In Defense of Smokers (2003, Lauren A. Colby. Version 2.5)

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Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:39

==Chapter 2: The Burden of Proof==
I am lawyer and, in particular, a trial lawyer. In the law, there is something called the burden of
proof. The anti-smoking crowd insists that smokers prove to them that smoking is not harmful. That's a
trap. Nobody can prove a negative, i.e., that something is not so.
Recently, a client wanted to know whether a particular document was filed with a government
agency. I told him my records did not show that it was filed and that I presumed that it wasn't. That
didn't satisfy him. He demanded a "yes" or "no": was it filed or wasn't it? I explained to him that I could
send a researcher to the agency, and if the researcher found a copy of the document in the agency's
files, that would prove, positively, that it had been filed. If, however, the researcher found nothing, it
would prove nothing. There would always be the possibility that the document was mislaid or that the
researcher overlooked it.
Tobacco companies know a lot about "burden of proof". That's why tobacco executives don't
deny there's a risk in smoking. In fact they even boast that there's a risk. One of their own employees
testified to the Waxman panel that he wouldn't want his daughter to smoke. You see, the tobacco
companies have frequently been sued by people suffering from lung cancer who claim that they got the
disease from smoking cigarettes. The conventional wisdom says that smoking does, in fact, cause lung
cancer, but the conventional wisdom is often wrong and, in this instance there is plenty of evidence that
it is wrong. The tobacco companies, however, don't need to buck the conventional wisdom in order to
defend lawsuits. The tobacco companies have found it easier to defend lawsuits by saying to the plaintiff
"Didn't you read the warnings on the cigarette packages? Didn't you listen to all the warnings from
prominent physicians and public officials? You went ahead and assumed the risk!".
Back in 1890, the conventional wisdom said that masturbation caused blindness. Suppose
some doctor dared to challenge the conventional wisdom, and advised a patient that the practice is
harmless. The patient takes the advice, goes ahead and masturbates and goes blind. He sues the doctor
and I'm hired to represent the doctor in court. Believe me, if I'm a good lawyer, I'm not going to
challenge the conventional wisdom and say the blindness had nothing to do with the plaintiff taking my
client's advice! A much better defense is to cross examine the plaintiff: "Haven't you read books written
by prominent authorities about the dangers of Onanism? Haven't you heard the preacher warn about it,
in church? Haven't you heard the lectures by prominent temperance authorities about this dangerous
vice? You proceeded at your own risk!"
Where smoking is concerned, it's obvious that if everybody who smoked developed lung
cancer, we could say, conclusively, that smoking "causes" lung cancer. But we all know that not
everybody who smokes develops lung cancer, and we also all know of many people who don't smoke
a day in their lives, but none-the-less develop lung cancer at an early age and die from the disease. Hal
Roach, the producer of the "Little Rascals" movies, was a heavy, 3 or 4 pack-per-day cigarette smoker
for his entire life, but died recently, at the age of 101, apparently from simple old age 1 . A former
governor of Virginia died recently of lung cancer; he was in his 50's and had never smoked. Just the
other day, CNN showed a picture of a Lebanese gentleman, who claims to be 134 years old. He was
vigorously puffing on a cigarette, burned down almost all the way to his lips. His formula for a long life:
smoking and drinking every day, along with the consumption of fresh vegetables. The world's oldest
woman, a 125 year old resident of France, smoked until she was 123.
In my own family, my aunt died recently in Florida, at the age of 78, from lung cancer. She'd
been a smoker in her youth, but gave it up about 25 years ago. A family friend, also a female, died in
New York at about the same time as my aunt died. The family friend was in her late 70's or early 80's,
and had never smoked a day in her life. Thus, these little old ladies became statistics. Or did they?
Actually, it may surprise the reader to learn that death certificates never contain any information
concerning the life-styles of the decedents. Therefore, while the Public Health Service keeps certain
records showing the cause of death from various diseases, nobody, but nobody keeps any records to
show whether the decedents were or were not smokers!
There is an Internet News Group devoted to smoking (alt.smokers). Recently, a participant
called the Office of Smoking or Health, in an effort to find out how the government arrives at its
estimate of 450,000 annual smoking related deaths. After repeated calls to different individuals within
the government, it turned out that nobody really knew how the figures are compiled. Some bureaucrat
said he thought the calculations might come from a book, "Foundations of Modern Epidemiology", by
David Lilienfeld. They don't. I'll discuss this and other interesting statistical manipulations, later.
Before leaving this subject, however, a recent (04/19/95) letter to the editor of the San Jose,
Ca., *Mercury News* sheds some light on the methods used by the anti-smoking lobby to generate
false reports of "smoking related" deaths. The author of the letter, Mary Ellen Haley, reported that a
loved one died of adenocarcinoma. Only 17 days elapsed from the deceased's first visit to the doctor to
the day of his death. The letter writer was provided with the information for the death certificate, which
she took to the attending physician for completion.
On the death certificate there was a line for the doctor to insert the immediate cause of death,
and then three lines for "due to". The doctor inserted "cigarette smoking" under "due to". The letter
writer questioned the doctor: was he sure the tumor was caused by cigarette smoking? The doctor said
he wasn't sure about that, but there were guidelines issued by the American Cancer Society, and that
when a person dies of certain conditions and has smoked, the doctor is instructed to list the "due to" as
"smoking". In this instance, Ms. Haley persuaded the doctor to omit the usual "due to cigarette
smoking", but obviously, this was a rare occurrence. The willingness of the medical profession to blindly
observe "guidelines", issued by the Cancer Society generates a continuous stream of death certificates,
validating the official line that cigarette smoking causes everything from heart disease to uterine cancer;
yet, there is no shred of scientific evidence to validate any of the certificates; they are based on nothing
more than official instructions to put down smoking as the cause of death!
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:41

==Chapter 3: The World Scene==
As I indicated in the last chapter, neither I nor anybody else can prove a negative. Therefore,
I'm not going to try to prove that smoking does not cause hangnails, or heart disease or anything else.
The burden of proof rests on those who assert that there is, in fact, a smoking/disease connection. The
connection most often alleged is the connection to lung cancer. I will concentrate on that connection, in
the following pages.
The *Oxford Atlas of the World*, ISBN 0-19-520955-9, published in 1992, gives figures for
cigarette consumption in different countries during the time period 1986-1988. The figures are in annual
consumption of cigarettes per capita. I have taken them from a graph and have attempted to interpolate
between dividers; however, the interpolation errors should be negligible. Here are the figures:
Country:
Hungary
Japan
USA
South Africa
UK
France
USSR
Brazil
Philippines
Venezuela
Zaire
India
Consumption:
2515
2510
2020
1950
1700
1690
1650
1200
1150
950
150
100
To draw any conclusions concerning the influence of smoking upon lung cancer in these
countries, we need figures on lung cancer death rates (LCDR's). Fortunately, the World Bank puts out
a book which gives statistics for a number of countries which give disease statistics in a form known as
"45Q15". The "45Q15" number represents the percentage risk of someone who is 15 years old dying
from a particular disease by the time he or she is 60. Figures are not available for all countries; such
important ones as the former USSR and India either don't report at all or don't break down deaths from
cancer into different types of cancer. Never-the-less, we do have LCDR's for some of the countries for
which we have smoking consumption figures. All of the following statistics are in 45Q15 format, which
means they are risk figures in percentages.
In the United States, the male LCDR is 1.4%, the female risk is 0.7%. Hungary, with the
highest rate of cigarette consumption of any country, has a male LCDR of 2.4; female 0.5%. Hungary
shares the highest rates with its neighbor, Czechoslovakia, where the male rate is 2.4% and the female
rate is 0.3%. Prima facie, these figures indicate that a high smoking rate is associated with a high
LCDR. Or do they?
Let's look at Japan. As we have seen, Japan is practically tied with Hungary for the highest rate
of cigarette consumption in the world. It turns out, however, that the male LCDR in Japan is 0.5%.
That's approximately one-fifth the rate in Hungary; approximately one-third the U.S. rate. The LCDR
for females in Japan is also astonishingly low, 0.2%.
Furthermore, although they have the highest smoking rate of any major nation, the Japanese are
remarkably healthy! At birth, a Japanese male has a whopping life expectancy of 75 years (as opposed
to 72 in the U.S.A.). Japanese girls, at birth, have a life expectancy of 80 years. Those are the highest
life expectancies in the entire world.
Another heavy smoking nation is China. The authors of the World Bank book tell us so, and a
recent PBS special concentrated on the "alarming" rate of smoking in China. In fact, in China, the
government grows tobacco and receives much of its revenue from cigarette sales. In China, however,
the LCDR is about the same as in Japan: 0.56% for men; 0.39% for women, in 1988, the last year for
which we have World Bank information.
Interestingly, some nations in the tropical and sub-tropical belts have very low LCDR's,
notwithstanding evidence suggesting that smoking is widespread in these countries. In Mauritius, an
island in the Indian Ocean where tobacco is an important crop, the LCDR for males is only 0.4; for
females it is 0.1. In Barbados, the male LCDR is 0.5; the female rate is zero. In the Seychelles, an
island paradise in the Indian Ocean, the male LCDR is 0.4; the female LCDR is 1.0, making that nation
the only one in the entire world, where the female rate exceeds the male rate.
At least one researcher has suggested that the low LCDR's in the tropical and sub-tropical
countries are attributable to the exposure of the residents to sunshine, which raises vitamin D levels.
That theory, however, fails to explain the very low LCDR's in China and Japan which are not tropical
or sub-tropical countries.
One possible explanation may relate to the diagnosis of lung cancer. Sri Lanka (formerly)
Ceylon) has the lowest male LCDR of any country in the world (0.1%), and a female rate of zero. So,
if you're worried about lung cancer, you should catch the next plane to Sri Lanka. Before you do,
however, you should be aware there is a disease category called "Senile and ill defined". The male
death rate from "ill defined" illness in Sri Lanka is 3.4%; the female rate is 2.2%. These figures are many
times greater than those for another country (for example, the male rate in the U.S. is 0.3%; in Hungary,
it is zero). Clearly, the doctors in Sri Lanka are not doing a very good job of diagnosing causes of
death. By comparison, in Hungary (which has the largest number of doctors per capita of any country in
the world), every death is accounted for, positively. There are no deaths attributed to "ill defined"
causes.
Diagnosis, alone, however, cannot be the whole answer. Japan has an excellent medical
system, and cases of lung cancer are surely and accurately diagnosed. The death rate from "ill defined"
illnesses in Japan is only 0.1% for males; zero per cent for females. In China, also, there is a rigorous
effort to pin-point causes of death; the rates of death for males and females from "ill defined" causes are
less than 0.1%. Yet, as we have seen, the LCDR's in China and Japan are very low, despite very high
rates of smoking. Moreover, the LCDR figures cannot be dismissed as resulting from poor diagnosis,
since the low rate of "ill defined" illness in each country proves that a vigorous effort is being made to
accurately pin point exact causes of death.
Possibly, genetic factors are at work. Hungary and Czechoslovakia, each with high LCDR's,
are contiguous countries, inhabited largely by fair skinned, blue eyed people. Japan and China, which
have very low LCDR's, are separated only by the narrow Sea of Japan, and populated by people with
relatively similar racial characteristics. Few figures are available on LCDR's in the developing nations in
the tropical and sub-tropical zones, but the available figures suggest that lung cancer rates are small in
these countries, which are largely inhabited by Blacks 2. Can it be that certain races of the world are
genetically more susceptible to lung cancer than others?
I don't know. I can, however, say with certainty that smoking doesn't cause lung cancer in
Japan and China. If it did, the LCDR's in these countries, which are populated by heavy smokers,
could not possibly be so low!
Addendum (2002):
When I wrote this Chapter in 1996, the only information I was able to get on smoking and
disease came from a book published by the World Bank. The World Bank used a very peculiar
method of computing lung cancer death rates (LCDRs), based on a percentage likelihood that
somebody would die by a certain age, from the disease. Also, the Bank didn’t have figures for many
countries.
With the continued development of the Internet, figures have become available which allow for
a comparison of LCDRs, smoking rates, and life expectancies in may countries. A Dutchman, Kees van
der Griendt, has compiled date for 87 countries, using data from the World Health Organization and
the CIA Fact Book. The complete study is at his web site:
http://www.kidon.com/smoke/index.html
It turns out that a high rate of smokers prevalence translates, in many cases, to long life
expectancy and low rates of lung cancer. For males, in 1994, the country with the highest life
expectancy (76.6 years) was Iceland, where 31% of the men smoked. The next runner-up was Japan,
where 59% of the men smoked, and life expectancy was 76.5 years. Other countries with high rates of
male smoking and long life expectancies included Israel (45%, 75.9 years); Greece (46%, 75.2 years);
Cuba (49.3%, 74.7 years) and Spain (48%, 74.5 years).
Clearly, these figures rebut the hysterical claims of anti-smoking organizations. Figures bandied
about in this country, and never challenged, estimate that smoking costs the smoker at least seven years
of life expectancy. Figures circulated in Europe and cited on Mr. Van der Griendt’s web page, claim as
much as 20 to 25 years of loss of life expectancy. But the official vital statistics from countries with high
rates of smoking fail to validate these claims. To the contrary, it turns out that some of the countries with
the highest rates of smoking have the longest life expectancies. This is important, not only from the
standpoint of lung cancer, but also from the standpoint of heart disease. If, as is frequently claimed,
smoking leads to heart attacks, the effects should be clearly show up in the form of greatly reduced life
spans in countries where a lot of people smoke. They don’t.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:44

