Has anyone read the book “Dying for a Hamburger,” which tries to show a causal link between modern meat-processing techniques and the prevalence of Alzheimer’s disease in industrialized societies? Basically, the theory is that BSE (or other prion diseases spread through meat and animal by-products) is the actual cause of Alzheimer’s, and since we don’t really have any good way of testing for BSE, it has actually become a pandemic across the country, but the latency period of the disease is so long that no causal link has been established–not to mention that we don’t have any in vivo tests for prion diseases.
If you’ve read the book, what do you think of it? I keep reading that it’s controversial, but I haven’t found any sites talking about the major flaws in its logic or research.
Some of the book’s main points:
The symptoms of Alzheimer’s disease (dementia, plaques in the brain) are very similar to symptoms of prion diseases–Creutzfeld-Jakob Disease, Bovine Spongiform Encephalopathy, kuru, scrapie, etc.
Dementia associated with old age was, judging from a review of medical literature, virtually unknown until the middle of this century. AD itself wasn’t diagnosed until the late 19th century. Medical texts mention dementia in other contexts, such as describing it as a symptom of syphilis, but make absolutely no mention of dementia associated with old age. They do describe other diseases of old age, but not dementia.
It might be argued that Alzheimer’s rates are rising due to the higher average life expectancy–people in previous centuries died of other causes before they could come down with Alzheimer’s. However, the book shows some population graphs that demonstrate that the lower average life expectancy was mostly due to a very high rate of infant and youth mortality–above the age of 50 or so, the percetage of people surviving to 60, 70, 80, 90 or older was actually very similar to today’s rate.
Alzheimer’s is still extremely rare in non-industrialized countries such as Nigeria, where people eat less meat generally and definitely far less meat processed the way it is in America/Canada/Europe/Japan, and in India, where meat consumption rates are very low.
Prions cannot be destroyed by any known sterilization techniques and are extremely infectious–a tiny amount of prions is enough to bring on a full-blown case of CJD
Prion diseases such can have a very long latency period (such as kuru, with a lapse of decades between infection and the first appearance of symptoms), so people could carry a disease and infect others for decades through surgeries, blood transfusions, etc.; these people in turn infect others, and so on. Because of the latency period and lack of testing, there’s no way to check whether someone is infected, try out cures, or enforce quarantines.
Prion diseases can leap across species barriers
Due to modern meat-processing techniques, prions from a single infected cow could end up infecting millions of people. Its meat is often ground up and mixed with meat from other cows on a large scale; its blood contaminates the entire processing plant; its remains are rendered and turned into all kinds of by-products–blood and bone meal that can be fed to other types of animals, which in turn can be ground up and fed back to cows; pet food, gelatin, and so on.
Anyway, lots of stuff to address, but I’d like to start with this one:
Dementia is a symptom of many neurodegenerative diseases, and is therefore nonspecific.
Plaques in the brain may also be seen in a variety of conditions. Plaques in prion diseases are generally immunoreactive for PrP. Since this is one method of confirming the diagnosis of a prion disease in a brain tissue sample, it shouldn’t be too hard to run the same assay on morphologically-diagnosed Alzheimer’s disease tissue and see if it’s also reactive. Did the book say if someone had done so?
Spongiform change, the hallmark of CJD and BSE, is not generally a feature of Alzheimer’s disease in my experience.
One thing I noticed from your description: He says that, because of the long latency period, no causal link has been established. If that’s the case, then how can he claim there is a causal link (since none has been established)?
It’s a fairly ridiculous theory. Enough cattle are tested for BSE when they’re slaughtered that a only a very tiny rate of infection is statistically possible given the number of actual positives that have been found. When BSE was very prevalent (in Britain) it was also very noticeable.
Did this author say how he tested his hypothesis that it was less well known last century? For example did he select a geriatric disease that we know from human remains was common 200 years ago (cataract would be a good comparison point) and do a comparison on the frequency of references? If not then his idea simply isn’t scientific. It’s an argument from assertion with no attempt made at testing or falsification. Hence I would be highly suspicious of his hypothesis.
A review of the medical literature will find very little about anything associated with geriatrics prior to this century. Old people were expected to get progressively and chronically ill, and then die. Nobody much studied it or wrote about it because there was little benefit in it. Conditions that were untreatable and unpreventable met the same fate. So I’d expect there to be no more written about senile dementia than is written about dementia caused by strokes in the medical literature.
