before adjusting for 
dietary PCB.
CONCLUSION: Exposure to PCBs was associated with increased risk of myocardial
infarction, while some beneficial effect was associated with increasing EPA and
DHA intake. To increase the net benefits of fish consumption, PCB contamination
should be reduced to a minimum.
 
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
 

PMID: 25679993

 

 

------------
[2]  EFSA Journal 2010; 8(7):1701. [35 pp.]. doi:10.2903/j.efsa.2010.1701.
 
European Food Safety Authority; Results of the monitoring of non dioxin-like PCBs in food and feed.
 
 
ABSTRACT
 
Non dioxin-like polychlorinated biphenyls (NDL-PCBs) are persistent organic chemicals that
accumulate in the environment and humans and are associated with a broad spectrum of health effects.
Processing and distribution of PCBs has been prohibited in almost all industrial countries since the late
1980s but they still can be released into the environment from electrical appliances, building paint and
sealants and waste sites that contain PCBs. In 2002 the European Commission prescribed a list of
actions to be taken to reduce the presence of dioxins and PCBs in food and feed and Member States
were recommended to monitor the situation. A total of 12,563 food and feed samples collected in the
period 1995 - 2008 from 18 EU Member States, Iceland and Norway were retained for a detailed
analysis of the occurrence of the six indicator NDL-PCBs (# 28, 52, 101, 138, 153, and 180). Overall,
18.8% of the results for single congeners were below the limit of quantification (LOQ) but their
distribution varied highly between food and feed groups. PCB-153 and PCB-138 were the most
commonly detected congeners. In food, the highest mean contamination level was observed in fish and
fish derived products followed by eggs, milk and their products, and meat and meat products from
terrestrial animals. The lowest contamination was observed in foods of plant origin. A similar pattern
was observed in feed where high contamination was reported in feed containing fish derived products
and comparatively very low levels in feed of plant or mineral origin. The sum of the six NDL-PCBs
was on average close to five times higher than the sum of the 12 dioxin-like PCBs. This relationship
varied across food groups and is presumably related to the origin of samples and the contamination
source. Country-specific clustering has been observed in several food and feed groups.

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P.S. I didn't realize it at first, but the same group of Swedish researchers who studied PCBs and heart attack in women described above, repeated the same analysis with a male cohort of Swedes [1], with virtually identical results.

 

Specifically, dietary PCBs were associated with an increase in heart attack risk. Dietary DHA/EPA was associated with a decreased risk of heart attack, but the two combined (i.e. in fish eaters getting both a lot of PCBs and DHA/EPA), resulted in a net increase in heart attack risk of about 20%. Like the women, lean men were worse off as a result of PCB intake than heavier men.

 

--Dean

 

---------

[1] Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction in men - A population-based prospective cohort study.

 

Bergkvist C, Berglund M, Glynn A, Julin B, Wolk A, Åkesson A.
 
Environ Int. 2015 Dec 12;88:9-14. doi: 10.1016/j.envint.2015.11.020. [Epub ahead of print]
 
PMID: 26690540
 
 
Abstract
 
BACKGROUND:
 
Major food contaminants such as polychlorinated biphenyls (PCBs) are proposed to play a role in the etiology of cardiovascular disease (CVD), but to date the impact of PCBs on cardiovascular health need to be explored.
 
METHODS AND RESULTS:
 
We assessed the association between validated food frequency questionnaire-based estimates of dietary PCB exposure and risk of myocardial infarction, ascertained through register-linkage, among 36,759 men from the population-based Swedish Cohort of Men, free of cardiovascular disease, diabetes and cancer at baseline (1997). Relative risks were adjusted for known cardiovascular risk factors, long-chain omega-3 fatty acids (eicosapentaenoic and docosahexaenoic acids) and methyl mercury exposure. During 12 years of follow-up (433,243 person-years), we ascertained 3005 incident cases of myocardial infarction (654 fatal). Compared with the lowest quintile of dietary PCB exposure (median 113ng/day), men in the highest quintile (median 436ng/day) had multivariable-adjusted relative risks of 1.74 (95% confidence interval [CI], 1.30-2.33; p-trend<0.001) for total and 1.97 (95% CI 1.42-2.75; p-trend<0.001) for non-fatal myocardial infarction. In mutually adjusted models, dietary PCB exposure was associated with an increased risk of myocardial infarction, while the intake of long-chain omega-3 fish fatty acids was associated with a decreased risk. We also observed an effect modification by adiposity on the association between of dietary PCB exposure and myocardial infarction, with higher risk among lean men (p value for interaction =0.03).
 