==Chapter 4: The U.S.: A Smoking Laboratory==
Many people believe that the current concern over smoking and health began with the
publication of the first Surgeon General's Report, in 1964. Not so! As early as 1952, the American
Cancer Society, frustrated by the inability of medical science to find a cure for cancer (or even find the
root causes of the disease), began pointing an accusing finger at smoking. In that year, the ACS began
a study of a group of volunteers allegedly to find out whether smoking was related to lung cancer but
actually, to prove that it was. They had the support of the Surgeon General at that time, Dr. Leroy E.
Burney, who, in an article in the Journal of the American Medical Association, opined that cigarette
smoking causes lung cancer and that cigarette smoking is 7 times worse than cigar smoking and 3 times
worse than pipe smoking. In the following pages, I will be discussing the relationship (if any) between
smoking and lung cancer. Before doing so, however, it needs to be pointed out that, despite the claims
of the anti-smoking movement, there is no "pandemic" of lung cancer in the United States. In the United
States, there are about 2,140,000 deaths from all causes, each year. Of these deaths, less than
120,000 are from lung cancer 3. Thus, despite what you may have read or heard, lung cancer is not a
common illness.
According to the Surgeon General's Report, released in 1964, cigarette consumption in the
United States was 50 cigarettes per capita per annum in 1900; 138 in 1910; 1965 in 1930; 1828 1940
and 3322 in 1950. In 1961, according to the Report, cigarette consumption reached a "peak" at 3986.
In that year, according to the Report, 68% of all males in the United States over the age of 18 were
smokers 4. The interesting word in the "Report" is the word "peak". By 1964, when the Report was
issued, the ACS campaign against smoking was already taking hold, and consumption was already
declining. By the time period 1986-88, according to the figures published in the *Oxford Atlas of the
World*, which I've previously cited, it was down to 2020 cigarettes per capita per year, or just slightly
over half the peak rate achieved in 1961. A Surgeon General's Report, issued in 1980, reported that in
1965, 51.1% of adult men smoked and 33.3% of women. According to the same source, the figures in
1979 were 36.9% for men; 28.2% for women5. According to the CDC (Centers for Disease Control),
26.5% of all Americans were smokers in 1992. Of these, 22.1% were regular smokers, while 4.4%
were occasional smokers.
There are approximately 180 million Americans over the age of 18. Assuming that the average
smoker smokes a pack a day (20 cigarettes), we can calculate annual per capita cigarette consumption
by taking 26% of 180 million to get the number of smokers (which equals 51 million), multiplying by
365 days to get the annual consumption of all 51 million smokers and dividing by 180 million to get the
per capita annual consumption. This gives a result of 2069 cigarettes per annum per capita, which is
very close to the number supplied in the *Atlas* 6. The United States, therefore, has been turned into a
giant laboratory for the evaluation of a cigarette/lung cancer link. If, in fact, cigarettes do, in fact,
"cause" lung cancer, we should see a decrease in the LCDR's over the time period between 1961 and
the present, corresponding to the approximately 50% decline in cigarette consumption, and the
comparable decline in smoking. The problem is, we don't!
The Statistical Abstract of the United States, published by the Commerce Department, 1993
Edition, gives statistics for cancer death rates in men and women during the time period from 1970 to
1990. Unlike the international statistics, reported in the previous chapter, the figures in the Statistical
Abstract are not percentages. Rather, they represent the number of deaths per 100,000 of population.
Where the figures refer to a particular age group, they refer to the number of deaths per 100,000
population in that particular age group. Thus, the figures are automatically "age adjusted" 7.
It turns out that in every important age grouping, LCDR's have increased, steadily, between
1970 and 1990, notwithstanding the decline in smoking! Here are the figures from the Statistical
Abstract:
For Men For Women:
Age
Group
1970 1980 1990 Age
Group
1970 1980 1990
35-44 17.0 12.6 9.1 35-44 6.5 6.8 5.4
45-54 72.1 79.8 63.0 45-54 22.2 34.8 35.3
55-64 202.3 223.8 232.6 55-64 38.9 74.5 107.6
65-74 340.7 422.0 447.3 65-74 45.6 106.1 181.7
75-84 354.2 511.5 594.4 75-84 56.5 98.0 194.5
85 + 215.3 386.3 538.0 85 + 56.5 96.3 142.8
Particularly interesting are the figures for women. They show dramatic increases in LCDR's, in
the key age groups where lung cancer is most prevalent, notwithstanding a steady decline in smoking
rates. The most obvious interpretation to be given to these figures is simply that the decline in smoking
has not produced any decrease in LCDR's and that, in fact, in most age categories, the LCDR's have
gone up. The anti-smoking people have an answer to everything, however, and, to combat the obvious
implications of the statistics, they have developed a new theory: the "incubation period" theory.
According to that theory, lung cancer is caused by smoking, and there is an "incubation period",
variously given as 20 years, thirty years, or some other number, during which cancer develops in the
lungs of smokers. According to this theory, the dramatic increase in LCDR's in women simply confirms
that smoking causes lung cancer, because women began to smoke more recently than men, and the
effects are just starting to show up in the figures.
There are a number of problems with the "incubation period" theory. The first is simply that,
contrary to the assumptions advanced by the proponents of the theory, women are not newcomers to
smoking, in America. A Gallup poll, taken in 1944, revealed that 36% of the women in the U.S. over
the age of 17, smoked" 8. In 1959, the Department of Agriculture estimated that 47% of the overall
population of the U.S., over the age of 14, smoked, and that men smoked an average of 24 cigarettes
per day while women smoked 19" 9. I have found no reliable statistics for female smoking earlier than
1944" 10, but would remind the reader that in films, books, etc., the female "flapper" of the 1920's was
usually depicted with a cigarette in her mouth, often in a long white holder. Anyway, various surveys,
taken between 1955 and 1985 and cited in *International Smoking Statistics* show female smoking
rates as low as 27% and has high as 37%, with the latest surveys (1985) at 25% or 28% (according to
which survey you believe). The notion that women were shy abstainers from tobacco use until recent
years simply is not supportable.
A second, even more serious problem for the "incubation period" theory is that the statistics for
LCDR's in women just don't add up when compared with the overall cancer death rate in women, i.e.,
the rate of death from cancers of all kinds, combined. According to the Statistical Abstract, that overall
cancer death rate, age adjusted, has remained practically constant over the years. In 1970, it was
108.8; in 1990, it was 112.7. But how is this possible, given the dramatic rise in LCDR's in women?
To answer that apparent paradox, we must remember that we're talking death rates, not rates
of incidence of disease. The death rate in females from heart disease has declined significantly in recent
years. Here are the rates, by age groups, for ischemic heart disease (the major killer in that category):
Age Group 1970 1980 1990
45-54 84.0 52.2 33.6
55-64 299.1 164.5 135.4
65-74 978.0 430.1 415.2
75-84 2866.3 1842.7 1287.6
85 + 6951.5 5280.6 4257.8 11
Furthermore, medical science has made considerable progress in curing some of the kinds of
cancer which afflict women. Thanks to pap smears and mammography, cancers of the genital organs
and breast can now be detected early and often successfully treated. Thus, more women are living to
the ripe old age where lung cancer usually strikes. Progress has also been made in prolonging the lives
of lung cancer victims through chemotherapy, which may well account for the slight reduction in lung
cancer rates in younger women (and men). The anti-smoking crowd, however, refuses to even consider
these factors. They are committed to the belief that if smoking were just prohibited, disease, of all sorts,
would be practically eliminated. When the statistics fail to show that the drastic decline in smoking has
brought about a corresponding decline in LCDR's, the anti-smokers simply postulate longer, and longer
"incubation" rates for lung cancer (forgetting, by the way, that on that theory, there also has to be an
"incubation period" for the disease in the thousands of non-smokers who develop lung cancer!).
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:46

==Chapter 5: Some Studies that Went Wrong!==
In February, 1991, a paper was published in the Journal, Cancer, entitled "Comparative
Epidemiology of Cancer Between the United States and Japan". The authors, Ernst L. Wynder, M.D.,
et al, started out with the assumption that smoking causes lung cancer. In fact, Dr. Wynder has been
crusading against smoking since the 1950's and the authors' report was paid for by the anti-smoking
National Cancer Institute. As we will see, the authors took some liberties with the figures presented in
their report, so as to try to make the data fit their preconception that smoking causes lung cancer, but
eventually had to admit that the data did not support that assumption. The highlight of the Wynder
Report is a graph, which purports to show per capita cigarette consumption in the United States and
Japan for the time period 1920 to 1985. The graph relies upon data, plotted at five year intervals. It
purports to show a sharp dip in consumption during World War II, to less than 1/3 the pre-war rate.
Also, amazingly, it purports to show that for the entire time period between 1920 and 1985, per capita
cigarette consumption in Japan was always less than in the U.S.
As we will shortly see, the authors of the Wynder Report presented data which they themselves
acknowledged to be in contradiction with their own graph. Before discussing that matter, however, it
will be helpful to consider a basic problem in epidemiology, i.e., the difficulty of comparing data for two
differing populations.
Suppose we postulate that people who eat jellybeans are prone to develop more carbuncles
than people who don't. To test the theory, we decide to study jellybean consumption in two different
countries: country A and country B. Both countries have populations of 1,000,000 divided equally
between men and women. Jellybean consumption in both countries is 1,000,000 beans per day,
yielding a per capita consumption figure of one jellybean per person per day. There is, however, a
difference. In Country A, only men eat jellybeans, while in Country B, both men and women eat
jellybeans. Obviously, in Country A, the jellybean consumption for men is 2 per day, while in Country
B it is one. In Country A, the daily jellybean consumption for women is zero, while in country B it is
one. Any comparison of the two countries must take this into account. Dr. Wynder and his colleagues
presented data on relative smoking rates for men and women in Japan and the United States. The rates,
expressed in terms of the percentage of each sex who smoke, are as follows:
Year: 1955 1965 1976 1980 1985
U.S. Males 52.6 52.1 41.6 37.9 33.2
U.S. Females 24.5 34.2 32.5 29.8 27.9
Japanese Males 81.4 82.3 75.1 70.2 64.6
Japanese Females 12.8 17.7 15.4 14.4 13.7
Likewise, the authors presented statistics for 1970, 1980, and 1986, showing that Japanese
males smoke more cigarettes per day than U.S. males, while Japanese females smoke fewer cigarettes
per day than their counterparts in the U.S. Clearly, the total consumption figures given in the graph,
accompanying the report, need to be adjusted to take into account the differing rates of smoking among
males and females in Japan and the US. Otherwise, the authors are comparing apples and oranges. No
adjustment was made but, if one had been made, so as to compare only Japanese males with US
males, the graph would most assuredly have shown much higher per capita consumption in Japan than
in the U.S. This is so because, in Japan, where few women smoke, the large number of non-smoking
women "waters down" or dilutes the per capita consumption figures for the population, taken as a
whole.
Other data presented in the report compared the lung cancer death rates in Japan and the U.S.
For some reason, the authors elected to give figures only for white U.S. males and females, excluding
African Americans and American Indians (probably, the inclusion of that data would have interfered
with some pre-conceived notions). Whatever the case, the male lung cancer death rates, age adjusted,
for 100,000 of population were presented as follows:
Year: 1955 1965 1975 1985
U.S. 90 130 160 165
Japan 15 35 45 50
At the time of the release of the report, there were interviews on TV with Japanese doctors, who
sought to explain the high rate of smoking in Japan and the low rate of lung cancer by declaring that in
Japan, cigarettes were hard to get, during World War II. The graph, prepared by Dr. Wynder and his
colleagues, seems to support that claim, showing as it does a big dip in cigarette consumption during the
War.
The graph is, however, tricky. The data is plotted at five year intervals, and 1945, the last year
of the war, is one of the years used. Simple interpolation was used to indicate the data between 1940
and 1945, and between 1945 and 1950; in other words, the authors drew two straight lines, one
between 1940 and 1945, and another between 1945 and 1950.
Actually, data is available for annual cigarette consumption in Japan for every year from 1920
to 1990, based upon sales. Those figures come from a book, *International Smoking Statistics*,
published by the Oxford University Press in 1993. The figures show that in Japan, as in the U.S., there
was a switch from machine made cigarettes to hand rolled cigarettes during World War II. Taking that
into account (which the Wynder authors apparently did not), the Japanese consumed 71,158 million
cigarettes (of both kinds) in the last year before the War, 1941. Consumption continued unabated until
1944, when 64,280 million cigarettes were consumed. In 1945, consumption dropped to 31,021
million cigarettes. It then rose steadily until 1950, when 75,138 million cigarettes were consumed. So
there was a dip, but it lasted only 5 years, and was not nearly as pronounced or as lengthy as the
Wynder chart would make it seem.
The bottom line, however, was the concession of Dr. Wynder that the data did not support
smoking as a cause of lung cancer in Japan. That concession did not come without a few confusing
gyrations. In discussing cancer of the larynx, the authors say that "The age adjusted mortality rates for
laryngeal cancer during 1955 are higher in U.S. Whites than in the Japanese. These differences can be
partially explained by the higher levels of cigarette consumption and alcohol consumption in the U.S.".
The authors discuss cancer of the esophagus, saying that "In spite of the higher tobacco and alcohol
consumption in the U.S., Japanese males have higher esophageal cancer mortality rates, which suggests
that other risk factors are of importance". Thus, in their discussions of these two types of cancer, the
authors assert that smoking and alcohol use are greater in the U.S. than in Japan, using that "fact" in one
instance to justify their preconceived belief as to the cause of laryngeal cancer, and dismissing the "fact"
as irrelevant when it comes to the other cancer (esophagus), where the figures just don't bear out the
preconception.
When it comes to lung cancer, however, the authors state that during 1955 to 1985, lung
cancer death rates are "higher in US White men than in Japanese men which is discrepant with the
higher prevalence of cigarette smoking among Japanese males for the same period of time". Exactly!
According to the authors' own figures, the lung cancer rate among Japanese males is less than one third
the rate among US White males, and as early as 1955, 81.4% of Japanese men were smokers
(compared to 52.6% in the U.S.). That is, indeed, a big discrepancy. The Wynder authors must have
had to write that word "discrepant" through gritted teeth, but at least they had the honesty to do it.
On January 13, 1995, the *Wall Street Journal* reported another study, this one involving
animals and funded, in part, by the U.S. National Institutes of Health. According to the report, the study
was inspired when a researcher in Buffalo, John Pauly, was studying some tissue from a smoker and
lung cancer victim and found a tiny particle of cellulose acetate, the material used to make cigarette
filters. He apparently decided that pieces of cigarette filters, imbedded in the lungs, are the cause of lung
cancer and decided to do an experiment with mice. He implanted pieces of filters, coated with
cigarette tar, in the lungs of six mice and found that they remained intact in the lungs for six months. This
finding was haled as a great break-through, demonstrating that pieces of cigarette filters may lodge in
the lungs and cause cancer. What this ignores, however, is a simple fact: no cancers were found in the
mice! What the study really proves, therefore, is merely that implanting pieces of cigarette filters,
drenched with tar, in the lungs of mice does the mice no apparent harm!
Before leaving this subject, i.e., studies which don't bear out the smoking/lung cancer
connection, it's worth mentioning a couple of studies that involve Native Americans. Some of the
heaviest smokers (and drinkers) in America are to be found among the Native Americans. In fact, a
1992 study by the CDC showed that 39.5% of American Indians smoked, as opposed to 25.6% of the
general population. Knowing this, I have been looking for some statistics on lung cancer among Native
Americans.
Turns out there have been at least two such studies. The first was conducted by J.M. Samet, et
al, of the University of New Mexico School of Medicine and published at *Am J Public Health* Sept.,
1988, 79(9) 1182-86. The study dealt with both Hispanics and Native Americans. The authors
concluded that in the study \ period (1958-82), "[in whites] age adjusted mortality rates from lung
cancer and from chronic obstructive pulmonary disease increased progressively in males and females.
Mortality rates for both diseases increased in Hispanics during the study period, but the most recent
rates for Hispanics were well below those for Other Whites....in Native Americans, rates for both
diseases were low throughout the study period, and did not show consistent temporal trends."
The second study was conducted by M.C. Mahoney, et al., of the New York State
Department of Health, using data from Native Americans in upstate New York, during the time period
1980-86. It is published in the *Int J Epidemiology*, June, 1989, 18 (2) 403-412. The authors came
to the same conclusion as Samet, et al. They stated that the principal causes of death among the Native
Americans were TB, diabetes, pneumonia and cirrhosis. However, "fewer than expected malignant
deaths occurred among both Native males and females [and]... A deficit of deaths was observed for
colon and lung cancer deaths among Native males and for colon and breast cancer deaths among
Native Females...".
In short, Native Americans smoke more than the general population but suffer from less cancer
and, in particular, less lung cancer.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:49