Outside the medical literature of course geriatric dementia was well known. While we can’t know whether this was caused by Alzheimer’s we can certainly say that it was expected that most people would become demented with sufficient age. Consider Shakespeare for example.
The idea of old men being devoid of their wits is considered to be as obviously true as the idea that old men have grey beards and wrinkles. That hardly suggests that geriatric dementia was unknown prior to last century does it?
Neither was influenza, cholera, malaria or almost any other disease you care to name. Remember in the mid 19th century it was still believed that diseases were caused by foul air. Diagnosis was at best made by symptom, so that “flux” and “consumption” and “ague” were considered diagnoses rather than malaria or cholera or TB specifically. That AD itself wasn’t specifically diagnosed as a separate disorder until slightly after cholera and influenza is hardly a surprise. But as you say, ‘dementia’ as an equivalent to ‘ague’ or ‘flux’ was diagnosed and well known for centuries.
But how common are these references to other diseases of old age? Are they significantly more common, or does chronic leukaemia get one mention, and cataracts one mention and senile dementia none? And were these other diseases also untreatable? And how did the author characterise a ‘disease of old age”? Did he include ‘rheumatism’ for example, which isn’t a disease of age? Unless he makes these things explicitly clear then he isn’t attempting a scientific discussion, he’s simply cherry picking.
And how did he derive those graphs? Careful records weren’t kept back then except for the nobility so what is the source of this data. Colour me sceptical. I’ll believe the rates for 40-60 would be the same, but he is saying that if we removed all medical care form people over 60 right now less than 5% of them would die in the next 10 years. In essence he is saying that modern medical care is keeping less than 5% of 60 year olds alive. That is clearly bollocks.
Yes, and life expectancy is concomitantly shorter. Once more, ask yourself if this man is doing science or is simply cherry picking. Did he include a comparative analysis for the rates of other geriatric diseases in Nigeria and India, and were those rates statistically identical to the rates of those diseases in the US?? If not then this simply isn’t science.
Well that’s simply bollocks. If he made that claim you can throw the book out. He clearly hasn’t done even basic research. “ Prions can be destroyed by 150 degrees autoclaving or treatment with 1M sodium hydroxide”. Prions are certainly tougher than many viruses and bacteria, but it’s not even close to true to say they cannot be destroyed by any known sterilization techniques
Good times! (tiltypig here, I’m just using my boyfriend’s computer.) Bear with me if I’m being vague or inaccurate in describing the book’s main points. I was really hoping to find input from someone who had read the book, so that I wouldn’t have to summarize the book section by section, with cites. I posted originally during my lunch hour, without the book on hand.
The author says that dementias can be categorized into four main forms, only one of which (multi-infarct dementia) existed in the past:
Multi-infarct dementia, partly caused by lifestyle (arteriosclerosis in the cerebral blood vessels causing brain cells to die off)
HIV/AIDS dementia (viral)
Dementia with Lewy bodies
Alzheimer’s disease
There is a mention of PrP and a description of how it works, but–now that I read it more closely–the book just says, “Prions are sometimes compared to beta amyloid protein, particles that form insoluble plaques in the brains of Alzheimer’s disease victims. Prions fold into structures called beta-pleated sheets in a pattern similar to amyloid found in AD.” There doesn’t seem to be any mention of PrP immunoreactivity. I thought the book had mentioned spongiform tissue degeneration associated with Alzheimer’s, but when I went back and looked, it just talked about the plaques and tangles looking similar, and mentioned multiple cases of CJD brains being initially misdiagnosed as AD or vice versa because they were so similar.
Manduck: sorry–I described it incorrectly. The author is trying to posit a link between prions and Alzheimer’s, but is not providing a smoking gun or any new research. It’s just a review of evidence gathered from various scientific studies. The second-to-last chapter cites Dr. Chi Ming Yang, “one of the world’s leading experts in prion research,” as saying his research suggests “…a common putative mechanism underlying the initiation stages of sporadic Alzheimer’s disease and both sporadic and genetic forms of prion diseases.” The author concludes from this, “In other words, a prion may provide the initial push required for the onset of these diseases.” Which, now that I’m looking at the sentence again, doesn’t really seem to be exactly the same thing as what Dr. Yang was saying.