CONCLUSIONS:
 
Exposure to PCBs via diet was associated with increased risk of myocardial infarction in men.
 
KEYWORDS:
 
Dietary; Epidemiology; Myocardial infarction; PCB; Population-based; Prospective cohort; n-3 fish fatty acids

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Hi Dean,

 

Firstly, let me thank you for all of your very interesting and well thought out posts. I'm going through the admittedly short archive just to see what I missed.

 

Regarding PCB, you made me go look to see how bad this could be. Google scholarlying on "pcb mortality", it seems like the overall effect is not that bad. Total mortality on relatively small and not greatly designed studies (mostly retrospective analysis) seems to not be any higher than on the normal population. Would you not expect for mortality to be clearly higher if the effect on MI was so strong? What is a reasonable synthesis merging both views?

 

Here are a few of the abstracts:

 

One on acute contamination showing higher liver cancer, as you would expect, but not higher total:

 

http://www.tandfonline.com/doi/abs/10.1080/00039896.1996.9936040

 

A Cohort Study on Mortality and Exposure to Polychlorinated Biphenyls
 
DOI:10.1080/00039896.1996.9936040
Shu-Feng Hsieha, Yea-Yin Yenb, Shou-Jen Lanc, Chung-Cheng Hsiehde, Chien-Hung Leec & Ying-Chin Ko M.D.c
pages 417-424
 
In 1979, an outbreak of food poisoning (“Yu-Cheng”) occurred in Central Taiwan, ROC, involving more than 2 000 people. The event was caused by ingestion of rice oil contaminated with polychlorinated derivatives of biphenyls, dibenzofurans, and quaterphenyls. A retrospective cohort study on mortality was undertaken, and possible long-term health effects in the affected individuals were studied. The mortality experience of 1 940 victims (929 males, 1 011 females) between 1980 and 1991 was compared with the expected numbers, which were calculated from national and local mortality rates. By the end of 1991, 102 deaths were identified, thus producing a standardized mortality ratio (SMR) of overall mortality of 0.99 for males and 1.34 for females. Total cancer mortality was lower than in each comparison group. Mortality from liver diseases was elevated significantly (SMR = 3.22), especially during the first 3 y after the food-poisoning event (SMR = 10.76). Increased clinical severity of polychlorinated biphenyl intoxication was associated with increased mortality from all causes and from liver diseases. In summary, there was a positive association between mortality and intoxication dose, and severe polychlorinated biphenyl poisoning acutely affected mainly the liver. A continued follow-up of this cohort would be valuable in the study of long-term health effects of polychlorinated biphenyl poisoning.
 
 
One from chronic exposure due to working in a transformer plant, finding increased pancreatic cancer but also with no increased total mortality:
 
 
Cancer mortality in workers employed at a transformer manufacturing plant
Annalee Yassi MD, MSc, FRCPC1,*, Robert Tate MSc2 andDavid Fish PhD3
Article first published online: 19 JAN 2007
DOI: 10.1002/ajim.4700250310
Copyright © 1994 Wiley Periodicals, Inc., A Wiley Company
Issue American Journal of Industrial Medicine
American Journal of Industrial Medicine
Volume 25, Issue 3, pages 425–437, March 1994
 
This study examined mortality to December 31, 1989 in a cohort of 2,222 males employed between 1947 and 1975 at a transformer manufacturing plant in Canada, where there had been extensive use of transformer fluid, some containing polychlorinated biphenyls (PCBs). A combined cohort list of 2,222 names was independently obtained from plant management and union officials. Mortality of 1,939 workers with known birthdates was ascertained by record linkage with the Canadian Mortality Database.
 
Standardized mortality ratios (SMRs) for different criteria for acceptance of the death certificate link and for cohort membership (based on work history) ranged from .71–1.05. There was no significant increase in overall cancer deaths. The only significant site-specific increased mortality was pancreatic cancer (11 deaths), with SMRs ranging from 2.92–7.64 and higher mortality risk in those who entered the cohort prior to 1960. All but one of these deaths had a latency period of at least 10 years, and greatest SMRs were found in departments with the greatest exposure to transformer fluid.
 