==Chapter 6: The Propaganda Machine==
Beginning in the early 1950's, the American Cancer Society started to wage war against
smoking. Later, the government took up the cudgel and, today, there is a government agency, the
Office of Smoking and Health, dedicated to stamping out smoking. Unfortunately, the government
propaganda is often predicated upon assertions which are simply untrue. In many instances, these are
examples of the "LaLonde effect".
Marc LaLonde was formerly the Canadian Minister of National Health and Welfare. He argued
that health messages should be vigorously disseminated, and should be "loud, clear and unequivocal"
even if unsupported by scientific evidence. If a particular study showed that smoking might be related to
a particular disease, it made no difference to LaLonde whether the study was seriously flawed, or not.
He felt that releasing the study was always justified, if it would convince people to stop smoking, since
everybody knew that smoking was bad for people.
The LaLonde effect is by no means new. As early as 1955, J. Neyman wrote an article in
*Science Magazine*, entitled "Statistics - servant of all sciences". In the article, he commented upon a
statistical study of smoking and cancer and concluded that the study was possibly flawed.
None-the-less, he felt obliged to remark, in a footnote, that "A referee warns me that in spite
of the fictitiousness of the figures in Table 1 and in spite of the emphasis on the methodological
character of my remarks, the `tobacco people' may pick up the argument and use it for publicity
purposes" 12.
Every year, the government releases figures on the number of "smoking related deaths" in the
United States. The most recent figure is 470,000, although Congressman Waxman recently said
500,000. Most people assume that there is some scientific basis to that figure. Not so! The government
"scientists" simply take a flat percentage of the number of people who die from a particular disease, and
assume that to be the number whose death was caused by smoking. There are no autopsies, no studies
on actual human beings.
Dr. Bernard M. Wagner, the editor of Modern Pathology, recently wrote, "Are there 450,000
smoking-related deaths per year in America? Maybe...but no human beings are ever studied to find
out". Wagner went on to say the biggest obstacle to knowing what is actually going on is the low
autopsy rate in this country, about 10%.
Perhaps the best (or maybe the worst) example of the LaLonde effect is the recent report of the
Environmental Protection Agency on the "dangers" of second-hand smoke (ETS).
In an article published in the Winter 93-94 issue of Bostonia, a magazine published by Boston
University, the EPA Report was vigorously attacked by Dr. John C. Luik, a non-smoker, and a senior
associate of the Niagara Institute, Ontario, Canada. As Luik showed, the EPA study was based on
some 30 studies from several different countries. These studies dealt, essentially, with the effect of
smoking by a smoking husband or wife on a non-smoking spouse. Of the thirty studies, 24 showed no
statistically significant connection between ETS (environmental tobacco smoke) and lung cancer.
However, while the EPA saw fit to discuss and refer to all 30 studies, it made a statistical analysis of
only 11 U.S. studies. EPA conceded that ten of these studies also showed no statistically significant
increase in lung cancer risk. One study alone showed such a risk, but to show such a risk, the EPA was
obliged to reduce the statistical "confidence factor" which it normally uses in such analyses from 95% to
90%!
The EPA then went on to merge all of the eleven studies together (a statistically invalid
procedure since the studies were not all structured the same way), and to reanalyze the results, using
the newly reduced "confidence factor". By folding, mutilating and stapling the data, the EPA decided
that the spouses of smokers had a risk of developing 119 lung cancers, as opposed to a risk of 100
such cancers in the spouses of non-smokers. Without the reduction in the "confidence factor", no
statistically significant risk could have been shown. None-the-less, the EPA branded ETS a
"carcinogen".
Writing in *Toxological Pathology*, Alvan Feinstein, a Yale University epidemiologist quotes
another prominent epidemiologist as saying this about the EPA report: "Yes, it's rotten science, but it's
in a worthy cause. It will help us to get rid of cigarettes and become a smoke-free society". The
"LaLonde Effect" is alive and well!
Meanwhile, the propaganda machine continues to spew out all kinds of spurious information
and distortions. On July 13, 1994, an obituary in the *Washington Post* reported the death, at age 60,
of Richard Joshua Reynolds, III, an heir to the founder of the R. J. Reynolds Tobacco Company. The
headline, and an accompanying photograph showed the deceased holding a lighted cigarette, implying
that Reynolds died from emphysema, caused by smoking. Reading the body of the obituary, however, it
turned out that he had quit smoking eight years before his death; that there was a family history of
emphysema and the deceased's own father had died from the disease at the age of 58; and that his
doctor was unable to state the "immediate cause" of his death!13
Recently, also, the Post Office released a postage stamp, honoring a deceased jazz musician.
The likeness of the musician is on the stamp, and is based on a photograph, taken while he was alive.
The original photograph showed the musician with a cigarette dangling from his lips. But the cigarette
has been airbrushed out in the postage stamp!
Recently, on Maryland Public TV, an official of the Maryland Cancer Society made the
statement that the smoking/lung cancer connection had been established in "laboratory experiments". Of
course, it has not, but nobody challenged him.
Similarly, in a recent CNN television program about smoking, a lady was presented who had
lost her larynx to cancer and had to use an artificial voice box. In the course of the program, it came out
that the lady was a life long non-smoker. The moderator, however, proceeded to explain that the
cancer had been caused by second hand smoke!
Whenever anybody challenges the view that "tobacco kills", they are immediately confronted
with the argument that they are tools of the giant tobacco companies. Supposedly, these companies
spend millions to spread lies and disinformation concerning smoking.
The truth is that the anti-smoking lobby has successfully demonized the tobacco companies to
such an extent that few public officials would dare accept contributions from tobacco companies, lest
they be charged at election time with accepting "tobacco money". The truth is, moreover, that there is a
lot of money to be made in the anti-smoking movement, and lots of people are benefitting, financially,
from that movement.
In 1994, the Labor Commissioner for the State of Maryland proposed a state-wide smoking
ban. It was far reaching indeed, and, in its original form, would have prohibited people from smoking,
even in their own hotel rooms, on the theory that the maid might come in to clean up, sniff some
second-hand smoke and suffer lasting injury.
At the time the ban was originally proposed, a stream of U.S. government officials poured into
Maryland, conducting seminars and public meetings to whip up support for the ban. These officials,
from such agencies as the Office on Smoking or [sic] Health, EPA, FDA, etc., make a good living,
"educating" the public in the dangers of tobacco. Furthermore, the months leading up to the ban were
filled with television spots, featuring animated skeletons, demonstrating the "dangers" of smoking. These
spots were paid for with taxpayer monies. A similar television spot campaign runs in California, also
paid for with taxpayer dollars.
At the time the Maryland ban was first proposed, William Donald Schaefer was Governor. In
November, 1994, an election was held for a new governor, and the smoking ban became a campaign
issue. The Maryland "hospitality industry", consisting of owners of restaurants, bars, convention
promoters, etc., was terrified that the ban would drive business out of the state to such nearby
jurisdictions as the District of Columbia, Virginia, Delaware, West Virginia and Pennsylvania. Ellen
Saurbrey, the Republican, promised to do away with the ban. Her Democratic opponent, Parris
Glendening, promised to provide exemptions for small businesses, taverns, restaurants, etc.
Glendening won the election by a whisker-thin margin, amidst charges of voter fraud. Upon
assuming the governor's office, he forgot all about his campaign promises, and set about to impose what
amounted to an all-encompassing ban. At a meeting of anti-smoking forces in the state capital, the
governor appeared with Victor Crawford, a self-styled former lobbyist for the tobacco industry, who
now has throat cancer and attributes it to his former smoking habit. At the same rally, the Governor
declared that 3,000 Marylanders die every year from second-hand smoke (a figure which is a
fabrication, pure and simple: remember, even in its highly flawed report on second hand smoke, the
EPA claimed no more than 3,000 deaths, annually, in the entire nation). The governor went on to claim
that Maryland has the highest rate of cancer in the nation. On the basis of death certificate records,
that's technically true; however, the Governor neglected to mention that Maryland has many large
cancer treatment centers, e.g., NIH, Bethesda Naval Hospital, and John Hopkins University Hospital,
and that when people die from cancer in these institutions, their death certificates are issued in
Maryland, even though the deceased may have come here from Iowa!
Ultimately, the state legislature passed legislation, exempting some bars and restaurants from the
ban, and the governor compromised, declaring, however, that he would come back later and remove
the exemptions. Meanwhile, however, Victor Crawford had a field day with the press. He was featured
in editorials and in a "60 Minutes" television interview with Leslie Stahl. In the interview, Crawford
asserted that he had served the tobacco companies by "turning out the troops" for pro-smoking rallies;
(b) presented false laboratory reports; and (c) presenting false information on poll results, affecting
smoking.
The Tobacco Institute has denied that Crawford did any significant amount of work for them.
Moreover, in the 22 years that I've lived in Maryland, I never heard about any pro-smoking rallies, or
any polls dealing with smoking, or any "laboratory reports". So, I searched the archives of the
Baltimore Sun. There were five references to Crawford: three dealing with his present claims that he
lied on behalf of the tobacco companies, one dealing with a property dispute, and another, which
identified him as a prominent criminal lawyer, who had been involved in 33 capital cases. There were
no references to any pro-smoking rallies, or polls dealing with smoking, or lab studies dealing favorably
with smoking. So, if Crawford organized rallies, they must have been kept very quiet and, if he
distributed information about polls or lab studies, that information must have been kept very quiet.
Crawford, of course, is a confessed liar. In fact, on "60 Minutes", he bragged about the lies he
supposedly told. The question I have is whether a confessed liar can be believed, when he says that
he's now telling the truth. Is it possible that he was paid for his appearances with the Governor?
Crawford's name surfaced again in the September 23, 1995 edition of the *Washington Post*.
There, a story appeared about a prostitute who said she had sex with a Montgomery County judge and
that her own attorney offered her $10,000, if she would leave Maryland after the investigation began.
The attorney? None other than Victor Crawford. Crawford denied the allegation of course, but his
denial shows that he still has tobacco on his mind. In a telephone interview from Denver, Crawford
said, "Somebody's got their facts awfully screwed up if they think I'm involved with this...Ten thousand
dollars? Somebody has really been smoking some funny cigarettes on this one...".
The story goes on to say that Crawford gained national attention this summer when he was
profiled by the CBS News program, "60 minutes" for abandoning his life as an Annapolis lobbyist for
the tobacco industry. Apparently, the *Post* forgot that, in their March 4 Edition, Crawford admitted
that he really never had a "life" as a tobacco lobbyist in Annapolis or any place else. In an interview, he
disclosed that he lives in the posh Washington, D.C., suburb of North Chevy Chase (some 60 miles
from Annapolis), and that his career as a tobacco lobbyist consisted solely of working on contract for
the Tobacco Institute for 6 years in the late 1980's. In the same interview, he claimed that he received
"about $20,000" for his services, at a rate of "up to"
$200.00 per hour. That meant that, if he can be believed, he devoted approximately 17 hours per year
to tobacco lobbying.
Many anti-smoking "experts" are paid, and paid very well. There are grants available from the
cancer societies and from governments, for anti-smoking research and "education", and many people
benefit from these grants. In California, Proposition 99, passed in 1988, has turned out to be a mother
lode for the anti-smoking lobby. Under its provisions, there is so much to dole out that practically
anyone with a harebrained scheme can profit, so long as their ideas can be viewed in some way as
furthering the anti-smoking cause. Thus, camping trips are funded and the hikers clothed with tee-shirts
bearing anti-smoking massages. One group built a race car with anti-smoking slogans on it and now
tour the racing circuit at smokers' expense. Swimming pools are built for schools on the condition that
smoking be banned throughout the property, including in teachers' cars on the parking lot.
If Crawford is the "Poster Boy" for the anti-smoking movement, Stanton Glantz is the
movement's high priest. Glantz is a professor at UCSF, in California. In addition to his salary, Glantz
gets generous government research grants as well as speaking fees from numerous groups such as the
American Heart Association. Glantz recently came up with a figure of 53,000 deaths per annum in the
U.S. from second hand smoke. In truth, Glantz did not support his estimate with any scientific data; he
didn't have to. His adoring audiences will believe anything he says, and he gets paid to say it, so long as
he tells the audiences what they want to hear.
Before leaving this subject of propaganda, mention should be made of the oft-repeated canard
that smoking imposes costs upon society, which must be paid by non-smokers. The State of Florida,
among others, is suing the tobacco companies for the medical costs which it claims to have incurred as
a result of the smoking habits of its residents.
Now, I do not happen to think that smoking causes any disease. Assuming, however, solely
arguendo, that smokers do, in fact, die prematurely from smoking-related diseases, there is a
considerable saving to society because these dead smokers do not collect their full social security
and/or pension benefits. Moreover, smokers pay cigarette and tobacco taxes, both to the states and the
federal government, which non-smokers do not pay.
In 1991, Willard G. Manning, et al., published a landmark study on the costs to society of
alcohol and tobacco 14. Manning and his colleagues were no friends of tobacco. They assumed that
smoking causes premature death, extra sick leave, and fires. Never-the-less, when all of the costs
attributed to smoking by Manning are added up and offset against the benefits, it is clear that smokers
pay more to society than they take from society. In the following table, a minus sign denotes a cost to
society, while a positive sign denotes a saving or benefit. All of the figures are expressed in cents per
pack of cigarettes smoked:
Additional medical expenses from smoking -26
Sick leave costs -01
Group life insurance -05
Fires caused by smoking -02
Lost tax revenues due to premature death -09
Reduced use of retirement pensions +24
Reduced use of nursing homes +03
Federal cigarette tax +24
State and local taxes 15 +26
Net Benefit to Society +34
This is, perhaps, a convenient place to mention another benefit to society which formerly
accrued from smoking, but no longer exists, because of the ban on smoking in commercial airplanes. In
these aircraft, devices known as "packs" are used to filter the air in the passenger cabins. When
smoking was allowed, the airlines used up to six packs to filter the air in first class; a fewer number in
economy class. Packs, however, cost the airlines money, because they decrease fuel economy. The
smoking ban enabled the airlines to reduce the number of packs they used, and they did so,
enthusiastically, since, without the odor of smoke, passengers could not tell whether the air was being
efficiently filtered, or not. As a result, the air in commercial airliners is likely to be filthy, and laden with
viruses, bacteria, and other unpleasant things. It's no coincidence, therefore, that stories have started
cropping up in the newspapers about stewardesses who transmitted tuberculosis to passengers and
other crew members 16. The odor of tobacco smoke formerly served the same function as the odor that
gas companies add to natural gas. It warned of insufficient ventilation.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:52