Gorsnak: Do you really think so? In the United States? If I remember correctly, the main response by the US government when mad cow disease was found in the States was to ban the sale of downer cows for human consumption, ban ruminants being fed to other ruminants (but not to non-ruminants and vice versa) and to encourage people not to eat cow brains or nervous systems (regardless of the possible contamination of meat processing equipment, what with spines getting sawed through, nerves being ground up into sausage, and such). Of course, when the government was advising consumers on imported beef, it was a different story–“don’t eat it! don’t eat it! It’s EEEEVIL!” :rolleyes: The current USDA goal is to test 12,500 cows per year for BSE. Um, what? They estimate that the US currently has 45 million adult cows. That means we’re only currently testing around 0.03 percent of our nation’s cattle. It’s not at all surprising to me that we haven’t found many positives.
Blake: The authors first describe some very “thorough” medical texts from the last century–books by Sir William Osler, or by Dr. William Boyd; French’s Index of Differential Diagnosis; “A Manual of Diseases of the Nervous System,” the “recognized standard text of neurology [in 1888]”–and note that they either don’t mention senile dementia at all, or devote maybe one sentence to mention it in passing. They then review the Index Medicus (an annual indexed listing of all medical articles published each year) from its start in 1880 to the present day. Until 1921, there are no citations on the subject of dementia, and only a few each year for “senile insanity” (which they say does not relate to Alzheimer’s disease.) They say that only in the 1930s did articles on what may have been Alzheimer’s begin to appear. They take various quotes from world literature and conclude that , in general, two main themes appear in talking about the elderly:
old people are wise and worthy of respect
old people are physically debilitated and have cranky or irritating personalities.
They say that there are many mentions in ancient literature of old people being physically weak, shrunken, and wrinkled, but seldom, if ever, are they described as being demented, forgetful, or senile.
There aren’t graphs in the book that go back to previous centuries to count instances in the medical literature of dementia vs. other diseases of old age. They do give a graph from 1966 to 2000 that shows a very steep increase in the number of articles in the U.S. National Library of Medicine’s bibliographic database on Alzheimer’s (5000x increase) as compared to hip fractures (100x increase) and prostate cancer (6x increase).
As for the graphs, the authors do mention the unreliability of many statistics gathered before 1800, but say that some English church parishes kept good records, and Scandinavian countries also kept good civilian records starting from around 1750; they also give a chart based on the life expectancies of the English aristocracy (which was well documented) from 1200 to 1745. I don’t know where the numbers they graphed for France came from originally–the citations they give are for books about European population patterns and social history.
One of the studies the authors cite with regards to AD in non-industrialized societies is “The Nigerian/American Study,” which compared more than 2000 Yoruba people living in Nigeria to a comparable population of African-Americans living in Indianapolis. All the participants were aged 65 or older and did not have dementia at the beginning of the study. They conducted a first study and then two follow-up studies, after two years and five years. Alzheimer’s disease appeared in the Yoruba population at a rate of 1.15 percent, and in the African-American population at a rate of 2.52 percent. They also cite a study of people aged 65 and over in rural Ballabgarh, India vs. a reference US population in rural Pennsylvania. The rate of AD in India was 4.7 per 1000 person-years; in Pennsylvania, it was 17.5 per 1000 person-years. Since the populations being studied were all over within a certain age range, with follow-ups being performed at the same intervals, rather than the statistics being based on incidence over the entire population over the subjects’ entire lifespans, does it really matter that life expectancy is shorter in these other countries?
The authors state that prions have survived autoclaving (I can’t find the reference right now) and have infected people in cases such as the initial trials of human growth hormone. The process designed to extract and purify the hGH should have killed all known pathogens.
Dementia itself as a word wasn’t even invented until 1806, so it’s hardly surprising it didn’t get much use until 100 years ago. I would like to think that when the author says that dementia doesn’t get a mention he doesn’t mean literally ‘dementia’. But we have no reason to believe he doesn’t. Honestly, a claim that these works don’t mention dementia is like a claim that they don’t mention viruses.
This still isn’t science. There is simply no way of falsifying this claim or attempting to give any statistical value to pour confidence in the claim. It’s neither more nor less than an argument from assertion. It would be simplicity itself to conduct a statistical analysis of mentions of what could be senile dementia in those works vs. mentions of something like cataracts that we know existed. Yet the author never did this. That is highly suspicious and makes this work, if not actual pseudoscience, then at best weak science.
