🚀 go-pugleaf

Ian Goddard <igoddard@erols.mom> wrote:

> 
>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>
Big problem Tofu contains other things besides soy.
Frequently aluminium sulphate or alum is illicitly included in the
coagulant used to gell the soy. The addition of aluminium helps to
give the tofu a much firmer texture.

Surely this must complicate any statistical research demonstrating
neurotoxicity of Tofu products.

Bob M

On Thu, 07 Aug 2003 05:47:54 GMT, molab@ww.co.nz (R Molony) wrote:

>>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>>
>Big problem Tofu contains other things besides soy.
>Frequently aluminium sulphate or alum is illicitly included in the
>coagulant used to gell the soy. The addition of aluminium helps to
>give the tofu a much firmer texture.
>
>Surely this must complicate any statistical research demonstrating
>neurotoxicity of Tofu products.

This raises the question as to whether soy bean products generally may
be tarnished by research findings that are properly applicable only to
tofu. Certainly my initial reaction was to fall into that groove.
---
Richard Schulman
Remove antispamming "-xyz" for email reply

"Richard Schulman" <ra.schulman-xyz@verizon.net> wrote in message
news:chc4jvo8paet3c2h0eapp6lnha0sen00gb@4ax.com...
> On Thu, 07 Aug 2003 05:47:54 GMT, molab@ww.co.nz (R Molony) wrote:
>
> >>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
> >>
> >Big problem Tofu contains other things besides soy.
> >Frequently aluminium sulphate or alum is illicitly included in the
> >coagulant used to gell the soy. The addition of aluminium helps to
> >give the tofu a much firmer texture.
> >
> >Surely this must complicate any statistical research demonstrating
> >neurotoxicity of Tofu products.
>
> This raises the question as to whether soy bean products generally may
> be tarnished by research findings that are properly applicable only to
> tofu. Certainly my initial reaction was to fall into that groove.
> ---
> Richard Schulman
> Remove antispamming "-xyz" for email reply


Interesting article I found against SOY. I cannot comment to it's accuracy.