==Chapter 7: The Surgeon General's Reports==
At this point, the reader will likely ask, "But what about the Surgeon General's Reports? Don't
they prove that smoking causes lung cancer?" Actually, they don't.
It's not easy to get copies of these Reports. When I started my research, I combed the local
libraries without success, and called major libraries all over the country. Nobody had any copies. One
reason the Reports may be so difficult to obtain is that they contain material which might be
embarrassing to the anti-smoking lobby, e.g., the data on pipe and cigar smoking. Ultimately, I found a
small company in Alexandria, VA, which was able to supply copies of the reports from 1964 through
1982, on microfilm. During that time frame, there were a total of 15 Reports, issued sporadically
between 1964 and 1982. The largest , most massive Report was issued in 1979, and dealt with
programs to "educate" (force) people not to smoke. The last Report that I have was entitled the
"Changing Cigarette", and dealt with such things as filters, tar content, etc. The basic "science",
purporting to show that smoking causes lung cancer was set forth in the first Report, in 1964, and for
that reason I will concentrate here on an analysis of the 1964 Report.
The 1964 Report was issued by a committee of ten "scientists", picked from a list of 150
scientists and physicians, heavily weighted towards government agencies and large organizations active
in public relations, with a low representation from the scientific community. There were no statisticians
on the panel, although statistical expertise was essential to a proper analysis of the epidemiological
studies, which formed a large part of the "evidence" which was studied. In 1965, a prominent
statistician, K.A. Brownlee, of the University of Chicago, wrote a scathing review of the Report,
pointing to many discrepancies in the statistical data. I will refer to that later 17.
Prior to the writing of the Report, numerous experiments had been conducted, attempting to
induce lung cancer in laboratory animals by painting their lungs and trachea with cigarette tars, forcing
the animals to inhale vast quantities of tobacco smoke, etc. All of these experiments failed, miserably!
Consequently, at page 165 of its Report, the Committee was obliged to concede that "Broncho genic
carcinoma has not been produced by the application of tobacco extracts, smoke, or condensates to the
lung o r the tracheobronchial tree of experimental animals with the possible exception of dogs".
The phrase "possible exception of dogs" related to a single experiment, of which the Committee
wrote that "this work has not yet been confirmed". To this day, it remains unconfirmed and it remains
true, to this day, that despite hundreds of experiments 18, nobody has been able to induce a single
cancer in lab animals by exposing them to ordinary tobacco products or smoke.
Other researchers attempted to induce lung cancer in lab animals by using nasty combinations
of industrial strength carcinogens. They used mixtures of ozonized gasoline and mouse-adapted
influence viruses; polycyclic aromatic hydrocarbons, directly applied to the lungs of rats; mixtures of
benzo(a)pyrene and iron oxide dust; radioactive cerium; and beryllium oxide. Even with these noxious
brews, the results were not entirely successful. For one thing, some of the experimenters reported
"distant metastases", i.e., tumors occurring in sites far from the lungs (which makes me wonder whether
the "treatments" had simply weakened the animals' immune systems to the point at which cancers were
springing up spontaneously throughout their bodies). Moreover, no t all the animals got sick. For
example, two out of ten rhesus monkeys injected with beryllium oxide developed cancers but 8 did not.
The animal experiments having failed, the Committee was left with retrospective studies and
prospective studies. Retrospective studies are studies in which cancer patients are interviewed about
their smoking habits and compared with another group of controls from the general population, whose
smoking habits are likewise identified. In prospective studies, a population is sampled, their smoking
habits are ascertained, and they are then followed for a number of years, to determine who develops
the disease.
The Committee had a number of retrospective studies available, but wisely decided not to rely
much upon them, because of well known problems with such studies. Instead, it chose to rely upon
seven prospective studies, as follows:
(1) British doctors, a questionnaire having been sent to all members of the medical profession in
the U.K. by Doll and Hill, in 1956.
(2) White American men in 9 states, enrolled by American Cancer Association volunteers, each
of whom enlisted 10 white males between 50 and 60 years of age. Hammond and Horn, 1958.
(3) Policy holders of U.S. Government Life Insurance policies. Dorn, 1958.
(4) Men, 35-64 in nine occupations in California which were suspected of having a high
occupational risk of lung cancer. Dunn, Linden and Breslow, 1960.
(5) California members of the American Legion and their wives. Dunn, Buell, and Breslow,
1961.
(6) Canadian War Veterans. Best, Josie and Walker, 1961.
(7) American men in ten states, enrolled by volunteers from the American Cancer society, each
of whom was asked to enroll about ten families containing at least one person over 45. Hammond,
1963 19.
Now, right off the bat, there were several sources of bias immediately apparent in the manner in
which the surveys were conducted. It was obvious to everyone, including the participants and their
doctors why these studies were being conducted, i.e., to prove that smoking causes lung cancer. Thus,
an element of detection bias was introduced. I'll return to that point shortly.
There was also the matter of the selection of the survey participants. Not all the holders of U.S.
Government Life Insurance policies participated; not all the British doctors participated, etc. Taking the
five studies for which it had data on the non- response rate, the Committee concluded that the average
non-response rate was about 32%. Then, at page 116 of its Report, the Committee made the following
curious observation. Citing a paper by Berkson 20, the Committee said, "The death rate in the complete
population (3.000) was 42% higher than the respondent death rate. The non-smoker death rate was
over 38 times as high among non-respondents as among respondents (60.1221/1.553), whereas among
smokers it was only 1.8 times as high. [Berkson's] calculations referred to an early year of the study, in
which the differential entry of ill persons among smokers and non-smokers are likely to be most
marked. Further, as we interpret his writing, the example was intend ed as a warning against the type of
subtle bias that can arise whenever a study has a high proportion of non respondents, rather than a
claim that this numerical estimate of the bias actually applied to these studies".
Thus, the Committee was confronted with what should have been a red flag: a finding that the
death rate amongst non responding non-smokers was 38 times as great as the rate amongst responding
non-smokers, whereas the death rate among non-responding smokers was only 1.8 times as great as
the death rate among corresponding respondents. It is apparent, even to a layman, that such a major
discrepancy could greatly skew the results of the surveys. Yet, the Committee brushed the point aside,
saying, in substance, that it didn't think that Berkson meant what he wrote!
There were troublesome discrepancies. The Committee found that the most potent carcinogen
present in tobacco smoke is benz (a) pyrene (p. 27). According to the Committee, cigar smoke has 4
times as much benz (a) pyrene as cigarette smoke, and pipe smoke ten times as much as cigarette
smoke (p. 58). Yet, the Committee found pipe and cigar smoke to be pretty much innocent of causing
lung cancer, and even concluded that pipe smokers live longer than non-smokers (unless they quit - the
Committee concluding that those pipe smokers who quit had done so because they were already ill).
Some would argue, of course, that cigar and pipe smokers inhale less than cigarette smokers
(although, in my case, I inhale both pipes and cigars). If, however, inhalation is a factor in the
development of disease, it should show up in relative inhalation rates for cigarette smokers. A study
was, in fact, conducted by Hill and Doll, which sought to classify cigarette smokers as inhaling vs.
non-inhaling. At page 188 of the Report, there is a reference to a "negative association" between
inhaling and lung cancer, based on the "early" Hill and Dole studies.
In 1959, in fact, R.A. Fischer analyzed some of the Hill and Doll data and concluded that
inhalers have a lower rate of lung cancer than non-inhalers 21. Fischer's findings were incorporated into
Table 8 of the 1982 Surgeon General's Report, but the Report did not deal with this apparent paradox.
The Committee did, to some extent, recognize the effect of socio-economic status on the
various prospective studies which it analyzed. Table 26 at page 109 of the Report showed incidents of
morbidity, derived from all seven prospective studies, for 25 different causes of death. In all but two
categories (cancer of the rectum and intestines), smokers showed an increased risk of death, as
opposed to non-smokers. Indeed, it was claimed that smokers have increased risks of dying from such
diverse causes as accidents and suicide, cirrhosis of the liver and bladder cancer, as opposed to non
smokers. This troubled Brownlee, because he failed to see the "specificity" of smoking to the disease
which the Committee claimed to be "caused" by smoking, i.e., lung cancer. After all, common sense
would seem to show no connection between smoking and prostate cancer, or smoking and cirrhosis of
the liver. Perhaps, what the studies were really studying was social class. Cigarette smokers tend to
come from lower socio-economic strata than cigar or pipe smokers, or non smokers. Perhaps it is
socio-economic status that accounted for the paradoxical finding that pipe smokers lived longer than
non smokers and that cigar smokers lived the same.
Studies published in recent years (and therefore not available to the 1964 Committee) bear out
the relationship between socio-economic status (SES), smoking and morbidity. A 1990 study 22
showed the following relationships between smoking and levels of education:
Percentage who Smoke (U.S.)
Years of Education Males Females
less than 13 41 36
13-15 30 24
16 25 15
>16 18 17
A 1973 Study 22a correlated morbidity with educational levels, as follows:
Ratio of Observed to Expected Deaths, U.S., ages 21-65
Years of Education Males Females
16+ 0.70 0.78
13-15 0.85 0.82
12 0.91 0.87
9-11 1.03 0.91
8 1.07 1.08
5-7 1.13 1.18
less than 5 1.17 1.60
What these studies show is that low class people tend to smoke more than higher class people,
and that low class people tend to die sooner than high class people: considerably sooner. There may be
many reasons for the higher death rates in people with lower SES. They tend to work in hazardous
occupations, exposed to hazardous fumes and chemicals. They eat a different diet, tend to become
obese, tend to receive less medical care and lower quality care. Moreover, they tend to suffer more
from mental depression 23. So the Committee's concern that the study results might be biased by SES
turns out to have been well founded. Subsequent studies confirm that, smoking aside, it is risky to
belong to the lower socio-economic strata.
While the Committee did, in fact, acknowledge the possibility of bias due to SES, it appears to
have overlooked entirely another important source of bias. That is detection bias. Remember,
everybody enrolled in the studies knew what was being studied, and their doctors knew that, also.
Thus, everybody was waiting with baited breath for the smokers to develop lung cancer. I will discuss
the role of detection bias in more detail in the next chapter. It should be noted, however, that the
methodology followed in the SG's studies was calculated to exaggerate the possibility of detection bias,
because the researchers were concentrating heavily upon the hypothesis that smoking causes lung
cancer.
In the British Doctor's study, for example, all deaths in which lung cancer was a contributing
cause were classified as deaths from lung cancer, even though the direct cause of death may have been
something else (Report, page 101). It is interesting, in that regard, that the British Doctor's study was
the one which purported to show the highest risk for lung cancer, from smoking 24.
There was, however, another indication of trouble, which has been heretofore overlooked. This
troublesome indicator is best illustrated by a more detailed discussion of one of the 6 cancer society
studies discussed in the 1964 Surgeon General's Report.
During the time period from October 1959 through February 1960, the American Cancer
Society enrolled men in a smoker survey, described in the Report as the "Men in 25 States" study.
Female volunteers were each asked to pick ten families among their acquaintances, each with at least
one person over the age of 45, and study them to find out whether they would die during the survey
period and, specifically, whether they would die from lung cancer.
There were 448,000 useable replies, representing 448,000 men between the ages of 35 and
89. We don't know how many replies were rejected as unusable because each volunteer was free to
use her own criteria. We also don't know how many smokers were studied as opposed to
non-smokers because the results, published in the 1964 Surgeon General's Report, don't furnish that
information. We do know that during the approximately 22 months that the survey lasted, there were
11,612 deaths. As the Surgeon General acknowledged, this translates to a death rate for both smokers
and non-smokers, considerably below the overall death rate for white males, meaning that the
participants in the survey were considerably healthier than the average person. At least, that's what the
Surgeon General thought that it meant. I have other ideas.
The observed mortality ratios for different types of smokers, as opposed to non-smokers, were
as follows:
+ Cigarettes only 1.83
+ Cigarettes and other 1.54
+ Cigars only 0.97
+ Pipes only 0.86
Thus, once again, as with Doll's study, it appears that cigar and pipe smokers actually lived
longer than non-smokers - something that modern anti smokers would vigorously dispute.
The SG's Report does not list the number of lung cancer deaths which were recorded by the
Cancer Society volunteers. Instead, the results are lumped in with five other studies (some or all of
which also seem to have been organized by the cancer societies ), and Doll's study of British doctors.
Lumping all of the studies together, there were 26,223 smoker deaths and 11,168 non-smoker deaths.
Of these, 1,833 deaths from cancer of the lung occurred in smokers while only 123 occurred in
non-smokers, yielding a mortality ratio of 10.8 for death from lung cancer among smokers as opposed
to non-smokers.
Table 15 of the Report shows that for all of the various studies, the age-adjusted death rates
for the study subjects were much lower than the age adjusted death rate of 22.9 per 1000 man years
for U.S. white males, in 1960. In the case of the 25 States study, the death rate for the non smokers
was 12.8, for smokers of less than a pack a day, 18..5, and for smokers of 1 pack or more, 19.2.
These results were similar to the 5 other cancer society studies, but the Men in 25 States results bear a
footnote saying that "These results may be too low by about 1.7%, since the person-years used in the
computation included some contribution by men who had not been full traced".
Table 2 at page 85 of the Report gives the mortality ratios for current smokers for various
studies, including Men in 25 States. We are assured by the Surgeon General that the figures were age
adjusted. Thus, we might expect that all figures given in th e Report would be age adjusted and
represent current smokers. It turns out, however, that this is not the case.
Table 19 at page 102 shows the number of deaths from each of 25 different causes (ranging
from lung cancer down to cancer of the intestines). The figures given in Table 19 represent the sums of
all of the deaths recorded in all of the seven studies. It b ears a footnote, reading: "Current cigarettes
only for four studies: all cigarettes (current and ex-) for the two California studies and Men in 25
States". That little word "ex" has tremendous significance. It means that for purposes of calculating the
lung cancer death rate, the Cancer Society dropped the practice of classifying only current smokers as
"smokers" and chose, instead, to treat anybody who had ever smoked a cigarette as a "smoker".
In 1961, 68% of the men in America smoked. Therefore, by the time a man reached the age
where lung cancer becomes a problem (essentially 50+), the likelihood that he would have smoked, at
some time in his life, surely approached or even exceeded 90%. It should not have been a surprise,
therefore, nor did it prove anything, that 90% of the lung cancer deaths were in "smokers" since, if a
smoker was defined as anybody who had ever smoked, 90% of the population susceptible to lung
cancer was comprised of "smokers".
Lumping the seven studies together was also a statistical mistake. Each had different
methodologies. Different age groups were studied and different populations (British doctors, U.S.
Veterans, etc.). To really sort out what was going on, we need to see the numbers for each individual
study but, at this late date, we probably never will.
The fact that there were so few deaths during the study period, compared to the deaths that
would be observed in a cross section of ordinary white males, worried the Surgeon General. I gather
that the footnote, suggesting that the figures from Men In 25 States might be a bit low, was part of an
effort to explain the discrepancy but, if so, it was a misplaced effort since all of the figures from the
other 5 cancer society studies were in the same ball park. Still, the Committee found it necessary to
speculate, at some length, concerning the discrepancy, suggesting, among other things, that people who
were already sick might not have been chosen as study participants, by the volunteers.
One thing that did not occur to the Committee or, if it did, was not mentioned, is that the
reported data, itself, may have been wrong or incomplete. This seems to me to be the most logical
possibility. According to the Surgeon General, the ladies who conducted the study were free to weed
out any responses which, for any reason, they felt to be inappropriate. Also, according to the Surgeon
General, the ladies were expected to get a death certificate when a death was reported. I have a feeling
that the reason there were so few deaths, particularly among non-smokers, was simply that the ladies
didn't report all the deaths. Getting a death certificate would have been as lot of trouble and, if
somebody died from some cause which seemed totally unrelated to smoking, the ladies might well have
concluded that it wasn't really relevant, and wasn't worth reporting.
In any event, in all of the cancer society studies, the overall death rates, for smokers and non
smokers alike, but especially for non smokers, were much, much lower than the death rates for the
general population. This should have been a red flag: it should have at least raised questions concerning
the quality and/or completeness of the data. But to the Surgeon General's Committee, bent on proving
that smoking causes lung cancer, it suggested only that the study subjects were, for some reason,
exceptionally healthy.
In 1991, Doll did a forty year followup of the doctors in his study, which is available on line at:
http://www.bmj.com/cgi/content/full/309/6959/901
There, we are told that most of the doctors who were smokers of cigarettes only (as opposed
to cigars and pipes) at the time the study began had given up smoking by the time of the followup, so
that only 6% continued to smoke. Indeed, most gave it up within a few short years after the study
began. This, however, did not deter Doll, who continued to try to estimate the number of pack years
smoked by the quitters, and to try to develop correlations to lung cancer. To do this, he had to go by
the recollections of those interviewed by mail at infrequent follow-ups, as to how long they had smoked
and when they gave it up. This seems to me to be a fallacious approach, since it introduces the very
element of recall bias that the prospective studies were supposed to avoid. The same approach also
required Doll to make numerous adjustments to take into account the effects of quitting - adjustments
which, wittingly or not, allowed his biases to get in the way of objective analysis.
Perhaps, however, the most damaging element of the Doll study is an admission that he made
when the study was finally terminated, in 2001. Writing in the December, 2001, issue of the British
Medical Journal, Doll explained that the study was "devised by Sir Austin Bradford Hill to achieve
maximum publicity for the critical link between smoking and lung cancer". In short it was never intended
as a serious scientific study to test the hypothesis that smoking may cause lung cancer. From the
beginning, it was just propaganda - well intended, perhaps, but propaganda none-the-less.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:54