Several previous studies have found excess pancreatic cancers in association with oil exposures and electrical equipment manufacturing. The need to further investigate pancreatic cancer in transformer manufacturing and related exposures is evident. © 1994 Wiley-Liss, Inc

 

And one more properly relevant using fishermen, which also finds no effect on total mortality, and even slightly lower ischemic heart disease risks

 

http://www.jstor.org/stable/40966338?seq=1#page_scan_tab_contents

 

I can't cut'n'paste that content since it's an image, but is similar in design to the others (3000 people compared to cohort)

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Thanks Ale!

 

And welcome to the CR Society Forums!

 

Thanks for pointing out via these studies that PCBs do their most harm through damaging and causing cancer of the liver and pancreas. Admittedly these are studies where subjects were exposed to much higher doses than one can conceivably get from eating fish, but a 3x increased rate of pancreatic cancer and 10x increased rate of liver cancer, both of which are quite deadly, is very dramatic increase. This is a risk I'd prefer to avoid, even if much attenuated. 

 

Regarding cardiovascular mortality, these studies are small compared to the Swedish study (a factor of 15 fewer subjects), so I'm not too surprised a significant increase in cardiovascular mortality risk was not observed. I didn't look at all three studies, but here is the relevant table of causes of death from the full text of the first one [1] (please include the PMID # when available Ale when referencing a paper, for ease of later searching).

 

Ta67gN1.png

 

I've highlighted some interesting cells. Overall, from the OBS columns, you can see not too many people died in this cohort, so there are pretty wide error bars (confidence intervals) across the board. You can see an increase liver related cancer and diseases and a large increase in "ill-defined diseases", whatever that means...

 

But also note that there is a trend towards higher cardiovascular disease rates, at least in men, who were exposed to PCBs. Overall, the confidence interval for cardiovascular disease seen in this study in both men and women spans the 20-50% increase in CVD risk observed in the much larger studies I listed above.  Plus, cardiovascular disease takes many years to manifest, and is (therefore) a disease of old age. This study was done over the 12 years immediately after the PCB exposure, so the increased risk of CVD was unlikely to have had time to manifest itself as an overt increase in CVD incidents which then progressed to the point of being fatal.

 

Finally, the body may deal much differently with mild, chronic exposure to PCBs than it does with acute exposures like the studies you point to. The former may make the body more prone to CVD.

 

So those are some of the possible ways to explain/interpret the apparent discrepancy between the studies I cited showing increased risk of CVD associated with higher PCB levels in the blood, and your studies showing no such clear association as a result of exposure to high concentrations of PCBs.

 

Finally, it seems like the increase of various organ cancers (liver, pancreas, kidney) as a result of acute PCB exposure demonstrated by your studies provides all the more reason to avoid PCBs if possible. For me that means getting DHA/EPA from algae sources, but even purified fish oil would seem better from a PCB (and mercury) perspective than eating fatty fish flesh.

 

--Dean

 

---------

[1] Arch Environ Health. 1996 Nov-Dec;51(6):417-24.

A cohort study on mortality and exposure to polychlorinated biphenyls.

Hsieh SF(1), Yen YY, Lan SJ, Hsieh CC, Lee CH, Ko YC.

Author information:
(1)Graduate Institute of Medicine, School of Public Health, Kaohsiung Medical
College, Kaohsiung City, Taiwan, ROC.
 
Full text: http://www.tandfonline.com.sci-hub.io/doi/abs/10.1080/00039896.1996.9936040

In 1979, an outbreak of food poisoning ("Yu-Cheng") occurred in Central Taiwan,
ROC, involving more than 2000 people. The event was caused by ingestion of rice
oil contaminated with polychlorinated derivatives of biphenyls, dibenzofurans,
and quaterphenyls. A retrospective cohort study on mortality was undertaken, and
possible long-term health effects in the affected individuals were studied. The
mortality experience of 1940 victims (929 males, 1011 females) between 1980 and
1991 was compared with the expected numbers, which were calculated from national
and local mortality rates. By the end of 1991, 102 deaths were identified, thus
producing a standardized mortality ratio (SMR) of overall mortality of 0.99 for
males and 1.34 for females. Total cancer mortality was lower than in each
comparison group. Mortality from liver diseases was elevated significantly (SMR =
3.22), especially during the first 3 y after the food-poisoning event (SMR =
10.76). Increased clinical severity of polychlorinated biphenyl intoxication was
associated with increased mortality from all causes and from liver diseases. In
summary, there was a positive association between mortality and intoxication
dose, and severe polychlorinated biphenyl poisoning acutely affected mainly the
liver. A continued follow-up of this cohort would be valuable in the study of
long-term health effects of polychlorinated biphenyl poisoning.