Jack N Dalton

The Trouble With Tofu: Soy and the Brain
By John D. MacArthur
"Tofu Shrinks Brain!" Not a science fiction scenario, this sobering soybean
revelation is for real. But how did the "poster bean" of the '90s go wrong?
Apparently, in many ways - none of which bode well for the brain.
In a major ongoing study involving 3,734 elderly Japanese-American men,
those who ate the most tofu during midlife had up to 2.4 times the risk of
later developing Alzheimer's disease. As part of the three-decade long
Honolulu-Asia Aging Study, 27 foods and drinks were correlated with
participants' health. Men who consumed tofu at least twice weekly had more
cognitive impairment, compared with those who rarely or never ate the
soybean curd. [1,2]
"The test results were about equivalent to what they would have been if they
were five years older," said lead researcher Dr. Lon R. White from the
Hawaii Center for Health Research. For the guys who ate no tofu, however,
they tested as though they were five years younger.
What's more, higher midlife tofu consumption was also associated with low
brain weight. Brain atrophy was assessed in 574 men using MRI results and in
290 men using autopsy information. Shrinkage occurs naturally with age, but
for the men who had consumed more tofu, White said "their brains seemed to
be showing an exaggeration of the usual patterns we see in aging."
Phytoestrogens - Soy Self Defense
Tofu and other soybean foods contain isoflavones, three-ringed molecules
bearing a structural resemblance to mammalian steroidal hormones. White and
his fellow researchers speculate that soy's estrogen-like compounds
(phytoestrogens) might compete with the body's natural estrogens for
estrogen receptors in brain cells.
Plants have evolved many different strategies to protect themselves from
predators. Some have thorns or spines, while others smell bad, taste bad, or
poison animals that eat them. Some plants took a different route, using
birth control as a way to counter the critters who were wont to munch.
Plants such as soy are making oral contraceptives to defend themselves, says
Claude Hughes, Ph.D., a neuroendocrinologist at Cedars-Sinai Medical Center.
They evolved compounds that mimic natural estrogen. These phytoestrogens can
interfere with the mammalian hormones involved in reproduction and growth -
a strategy to reduce the number and size of predators.
Toxicologists Concerned About Soy's Health Risks
The soy industry says that White's study only shows an association between
tofu consumption and brain aging, but does not prove cause and effect. On
the other hand, soy experts at the National Center for Toxicological
Research, Daniel Sheehan, Ph.D., and Daniel Doerge, Ph.D., consider this
tofu study very important. "It is one of the more robust, well-designed
prospective epidemiological studies generally available. . . We rarely have
such power in human studies, as well as a potential mechanism."
In a 1999 letter to the FDA (and on the ABC News program 20/20), the two
toxicologists expressed their opposition to the agency's health claims for
soy, saying the Honolulu study "provides evidence that soy (tofu)
phytoestrogens cause vascular dementia. Given that estrogens are important
for maintenance of brain function in women; that the male brain contains
aromatase, the enzyme that converts testosterone to estradiol; and that
isoflavones inhibit this enzymatic activity, there is a mechanistic basis
for the human findings." [3]
Although estrogen's role in the central nervous system is not well
understood, White notes that "a growing body of information suggests that
estrogens may be needed for optimal repair and replacement of neural
structures eroded with aging."
One link to the puzzle may involve calcium-binding proteins, which are
associated with protection against neurodegenerative diseases. In recent
animal studies at Brigham Young University's Neuroscience Center,
researchers found that consumption of phytoestrogens via a soy diet for a
relatively short interval can significantly elevate phytoestrogens levels in
the brain and decrease brain calcium-binding proteins. [4]
Concerns About Giving Soy to Infants
The most serious problem with soy may be its use in infant formulas. "The
amount of phytoestrogens that are in a day's worth of soy infant formula
equals 5 birth control pills," says Mary G. Enig, Ph.D., president of the
Maryland Nutritionists Association. She and other nutrition experts believe
that infant exposure to high amounts of phytoestrogens is associated with
early puberty in girls and retarded physical maturation in boys. [5]
A study reported in the British medical journal Lancet found that the "daily
exposure of infants to isoflavones in soy infant-formulas is 6-11 fold
higher on a bodyweight basis than the dose that has hormonal effects in
adults consuming soy foods." (A dose, equivalent to two glasses of soy milk
per day, that was enough to change menstrual patterns in women. [6]) In the
blood of infants tested, concentrations of isoflavones were 13000-22000
times higher than natural estrogen concentrations in early life. [7]
Soy Interferes with Enzymes
While soybeans are relatively high in protein compared to other legumes,
Enig says they are a poor source of protein because other proteins found in
soybeans act as potent enzyme inhibitors. These "anti-nutrients" block the
action of trypsin and other enzymes needed for protein digestion. Trypsin
inhibitors are large, tightly folded proteins that are not completely
deactivated during ordinary cooking and can reduce protein digestion.
Therefore, soy consumption may lead to chronic deficiencies in amino acid
uptake. [8]
Soy's ability to interfere with enzymes and amino acids may have direct
consequence for the brain. As White and his colleagues suggest, "isoflavones
