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[A1CR]

Posted for MR:

All:

CRONie_TP wrote:
>> >>2. J Clin Invest. 2006 Jan;116(1):209-16
>> >>Soy diet worsens heart disease in mice.
>> >>Stauffer BL, Konhilas JP, Luczak ED, Leinwand LA.

>> >>We report that dietary modification from a soy-based
>> >>diet to a casein-based diet radically improves disease
>> >>indicators and cardiac function in a transgenic mouse
>> >>model of hypertrophic cardiomyopathy.

>> >>PMID: 16395406
> >
> >
> > Wow, this comes as a real shock to me. The China Study
> > would seem to show the reverse.

First, I expect that you're confusing cardiomyopathy with cardiovascular
disease; Wiki them if need be.

Second, one (hopefully last) time: the China Study was crummy,
population-comparison ecological crap, not proper prospective
epidemiology; please, folks, ignore it and any conclusions drawn from it.


To reiterate: the China Study was crummy, population-comparison
ecological crap, not proper prospective epidemiology. In a real
prostpective epidemiological study, you take a group of individuals and
ask each of them INDIVIDUALLY about hir dietary and other exposures at
time X, and then follow them all up for several years and see their
health outcomes; then, you correlate specific exposures to specific
outcomes. If you see such correelations (eg, people who consumed more
cooked tomato products were less likely to develop aggressive prostate
cancer), then because you have a range of other information about EACH
of these people as INDIVIDUALS, you can double-check for false positives
on an individual-by-individual basis: eg, you can say, "were cooked
tomato product users mostly of Italian descent (possible genetic
influence)? Were they less likely to smoke, or eat a lot of saturated
fat? Did they tend to have their cooked tomato products with salads, or
eat more vegetables generally?" Etc. The combination of a prospective
design and the existence of a range of info about EACH PERSON'S
lifestyle gives such studies great power to test for real causal
connections -- not definitive proof, but strong evidence.

The China study was not prospective epidemiology, but an "ecological"
study, which aggregates entire populations. That is, they looked at how
much meat was consumed in an ENTIRE PROVINCE, and the rates of heart
disease in the province AS A WHOLE, and then compared the two variables
in another province; if provinces with more meat consumption also have
more heart disease, they inferred that meat causes heart disease. As
I've often harped in the past, these kinds of studies are MEANINGLESS.
The Japanese smoke more than the Americans; they also die less of lung
cancer. That doesn't mean that smoking is protective against lung cancer
-- and you can prove this with proper, prospective epidemiology, because
WITHIN *either one* of those populations, INDIVIDUALS who smoke at time
X are more likely to die of lung cancer several years down the road.

I hate to be a grouch, but I've said this many, many times before, and
I''m very tired of repeating myself; it's very frustrating go through
endless iterations of this on the List, as not only newcomers but folks
who have been on the List for YEARS continue to take these kinds of
bullshit studies seriously. One such exchange, slightly edited:

-----------
http://lists.calorierestriction.org/cgi-bin/wa?A2=ind0107&L=crsociety&P=R6850

"CRONie_TFS" wrote:
> > > How come [the Okinawans] (who eat lots of
> > > soy) have lower rates of dementia, ...???

[MR responded:}
> > http://groups.yahoo.com/group/crsociety/message/8989

> I still fail to understand why more Okinawans don't have dementia
> (CR or no CR) if there's a link between it and soy. You say that
> such statistics are meaningless,

Right. Again: your line of reasoning is:

"They" say that soy causes dementia. Yet the Okinawans eat more soy than
the Japanese or North Americans, and have LOWER rates of dementia than
people from those groups. Therefore, clearly, soy does not cause dementia.

But the same logic applies all over the place, in places wehre it
clearly ain't so, as eg:

"They" say that smoking causes lung cancer deaths. Yet the Japanese
smoke more cigarettes than North Americans, and have LOWER rates of lung
cancer death. Therefore, clearly, smoking does not cause lung cancer death.

