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Tuesday, 5 May 2015

Chemical Atherogenesis - the alternative hypothesis.



In 1977, when I was 19, and shortly before I cut my hair and joined a punk group, I worked as an apple picker in Upper Moutere, near Mapua, in the Tasman district of New Zealand.
The orchard was an eerie pace - no insects, no weeds, it even seemed that birds didn't fly over it, they certainly never ate the fruit. The fruit we picked had a white film on it. One of the guys I worked with drove the spray tractor, and he complained that he was loosing his vision due to the effects of the spray. None of us had protective gear. Our fires at night, fueled with cut-down apple trees, smelled like burning tyres. The factory that made some chemicals, including DDT, DDD, and which processed others, including 2,4,5-T and 2,4-D, was only 8 kilometres away, as the crow flies. Crows were probably the only thing that flew there.
There is a short report on this factory here. You can see that environmental standards were non-existent in New Zealand during the heyday of the persistent organochlorine pesticides and herbicides, which were used on the food everyone ate. Those who lived near or worked on farms were exposed to the highest levels, and urban workers were not exempt because PCBs were used in multiple industries and very similar organochlorine chemicals were added to petrol as "anti-knock" agents (they were, and probably still are, used in proprietary formulations such as STP).
My boss was a fit and hard-working guy, a non-smoker, who looked to be about 50. He was completely positive about the pesticides; it was as if he had a death-wish, or even an addiction. If Apocalypse Now had been released back then, I can imagine him saying "I love the smell of Dieldrin in the morning!" on a daily basis. I always assumed he sprayed Dieldrin for insects, because DDT was becoming less popular by 1977, even in New Zealand. He used to stand in the orchard while we worked and sneeze, loudly and often. He'd tell us how good sneezing made him feel - "like an orgasm!" - as he stood there in his shorts and plaid shirt, braced with his hands to his sides, like a jolly scoutmaster.
I only worked there for a month or so, but shortly after I left I had problems with recurrent flus, chronic fatigue, and headaches that lasted a long time. After a year or two I got word that my employer had died of a heart attack.
It never occurred to me for a moment that the butter in his diet had killed him. Obviously his blithe disregard for the dangers inherent in pesticide use had done him in.

Here is the NZ graph for mortality trends in CHD among people in their 50s. This is the historical ecological data cited by epidemiologists like Rod Jackson to make the case against saturated fat.


Saturated fat consumption in NZ increased between 1950 and 1970, but saturated fat consumption was always high - the increase did not represent a huge spike, and besides atherosclerosis is supposed to take 20 years or more. And women also ate more saturated fat - we are talking about the end of rationing and a new prosperity - yet the spike in CHD for women is minute - and this was the period when women started smoking in greater numbers. Sugar consumption skyrocketed at the end of rationing in 1950, polyunsaturated fats (and vitamin E) began to increase during the 1970's, selenium began to increase during the 1980's. I remember that women in the 1960's and 1970's often avoided sugar - saccharine and other artificial sweeteners were popular products specifically marketed to women in those days.

Meanwhile there was a growing awareness of the dangers of persistent pesticide use, the dangers of smoking, and the dangers of air pollution. New Zealand, despite its socialist politics, was completely dependent on primary industry - agriculture and manufacturing. The tourism and film industries, which benefit from pristine natural reputation, were insignificant. Not to put too fine a point on it, the situation was a messy scandal which few people want to go near even today. Proper records were not kept, guidelines were not followed, laws were ignored. It was only cleaned up slowly by a combination of a groundswell of increasing "green" criticism, the exposure of the Agent Orange scandal in South East Asia (involving the same chemicals we used for agricultural weed control in New Zealand) and, perhaps more important than any other factor, the rise of Monsanto, who had new and less persistent toxins to sell, and were actually in a position to convince the die-hards that the old poisons needed replacing.


All this would be moot if there was no evidence that organochlorines cause atherosclerosis. However, it is quite clear that they do.
This lovely document came out last year:


Review

Chemical Atherogenesis: Role of Endogenous and Exogenous Poisons in Disease Development.  MK AT, LC. Toxics 2014, 2(1), 17-34; doi:10.3390/toxics2010017


Chemical atherogenesis is an emerging field that describes how environmental pollutants and endogenous toxins perturb critical pathways that regulate lipid metabolism and inflammation, thus injuring cells found within the vessel wall. Despite growing awareness of the role of environmental pollutants in the development of cardiovascular disease, the field of chemical atherogenesis can broadly include both exogenous and endogenous poisons and the study of molecular, biochemical, and cellular pathways that become dysregulated during atherosclerosis. This integrated approach is logical because exogenous and endogenous toxins often share the same mechanism of toxicity. Chemical atherogenesis is a truly integrative discipline because it incorporates concepts from several different fields, including biochemistry, chemical biology, pharmacology, and toxicology. This review will provide an overview of this emerging research area, focusing on cellular and animal models of disease.
[N.B. the authors mention saturated fat as an endogenous atherogenic factor - not a dietary one. However their reference 18, cited to support this claim, a tasty review of ApoE knockout mouse research, doesn't really back it up - maybe because the experiments it cites rely on dietary fat, not endogenoous SFA].