in tofu and other soyfoods might exert their influence through interference
with tyrosine kinase-dependent mechanisms required for optimal hippocampal
function, structure and plasticity." [2]
High amounts of protein tyrosine kinases are found in the hippocampus, a
brain region involved with learning and memory. One of soy's primary
isoflavones, genistein, has been shown to inhibit tyrosine kinase in the
hippocampus, where it blocked "long-term potentiation," a mechanism of
memory formation. [9]
Tyrosine, Dopamine, and Parkinson's Disease
The brain uses the amino acids tyrosine or phenylalanine to synthesize the
key neurotransmitters dopamine and norepinephrine, brain chemicals that
promote alertness and activity. Dopamine is crucial to fine muscle
coordination. People whose hands tremble from Parkinson's disease have a
diminished ability to synthesize dopamine. An increased incidence of
depression and other mood disorders are associated with low levels of
dopamine and norepinephrine. Also, the current scientific consensus on
attention-deficit disorder points to a dopamine imbalance.
Soy has been shown to affect tyrosine hydroxylase activity in animals,
causing the utilization rate of dopamine to be "profoundly disturbed." When
soy lecithin supplements were given throughout perinatal development, they
reduced activity in the cerebral cortex and "altered synaptic
characteristics in a manner consistent with disturbances in neural
function." [10]
Researchers at Sweden's Karolinska Institute at the National Institutes of
Health and are finding a connection between tyrosine hydroxylase activity,
thyroid hormone receptors, and depleted dopamine levels in the brain -
particularly in the substantia nigra, a region associated with the movement
difficulties characteristic of Parkinson's disease. [11-13]
Soy Affects the Brain via the Thyroid Gland
Tyrosine is crucial to the brain in another way. It's needed for the body to
make active thyroid hormones, which are a major physiological regulator of
mammalian brain development. By affecting the rate of cell differentiation
and gene expression, thyroid hormones regulate the growth and migration of
neurons, including synaptic development and myelin formation in specific
brain regions. Low blood levels of tyrosine are associated with an
underactive thyroid gland.
Scientists have known for years that isoflavones in soy products can depress
thyroid function, causing goiter (enlarged thyroid gland) and autoimmune
thyroid disease. In the early 1960s, goiter and hypothyroidism were reported
in infants fed soybean diets. [14] Scientists at the National Center for
Toxicological Research showed that the soy isoflavones genistein and
daidzein "inhibit thyroid peroxidase-catalyzed reactions essential to
thyroid hormone synthesis." [15]
Japanese researchers studied effects on the thyroid from soybeans
administered to healthy subjects. They reported that consumption of as
little as 30 grams (two tablespoons) of soybeans per day for only one month
resulted in a significant increase in thyroid stimulating hormone (TSH),
which is produced by the brain's pituitary gland when thyroid hormones are
too low. Their findings suggested that "excessive soybean ingestion for a
certain duration might suppress thyroid function and cause goiters in
healthy people, especially elderly subjects." [16]
Thyroid Hormones and Fetal Brain Development
Thyroid alterations are among the most frequently encountered autoimmune
conditions in children. Researchers at Cornell University Medical College
showed that the "frequency of feedings with soy-based milk formulas in early
life was significantly higher in children with autoimmune thyroid disease."
[17] In a previous study, they found that twice as many diabetic children
had received soy formula in infancy as compared to non-diabetic children.
[18]
Recognizing the risk, Swiss health authorities recommend "very restrictive
use" of soy for babies. In England and Australia, public health agencies
tell parents to first seek advice from a doctor before giving their infants
soy formula. The New Zealand Ministry of Health recommends that "Soy formula
should only be used under the direction of a health professional for
specific medical indications. . . Clinicians who are treating children with
a soy-based infant formula for medical conditions should be aware of the
potential interaction between soy infant formula and thyroid function." [19]
Thyroid hormones exert their influence during discrete windows of time.
Inappropriate hormone levels can have a devastating effect on the developing
human brain, especially during the first 12 weeks of pregnancy when the
fetus depends on the mother's thyroid hormones for brain development. After
that, both maternal and fetal thyroid hormone levels affect the central
nervous system.
A 1999 study published in the New England Journal of Medicine showed that
pregnant women with underactive thyroids were four times more likely to have
children with low IQs if the disorder is left untreated. The study found
that 19% of the children born to mothers with thyroid deficiency had IQ
scores of 85 or lower, compared with only 5% of those born to mothers
without such problems. [20]
Thyroid, Brain, and Environmental Toxins
Children exposed prenatally and during infancy to common environmental
toxins like dioxin and polychlorinated biphenyls (PCBs) can suffer
behavioral, learning, and memory problems because these chemicals may be
disrupting the normal action of thyroid hormone. [21]
Soybeans grown in the United States contain residues of the pesticide
dieldrin, an organochlorine similar to DDT. Although both chemicals were
banned in the 1970s, dieldrin still persists in soils and is absorbed