==Chapter 8: Smoking Myths and the Role of Detection Bias==
A common myth about smoking assert that the lungs of smokers become brown or even black
from years of accumulation of tars and goo. Not true, according to Wray Kephart. Mr. Kephart
presently works as an engineer but he previously worked in a hospital, performing autopsies, most of
which were paid for by insurance companies, seeking to determine whether the deceased committed
suicide, or died from "natural causes". Kephart tells me that he's done approximately 1560 autopsies,
and he's seen some strange things, such as the lungs of auto painters, which were "effectively sealed
with catalyzed lacquers".
Kephart insists, however, that it is normally impossible to tell, from autopsy, whether the
deceased was or was not a smoker. Upon resection, the lungs are always clear, unless the deceased
lived in a large city where there was significant industrial pollution. In that event, carbon deposits may
be found, but these are unrelated to smoking. So the "brown lungs" myth is exactly that: a myth.
Recently, I posed a question to Ed Uthman, M.D., a pathologist practicing in Dallas, TX. The
question was whether a surgeon, at autopsy, could determine from an examination of the deceased's
lungs, whether the deceased was or was not a smoker. Here is Dr. Uthman's response: I don't think
one can tell if the deceased were a tobacco smoker or not by the appearance of the lungs. The absence
of any black pigment suggests that the person was either a nonsmoker or a very light smoker. Heavy
black pigmentation suggests that the person was either a heavy smoker, or lived in a city with heavy
particulate air pollution, or was a coal miner, or some combination of the three. The black pigment in
question is elemental carbon, which most investigators believe to be inert in its effects on the lungs
(although in the extremely heavy doses that coal miners used to get, it may have had a partial role in
coal-workers' lung disease).
When I point these things out to anti-smokers, they frequently say, "But I've seen photographs
of smoker's lungs that were shown to me in grade school, and they looked simply horrible." I've seen
these photographs also, but they are phonies. A popular Internet web site features side by side
photographs of two lungs. One is labeled "Smoker's lung - dead at 50". The other is labeled
"Non-smokers's lungs, alive at 70". The problem is simply that the photograph of the smoker's lung is a
photograph of a lung ravaged by lung cancer; it is not a photograph of the lung of some smoker who
died from some other disease. Therefore, even if the cancerous lung is from somebody who smoked,
and the "healthy" lung is from somebody who did not, the photographs prove nothing except that
cancerous lungs look different from non-cancerous lungs.
Of course, both photographs are photographs of dead people's lungs, because it's not possible
to take a photograph of the lung of a living person. Also, rather obviously, the photographs show the
outside surface of the lungs. The outside surfaces of lungs are not exposed to either air or smoke;
therefore, it would be impossible for smoke to stain those surfaces.
Another myth, propagated by the anti-smoking crowd, is the notion that lung cancer was a rare
disease in this country until some time in the 1930's, when it began to raise its ugly head as the result of
smoking. Not long ago, George Will told a story on TV about a physician in the early part of the
century who ran across a case of lung cancer and declared it to be such a rare disease that he
assembled the medical students to witness the autopsy, believing it to be a rare opportunity.
The story may be true, but it proves nothing, because, in the early part of this century, the
diagnosis of lung cancer was complicated by the "consumption factor". "Consumption" was a name
applied to any disease characterized by emaciation, wasting away and coughing. It doubtless included
the disease which we now know as "tuberculosis", but it also included other diseases, as well.
Funk and Wagnalls Encyclopedia, published in 1912, has an entry for "consumption". It says,
"See: Pthisis". Under "Pthisis" we are told that "strictly speaking, the name includes a group of
affections, but it is generally used to indicate pulmonary consumption, i.e., a more or less advancing
process of lung destruction, associated with progressive emaciation and other characteristics and
symptoms. This is a disease of grave importance, from its frequency and fatal tendency. It has been
estimated that consumption is responsible for one-seventh of the mortality of Europe. "
"Tho pthisis was early recognized as a definite disease, and its clinical course fairly well studied,
much obscurity has rested over its causation. Medical opinion was divided until 1882, when Koch
announced the fact that he had discovered an organism, which he believed to be present in all cases of
consumption proper. This organism, the bacillus tuberculosis, is a minute rod-like structure, capable of
cultivation outside the human body, and easy of demonstration in the expectorants of consumptive
patients...".
"Any condition that weakens the constitution favors the development of pthisis. Thus,
malnutrition, syphilis, overcrowding, lack of fresh air, and defective hygiene, are all factors in the
causation of pthisis. More especially is this true of occupations whose performance necessitates the
inhalation of dust particles, e.g., stone masonry, knife grinding, metal polishing, wood carving, etc...."
"The early symptoms vary much. There may be nothing but a gradual loss of strength, it may be
of flesh; there may be slight discharge of blood from the throat or chest; there may be a more or less
persistent tickling cough; there may be breathlessness, with or without pain; or there may be little except
a tendency to take cold easily...."
Clearly, the state of medical knowledge about "pthisis" was confused. The article implies that all
cases of the disease were caused by the tuberculosis germ, discovered by the great Dr. Koch. But
many of the symptoms described are applicable to lung cancer and, in 1912, most people were treated
by family physicians who made house calls, and probably diagnosed most disease from the symptoms,
rather than from any sort of laboratory analysis.
The Historical Statistics of the United States, published by the Government Printing Office, give
cancer statistics from 1900 to 1970, but these statistics do not differentiate between different types of
cancer. The following table, derived from the Historical Statistics, shows the number of deaths per
100,000 of the population, for tuberculosis, influenza and pneumonia, and malignant neoplasms
(cancer), for the years from 1900 to 1970:
YEAR Tuberculosis Cancer flu pneumonia
1970 2.6 162.8 30.9
1960 6.1 149.2 37.3
1950 22.5 139.8 31.3
1940 45.9 120.3 70.3
1930 71.1 97.4 102.5
1920 113.1 83.4 207.3
1910 153.8 76.2 155.9
1900 194.4 64.0 202.2
The government statistics contain no item for "consumption" or for "pthisis". However, as we
have seen, "consumption" was still a recognized disease as late as 1912 (and probably later). No doubt,
those early death certificates which listed the cause of death as "consumption" have been classified as
"tuberculosis", in the later years. Note the nice, linear and inverse relationship between cancer deaths
and deaths from "tuberculosis" ("consumption") over the time period covered by the chart. There is no
doubt that some of the early deaths reported from "consumption" were really lung cancer. I've also
thrown in the figures for influenza, because, in the early years, some terminal lung cancers may have
been diagnosed as pneumonia, and also because it's simply interesting to note the devastating impact of
influenza and pneumonia in the early years.
It is generally assume that today, doctors can easily recognize lung cancer when they see it. But
can they? In 1959, in England, Heasman and Lipworth 25 surveyed reports from 75 hospitals of the
National Health Service. Attending physicians diagnosed 338 cases of cancer of the lung, while
pathologists discovered 417 cases, by post mortem autopsy. The attending physicians and the
pathologists agreed, however, in only 227 instances. If the pathologists were correct, 111 (33%) of the
diagnoses of the attending physicians were false positive, while 190 genuine cases of lung cancer (46%)
were missed.
A similar result was obtained by Feinstein, in a study conducted at the Yale University School
of Medicine, and published in September, 1986, in the Archives of Internal Medicine 26. Researchers at
Yale obtained records on 3,286 adults who had died between 1971 and 1982. 153 of these patients
were found, upon autopsy, to have died of lung cancer. The researchers then went back and obtained
the death certificates for these 153 patients and attempted to obtain information about their smoking
habits. For 13 patients, adequate smoking information was not available, so they were thrown out of the
survey. The researchers reported, however, that out of these 13 patients, seven had been correctly
diagnosed as having lung cancer during life, but 6 had not.
Working with the remaining 140 cases, it turned out that there were 37 "surprise" cases of lung
cancer, i.e., cases which had not been correctly diagnosed during life. 57% of these cases involved
non-smokers; 30% involved moderate smokers; but only 16% involved heavy smokers. The
researchers concluded that there was a detection bias; that doctors were very ready to diagnose lung
cancer in a smoker; very reluctant to make the diagnosis in a non-smoker.
Before leaving this study, it is important to point out that, by reason of the methodology used,
working from autopsies backwards to death certificates, the study could only expose false negatives,
i.e., cases of lung cancer which had not been discovered during life. It is a pity that the researchers
could not have conducted another study, working from death certificates forward to autopsies. That
would have yielded a number for false positives, i.e., the number of cases diagnosed as having lung
cancer which, upon autopsy, turned out not to be lung cancer.
At the beginning of this book, I said I would describe the work of a British medical researcher,
who questioned the hypothesis that smoking causes disease. The researcher was the late Philip R. J.
Burch, a professor of Medical Physics at the University of Leeds. He was a non-smoker, whose
principal life work was an attempt to develop a unified theory of cancer.
In 1976, Doll and Peto issued a paper in which they reported that daily cigarette consumption
by the British doctors who had been studied in connection with the 1964 SG's report had declined from
9.1 in 1951 to 3.6 in 1971. Doll and Peto claimed that, as a result there was a 38% reduction in lung
cancer death rates amongst the doctors. In a paper 27, however, Burch
showed that Doll and Peto had compared the lung cancer death rates among the doctors with the lung
cancer death rates for the entire British male population. Burch re-plotted the data to compare the
doctors with themselves and showed that, on that basis, the risk for lung cancer amongst the doctors
had actually increased by 31%.
Burch may have been on to something here, even beyond what he, himself, saw. His chart
shows that during the time period 1955 to 1971, the risk of lung cancer amongst all men in England and
Wales more than doubled, while the risk amongst the doctors increased only 31%. Remember our
earlier discussion of socio-economic status? The doctors, of course, were, as a group, in a
socio-economic class far higher than most other men. They worked indoors at a sedentary occupation,
ate different food, and were not as susceptible to depression. Could these factors account for the
difference between the doctors and ordinary men?
In the same paper, Burch plotted cigarette consumption for women and men in England and
Wales against lung cancer death rates, during the period 1890 to 1971. He showed that the largest
increases in LCDR's in both sexes came during the time periods 1916- 1920 and 1931-35, when at a
time when cigarette consumption among women in England and Wales was very small. From this Burch
concluded that the rise in lung cancer was due to improved diagnosis, not smoking. In England and
Wales, there was, in fact, a 30 year gap between the time when males began smoking and females. So
it is not surprising that the anti-smoking crowd in Britain made the argument that recent (in 1966)
increases in lung cancer among women resulted from a "30 year incubation period". Burch effectively
refuted that argument by plotting lung cancer rates for males in 1906 through 1926, against female rates
for 1936 to 1966, and showing that while, if the incubation theory was correct, the two curves should
have been synchronous, they were in fact completely dissimilar.
Burch also wrote, extensively, about the problem of "detection bias". Primary lung cancer can
be simulated by pulmonary metastases from carcinoma of the pancreas, kidney, stomach, breast and
thyroid, and by malignant melanoma. He suggested that many cases diagnosed as "primary lung cancer"
are not, in fact, "primary lung cancer", but simply metastasized tumors, originating in some other site 28.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:57