So here we have the alternative hypothesis to explain the late 20th century rise and fall in CHD mortality. As cities and the countryside became more polluted, with particulate pollution, smoking, and organochlorines in agriculture and industry, which seeped into the food supply and home furnishings, heart disease rose. It rose significantly more in men because men - almost exclusively - worked in the industries, and at the automotive and electronic hobbies, that increased exposure to these pollutants the most. A few years after the publication of Silent Spring, as use of the most egregious pesticides lessened, it began to fall. As the rate of use, and the persistence of these chemicals fell further, CHD rates steadily dropped. The Clean Air Acts and improving Vehicle Emissions Standards of the 1970's-2000's, and the invention of the catalytic converter gradually reduced exposure to particulates and anti-knock additives, and lead was eliminated from petrol and paint. Better antioxidant and other micronutrition and the war against smoking also played an important role in its decline, and we can only hope that medicine was improving too, because some of the atherogenic chemicals were likely to have been drugs in common use - this is still a problem with SSRIs and antipsychotics today.

What is the role of sugar? Still not likely to be good. Not everyone had heart attacks from pollutant exposure; the dietary and hormonal drivers still operate. What about saturated fat?
This is likely to be bidirectional. Hence there is no association in prospective population studies. Saturated fat, when it increases LDL-cholesterol, is giving more hostages to fortune; but it is also less prone to oxidation than other lipids (though MUFA is no slouch in this regard), and it decreases gut permeability, reducing uptake of some swallowed atherogenic factors, and makes the liver less sensitive to toxins. Thus it can help some and harm others, so that the net effect is a wash-out at a population level. Maybe. A further factor is, that the atherogenic organochlorines were all lipid-soluble, and perhaps accumulated in animal fat (though the amount left on bought fruits and vegetables was sometimes visible to the naked eye), and at least one of the atherogenic factors, acrolein, is formed from the glycerol in burning fat - possibly helping to account for the differential CHD associations of meat SFA (always cooked, often burnt) vs. dairy SFA (usually eaten uncooked, and rarely burnt).

And this is my picture.

9 comments:

Dea Roberts said...

About 15-20 years ago, there was a bit of talk of rapid and substantial weight loss being of concern re: release of lot of fat-soluble toxins from adipose tissue. This never caught hold as a topic and it just does not seem to be in evidence as an area of concern at present - seems not on the radar. In practice, difficult to know to check out this concern as access to relevant testing is not available through the usual lab channels. Is all the more reason to avoid toxins and take a broad, multi-factorial approach to health and resilience.
A related topic is lead coming out of bones any time there is substantial loss of bone density/calcium. The lead is incorporated in bone due to it's similarity to calcium. Menopause, prolonged bed rest, reduction from large muscle mass in those previously athlete or heavy physical work - these are some examples of times when lead could be coming out of bone in significant amounts.
Thanks for another great article, George.

Steven Hamley said...

Excellent post George. Another factor regarding the decline in CHD mortality is probably smoking, which greatly decreased in prevalence (mainly in men) during the second half of the 20th century
http://www.tobaccoinaustralia.org.au/1-3-prevalence-of-smoking-adults

Denise said...

And on the same day, this article appeared in my reader:

http://nourishingplot.com/2015/05/06/studies-confirming-source-of-health-issues/

George Henderson said...

@ Steve,
The chemical atherogenesis hypothesis encompasses smoking as well; in fact, tobacco was grown with DDT long after its use was banned on food crops.

Zeliger has an interesting theory about the interrelationship between different classes of pollutant.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798856/

We can see that the science is only just coming up to speed to link DDT and CVD
https://apha.confex.com/apha/140am/webprogram/Paper267912.html

And that's in women, who I'm pretty sure had lower exposure to the POPs in the workforce and through hobbies.

It's easy now to test a new toxin for cancer and birth defects, there is no Ames test for atherosclerosis, heart rhythm or clotting defects.

@ Dea,

The whole field was left to the quacks and the Orthomolecular theorists, who at least had the imagination to sense the possibilities. Atkins wrote a bit about it. For government, it wasn't convenient to explore - too much liability, too complex except as an environmental issue (birds can't sue).

@ Denise - how shocking that people can still be exposed to DDT in the USA.
If Zeliger is right, the persistent lipophilic pollutants like DDT and PCBs increase sensitivity to the hydrophilic pollutants like glyphosate.
He is an expert on multiple chemical sensitivity and the various toxic effects of pollutants.
The more I read this stuff, the better saturated fats look.

shtove said...

Cheers.

Publicity today in UK for an inquiry into organo-phosphate effect on farmers from sheep dip - looks like our government will go ahead. The effects seem terrible. No doubt a big concern in NZ too.

ps. Anyone know if itsthewooo is still active?

George Henderson said...

Acute cardiac events from organophosphates
http://www.ncbi.nlm.nih.gov/pubmed/15284933

Alas no new woo for a time but try https://twitter.com/itsthewooo

annlee said...

New post from Wooo up today.

Jacquie said...

Hi George,

I've been reading your terrific blog for several years, but never felt I had anything particularly worthwhile to contribute, so haven't commented previously. Today I came across an article that I imagined you and/or some of your other readers might find as fascinating as I did, mainly as a history lesson in the diagnosis of liver disease via physical exam.

I did a fast and dirty search of your blog and didn't find mention of the article, "The Liver has a Body—A Cook’s Tour," (my apologies if I missed it) so I offer the link:

http://onlinelibrary.wiley.com/doi/10.1002/hep.20597/pdf

Just thought you might like to add this article to your collection.

Best regards from the New Jersey shore, USA.

George Henderson said...

Thanks Jacquie, I look forward to reading that - it looks amazing!