excellent article above, written by fellow "skeptic" Jerome
Sullivan, was published today in RedFlagsWeekly and is posted at http://www.redflagsweekly.com/features/2002_august12.html
Also, a rebuttal from another fellow skeptic, Stephen Byrnes, to the
Ornish/Pritikin responses to the Gary Taubes NYT feature is also in
today's issue and is
posted at http://www.powerhealth.net/protein2001.htm
Thanks for sending this. The
universal acceptance that female hormones protect against CHD has been a
source of some amazement to me to for time, given that all evidence to
support this hypothesis, thus far, has been absolutely contradictory. As
outlined in Jerome's paper.
However, I have a problem with the proposed excess iron hypothesis for
There are populations in the world where women suffer a higher rate of CHD
than men (Brazil, for example) Within most populations groups studied,
male diabetics (type II) have the same rate of CHD as male diabetes (type
II). I cannot see where iron plays a
part in this. Scottish women suffer twice the rate of CHD as French men,
age matched. Why doesn't iron depletion protect Scottish women? (Or, what
hypothesis can be devised to explain away this fact). The ratio of CHD
between men and women varies between 10:1 (NZ in the 1970s) to 1:1.
Brazil. I can't see how the iron depletion hypothesis can explain a 10
fold difference in rates?
Thank you for supportive comments regarding the redflagsweekly article.
I don't have much to add to my many previous replies to your other points.
These replies, in my view, adequately answer your arguments as I
them (your present formulations appear to be burdened with contradictions
and to lack adequate documentation). I do not agree that these arguments
invalidate the iron hypothesis.
In general, your examples do not speak directly to iron levels. This is
surprising considering that you are debating the hypothesis that iron
depletion is a primary protective factor against ischemic heart disease.
Simply specifying gender does not specify iron status.
You seem to consider each modifying factor to be equivalent to an ad hoc
argument. Iron levels really are influenced by gender and age as well as
genetic and environmental factors. Heart disease rates are also modified,
sometimes for reasons that we do not yet understand, by an equally broad
set of factors.
As an example, it is not an ad hoc argument to note as I have done before
with respect to the Masai that iron deficiency can coexist with a high
level of iron intake. Your sweeping conclusions do not take into account
actual iron levels in the men and women in the populations in question.
These levels vary with genetic polymorphisms, cultural practices and
secularly through time, to name a few influences. I have not even alluded
to uncertainties relating to varying diagnostic practices in various
locales at various times.
(Please refer to previous messages and citations.)
Best regards, Jerome
I am not certain if this discussion forum requires endless referencing of
materials. I am also aware that if I state, as fact, that Scottish women
suffer more CHD than French men, several members of this group will remind
me that all statistics on CHD are meaningless.
Anyway. If you want up-to-date statistics on CHD that, in my opinion, are
reasonably robust, the British Heart Foundatation has them. Just type BHF
into Google, or look up the statistics from the Monica study. (Here you
also find huge variability in the ratio of male and female deaths from CHD
between different countries.)
My point, however, is that Scottish women suffer more CHD than French men,
age matched. Scottish women have periods, French men don't. If you are
suggesting that Socttish women have cultural practices, genetic
polymorphisms and secular variability (or some form of dietary factor)
makes them uniquely at risk then you have to provide evidence that this is
so. You can't just say that it is probably so and ignore it. As it stands,
the French and Scottish statistics directly contradict the hypothesis that
iron depletion protects against CHD. There may be an ad-hoc hypothesis
can explain this problem with the iron-depletion hypothesis, but I can't
currently see what it is.
To quote Carl Popper 'A biologist proposes the conjecture that all swans
white. When a black swan is found in Australia, he says that it is not
refuted. He insists that these black swans are a new kind of bird since it
is a part of the defining property of a swan that it is white. In other
words he can escape the refutation, though I think he is likely to learn
more if he admits that he is wrong.'
Currently, I can see too many refutations to your 'iron-depletion'
hypothesis to accept it as more than a conjecture - perhaps all of these
refutations can be explained away. Of course others may disagree, and,
taking a broader veiw, it is not important that you convince me. But I
suspect that others will have the same problem with your conjecture. I
that I am raising specific points e.g. Scottish women and French men, and
you are providing a general refutation. 'Your sweeping conclusions do not
take into account actual iron levles in the men and women in the
in question....' Well, what are the iron levels in Scottish women and
Bravo! A lot of golf is being played in our group.
Correlation is never equal to causation and selective correlation is
equivalent to propaganda.