==Chapter 9: Smoking Animals==
Remember the smoking beagles? Movietone News, the old newsreel company, featured a
piece on these cute little dogs, shot some time in the 1950's or 60's. It's sometimes re-run on late night
TV, even today.
Actually, the experiment was rather cruel (although not nearly so much so as later ones). The
beagles were strapped side-by-side to a long bench, in a rather unnatural upright position. They were
fitted with face masks, which forced them to inhale and exhale smoke from lighted cigarettes. A
mechanical device lit a new cigarette and dropped it into the air line, as soon as an old one was used
up. Although the Surgeon General later claimed that the smoking machines did not force animals to
inhale and exhale deeply, the newsreel footage sure made it look as if the dogs were inhaling and
exhaling very deeply.
It was, perhaps, the smoking Beagles that were referred to in the 1964 SG's Report, when the
Committee made the observation that with the "possible exception of dogs", the animal experiments had
all failed to induce lung cancers. Whatever the case, in the 1971 Report, the Surgeon General
conceded that the experiments with dogs, using smoking machines, had failed. However, also in the
1971 Report, the SG described a new experiment, conducted by a government physician, Oscar
Auerbach, and others, in which the Beagles were forced to smoke in what the SG described as a "more
natural" manner.
Specifically, Auerbach claimed to have slit the throats of 78 Beagles and inserted
tracheotomies. He claimed that he had been able to train the dogs to smoke cigarettes through those
tracheotomies. A table was presented, showing the number of dogs that managed to survive for 875
days, smoking either regular cigarettes or filter tips or no cigarettes at all. Amongst the 8 controls who
did not smoke, there were no deaths. Among the smokers, however, there were 24 deaths from
various causes, variously listed as "aspiration of food", lung fibrosis, etc. Although Auerbach did not
claim that any of the dogs died from lung cancer, he did in fact claim that 2 of the animals, who smoked
non-filter cigarettes, had developed early invasive squamous cell carcinoma in the bronchi.
Auerbach's experiment was again described and the table again presented in the 1977 SG's
Report (which was just a reprint of portions of earlier reports). In the 1982 Report, however, the SG
described Auerbach's experiment again but this time the SG remarked that Auerbach's "observation has
not been repeated so far".
When a scientist says that an observation has not been repeated, it is a polite way of saying that
the initial experiment may have been fraudulent. It would be nice to know why Auerbach's experiment
was not replicated. Were others unable to train Beagles to smoke through tracheotomies, or were
others able to do so, but no harm was done to the dogs? We do not know and the SG does not tell us.
At page 185 of the 1982 Report, there is a general discussion of the difficulties experienced in
trying to induce cancer in laboratory animals by forcing them to inhale smoke. We are told that there's
too much carbon monoxide in cigarette smoke to allow for continuous exposure, so that inhaling
machines must be used. But, we are told, "laboratory animals are not willing to inhale aerosols very
deeply and are especially reluctant to inhale tobacco smoke. Rhesus monkeys and baboons have been
trained to smoke cigarettes. This approach does not yield neoplasms [cancers] because of insufficient
exposure time and because of the tendency of the animals to puff rather than to inhale". Maybe so, but
the old newsreel pictures of the smoking Beagles surely seemed to show them inhaling, deeply!
Also, at pages 185 and 186 of the 1982 Report, there is a description of some failed
experiments with Golden hamsters, explaining why tobacco smoke had failed to induce lung tumors.
Never-the-less, interleaved into all of these discussions of failures, there is a description of an
experiment which, allegedly, succeeded. At page 185, we are told that in 1980 experimenters at the
Oak Ridge National Laboratories, using a newly developed "advanced inhalation device" were able to
induce tumors of the "respiratory tract" in rats. The Report states that "...seven of the 80 smoke
exposed rats had tumors.." and that one of 30 "sham exposed rats" had tumors 29.
Apparently, the "advanced inhalation device" referred to by the SG is the "Maddox-oral
smoking machine". It is referred to in an article by A.P. Wehner, et al., which appeared in 1981 in
*Toxicology and Applied Pharmacology* at pages 1-17. There, the authors describe an experiment in
which 80 female rat were forced to consume 8 cigarettes per day, seven days per week, for 2 years.
One of the rats developed a carcinoma of the lung.
Before getting too excited about these experiments, however, we need to consider this: the
largest known rats weigh no more than an average of one pound. Forcing a one pound rat to smoke 8
cigarettes per day is the equivalent of forcing a 160 pound human to smoke 1280 cigarettes per day
(64 packs). Such experiments are not realistic and in no way replicate exposure to ordinary tobacco
smoke. Given the enormous concentrations of smoke used by the experimenters, it is wonder that any
of the animals even survived the ordeal; yet, they did, and only a small percentage developed tumors.
Strangely, despite exhaustive research in medical databases, I have been unable to find any
additional rat experiments (or experiments with any other animals) conducted in the years since 1980,
which replicate the above reported experiments. A 1989 article in *Toxicology and Applied
Pharmacology* 30, describes an experiment in which rats of both sexes were forced to inhale
cigarette smoke in high concentrations for 22 weeks. The rats were then killed, and investigations made
to determine the effect of the smoke on the level of "DNA adducts". The experimenters concluded that
"inhaled cigarette smoke induces lung DNA adducts which may play an important role in cigarette
smoke-induced lung carcinogenesis" (emphasis mine). But the experimenters stopped short of claiming
that the smoke actually induced any tumors.
A report of a similar experiment with rats forced to smoke for 8 weeks appears in 1985 in the
Journal, *Cancer Research* 31. Here again, however, the researchers did not claim that the smoke did
the animals any direct harm. They claimed, instead, that the smoke reduced the level of production of
cytotoxin, a substance thought to be toxic to certain types of tumor cells. My question is simply this:
why haven't the 1980-81 rat experiments been repeated? Was there something wrong with them? Did
the researchers conclude that because of the extremely high concentrations of smoke given to the
animals, and the large number of animals that were unharmed, the experiments failed to prove their
point? Or was there some other reason? I'm afraid I don't have the answers.
In recent years, new smoking machines have been devised that subject rats to second hand
smoke. In an article in the May 28, 1994 issue of *The Los Angeles Times*, writer Sheryl Stolberg
describes experiments that have been going on for three years, exposing rats to continuous
concentrations of smoke as high as 4,000 micrograms per cubic meter, concentrations many times the
concentrations encountered in the real world, even in times of brief exposure, e.g., bars. Bottom line: no
significant harm to the animals has been shown, although one researcher at UC (Davis) claims a 6%
reduction in birth weight for the offspring of the exposed animals.
In earlier versions of this book, I left the subject of the animal inhalation experiments with
unanswered questions. It appeared that there had been two experiments - never repeated - one of
which induced a single carcinoma in a rat, and other of which supposedly induced "tumors" in a very
small percentage of rats. In 1998, however, an event took place which enables me to resolve the
unanswered questions. In that year, the State of Minnesota brought a lawsuit against tobacco
companies to recover damages to the State, allegedly caused by smoking. The case was settled before
any judgment could be rendered, but not before a few trial sessions were held.
At these sessions, testimony was taken from experts for both the plaintiff (the State) and the
Defendants (the tobacco companies). Experts for both sides agreed that, despite many, many animal
inhalation experiments over a period of many years, all of the experiments had failed, i.e., nobody has
ever been able to demonstrate, through animal experiments, that inhaling tobacco smoke - no matter in
what quantities or concentrations - causes lung cancer. These failures are powerful evidence, indeed. If,
as alleged, smoking causes lung cancer, training or forcing animals to smoke should produce lung
cancers. It doesn't.
Before leaving this subject, I ran into a couple of strange, weird studies while doing the research
on smoking animals. A 1993 study in Norway 32 reminds me of an old joke about a temperance lady
who comes to a school to do a demonstration. She has a worm, a glass of water and a glass of booze.
She drops the worm into the water and it swims about unharmed; then she drops the worm into the
glass of booze and it instantly shrivels up and dies. She asks the class, "Can anyone tells me what this
means?". Little Johnny holds up his hand and shouts "It means that booze is mighty good for you if you
have worms!".
Anyway, in the Norwegian study, investigators induced pneumonitis (lung inflammation) in rats
by exposing the animals to radiation. The animals were then exposed to tobacco smoke, and it was
shown that the smoke actually suppressed the inflammation in the lungs. In short, smoking is good for
you if you have pneumonitis (I guess) 33
The other weird study has little to do with smoking; I simply report it because it's interesting.
Recently, health food stores have begun selling green tea, because of its alleged health benefits. In fact,
some have suggested that the drinking of green tea accounts for the low rate of lung cancer in Japan
and China. A study published in 1990 in *Environmental Research* 34, however, claims exactly the
opposite. According to that study, females in Hong Kong had a 2.7 times greater risk of developing
lung cancer if they drank green tea than if they did not drink green tea. This just proves that you can
prove anything with statistics, which is another way of saying you can't prove anything with statistics.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:58