PMID: 9012319

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I guess the below papers the last of which is pdf-availed, SCI-HUB seems to be down, go towards backing up your contentions, Dean.

 

 

Mortality after exposure to polychlorinated biphenyls and polychlorinated dibenzofurans: a 40-year follow-up study of Yusho patients.
Onozuka D, Yoshimura T, Kaneko S, Furue M.
Am J Epidemiol. 2009 Jan 1;169(1):86-95. doi: 10.1093/aje/kwn295. Epub 2008 Oct 30.
PMID: 18974082 Free Article
 
Abstract
 
A 40-year follow-up study was conducted to examine mortality among 1,664 patients in Japan suffering from "Yusho," a disease caused by ingestion of rice oil contaminated with polychlorinated biphenyls and polychlorinated dibenzofurans. To evaluate the effects of exposure on mortality, the authors calculated standardized mortality ratios. National mortality rates for major causes of death were used as reference points. A total of 1,596 Yusho patients (95.9%) were followed until death or the end of the study (December 31, 2007). The standardized mortality ratios for most major causes of death were not significantly elevated, with the exceptions of all types of cancer (standardized mortality ratio (SMR) = 1.37, 95% confidence interval (CI): 1.11, 1.66), liver cancer (SMR = 1.82, 95% CI: 1.06, 2.91), and lung cancer (SMR = 1.75, 95% CI: 1.14, 2.57) in males. In addition, the standardized mortality ratios for all cancers, liver cancer, and lung cancer among males tended to decrease over time. Results from this study suggest that the carcinogenicity of polychlorinated biphenyls and polychlorinated dibenzofurans must be taken into account when evaluating mortality risk.
 
 
Yusho: 43 years later.
Yoshimura T.
Kaohsiung J Med Sci. 2012 Jul;28(7 Suppl):S49-52. doi: 10.1016/j.kjms.2012.05.010. Epub 2012 Jul 21. Review.
PMID: 22871602 Free Article
 
Abstract
 
The aim of the present study is to describe recent issues with Yusho disease in Japan, describe the state of dioxin accumulation and the intake of dioxin via food in Japan, and introduce the Japan Environment and Children's Study. Yusho disease manifested in western Japan in 1968. The causes of Yusho are believed to be dioxin-related compounds, mainly polychlorinated biphenyls (PCBs) and polychlorinated dibenzofurans (PCDFs), via the ingestion of rice oil produced in February 1968. As of March 31, 2011, there were 1961 registered Yusho cases, but of these 539 are deceased. A retrospective cohort study on registered Yusho cases reported that the standardized mortality ratios (SMRs) for the major causes of death were not significantly elevated, with the exception of all-cancer (SMR=1.26; 95% confidence interval [CI]: 1.03-1.53) and lung cancer mortality (SMR=1.56; 95% CI: 1.03-2.27) in males. The results of the Yusho mortality study show that the SMR for liver cancer in males tends to decrease over time. In 2011, the Ministry of the Environment of Japan reported that the average concentration of dioxins in the blood (2002-2010) of the Japanese people was 19 pg-TEQ/g-fat, demonstrating a range of 0.10-130 pg-TEQ/g-fat, and that the average dioxin intake from food (2002-2010) was 0.82 pg-TEQ/kg-body weight/day, demonstrating a range of 0.031-6.2 pg-TEQ/kg-body weight/day according to 2006 WHO TEFs. The Japan Environment and Children's Study Project was launched in 2011 and is supported by the Ministry of the Environment of Japan. In this project, 100,000 mother and child pairs will be recruited over 3 years from designated study areas. Follow-up examinations will be carried out from pregnancy until the children are 13 years of age (a so-called birth-cohort study). This project will be implemented by the National Center at the National Institute for Environmental Studies and is supported by the Medical Support Center at the National Center for Child Health and Development. Field operations will be performed at 15 designated regional centers nationwide.
 