We don't know whether atherosclerosis is a disease or simply a finding
several causes. The apparent weak ability of the statins to delay
their ability to lower cholesterol also is only a correlation, but it is
presumed by the cholesterol crowd to be strong evidence that lowering
cholesterol is good for you. Any interventional manoeuvre to attempt
demonstrate causality, to be reliable, must be selective in its effect.
seems probable that any beneficial effect of the statins is by
than lowering cholesterrol (?anti-inflammatory).
Let's keep "our minds open, but not so open that our brains fall out".
You evidently have better access to the Monica data that I do. The BHF
available to me does not have these data. The Monica site I have looked at
this morning does not have age vs disease data. This is critical for
evaluating the differences between heart disease rates in Scottish women
and French men. You emphasize age matched, however these do not appear to
be published as rate vs age curves. Combined age standardized rates do not
tell what happens below age 40.
Since most heart disease occurs in older persons, a straight comparison of
total rates for men with those of women obscures what happens in
premenopausal women. The focus of the iron hypothesis is on protection by
iron depletion, not on the nature of any particular quantitative
relationship between iron load and disease production (this point has been
elaborated repeatedly in my published papers). After iron depletion is
with cessation of menses, coronary rate will likely depend on risk factors
other than the level of storage iron.
Thus total coronary disease burden in Scottish women will reflect
overwhelmingly what happens to Scottish women after cessation of menopause.
A global disease rate that lumps pre- and postmenopausal women will hide
any protective effects of iron depletion in the premenopausal age groups.
The rate in all Scottish women compared to the rate in all French men will
shed little light on the bases for the sex difference in coronary disease
or the effects of menopause on disease.
COMPARISON WITH DISEASE RATES IN FAMILIAL HYPERCHOLESTEROLEMIA:
One situation in which this problem is seen with some clarity is in
heterozygous familial hypercholesterolemia. Women heterozygotes have more
coronary disease than normal men, if all ages are lumped together. Such
lumping however obscures a remarkable and unexplained pattern in
heterozygous familial hypercholesterolemia. Despite the enormous coronary
burden seen in later years, young female heterozygotes actually have a
lower coronary rate than normal young women of the same age. (This is not
misprint.) I have proposed that their iron losses protect the young female
heterozygotes more or less entirely from the otherwise cardiotoxic levels
of cholesterol. This pattern is particularly remarkable because the young
female heterozygotes have the same lipid phenotype as heterozygous men
birth. If anything the women have slightly higher cholesterol levels.
AN IMPROVED VERSION OF YOUR ARGUMENT:
Your Scottish vs French example can be made much sharper and more dramatic
if you point out that women with heterozygous familial
have a far higher coronary rate than normal men. By analogy with your
Scottish/French example, you would then argue that they bleed, the normal
men don't bleed, but the women have a dramatically higher coronary rate.
Thus the iron hypothesis cannot be true!
But, as you see, even this stronger version of your argument fails to
disprove the iron idea, because the younger female heterozygotes are
markedly protected. Their coronary rates are even slightly lower than
of normal women. The familial hypercholesterolemia example presents a
crucial challenge to the cholesterol hypothesis, but is quite consistent
with the iron hypothesis.
UNPROVED VS DISPROVED - STATUS OF THE IRON CONJECTURE:
I agree with you completely that the iron hypothesis is an unproved
conjecture. I do not agree that what is currently known disproves it. This
does not involve arguments on nomenclature. It is not a non-disprovable
idea. What is needed is a trial. We can continue the iron depleted state
women who undergo menopause by regular phlebotomy or other methods, and
what happens to coronary rates. As noted before, epidemiological data can
help us to generate new hypotheses, but is far less good at providing
If it is shown in a prospective trial that iron depletion significantly
lowers coronary rates, the existing epidemiological data may make a little
more sense, especially if taken together with a lot more data on iron
levels, and the effects of genetics, environment and age on iron levels
various populations. The example of the theory of continental drift may be
instructive. Before applying the continental drift idea, geologists had a
great deal of confusing information, for example, the similarity of
at a certain level in South America and Africa. The whole bewildering
picture might have been explained by a series of ad hoc explanations and
conjectures. But the new hypothesis of continental drift, even though it
seemed preposterous to geologists of the day, cut through the confusion
ad hoc suppositions and made sense of the otherwise confusing and
Yes, I agree with your comments.
But I tend to see AS as a process which starts within the intimal layer
due to some? metabolic defect/occurrence/consequence/local trigger, in
combination with a particular vascular wall hemodynamic anomaly, as
suggested by engineers. It is after all a local/focal phenomenon.
Have any of you followed a link I have sent few day ago to that paper
What is your opinion about the performance of CT in the assessment of AS,
and obviously how about nutritional arrest of AS?