The next problem is that there is a world of difference between not mentioning dementia, and not devoting much effort to it. One can be used as evidence that the condition was unknown. The other is simply evidence that it wasn’t considered interesting, and is actually evidence that it will be underrepresented in the other works.
The next problem is that we still don’t know what criterion the author used to define a mention of senile dementia. This once more make s it impossible to test or falsify his claims. The assertion becomes the argument, not science.
And what leads them to that conclusion? Given the nature of medical ‘science’ 150 years ago how could they possibly separate an old person who has gone insane and started wearing his underpants form his head from someone with precisely the same symptoms suffering from Alzheimer’s?
And did they take into account changing social patterns when reaching that conclusion? For example it was once considered so shameful that Granny went nuts and ran down the street naked that she was immediately either locked up in the house or sent to a funny farm. Neither was conducive to medical referencing. These things were shameful and were hushed up, they were not something people gave permission to be published.
Once more, was a comparative analysis conducted on other socially stigmatic illnesses, such as syphilitic insanity amongst married women? That would be a very simple analysis to conduct and provides some sort of statistical comparison. But merely noting that these things were more commonly written about as society becomes more liberal tells us nothing at all. The question is whether they are written about with a greater increase than equally shameful conditions.
If that is the conclusion then I contend that the book has been debunked already.
I have already provided one quote from Shakespeare describing old people as being demented, forgetful or senile. And literature is replete with numerous others. Quite clearly whoever made that claim hasn’t read much old literature, in which mentions of demented forgetful or senile old people is commonplace. Don Quixote himself displays all the classic signs of dementia.
The obvious problem with this type of claim is that ‘old’ people don’t often rate a mention at all, except if they are kings/heroes. And such people are not given to accurate histories. Nobody is likely to write that Odysseus was a mad old fool when he returned home, or that Faustus was senile. But what we do find is that mentions of common people make it fairly clear that having a ‘lack of wit’ is considered as normal as having grey hair.
Once more, unfortunately, this simply isn’t science. Once more a simple statistical comparison could have been carried out. All you would need to do is find something that is approximately as common amongst old people as senility or forgetfulness, and then compare references. Unfortunately because the author has apparently made no attempt to do this we have something that is simply not science.
But once again, no attempt has been made to make this falsifiable or even analysable.
What was the rate of increase in new methods to diagnose Alzheimer’s vs. new methods of diagnosing hip fractures? What was the rate of increase for the number treatments for Alzheimer’s, vs. the number of new treatments for hip fractures? How many new theories do we have now concerning the cause of hip fracture vs. the cause of Alzheimer’s?
If modern medicine has provided new treatment regimes, new diagnostic tools and new theories of causation and progression then of course those things will all be published and debated, leading to far more articles being published. And doesn’t it seem likely that the treatment, diagnosis and causation of Alzheimer’s has changed more in the last 40 years than the causes, treatment and diagnosis of hip fracture?
Did the author do the most obvious comparison? Did he look at other diseases we know existed 200 years ago, like for example glaucoma or chronic leukaemia and see how much they increased? Broken bones are probably the worst possible example. They are diagnosed today just as they were in 1920: by an x-ray. And they are treated exactly the same way: with traction. The only difference is the use of antibiotics for secondary infection and the possible later replacement with artificial joints. So of course there hasn’t been any great increase in the number of articles published. So why not compare apples and apples rather than apples and wheelbarrows? Why not compare a disease with massive advances in treatment technology since 1960 with a similar disease?
Sloppy, sloppy reasoning and even sloppier science. Sorry, but this sort of thing doesn’t thrill me with confidence on the strength of this hypothesis. It stinks of cherry picking.
How many problems can you see with this technique?
The first problem is that is he is using British parish records and Scandinavian (esp Icelandic) records he is blatantly contradicting al other analyses. Those records all show that, for example, tri-generational families were exceedingly rare. I’ll provide multiple references for that if you like. That can not be explained by childhood mortalities, since everybody who had a young child had obviously already survived childhood. Yet almost nobody with a child still had a living parent. Quite clearly there was considerable death in early middle age. Yet this author has concluded exactly the opposite to every other analysis I have ever seen.