 
Mortality after exposure to polychlorinated biphenyls and polychlorinated dibenzofurans: a meta-analysis of two highly exposed cohorts.
Li MC, Chen PC, Tsai PC, Furue M, Onozuka D, Hagihara A, Uchi H, Yoshimura T, Guo YL.
Int J Cancer. 2015 Sep 15;137(6):1427-32. doi: 10.1002/ijc.29504. Epub 2015 Mar 16.
PMID: 25754105
 
Abstract
 
Both Yucheng and Yusho were events of accidental exposure to highly doses of polychlorinated biphenyls and dibenzofurans in Asian people. Mortality experiences caused by various diseases were reported in both cohorts with similar and dissimilar findings. We thus conducted a meta-analysis of two cohorts to reevaluate the effects of PCBs and PCDFs on major causes of mortalities. Two recently updated Yucheng and Yusho mortality studies were included. For selected diseases, standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were extracted. Meta-analyses were conducted using a random-effects model only when heterogeneity (I(2)  > 50% and/or p value <0.10 by the Q test) was not found. A total of 1,803 Yucheng subjects (male, N = 830; female, N = 973) with 48,751 person-years of follow-up and 1,664 Yusho subjects (male, N = 860; female, N = 804) with 50,773 person-years are included. An increase in all-cause mortality (pooled SMR=1.2, 95% CI: 1.1-1.3, I(2)  = 0.0%), all cancers (pooled SMR=1.3, 95% CI: 1.1-1.6, I(2)  = 0.0%), lung cancer (pooled SMR=1.7, 95% CI: 1.2-2.3, I(2) =0.0%), heart disease (pooled SMR=1.3, 95% CI: 1.0-1.7, I(2)  = 43.4%) and hepatic disease (pooled SMR=1.9, 95% CI: 1.3-2.8, I(2)  = 0.0%) were found in pooled males. Significant elevation from liver cancer was found in pooled females (pooled SMR=2.0, 95% CI: 1.1-3.6, I(2)  = 0.0%). This meta-analysis of Yucheng and Yusho cohorts showed similar elevation from all cancer, lung cancer, heart disease and hepatic disease mortalities in exposed men. Furthermore, a new finding of elevated liver cancer mortality in exposed women was identified.

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Thanks Al,

 

I guess the below papers the last of which is pdf-availed, SCI-HUB seems to be down, go towards backing up your contentions, Dean.

 

Yes - it seems so. It nice when that happens :-). To highlight what you're referring to, from PMID 25754105, a meta-analysis of data from two of PCB-exposed cohorts Ale pointed to, but this time with 45+ years of followup:

 

 An increase in all-cause mortality (pooled SMR=1.2, 95% CI: 1.1-1.3, I(2)  = 0.0%), all cancers (pooled SMR=1.3, 95% CI: 1.1-1.6, I(2)  = 0.0%), lung cancer (pooled SMR=1.7, 95% CI: 1.2-2.3, I(2) =0.0%), heart disease (pooled SMR=1.3, 95% CI: 1.0-1.7, I(2)  = 43.4%) and hepatic disease (pooled SMR=1.9, 95% CI: 1.3-2.8, I(2)  = 0.0%) were found in pooled males.

 

This seems to vindicate my summary in the first post in this thread:

 

Summary: PCBs are bad sh*t.

 

--Dean

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Thanks Mike,

 

Yes, as I mentioned in the opening post of this thread, fish are often mislabelled - in particular farm-raised salmon are often labelled as 'wild'. We discussed the study your article points to in this thread. Saul, as usual, defended fish and his honest fishmonger. :-)

 

--Dean

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Thanks Dean and Al for the follow up. The mortality increase showing up on the meta-analysis is very interesting. It sounds like PCBs are something to look out for (which is a pity).

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The only fish I eat is wild-caught salmon from the Pacific Northwest (of North America). Sardines from that area would be OK too, but the canned ones available are usually sold in aluminum containers (with a lining, but still).

 

Zeta

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Zeta,

 

Given that fish, and salmon in particular, often get mislabeled as reference above, what process do you use to vet the salmon you purchase to make sure it is really what it is claimed to be?

 

I realize this question be posed for anything we eat (e.g. How do we really know a particular green tea comes from Japan and not China?), but salmon seem particularly prone to such mistakes, or dare I say, bait-and-switch tactics.

 

--Dean

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Ah, thanks Zeta.

 

I didn't realize you were referring to consuming canned wild salmon. If I ate fish, I too would trust the label on a can more than my local fishmonger, who has very little chance of getting caught (and quite a bit to gain) if he unscrupulously switches the tag on salmon fillets in the seafood section of his market so as to read "wild" rather than "farm-raised" salmon.  \

 

Further, it may not even be him who does the cheating, but the seafood wholesaler who sells him the supposedly wild salmon fillets...