To challenge you even more - have look at the paper by Rath and his famous
friend, in an obscure journal (not on the Medline)
JOURNAL OF APPLIED NUTRITION, VOLUME 48, NUMBER 3, 1996
Copyright - International Academy of Nutrition and Preventive
SUPPLEMENT PROGRAM HALTS
PROGRESSION OF EARLY CORONARY ATHEROSCLEROSIS
DOCUMENTED BY ULTRAFAST COMPUTED TOMOGRAPHY
Rath, M.D. and Aleksandra Niedzwiecki, Ph.D.
ABSTRACT: The aim of this study was to determine the
effect of a defined nutritional supplement program on the natural
progression of coronary artery disease. This nutritional supplement
program was composed of vitamins, amino acids, minerals, and trace
elements, including a combination of essential nutrients patented for use
in the prevention and reversal of cardiovascular disease. The study was
designed as a prospective intervention beforeafter trial over a 12 month
period and included 55 patients (age 4467) with various stages of coronary
heart disease. Changes in the progression of coronary artery calcification
before and during the nutritional supplement intervention were determined
by Ultrafast Computed Tomography (Ultrafast CT). The natural progression
rate of coronary artery calcification before the intervention averaged 44%
per year. The progression of coronary artery calcification decreased on
average 15% over the course of one year of nutritional supplementation. In
a subgroup of patients with early stages of coronary artery disease, a
statistically significant decrease occurred, and no further progression
of coronary calcification was observed. In individual cases, reversal
and complete disappearance of previously existing coronary
calcifications were documented.
is the first clinical study documenting the effectiveness of a defined
nutritional supplement program in halting early forms of coronary artery
disease within one year. The nutritional supplement program tested
here should be considered an effective and safe approach to prevention and
adjunct therapy of cardiovascular disease.
I read the paper by Rath and Pauling. It's a clever hypothesis, and
works on a number of levels. The problem that I have with it is that I
cannot see any way that it explains the pattern of CHD seen throughout the
world. If CHD is entirely due to a lack of vitamin C, then it should have
been far more prevalent hundreds of years ago than it is today. In
the Western World no-one (or hardly anyone) suffers a lack of vitamin C. Manufacturers
stuff it into everything, and have done so for as far back as I can
the Innuit eat absolutely no fruit or vegatables, yet suffer a rate
of CHD of almost zero. (I know they save the adrenal gland) If any
population was going to suffer a lack of vitamin C it would be them, yet
they don't get CHD. Explain that?
regard to the abstract below.'the natural progression rate of coronary
artery calcification before the intervention averaged 44% per year...' I'm
sorry but that doesn't actually mean anything at all.
I agree with you 100%, again!.
For the last 5 and a bit years I have been on high fat diet, my Vit C
intake has been relatively low, relatively to what it used to be and to
what other "healthy people" consume. The only reliable source of
it in my
weekly diet have been principally sour (fermented) cabbage, and an
occasional veg which resembles tomato, an orange or 2, raw onions, mainly
spring variety. Is there any Vit C in cooked potatoes?
Seasonally, I might have some berry fruits, like some Innuit or Yakut,
might have had, or in the case of most Yakuts still enjoy. (Surprisingly,
Soviet totalitarianism and collectivism was not as bad as the Canadian
democracy for their respective northern nations.)
Yet, neither I nor my family, nor many people I know who re on a similar
dietary "trip", have had no symptoms of Vit C deficiency. Some,
I know, apart from a lemon slice with tea, have no Vit C intake at all,
and have shown remarkable improvements in CV function. What is going on?To
me Vit C and other Vits may be important deferentially, depending on what
type of nutrition one follows. Let me recall Vit B1 again - it is
virtually totally dedicated to carbate metabolism, so it is almost
obsolete for those running on fat.However, you might be interested in
reading a discussion on Vit C & E and
post-transplant atherosclerosis in the Lancet letter section (10
August).Also, if you go to the website
from which I took an abstract below, you can download a whole paper. Let
me ask again, anyone! - is the CT assessment of AS any good? After all it
only "looks" at a surrogate marker of AS, buildup of Ca in a
tissue. I remember some marketing of such a method on TV, of course as
part of an impartial current affairs program.
A new study has just been published in a journal I can't get, which
implicates saturated fat with CHD in women. The abstract is below. They do
keep trying, don't they!