"They" say that dairy is protective against osteoporosis and fractures.
Yet many Asian cultures consume less dairy than North Americans, and
have LOWER rates of osteoporosis and fractures. Therefore, clearly,
dairy is not protective against osteoporosis and fractures.

The problem is that you CAN'T meaningfully isolate any one such factor
out of 2 aggregated populations and even begin to make causal
connections. Otherwise, you can pick any damned difference you like, and
point to it the factor causing any other damned difference that you
like. Eg: "The Chinese play more ping-pong than North Americans, and
they have a lower rate of heart disease than North Americans. Thus,
ping-pong is highly protective against heart disease." "The Japanese get
more stomach cancer than do North Americans, and they consume more green
tea. Thus, green tea cannot possibly be protective against stomach
cancer, and indeed, may CAUSE stomach cancer." ETC ETC.

You have to look WITHIN a cultural pattern, and see whether, WITHIN that
cultural pattern, INDIVIDUAL PEOPLE who do more X get less Y. If someone
will point me to a study in which individual Okinawans who consume more
soy get no more dementia than individual Okinawans who consume less,
after adjusting for education, income, occupation, age, and other
obvious covariates, then THAT will be interesting data. This just ain't.
----------

The same points are made in more formal fashion a webpage from the FDA,
of which I've appended edited sections at the end of this email; and
also, tho' in inadequate explication, here (note that study designs are
listed in order from strongest to weakest):

http://www.vetmed.wsu.edu/courses-jmgay/GlossClinStudy.htm

> the New York Times called it "the
> Grand Prix of Epidemiology."

The NYT is not a source of scientific evidence and shouldn't be treated
as one. And to make an important niggle: I guarantee that "the NYT" did
not say this; rather, some writer who happened to get an article
published IN the NYT said that in hir article. Evidently, the writer was
not a scientist (or perhaps s/he was a chemist, a geologist, or some
other scientist who would have no reason to have an understanding of
epidemiological study design -- cf the citing of "scientists" who don't
believe that anthropogenic C02 emissions are causing climate change who
have no actual background in climatology).

> > Aside from that main study, he has also published many on his
> > experiments with aflatoxin-induced cancer in rats which found
> > lower-quality proteins, like wheat, prevented and/or reversed
> > cancer progression, while high-quality proteins, like casein,
> > promoted it. Here is one reference [2]:

First, a quibble: (2) did not show that lower-quality proteins
prevented and/or reversed cancer progression, but that animals fed
lower-quality proteins developed fewer preneoplastic lesions of the
liver. That doesn't NECESSARILY show even less *liiver* CANCER, let
alone less TOTAL cancer or cancer deaths. This is just one risk factor
for one disese, not an effect on global health as indicated by a LS
study. Indeed, Ross and Bras (3) showed that higher protein consumption,
in either AL OR CR animals, led to longer mean and maximal LS, *and*
that the animals were more likely to die WITH tumors in their body --
AND that they were less likely to have *died* OF *CANCER* (see the
distinctioin? Like the harmless breast and prostate minitumors that are
so often needlessly removed after a suspicious PSA or mammogram, that
would never have resulted in a full-blown cancer, with the result that
increased PSA and mammograms have not actually reduced the death rates).
Thus, more protein INCRESED tumor prevalence at death, but was still
overall a good thing -- a remarkable finding, granted how often mice and
rats die of cancer.

Furthermore, the abstract of (2) says nothing about body weight or food
intake; many studies in the past have shown that protein restriction
induces mild 'spontaneous' CR, and this may be a similar case. Second:
an animal consuming low-quality protein, at the same "RDA" gram amount
as another animal consuming high-quality protein, has inadequate protein
for growth and development, because you need complete protein to build
tissue. This includes both healthy and cancerous tissue. So it's not
necessarily surprising that a low-quality protein might well reduce the
progression of cancer if it did -- because the animals would be mal-
(not just under-)nourished. Similar effects might well flow from being
deficient in any number of vitamins, minerals, or other essential
components of the diet. The questioin is whether you think it's sensible
to go around being deficient in essential nutrients in order to avoid
one specific disease risk factor.