 

--Dean

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Hi all!

 

My new favorite is farmed New Zealand king salmon.  This fish has won a lot of green awards for the excellent job done is the raising of the fish (one can probably look up figures for heavy metals, PCBs, etc. if you like).

 

Also:  Dean, you and however-you-spell-it haven't done any studies on contamination in vegetables (and fruit).  Not unlikely that there's at least as much junk in the veggies we eat (organic or not) as in fish or land animals.

 

That doesn't mean that we shouldn't eat our veggies.

 

:)xyz

 

  -- Saul

 

P.S.:  I agree thoroughly with Zeta.

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Saul,

 

Nice to have you back, but as usual, you are thoroughly misinformed. :-)

 
On 2/17/2016 at 8:35 AM, Saul said:

Dean, you and however-you-spell-it haven't done any studies on contamination in vegetables (and fruit).

 

Both I and Dr. Greger have spoken at length on contamination of plant foods. Here are just a few examples:

  • Here is a post I wrote analyzing, and largely debunking, the "Dirty Dozen" list of supposedly highly contaminated produce from the Environmental Working Group (EWG). 
  • Here is Dr. Greger's video on produce contamination and whether organic produce is worth it.
  • Here is a post in which I discuss a Rich Roll Podcast interview with Dr. Greger by Rich Roll, where Dr. G talks about fruit & vegetable contamination at 58:00. 
  • Here is a post in which I discuss Dr. Greger's video on green tea contamination.
  • Here is a whole thread on cadmium contamination of cacao products, which culminated in my extended quest to eliminate it by brewing, rather than eating, chocolate, discussed ad nauseum in this thread.

So quite clearly both I and Dr. Greger have thought and written quite a lot about contamination of plant foods.

 

On 2/17/2016 at 8:35 AM, Saul said:

Not unlikely that there's at least as much junk in the veggies we eat (organic or not) as in fish or land animals.

 

Have you even bothered to read this thread as you are posting to it Saul, or are you just jumping in to make random and unfounded comments as is your usual style?

 

If you had read the very first post in this thread (which BTW I started in order to clear up some stupid comments you've made on other threads on this topic), you'd see the graph below, which, also as usual, shows you're (still) totally ignorant of the facts in this case:

 

kY6mfCp.png

 

Notice the bar labeled "Fish" and the bar labeled "Fruit, Veg. Cereals"? Notice the former is 292x taller than the latter? Notice all the other animal products with the big bars as well? In short, PCBs (and other contaminants, like mercury) bioaccumulate in the fat of animals higher up on the food chain, and especially fish who are the unfortunate downstream recipients of all the man-made pollutants that get washed into lakes, rivers and oceans. Once again you're talking out your butt on this one :-).

 

On 2/17/2016 at 8:35 AM, Saul said:

That doesn't mean that we shouldn't eat our veggies..

 

Hey - something you're right about! I guess it had to happen eventually...

 

On 2/17/2016 at 8:35 AM, Saul said:

Dean, you and however-you-spell-it ...

 

I admire your willingness to refrain from using Dr. Greger's name due to your apparent ignorance of how to spell it - despite my repeated corrections to try to help you out.  Thanks for that. I only wish you would let that reluctance to speak on topics you know nothing about spill over into the rest of your posts... 

 

You're a religion person, right Saul - prone to suggesting we read and sometimes even quoting from the old testament? Perhaps you should listen to your good book more often, like proverb (10:19):

 

"When there are many words, transgression is unavoidable, But he who restrains his lips is wise."

 

:)xyz

 

--Dean

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All,

 

Here is a brand new meta-analysis [1] which identifies a further detrimental effects (on top of heart disease, discussed above) of fish, namely rapid weight gain and increased childhood obesity in children of moms who ate a lot of fish during pregnancy. Specifically they found that children of women who consumed more than 3 fish meals per week during pregnancy were over 20% more likely to be overweight/obese by age 6. Here is the graph from the free full text summarizing their findings:

 

42eJqQ5.png

 

The authors suggest it is likely a result of contaminants in fish. Here is their discussion of the likely cause:

 

Contamination by environmental pollutants in fish could provide an explanation for the observed association between high fish intake in pregnancy and increased childhood adiposity. In humans, fish consumption is a major source of exposure to endocrine-disrupting chemicals.26,27 Mixtures of persistent organic pollutants found in fish have been shown to increase fat storage in cultured adipocytes as well as weight gain in animals.28 It has been proposed that these toxicants may perturb signaling of several nuclear receptors and, through altered gene expression, influence adipocyte differentiation and fat metabolism.3,4

 

Obviously most of us aren't planning to get pregnant anytime soon :-), but it is more evidence that contaminants in fish can be deleterious for human health.