See also my reply to news that a high protein diet is nhealthy at http://bmj.com/cgi/eletters?lookup=by_date&days=1#24944
The original article is at http://bmj.com/cgi/content/full/325/7361/408/d?eaf
Eur J Clin Nutr 2002 Aug;56(8):786-92
Dietary fats and 16-year coronary heart disease mortality in a cohort of
men and women in Great Britain. Boniface DR, Tefft ME.University of
Hertfordshire, Hatfield, Herts,UK.
OBJECTIVE: The paper aims to investigate the relationships of dietary fats
to subsequent coronary heart disease (CHD) mortality in men and women
while taking account of other CHD-related behaviours. DESIGN: A cohort of
randomly selected men and women were interviewed in 1984-85 and monitored
subsequently for 16 y for deaths. The interview covered health,
health-related behaviours, physical measurements, socio-demographic
details and a dietary questionnaire. Appropriate exclusions left 1225 men
and 1451 women aged 40-75 with 98 and 57 CHD deaths, respectively.
Saturated, polyunsaturated and total fat intakes were estimated. SETTING:
The sample was randomly selected from households in Great Britain. The
interviews took place in participants' own homes.
RESULTS: Not consuming alcohol, smoking, not exercising and being socially
disadvantaged were related to high saturated fat intake and CHD death. Cox
survival analyses adjusting for these factors found that a level of
saturated fat 100 g per week higher corresponded to a relative risk for
CHD death for men of 1.00 (0.86-1.18) and 1.40 (1.09-1.79) for women. This
difference between the effects of saturated fat in men and women was
statistically significant (P=0.019). Results are also reported for total
and the relative effects of polyunsaturated and saturated fats.
CONCLUSIONS: Strong evidence was found for the within cohort relationship
of dietary fat and CHD death in women while no evidence was found for a
relationship in men. Possible explanations for this are discussed.
SPONSORSHIP: This study was supported by University of Hertfordshire using
funding made available by the UK Higher Education Funding Council.
but in this article it was stated that the urinary calcium excreted was
much higher. This is apparently an objective parameter that is not
debatable, so what is the mechanism to offset this calcium loss? Since
calcium comes from the bones, how does one claim that no studies have
shown that the development of osteoporosis over a long period of time
might not result? But then there is the problem of skinny white
women who do not have high protein diets, yet they are most at risk for
developing osteoporosis. How to resolve this conflicting
and Alice Ottoboni
You bring up a common argument against high dietary protein. However,
we think that in the long run, the studies showing that soy protein, but
not animal protein causes calcium loss will prove to be correct. Further, there is no difference in calcium balances between human subjects
on high or low animal protein diets.
The references are:
Fallon, Sally, Enig, Mary. Tragedy and Hype: The Third
Symposium. Nexus Magazine, 2000, Vol. 7, No. 3.
Hunt, JR, etal. High-versus low-meat diets. American Journal
Nutrition, 1995, Vol. 62, pages 621-632.
I have not read the full paper (anyone who has access to Kidney
International?), but my main objection against the study as it appears in
the abstract is that they have made the classical shortcut, to measure
surrogate outcomes. That urinary calcium excretion is increased during a
few weeks is not equivalent with osteoporosis or nephrocalcinosis or
calcium stone production. In the long run compensatory mechanisms may
only way to study that problem is to follow individuals with high and low
protein intake (in a cohort study for instance) and see if the high
protein eaters really develop these diseases more often than the
low-protein eaters. Lowering cholesterol is not equivalent with less
Uffe: I understand the necessary
study design to show the evidence
to prove/disprove the claim. But does anybody KNOW that compensatory
mechanisms kick in to preserve calcium and if this ever occurs? What
about the studies that John McDougall has always claimed show a large NET
urinary calcium loss even with calcium supplementation when the person is
on a higher protein diets?
Surely after 35 years of beating this horse there is some solid evidence
out there one way or the other and it does not require another study to
prove it? Alice and Fred Ottoboni send a message that it might be
soy protein rather than animal protein, but what possible mechanism could
account for this if the amino acids are broken down and absorbed?
Pardon me if I am behind the curve on this, but do you know something
brief to explain this Steve Byrnes?
Fred and Alice Ottoboni
Dr. Tom: With regard to soy protein, the probability is that it is not
protein per se
that is causing calcium loss, but rather another component of commercial
protein. A likely culprit is phytic acid, which is known to tie up
Please see my paper "Hypercholesterolemia due to ascorbic
acid"(PSEBM 151: 579,1976). In 1970, 40,000 people in the US
were examined for nutritional disorders and no cases of scurvy were found.