The problem with using the aristocracy should be obvious. The aristocracy, notably in Britain, ate massive amounts of meat, far more than is normal for people today. So they should in fact have had more instances of Alzheimer’s.
Re "The Nigerian/American Study. It’s hard to tell without the exact data, but to me a difference of 1% with paired sample sizes doesn’t seem to be significant. Did the author say that these results were significant? The problem is that you will expect differences in that range by pure chance. Equally importantly, since the study group was already aged was the death rate identical? If the author doesn’t mention that point then he is indeed cherry picking.
Re the Ballabgarh study, was the population makeup statistically the same, or were the stats weighted to reflect differences? 1000 person years in the US could easily be a dozen people with an average age of 75. In India it might be 15 people with an average age of 65. That makes one hell of a difference. And were the death rates in the two groups identical? Were they even mentioned?
Yes. It’s crucial.
To start with Alzheimer’s itself kills. A person with low level Alzheimer’s might easily wander in front of a bus, and yet unless these studies autopsied all subjects (which I doubt occurred) such a person would be unrecorded as an Alzheimer’s case. So it’s crucial that we know the life expectancies of that age bracket.
Alternatively imagine we have two groups of >75yo people with a pretty normal distribution from 75-120. Now imagine that in one group 99% of people die between ages 65 and 80, and in the other group 1% die in that age range. That’s; entirely possible since people will probably die of untreated heart disease in that range, while those with no heart disease will already have passed that danger point. Since the frequency of any disease increases with time (it’s just random chance after all) we would expect that the group where most people died in the younger age classes would have less of any disease. Yet somewhat paradoxically it will also end with a higher average age. So we really do need to know the life expectancy within the sample group. We also need to know the causes of death to get anything meaningful.
But realistically all this is somewhat academic. These are such small differences, especially the Nigerian study, that I doubt they are significant. It’s not enough to simply note that one group is 1% more likely to exhibit a trait. We need to be able to say whether that is just random chance, or if it represents a real correlation. Does the author by any chance reference the journals these studies appeared in so we can see if there is any statistical difference?
That’s right. And before viruses were discovered filtering should have killed all known pathogens. Every time a tougher pathogen is found the existing techniques will no longer kill all known pathogens. That’s how we know the new contender is tougher. That a far cry from claiming they can’t be killed by any sterilisation technique.
The problem is that this book doesn’t seem to be actual science. It appears to lack any ready method of falsification and it doesn’t seem to clearly define how it is using terms of defining what was or was not a dementia reference 150 years ago. Simple, valid comparisons have been completely neglected, while the author has chosen to emphasise other totally invalid comparisons with broken bones.
This theory doesn’t appear to have been published in any peer reviewed journals, and I think I can see why. It would get torn to shreds from what I have seen here, assuming any science journal would even accept it. I don’t have any immediate intention of reading this book. It seems like another sensationalist pop-sci novel in the vein of “Chariots of the Gods”. And it seems to suffer form much the same problems as CoTG, namely cherry picking and absence of falsifiability or ability for objective analysis.
This may interest you. Seems to put paid to the idea that there are no or few mentions of the disease prior to last century. I don’t have access to full text, but if you really want an rounded opinion on these claims you really should seek it out. And if this author doesn’t include it in his bibliography he really has been blatantly cherry picking.
Bolding mine.
Berchtold, N.C. 1998. Evolution in the Conceptualization of Dementia and Alzheimer’s Disease: Greco-Roman Period to the 1960s. Neurobiology of Aging. 19:3
Most histories of senile dementia commence with Alois Alzheimer’s description in 1906 of the first case of Alzheimer’s disease, yet the history of senile dementia before 1906 is quite rich, dating back to the ancient Greek and Roman philosophers and physicians. Over the 2500 years since ancient times, the concept of senile dementia has evolved from a rather vague notion that mental decline occurred inevitably in old age, to become defined today by a distinct set of clinical and pathological features with the potential for treatment and prevention within grasp. Throughout history, many elderly individuals with unpredictable behavior were sequestered in institutions, and the line between mental disorders and senile dementia was hazy at best. The identification of Alzheimer’s disease at the onset of the 20th century was a turning point for the understanding of senile dementia, and the concepts and histological findings presented by the early researchers of Alzheimer’s disease remain relevant still today. Indeed, these early findings are proving to be a continuing source of insight, as many of the issues debated at the turn of the century remain unresolved still today. This paper thus traces the history of the evolution of our current conceptualization of Alzheimer’s disease from the amorphous Greco-Roman concept of age-associated dementia.