 

--Dean

 

-----------

[1] JAMA Pediatr. Published online February 15, 2016. doi:10.1001/jamapediatrics.2015.4430

 

Fish Intake in Pregnancy and Child Growth - A Pooled Analysis of 15 European and US Birth Cohorts

 

Nikos Stratakis, MSc1,2; Theano Roumeliotaki, MPH1; Emily Oken, MD3; Henrique Barros, PhD4,5; Mikel Basterrechea6,7; Marie-Aline Charles, MD8,9; Merete Eggesbø, PhD10; Francesco Forastiere, PhD11; Romy Gaillard, PhD12; Ulrike Gehring, PhD13; Eva Govarts, MSc14; Wojciech Hanke, PhD15; Barbara Heude, PhD8,9; Nina Iszatt, PhD10; Vincent W. Jaddoe, PhD12; Cecily Kelleher, DMed16; Monique Mommers, PhD17; Mario Murcia, MSc7,18; Andreia Oliveira, PhD6,7; Costanza Pizzi, PhD19; Kinga Polańska, PhD17; Daniela Porta, MSc13; Lorenzo Richiardi, PhD19; Sheryl L. Rifas-Shiman, MPH3; Greet Schoeters, PhD20,21; Jordi Sunyer, PhD7,22,23; Carel Thijs, PhD17; Karien Viljoen, PhD16; Martine Vrijheid, PhD7,22,24; Tanja G. M. Vrijkotte, PhD25; Alet H. Wijga, PhD26; Maurice P. Zeegers, PhD2,27; Manolis Kogevinas, PhD7,28,29,30; Leda Chatzi, PhD1
 
 
ABSTRACT
 
Importance  Maternal fish intake in pregnancy has been shown to influence fetal growth. The extent to which fish intake affects childhood growth and obesity remains unclear.
 
Objective  To examine whether fish intake in pregnancy is associated with offspring growth and the risk of childhood overweight and obesity.
 
Design, Setting, and Participants  Multicenter, population-based birth cohort study of singleton deliveries from 1996 to 2011 in Belgium, France, Greece, Ireland, Italy, the Netherlands, Norway, Poland, Portugal, Spain, and Massachusetts. A total of 26 184 pregnant women and their children were followed up at 2-year intervals until the age of 6 years.
 
Exposures  Consumption of fish during pregnancy.
 
Main Outcomes and Measures  We estimated offspring body mass index percentile trajectories from 3 months after birth to 6 years of age. We defined rapid infant growth as a weight gain z score greater than 0.67 from birth to 2 years and childhood overweight/obesity at 4 and 6 years as body mass index in the 85th percentile or higher for age and sex. We calculated cohort-specific effect estimates and combined them by random-effects meta-analysis.
 
Results  This multicenter, population-based birth cohort study included the 26 184 pregnant women and their children. The median fish intake during pregnancy ranged from 0.5 times/week in Belgium to 4.45 times/week in Spain. Women who ate fish more than 3 times/week during pregnancy gave birth to offspring with higher body mass index values from infancy through middle childhood compared with women with lower fish intake (3 times/week or less). High fish intake during pregnancy (>3 times/week) was associated with increased risk of rapid infant growth, with an adjusted odds ratio (aOR) of 1.22 (95% CI, 1.05-1.42) and increased risk of offspring overweight/obesity at 4 years (aOR, 1.14 [95% CI, 0.99-1.32]) and 6 years (aOR, 1.22 [95% CI, 1.01-1.47]) compared with an intake of once per week or less. Interaction analysis showed that the effect of high fish intake during pregnancy on rapid infant growth was greater among girls (aOR, 1.31 [95% CI, 1.08-1.59]) than among boys (aOR, 1.11 [95% CI, 0.92-1.34]; P = .02 for interaction).
 
Conclusions and Relevance  High maternal fish intake during pregnancy was associated with increased risk of rapid growth in infancy and childhood obesity. Our findings are in line with the fish intake limit proposed by the US Food and Drug Administration and Environmental Protection Agency.

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