Broadly speaking, higher protein intake -- including (and usually
MOSTLY) animal (complete) protein intake -- has been shown in many
high-quality epidemiological and even controlled clinical trials to
reduce risk of many chronic diseases in humans, when saturated fat
intake and other potentially confouding risk factors are adjusted for or
actively controlled; some examples here:

http://lists.calorierestriction.org/cgi-bin/wa?A2=ind0405&L=crsociety&P=R33881

---------
FDA Office of Food Additive Safety
Redbook 2000
Toxicological Principles for the Safety Assessment of Food Ingredients
October 2001

http://www.cfsan.fda.gov/~redbook/red-vib.html

Epidemiology is the study of the distribution and determinants of
health-related states and events in specified populations, and the
application of this study to the control of health problems. The goal of
all epidemiology studies is to uncover relationships between exposure to
a specific agent and changes in health status. ...

There are two main categories of epidemiology studies, descriptive and
analytic. Descriptive studies are concerned with the existing
distribution of variables; they *do not* *test hypotheses* or *make
inferences concerning causality* . Analytic studies are designed to
examine associations, particularly hypothesized causal relationships,
and focus on identifying or measuring the effects of specific risk
factors...

1. Descriptive Epidemiology Studies
Descriptive epidemiology studies are relatively inexpensive to conduct
and are usually of short duration. However, such studies are limited in
their usefulness since no inferences can be made concerning causality.
Generally, descriptive epidemiology studies are sentinel devices used to
generate hypotheses or to provide evidence that indicates whether there
is sufficient cause for conducting a lengthier and costlier analytic study.

a. Correlational Studies
Correlational studies, also called ecological studies, use grouped
population data to relate exposure patterns of whole populations to
disease incidence or mortality rates for whole populations. Because
these studies do not examine the relationship between exposure and
disease among individuals, the studies have been traditionally regarded
as useful for generating, rather than definitively testing, a scientific
hypothesis. Thus, the results of correlational studies would be
insufficient to demonstrate a relationship without other types of data
to support them. ...

2. Analytic Epidemiology Studies
Although analytic epidemiology studies are more informative than
descriptive studies, they are expensive and time-consuming to conduct...

b. Prospective Studies
In prospective studies, also called cohort or follow-up studies, the
investigator selects a study population of exposed and non-exposed
individuals and follows both groups to determine the incidence of
disease. The group can be characterized by factors thought to influence
the development or course of the disease and by the presence or absence
of risk factors (e.g., exposure or nonexposure to some agent).
Prospective studies generally imply study of a large population, study
for a prolonged period of years, or both. This type of study design is
effective when there is good evidence of an association of the disease
with a certain exposure (from clinical observations or from descriptive
epidemiology studies), when exposure is rare, but incidence of disease
among the exposed is high, and when the time between the exposure and
disease is short. The major advantage of prospective studies is that the
incidence rates of the disease under study can be measured directly;
therefore, absolute and relative risks also can be measured directly. In
addition, it is possible to analyze the association of a particular
exposure with several diseases, and a temporal relationship between
exposure and disease can be established.


>>>>1. J Clin Invest. 2006 Jan;116(1):209-16
>>>>Soy diet worsens heart disease in mice.
>>>>Stauffer BL, Konhilas JP, Luczak ED, Leinwand LA.
>>>>PMID: 16395406


> 2. J Natl Cancer Inst. 1989 Aug 16;81(16):1241-5.
> Effect of dietary protein quality on development of aflatoxin B1-induced
> hepatic preneoplastic lesions.
> Schulsinger DA, Root MM, Campbell TC.
> PMID: 2569044 [PubMed - indexed for MEDLINE]

3. 1: Ross MH, Bras G.
Influence of protein under- and overnutrition on spontaneous tumor
prevalence in the rat.
J Nutr. 1973 Jul;103(7):944-63. No abstract available.
PMID: 4351915 [PubMed - indexed for MEDLINE]