Thanks! I’ve never heard of this Murray Waldman, but then again, I’m not a neuropathologist, so that doesn’t mean much.
I think this classification is, if not highly outdated, at least oversimplified. For starters, IIRC, many cases of “HIV dementia” turned out to be related to reactivated cerebral toxoplasmosis (infection) or development of central nervous system lymphoma (neoplasia).
Also, how far in the past are we talking about? Prior to the widespread histopathologic examination of autopsy brains, there would have been no way of identifying Lewy body dementia (a histologic finding). For that matter, prior to widespread gross examination of autopsy brains, it would have been pretty hard to tell multi-infarct dementia from Alzheimer’s based solely on clinical symptoms.
It’s certainly possible that cases of early CJD could be misdiagnosed as AD. I think the first sentence is a bit telling, though. It sounds like he’s saying that PrP behaves in vivo like beta-amyloid (forming insoluble plaques), but I notice he never actually declares whether or not they’re actually the same protein. (I’m pretty sure they’re not.) As I said before, it shouldn’t be hard to try to demonstrate PrP immunoreactivity in tissue from AD brains if it’s there.
As far as I can tell, Dr. Yang is saying something much more reasonable: that accumulation of insoluble plaques composed of beta-pleated protein sheets may be a common underlying mechanism for the development of dementia in both prion disease and sporadic AD (I notice he seems to specifically exclude familial AD). The author then takes the unwarranted leap of assuming that all beta-pleated protein sheets (and thus all plaques) are composed of prions, which AFAIK has yet to be shown.
Prions are pretty tough, but can be denatured (and thus rendered noninfectious) by using a concentrated bleach solution.
Well, I’ve got one: The Woodlanders, by Thomas Hardy. There’s an elderly character who becomes demented and imagines a tree is going to fall and crush the house:
He looked out of the window in the direction of the woodman’s
gaze. The tree was a tall elm, familiar to him from childhood,
which stood at a distance of two-thirds its own height from the
front of South’s dwelling. Whenever the wind blew, as it did now,
the tree rocked, naturally enough; and the sight of its motion and
sound of its sighs had gradually bred the terrifying illusion in
the woodman’s mind that it would descend and kill him. Thus he
would sit all day, in spite of persuasion, watching its every
sway, and listening to the melancholy Gregorian melodies which the
air wrung out of it. This fear it apparently was, rather than any
organic disease which was eating away the health of John South.
To ease his mind, his neighbors cut down the tree – and his mind promptly snaps.
I think the biggest empirical argument is quite simple: Alzheimer’s studies get quite a lot of money, because it’s a nasty disease and no one wants it. Tuhs far, these have no identified any prion. Nor have they linked it to any probably prion-related vectors. Granted, prions are not easy to identity, but it still seems mildly unlikely.
More to the point, while the symptoms of Alzheimer’s are similar to some prion-caused diseases, they seem to cause damage in quite different ways.
As I understand it, prions like Kuru or BSE attack the tissues of the brain, albeit slowly, and devour them bit by bit. Alzheimer’s adds plaques to neural pathways which eventually stifle the signals, but leaves the brain intact. But I could be wrong about that.
No! Should I?
Just another book by an author trying to push his theory and make a few bucks.
An anti-meat vegatarian?
A doctor told me it was due to having taken flu shots which contain(ed) mercury.
Small shots, small amount of Hg. Name your poison and take your chances.
I seriously doubt that anyone knows, but many speculate.
If you test 12500 cows and find 0 positives (the 2 positives were not from the 12500 semi-random tests, they were from downers), what’s the statistical probability of there being more than a 0.01% BSE rate? I don’t remember statistics well enough to do the math, but there simply is not a high rate of BSE in North American beef. Moreover, the tests are not of a random sample of slaughtered beef, but are from those animals most at risk at having developed BSE (read: oldest). The vast majority of slaughtered animals are under 2 years old and would be unlikely to have BSE even if BSE were rampant. So, while 12500 may not sound like a lot of tests, and there are undoubtably a few cases going undetected, there is no freaking way that BSE is widespread in North America.
I posted originally during my lunch hour, without the book on hand.