There also were 666,665 deaths from IHD. "It seems unlikely
that if IHD and scurvy share a common etiology...the diseases should be
distributed so unequally"
I like those two statistics. I think I would have been suspicious
people had died of IHD. Not only is that exactly two thirds of one
million, it is also the number of the beast, twice (spooky?) However, I am certain that, when confronted by such figures,
those who believe in the ascorbic acid theory will fall back on a position
such as: 'Ah, we never said
frank scurvy. We meant a more subtle form of ascorbic
acid deficiency that would not have been picked up by that test.'
'A lack of ascorbic acid does not necessarily show up symptomatically.'
(Insert supportive excuse of your choice here).
One thing is for sure. Once someone grabs hold of a theory, they cling on
for dear life, and never let it go. I often think it would be simpler to
reverse the direction of Earth's orbit than to change anyone's mind.
The most likely explanation is that the protein is not consumed with
fat-soluble vitamins to enable its absorption. When Spencer and Kramer did
their work on calcium loss and protein intake, they discovered that when
protein was eaten as real meat (and dietary calcium intake was adequate),
bone loss was detected, even over a long period of time. They did not
initially, there was a higher excretion of calcium in the urine in some
subjects, but that this quickly balanced out and no further losses were
detected. This might explain the higher loss in the new paper. As Uffe
pointed out, the study was only short-term. You may want to read this
paper on the subject by Fallon and Enig at
Its amazing how old lies never die. I'm reading Stafansson's book
of the Land" right now and he wrote back in the 1930s that:
"It was strongly and widely held that the less meat one ate the
would be for him. If one ate a good deal of it he was supposed to develop
rheumatism, hardening of the arteries, high blood pressure, with a
to breakdown of the kidneys--in short, premature old age. An extreme
had it that one would live more healthily, more happily, and longer if he
became vegetarian." pg 41
Does this sound familiar?
With regards to the bone loss issue, he also wrote that:
"It is written by many nutritionists and physiologists that Eskimos
necessary calcium by chewing bones. Their skeletons, as studied in our
museums, indicate a plentiful calcium supply . . . . There had certainly
been no sign of calcium deficiency after ten Arctic years, about half of
which were exclusively on meat and the other half on a preponderance of
meat." pg 77
"When a doctor looks for calcium deficiency, he studies bones. The
do then, was to examine the skeletons of people who had died at a
high age after living from infancy upon an exclusive meat diet. Such
skeletons of Eskimos who died before European influences came in. Dr.
reported no sign of calcium deficiency. On the contrary, there was every
indication that the meat eaters had been liberally, or at least adequately,
supplied." pg 85
Perhaps modern researchers who still cling to the meat=bone loss theory
should read Stefansson's work, published over 70 years ago.
Perhaps I missed something, but are you saying that protein
absorption does NOT occur in the absence of fat soluble vitamins?
I think I tend to agree with (some) of the Washington Post article. On the
basis that fat contains twice as many calories - per gram - as
If you eat 100g of fat you will be taking in more calories than if you eat
100g of carbs. As the body has no way (of which I am aware) of shedding
calories, other than through exercise and radiating heat, then if you eat
fat, you should get fatter than if you eat the same amount (in grams) of
If this is not true, then could someone please enlighten me as to why not.
Although others have already made quite an effort to explain why calories
ain't calories, let me add a bob or two.
As one of only few on this group, I feel uniquely qualified to comment, if
only because of what I eat - mainly fat.
Firstly, as I have already explained some months ago, using the results of
Kekwick & Pawan (see the atachment), our body can and does get rid of
unwanted energy and that process is much more efficient for fats. Up to
can be excreted compared with about only 6% when the energy is derived
mainly from carbate. So the body has the way of shedding calories!!! And
that process favours fat-derived energy.
Secondly, when one, like me, eats, lets say, 180 g of fat/day there is no
way one can possibly eat a lot of carbate and proteins at the same time.
The satiety is simply unbearable, and it lasts. You just can not eat too
much of energy when you get it as fat. So the scenario that one can
on fat, or even on protein when eating lots of fat is simply impossible.
one tries (sorry, but I have not) I am sure the diaphragm would be
And even assuming that one could get down 300 g of fat/day, the
physiological limit of intestinal absorption would not permit to absorb
more than about 15 g of fat/h, or 180 g/day. The rest would come out in a
certain loose way, just like what happens after taking the recently
approved inhibitor of lipid absorption.
Of course, the story is totally different with carbate. One can easily eat
300-500 g of carbate & protein in a single meal, and then assuming
most of it is absorbed (some will obviously travel to the colon undigested)
the body has no other option but to store it for later as fat, since the
calorie shedding mechanism is not as effective. To make matters worse,
few h after eating high carbate meal (not so with protein), one feels
hungry again, but not so after eating a nice fatty meal. I.E., - calories