==Chapter 10: Is there No Risk?==
So far, I have argued that the case that smoking causes lung cancer has not been proven. The
reader may ask, "Well, if smoking doesn't cause lung cancer, just what does?". Recent studies suggest
that the answer lies in the genes of those individuals who develop the disease. One must be cautious in
assessing the genetic evidence, because molecular biologists, many of whom are employed by the
rabidly anti tobacco government establishment, are not above the use of techno-babble in support of
the establishment position on smoking. In their book on gene therapy, *Altered Fates*, authors Jeff
Lyon and Peter Gorner quote scientist Philp Leder as saying that nicotine is a "mutagen par excellence".
A mutagen, according to them, is another way of saying "carcinogen". There are, however, absolutely
no studies showing that nicotine is a carcinogen. If it were, the FDA could scarcely have approved the
sale of the nicotine patches, used by smokers who choose to quit smoking.
Recently, the press gave much attention to a study by researchers at John Hopkins University
School of Medicine, dealing with head and neck cancers and the P53 gene. The P53 gene is called the
Guardian Angel gene because it is believed to protect against cells becoming cancerous. According to a
report in the March 16, 1995, edition of the *Washington Post*, the researchers studied tissue samples
from 129 people with head and neck cancers. The samples were divided into smokers,
smoker/drinkers, and total abstainers. About 58% of the tumors from the smoker/drinkers had P53
gene mutations, as opposed to 33% of the smokers who did not drink, and 17% from the abstainers.
What the press reports ignored, however, is that everybody who participated in the study had cancer.
83% of the abstainers had perfect P53 genes; yet they still had become ill. The real lesson of this study,
if there is one, is that the P53 gene won't keep a person from getting cancer; at least it won't do so if the
person is otherwise genetically predisposed to the disease.
A more informative study is described in the August 1, 1990 edition of the Wall Street Journal.
That study was conducted by researchers at Louisiana State University Medical Center in New
Orleans and Albert Einstein College in New York. The researchers studied 300 families in Southern
Louisiana, who had a history of lung cancer, and compared them with 300 controls. The researchers
concluded lung cancer is an inherited disease. Based upon retrospective studies (which I do not
necessarily accept as accurate) 35 the researchers concluded that if a person had two copies of the lung
cancer gene, his chances of getting lung cancer by the age of 50 would be 14% if he did not smoke,
increasing to 27% if he were a heavy smoker. In the more likely case of an individual having only one
copy of the gene, the researchers concluded that a non-smoker would have practically no risk of getting
lung cancer by age 50, but for a heavy smoker the risk increased to 5% by age 50, 16% by age 60,
and 25% by age 75.
In the same WSJ article, there is an interesting quote from Neil E. Caporaso, a researcher at
the government-owned National Cancer Institute in Bethesda, MD. According to Mr. Caporaso, one
out of eight smokers will be stricken with lung cancer (which is another way of saying that seven out of
eight will not). Considering the fact that one out of every five Americans dies from some form of cancer,
and that lung cancer is the most common form of cancer in persons between the ages of 45 and 74, and
the second commonest form in persons over that age, Mr. Caporaso's estimate of the risk seems very
modest and wholly at variance with the position taken by most government scientists, who shriek
hysterically that smoking "causes" lung cancer.
The fact remains that inheritance seems to play a major role in cancer. Pancreatic cancer is very
rare, but former President Jimmy Carter has seen it in at least four members of his family: his two
sisters, his brother and his father. His mother died from breast cancer which metastasized to her
pancreas. Diabetes is the scourge of my family. Three of my four grandparents died from
the disease. All were obese and all consumed a diet, which was rich in starches and sugars. As a young
man, I was obese and ate a lot of starches and sugars. I chose to go on a life-long diet, in which I
refrain from eating starches and sugars. Simply avoiding starches and sugars is enough to control my
weight (I weighed 240 lbs when I first went on the diet at the age of 38; now, I weigh 162 lbs). I
consider this a sensible precaution. If I had a history of cancer in my family, especially lung cancer, I
might choose not to smoke. However, I have no such history, so I puff away.
My wife, who is naturally thin, has no family history of diabetes and regularly consumes huge
quantities of starches and sugars. I would never presume to ask her to stop. I certainly would not favor
legislation to ban the eating of starches and sugars. Of course, the anti-tobacco crowd sees things
differently; they are not content with their personal decision not to smoke; they want to impose their
decision on everyone else, through widespread smoking bans. Curiously, however, as revealed in the
postings on the Internet, many of the anti-smokers are avid devotees of ***** smoking, which they
consider to be healthy. On a more consistent note, many seek legislation to outlaw or restrict the sale of
fatty meats, or red meats or vitamins or whatever. They consider themselves "liberals". Their hero is the
dour chief of the FDA, David Kessler.
Quite frankly, I do not know whether there is a risk to smoking, or not. I do know that "risk" is
not the same as causation. Philosophers, from Plato to Supreme Court Justice Louis Brandeis, have
been fascinated with the word "cause", and have written many learned treatises on the subject. My
great-grandfather was working on a bridge construction site in 1927, when a careless driver jostled
him. My great-grandfather became startled, lost his balance, and fell through a hole in the bridge. Not
being able to swim, he drowned in the river below. Was the cause of death (a) drowning; or (b) the
actions of the careless driver; or (c) the loss of balance; or (d) the existence of the hole in the bridge
flooring; or (e) not being able to swim? Just about every human activity involves risk. Walking across
the street runs the risk of getting hit by a car. Bungee jumping involves the risk that the bungee cord
may break or become detached from the supporting structure. If, however, a pedestrian is hit by a car,
it is far-fetched to say that the cause of death was walking across the street. If a bungee cord breaks
and someone is killed, the newspapers will not say that the deceased died from bungee jumping.
Rather, they will report that "Smith died when the bungee cord broke, and he descended 100 feet to
the ground below".
Anti-smokers are fond of repeating the mantra: "cigarettes are the only product which, when
used for their intended purpose, cause death". Nonsense! Firearms are specifically manufactured to
cause death in animals and humans. Automobiles, used carefully and driven properly, can still cause
death if a tie rod breaks at 60 mph. I don't know whether starches and sugars can cause death in a
person genetically susceptible to diabetes, but from personal observation, I feel there is a risk and,
because of the history of diabetes in my family, I choose not to take the risk. Before leaving this subject
of risk, a very interesting study was recently reported, which confirms that if there is a risk, it has been
grossly exaggerated by the anti-smoking movement. On May 23, 1995, the Associated Press reported
on a study made by Dr. Gary Strauss. Strauss analyzed 685 lung cancer patients seen at Brigham and
Women's hospital in Boston between 1988 and 1994. He found that 59% of the patients were
non-smokers at the time their cancers were diagnosed. Of these, 8% of the entire sample had never
smoked; 51% had smoked at one time but had given it up. Of the 51% who had quit, nearly one fourth
had been off cigarettes for more than 20 years. On average, the former smokers had been off cigarettes
for six years. As I have previously pointed out, lung cancer is not always diagnosed in non-smokers,
because doctors aren't looking for it. Currently, according to the CDC, 25% of the population are
smokers. In the study years (1988-1994), the percentage was as high as 30%. Thus, purely on the
basis of demography, we would expect between 25 and 30% of the sufferers from lung cancer, or for
that matter, hangnails or acne, to be current smokers. 41% of the cases studied by Strauss were current
smokers. Given the role of detection bias (doctors more likely to diagnose lung cancer in smokers than
non-smokers), the 41% figure suggests that the lung cancer risk for current smokers may be little or no
greater than for non-smokers. In the article, Dr. David Burns of the University of California, seems to
support the view that giving up smoking is not the "cure" for lung cancer. He is quoted as saying, "These
folks have done what we told them to do, yet they are still at substantially increased risk. What can we
do for them? We owe these people an answer." Burns suggested that it may be possible to device a
genetic test to spot lung cancer. I would go further and suggest a genetic test to spot the likelihood that
somebody will get lung cancer. Whether, in such an individual, giving up smoking would do any good, I
don't know, but such individuals probably would choose not to smoke, just as I choose not to eat
starches and sugars. The same article also reports that deaths from lung cancer have increased by 51%
between 1980 and 1994, despite a drop in the percentage of adults who smoke from 42% in 1965, to
25% in 1993. Isn't it about time to stop blindly adhering to the notion that lung cancer will disappear if
people simply give up smoking?
Actually, Dr. Burns is not the only medical doctor who has begun to question that simplistic
notion. Julian Whitaker, MD, is a practitioner of "alternative medicine", a writer of a monthly newsletter
on health and exercise, and no friend of smoking. However, in the October, 1995, issue of his
newsletter, "Health and Healing", Doctor Whitaker writes: "Since 1950, the incidence of all cancers in
people between the ages of 50 and 60 years has increased by 44%, with even higher increases in some
of the more deadly forms of cancer. Breast and colon cancer went up 60%, prostate up 100% and
testicular cancer for men between the ages of 28 and 35 went up 300%. Lung cancer has gone up
262%, an increase that is obviously not related to cigarette smoking, because over the same period the
number of people smoking cigarettes dropped from 50% to 25%..."
Doctor Whitaker expresses no opinion as to the reasons for the startling increases in cancer in
recent years. I, however, have an opinion. Medicine, over the past 40 years, has grown more and more
socialized. As late as 1950, people were largely responsible for paying their own medical bills, and
doctors hesitated to order expensive tests and treatments for those who couldn't pay the bills.
Today, almost all medical procedures are paid for by insurance or by federal funds, through
Medicaid and Medicare. Physicians, therefore, have a strong incentive to order every possible test and
treatment, because they know that they will be paid for doing so. As a result, there are no more
undiagnosed cases of cancer. Every case is always diagnosed. This will, in my opinion, show up in
future years, in the form of statistics which show a leveling off of the number of cancer cases. Only time
will prove whether I'm right or wrong.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 09:59

==Chapter 11: Is Nicotine Addictive?==
Much of the rhetoric of the anti-smoking movement seeks to demonize tobacco smokers as
"nicotine addicts". In the past, of course, the term "addict" has been generally applied only to
mind-altering drugs, e.g., heroin and cocaine. Even alcohol, which is mind-altering, is not generally
referred to as "additive". So, the argument is one of semantics. If nicotine is addictive, so are chocolate
candies, pies and cakes, etc. Indeed, if "addition" is defined as dependence upon some chemical,
everyone is addicted, to air! I am not going to engage in a philosophical debate over the definition of
"addiction". There is a question in my mind, however, as to whether nicotine is really the active
ingredient in tobacco smoke..
Nicotine is a chemical, C10H14N2, which is found in the tobacco plant. Anti-smokers are quick
to point out that pure nicotine is a poison, used as a pesticide. And it's true that pure nicotine (a
colorless, odorous liquid), is poisonous. According to the mens that to kill a 180 lb man, he'd have to
drink about 80 mg of the stuff. Many other common substances, however, also have minimum lethal
doses. According to the same source, ingesting a gram of caffeine is fatal.
In fact, many substances which are beneficial in small quantities are toxic in large quantities. My
mother suffered a stroke some years ago. Her life was saved, and she recovered, by taking a blood ll,
so he doubled it. My mother began hemorrhaging, and almost died from loss of blood. The blood
thinner, which is life saving in small quantities, proved toxic in large quantities. Of course, most of the
nicotine in tobacco is lost in the process of smoking. Only a little finds its way into the smoker's
bloodstream. That small quantity may account for some of the beneficial effects of smoking, e.g.,
improved mental concentration. Strangely, fine Havana cigars, when they were available, contained only
2% nicotine. If, in fact, nicotine is the reason why people smoke, it seems strange that people would
pay enormous amounts of money for Havana cigars, which contain so little nicotine.
I question, however, whether nicotine is the active ingredient in tobacco. If it were, nicotine
patches should satisfy a smoker's craving for tobacco; they don't! In prisons, where, as a part of the
punishment, smoking is sometimes forbidden, the inmates take to smoking corn silk, paper, string, etc.,
none of which contain any nicotine.
When I was a young man, there was a chain of tobacco stores which sold cheap cigars. They
were made almost entirely from brown paper, with only one outside wrapper made from tobacco. I
doubt they contained any significant amount of nicotine. Yet, they were a satisfying smoke.
Recently, anti-smoking forces have suggested taking the nicotine out of cigarettes, to
discourage smoking. This assumes, of course, that smokers smoke to get nicotine. In their book, "Life
Extension", health writers Durk Pearson and Sandy Shaw, take a different approach. Believing that
smoke is bad for health but that nicotine is not, Pearson and Shaw suggest that cigarettes be spiked
with extra nicotine, so that smokers will consume fewer cigarettes. It is not universally accepted,
however, that nicotine is the active ingredient in tobacco smoke. The authors of the widely respected
"Merck Manual" say only that it is "probably" the active ingredient. If, in fact, the anti-smokers finally
succeed in getting the tobacco companies to remove the nicotine from cigarettes, we will finally find out
the truth. My own bet is that a cigarette without nicotine will probably be almost as satisfying as one
with nicotine. The active ingredient in smoke is smoke.
Recent studies, reported by the National Institute on Drug Addiction (NIDA), seem to bear out
my hunch. These studies suggest that tobacco contains a monoamine oxidase inhibitor (MAOI).
MAOI's are anti-depressants, which work by increasing serotonin levels in the brain. They are used in
medicine to treat Parkinson's disease, which may explain why a number of studies have shown that
smokers have a far lower rate of Parkinson's than non-smokers. In any event, the MAOI in tobacco
smoke may play as great a role in smoking as nicotine.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 10:01

==Chapter 12: Smoking and Heart Attacks==
For many years, anti-smoking activists have insisted that smoking "causes" heart attacks. In
truth, there is no scientific evidence to support such a claim.
As early as the 1950's government scientists began conducting studies in Framingham, MA., to
assess the "risk factors" which lead to heart attacks and stroke. Early on, they identified three such risk
factors: Smoking, high blood pressure and cholesterol. As the years have gone by, however, other
researchers have identified still other risk factors. Taking estrogen pills has been identified as a risk
factor in women 36. Male pattern baldness has been identified as a risk factor in men 37. Vitamin and
mineral deficiencies have been blamed for heart attacks, as well as eating fatty foods and drinking too
much alcohol.
There are other obvious risk factors: 100% of all heart attack victims breathed air during the
time prior to their heart attack. 90% drove automobiles. 95% paid income taxes.
I am, of course, citing these "other obvious risk factors" in jest, to illustrate the absurdity of "risk
factor" analysis. If everything is a risk factor, then nothing is a risk factor, because there is no
conceivable way of determining whether (a) a particular heart attack or stroke was caused by one of
the risk factors and (b) if it was caused by a risk factor, which one.
Risk factor studies are, by their very nature, biased by the opinions of the people who conduct
such studies. That's because the researchers must select the factors that they consider risky, before the
study ever begins.
Consider this: It is a known fact that exercise sometimes causes heart attacks. I say "known
fact" advisedly, because there are many newspaper accounts of athletes and others, dying from heart
attacks brought on by exercise. A few years ago, my Congressman, Goodloe Byron, dropped dead of
a heart attack while jogging on the CO Canal. He'd been warned by his doctor that he had a weak
heart and should not over-exercise, but he disregarded the doctor's advice. Also, a few years ago,
Nelson Rockefeller suffered a fatal heart attack while exercising in bed in the company of two nubile
young women.
Yet, nobody has ever conducted a study to determine how many heart attacks are caused by
exercise. Why not? The answer, of course, lies in the conventional wisdom that "exercise is good for
you". Researchers don't conduct studies to link exercise with disease because everybody knows that
exercise doesn't cause disease, so there's no point in conducting such a study.
On August 18, 1995, the Wall Street Journal reported on an epidemiological study in England
by anti-smoking activist Richard Peto, which claimed that in people aged 30 to 49, smokers have a
heart attack risk 2.4 times that of non smokers. For that study to be meaningful, however, Peto would
have had to also study a multitude of other risk factors. Smokers tend to be from the lower
socio-economic strata of society, and people with low SES tend to be fat and work at hard manual
labor (the "exercise factor", again). They may consume too much alcohol and eat diets deficient in the
vitamins and minerals which some experts claim are protective against heart disease.
Peto selected smoking as the risk factor to be studied because he believed smoking causes
heart attacks. But he might just as well have selected SES, obesity, alcohol consumption, cholesterol,
estrogen consumption, diet, baldness, ear creases, etc. Even if he'd studied all of these risk factors, he
might still miss the right one, because the real cause of heart attacks may be something that nobody's
even remotely considered. After all, we now know that most stomach ulcers are caused by bacteria
and can be treated with antibiotics; yet, until just a few years ago, every responsible physician in the
world would have dismissed such a notion as total nonsense.
Just recently, researchers have suggested that the true cause of heart attacks may be surplus
iron in victim's diets. This iron, they suggest, oxidizes cholesterol and deposits harmful plaque deposits
on the artery walls. 38
In earlier chapters, I discussed the flaws in the 1950's and 60's studies that attempted to link
smoking to cancer and other diseases. Not the least of these flaws was the self-selection of the
participants and the failure to establish adequate controls. Take, for example, Doll's famous (or
infamous) study of British doctors. In 1951, Doll wrote to 59,600 physicians in the United Kingdom,
asking them to fill out questionnaires and become part of his study group, but only 40,70l of the
physicians responded 39. Thus, the participants selected themselves. Furthermore, all of the participants
were from the same highly select, elite profession, i.e., medicine. There was no control group,
representing the population at large.
In the mid 1970's, some researchers decided to do a study on the effects of smoking cessation
as well as other "healthy behaviors". They sought to avoid the flaws that had plagued other
epidemiological studies and, to that end, they sought to study groups that were not self selected, but
rather were selected, at least in part, on a random basis. The study group was called the "Multiple Risk
Factor Intervention Trial (MRFIT) Research Group".
12,866 high risk men, aged 35 to 57 years, were randomly assigned to one of two groups. One
group was treated to a special intervention program, consisting of drug-care treatment for hypertension,
counseling to stop cigarette smoking, and dietary advice for lowering blood cholesterol (I will call this
the "special intervention" or"SI group"). The other group, which I will call the "control group", was left
to smoke, eat, and have high blood pressure, without intervention.
The MRFIT Research Group rendered its first report in 1982, reflecting an average follow-up
time of 7 years. To the disappointment of the researchers, there was no statistically significant difference
between the mortality in the SI group, from that in the control group - despite the fact that, as a result of
the nagging, the participants in the SI group significantly "improved" their health habits, i.e., stopped
smoking, and lowered their blood pressure and cholesterol levels.40
In 1990, the MRFIT group produced another report, reflecting 10.5 years of research, using
the same two groups. This time, the results appeared to show a statistically significant reduction in
coronary heart disease (CHD) in the intervention group, but this was attributed not to smoking
cessation, but rather to reduction in hypertension 41. It turned out that there were more deaths from
ischemic heart disease in the SI group than in the control group (96 vs. 86 deaths). Moreover, there
were more deaths from cancer of the respiratory and intrathoracic organs in the SI group than in the
control group (66 vs. 55) 42.
It is amusing to read the explanations of the health establishment for the discrepancies reflected
in the MRFIT study. One group of writers tried to explain the higher incidence of lung cancer in the SI
group by pointing out that all of the deaths from primary lung cancer reflected in the 10.5 year trial
involved smokers or ex-smokers; there were no primary lung cancer deaths among "never-smokers" 43
. These writers apparently forgot that the participants in both groups were selected because they were
adjudged to be at "high risk", i.e., smokers and ex smokers. We could hardly expect to find any lung
cancer deaths involving "never smokers" in a group that didn't have any "never smokers"!
The MRFIT study is not the only study to use intervention to try to reduce coronary heart
disease (CHD) and cancer, by nagging people to improve their health habits. The World Health
Organization conducted a massive study. It involved 63,733 men aged 49 to 59 in 44 factories in
Britain, Belgium, Italy, Poland and Spain. The authors estimated that, as a result of smoking cessation
and other improved health measures, they managed to reduce the risk of heart attack by 14% in the
group as a whole and 24% in a high risk sub-group. Unfortunately, there was no equivalent reduction in
the number of heart attacks 44.
In 1982, Rose, Hamilton, Colvell and Shipley reported on a 10 year follow up study of middle
aged smokers, thought to be at high risk for cardiorespiratory disease. The smokers were divided into
two groups: a control group who were allowed to continue to smoke and an intervention group (a "SI"
group) who were encouraged to give up smoking. The intervention was very successful. In fact, in the
SI group of 714 men, the naggers succeeded in reducing the rate of cigarette consumption by half.
As in other studies, however, the results were negative. In fact, 17.2% of the 714 men in the
intervention group died during the study period, as compared to 17.5% of the 731 men in the control
group - an insignificant difference. There was also no significant difference in lung cancer. There were
25 cases in the control group and 22 in the intervention group. Interestingly, however, there was a
statistically significantly greater rate of "all other cancers" in the intervention group than in the control
group 45.
So nagging people to quit smoking - even successful nagging doesn't reduce the rate of either
cancer or heart attack.
Perhaps the final word on smoking and heart attacks came in 1998, when the results of a
massive study, financed by the World Health Organization, were released. The Monica Study, which
assessed 21 countries over ten years, found the incidence of heart disease dropping across Europe,
Australia, and North America. But scientists could find no statistical correlation between the reduction
and changes in obesity, smoking, blood pressure or cholesterol levels. They didn't look at antibiotic use
but maybe they should have, because at least one recent study showed that a course of treatment with
antibiotics appears to protect against heart attacks, suggesting that, like stomach ulcers, they may be
caused by bacteria.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 10:02

==Chapter 13: Smoking and Emphysema==
On July 13, 1994, an obituary in the Washington Post reported the death, at age 60, of Richard
Joshua Reynolds, III, an heir to the founder of the R.J. Reynolds tobacco company. The headline and
an accompanying photograph showed the deceased smoking a cigarette and implied that Reynolds died
from emphysema, caused by smoking. Reading the obituary in detail, however, it turned out that he had
quit smoking eight years prior to his death; and that there was a family history of emphysema, the
deceased's own father having died from the disease at the age of 58. Furthermore, the obituary
disclosed that the deceased's own doctor was unable to state the "immediate cause" of his death.
Medical opinion concerning emphysema has had an interesting history. My 1973 edition of
"Diagnosis and Treatment" (a standard medical textbook), states that emphysema is a disease which
involves destruction of the alveolar (lung) tissue but that the cause is unknown, although "many doctors"
think it is caused by "cigarette smoking". In 1973, Chromic Pulmonary Obstructive Disease (COPD)
had not yet been invented. COPD, while now discussed at length in modern medical textbooks, did not
exist in 1973.
Some time subsequent to 1973, a genetic cause of emphysema was discovered. In an article in
the latest on-line edition of Grolier's Encyclopedia, Howard Buechner, M.D., explains that a significant
number of the people with the disease lack a gene that controls the liver's production of a protein called
alpha-1 antitrypsin (AAT). This protein controls or degrades an enzyme called neutrophil elastase,
produced by the white blood cells. When the enzyme is left unchecked, it destroys alveolar tissue.
Evidently, the Reynolds, father and son, had genetic cases of emphysema, which may or may
not have killed the younger Reynolds, even thought he had not smoked for eight years prior to his
death. But this raises the question: if there any proof that there is any cause of emphysema other than
genetics?
The politically correct medical establishment dances around that question with all of the skill of
a lawyer. In the Merck Manual, 14th Edition (1982), we are introduced to a new disease, Chronic
Onstructive Pulmonary Disease, or COPD, and, at page 629, we are shown a diagram, showing that
the disease is combination of emphysema and bronchitis, and that some patients may have one disease
and some the other, but many will have both. Cigarette smoking is said to "presumably" play a role in
COPD. At page 630, we told about AAT deficiency, but this is described as a "rare condition"; it is not
clear whether the authors mean that AAT is a "rare condition" that causes emphysema, or that
emphysema is rarely caused by AAT deficiency. The language is, I think, deliberate vague.
By 1992, it becomes still more politically imperative to blame smoking for COPD and
emphysema. In the 16th Edition of the Manual (1992), it is explained that, yes, emphysema is caused
by destruction of lung tissue, caused by an unchecked enzyme. We are told, however, that smoking
lowers the body's defenses to the enzyme. No evidence or authority is cited for that proposition.
Thus, we are left with confusing conclusions. We have a new disease, COPD, the exact cause
of which is unknown (indeed, the definition of the disease is vague; it seems to be a case of "this patient
has something wrong with his lungs, but we don't know exactly what"). Cigarette smoking is thought to
play a role; yet the 16th Edition makes it clear that many cigarette smokers never develop the disease,
and the authors do not know why. I submit that the reason is very simple: smoking does not cause
emphysema.
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 10:04

==Chapter 14: Summation==
In this book, I have shown that the case for a smoking/lung cancer connection is by no means
proven. Certainly, there is no case whatever for a connection between ETS (second hand smoke) and
any disease, nor is there are any case for a connection between cigar and pipe smoking and lung
cancer. The case for a connection between cigarette smoking and lung cancer rests on the slim reed of
a science called epidemiology. But all epidemiological studies, predicated as they are on statistics, are
subject to so many co-factors and confounding factors as to be subject to innumerable different
interpretations.
Once an assumption is made that, say, eating jellybeans causes carbuncles, it is all too easy to
gather and/or manipulate data to support the theory. It is all too easy for researchers to ignore or
explain away data which points the other way. We have seen examples of this in the preceding
chapters.
In recent years, Americans have embarked upon an increasingly puritanical view of the world.
The War on Drugs has dramatically changed the way Americans view the use of ***** and cocaine
(and has also resulted in the U.S. having the largest prison population, per capita, of any major nation).
Last year, Surgeon General Jocelyn Elders was fired, essentially for daring to mention the word
"masturbation" at a televised conference.
The last time the country went on a binge of Puritanism, the result was Prohibition. The
enthusiasm for Prohibition was so overwhelming that when the Congress proposed the 18th
Amendment to ban booze, the Amendment was ratified by every state except Connecticut and Rhode
Island, and the total votes in the various State Senates were 84.6% for the amendment, while the total
votes in the lower houses were 78.5% for the Amendment.
We are moving in the direction of a National Prohibition of smoking. If it passes, we will see
bootlegging, smoking speakeasies, smoke police, raids on establishments and maybe even homes
where tobacco is believed to be stored or used. We will see the ultimate corruption of public officials
and law enforcement officers, bribed to allow illegal smoking establishments to continue in business.
This is a slippery slope! Once the role of government has been firmly established in regulating
the personal smoking behavior of its citizens, the next easy step is to begin regulating other forms of
personal behavior, deemed offensive to the majority. Soon, books, movies, videos, etc., deemed
offensive, will be banned, as well. Already, government regulations are coming into effect which will
require employers to limit the use of automobiles by their employees, and to require citizens in certain
parts of the county to purchase special types of gasoline which cost more than regular gas and yield less
mileage.
Government regulation tends to put people out of business and out of work. It is no coincidence
that Prohibition of Alcohol was followed by a market crash in 1929, followed by the horrible
depression of the 1930's. Prohibition destroyed the California wine and grape industry; it closed
thousands of restaurants and drinking establishments. Of course, it made Al Capone a wealthy man and
much admired by the American public, but that can by no means be counted a benefit!
The anti-smoking movement in this country and in the world at large is using unreasoning fear as
a weapon to achieve its objectives. An entire generation of Americans has been brain washed to
believe that if somebody lights up a cigarette in a room, everybody in that room will shortly come down
with a host of fatal ailments.
In their book, "Generations" 46, authors William Strauss and Neil Howe put forth a theory of
American thought, based upon a repeating 80 year cycle. The authors contend that we are presently in
a phase of the cycle which corresponds to the generational constellations which brought prohibition in
1919. The authors argue that the baby boomers, a generation of idealists, are now about to seize
power. Unlike their elders, the Silents, who valued tolerance and compromises, the boomers are grim
moralists, who have no hesitation to impose their values on others. On that theory, Newt Gingrich and
Hillary Clinton have more in common than they have in differences; their values may differ, but they
share the common view that values are good, and must be imposed, as Hillary did, when she banned
smoking in the White House.
If Howe and Strauss are right, we are entering a new era of Puritanism which, they claim, will
end only after the Puritans clash amongst themselves or with foreign enemies, resulting in a crisis - which
they say will occur sometime after the year 2004. Further, if the authors are right, facts will mean little in
this coming Puritanical age. The facts will simply be created to justify bans on smoking, drinking, and
other pleasurable things, and to justify the loss of many other personal freedoms. In short, if the authors
are right, I am in the position of King Canute, trying to hold back an inevitable force. Never-the-less, I
cherish the hope that some people, at least, will still value the facts which I've tried to present.
It is too much to hope that this book will be read by non-smokers. They will have no interest in
this tome. My hope is simply that smokers will read these pages, and arm themselves with facts to
refute the propaganda.
A medical doctor recently asked me "why do you insist on smoking?". I replied, "Because I
enjoy it". I'm afraid he just didn't "get it".
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Molia » 26 Iun 2010, 10:15

Cam atat. Sper in continuare sa apara astfel de lucrari si eventual sa fie citite, dar in situatia in care presedintele Statelor Unite se lasa de fumat cand nu-l mai ajuta imaginea si risca sa piarda campania electorala pentru ca era fumator, va trebui sa fim un pic mai agresivi.

Recomand calduros replica: [quote]Ca nefumator ma indoiesc ca sunteti mai bine documentat privind efectele fumatului. Va rog sa incheiati subiectul caci tin la sanatatea mea iar nesimtirea dumneavoastra imi provoaca hipertensiune.
Pana acum a mers.
Fişiere ataşate
New Bitmap Image.JPG
Molia
 

Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde zudo » 26 Iun 2010, 16:36

Consider ca ar fi mai utila sub forma tradusa in limba romana. Haideti sa facem un efort, sa luam fiecare cate un capitol si sa-l traducem. Il iau eu pe primul.
Cap. 1 - zudo
Cap. 13 - Lifelover
Cap.14 - molia (dupa ce se completeaza lista ma apuc)
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Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Radu-Mihai » 26 Iun 2010, 19:37

Asa da Zudo, "gand la gand cu bucurie"... :1)
[color=#FF0000]Micile vicii dau farmec unei vieti monotone![/color]
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Re: In Defense of Smokers (2003, Lauren A. Colby. Version 2.

Mesajde Lifelover » 29 Iun 2010, 10:57

Iau eu 13le, am o relatie speciala cu numarul asta.
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