through the roots. Today it is the most toxic residue found on domestic
soybeans. [22] In Silent Spring, Rachel Carson warned that dieldrin is
nearly 50 times as poisonous as DDT. In addition to disrupting hormones, it
can have long delayed neurological effects, ranging from loss of memory to
mania. [23]
Combinations of insecticides, weed killers, and artificial fertilizers -
even at low levels - have measurable detrimental effects on thyroid and
other hormones as well as on the brain. [24] EPA scientists now want to
upgrade the commonly used herbicide, atrazine, to a "likely carcinogen." In
animal tests, atrazine attaches to sites on the hypothalamus, a crucial
brain region involved with regulating levels of stress and sex hormones.
[25]
Individuals newly diagnosed with Parkinson's disease were more than twice as
likely to have been exposed to insecticides in their home, compared to those
without the disease. [26]
Soy formulas for infants can contain other neurotoxins: aluminum, cadmium,
and fluoride. Studies found that aluminum concentrations in soy-based
formulas were a 100-fold greater compared to human breast milk, while
cadmium content was 8-15 times higher than in milk-based formulas. In an
Australian study, the fluoride content of soy-based formulas ranged from
1.08 to 2.86 parts per million. The authors concluded that "prolonged
consumption (beyond 12 months of age) of infant formula reconstituted with
optimally-fluoridated water could result in excessive amounts of fluoride
being ingested." A study of Connecticut children revealed that
mild-to-moderate fluorosis was strongly associated with soy-based infant
formula use. [27-30]
In May 2000, Boston Physicians for Social Responsibility released their
report, "The Toxic Threats to Child Development." In the section on
neurotoxins, they concluded: "Studies in animals and human populations
suggest that fluoride exposure, at levels that are experienced by a
significant proportion of the population whose drinking water is
fluoridated, may have adverse impacts on the developing brain." [31]
Iodine vs. Fluorine
The thyroid gland uses tyrosine and the natural element iodine to make
thyroxine (T4), a thyroid hormone containing four iodine atoms. The other,
much more biologically active thyroid hormone is tri-iodothyronine (T3),
which has three iodine atoms. Lack of dietary iodine has long been
identified as the problem in diminished thyroid hormone synthesis.
According to the International Council for the Control of Iodine Deficiency
Disorders: "Iodine deficiency has been called the world's major cause of
preventable mental retardation. Its severity can vary from mild intellectual
blunting to frank cretinism, a condition that includes gross mental
retardation, deaf mutism, short stature, and various other defects. . . The
damage to the developing brain results in individuals poorly equipped to
fight disease, learn, work effectively, or reproduce satisfactorily."
This crucial role of iodine is another reason why the thyroid gland is
especially vulnerable today. Canadian researcher Andreas Schuld has
documented more than 100 studies during the last 70 years that demonstrate
adverse effects of fluoride on the thyroid gland. [32] Schuld says,
"Fluorine, being the strongest in the group of halogens, will seriously
interfere with iodine and iodine synthesis, forcing more urinary elimination
of ingested iodine as fluoride ingestion or absorption increases."
Fluorides were actually used in the past, specifically to reduce thyroid
function. In the 1930s through to the 1960s fluorides at 0.9mg to 4.5mg/day
were given as effective anti-thyroid medication to hyperthyroid patients."
[33] Russian researchers in the 1980s concluded that prolonged consumption
of drinking water with a raised fluorine content was a risk factor of more
rapid development of thyroid pathology. [34]
A major source of fluoride exposure in the United States is fluoridated
drinking water - including foods and drinks manufactured and processed with
this treated water. (Only about 5% of the world's population is fluoridated,
and more than half live in North America. 99% of western continental Europe
has rejected, banned, or stopped the addition of fluoride compounds to their
drinking water. [35]) Also, approximately 45 million pounds of hydrogen
fluoride are released from U.S. coal-fired plants every year into the
environment.
Soy Phytates Inhibit Zinc Absorption
Another way that soybeans may affect brain function is because of their
phytic acid content. Phytic acid is an organic acid present in the outer
portion of all seeds. Also known as phytates, they block the uptake of
essential minerals in the intestinal tract: calcium, magnesium, iron, and
especially zinc. According to research cited by the Weston A. Price
Foundation, soybeans have very high levels of a form of phytic acid that is
particularly difficult to neutralize - and which interferes with zinc
absorption more completely than with other minerals.
The soy industry acknowledges the problem, noting that "one-half cup of
cooked soybeans contains one mg of zinc. However, zinc is poorly absorbed
from soyfoods." As for iron, "both phytate and soy protein reduce iron
absorption so that the iron in soyfoods is generally poorly absorbed." [36]
Nutritionist Sally Fallon, author of Nourishing Traditions: The Cookbook
that Challenges Politically Correct Nutrition and the Diet Dictocrats, says
that as early as 1967, researchers testing soy formula found that it caused
negative zinc balance in every infant to whom it was given. Even when the
diets were additionally supplemented with zinc, there was a strong
correlation between phytate content in formula and poor growth. She warns
that "a reduced rate of growth is especially serious in the infant as it
causes a delay in the accumulation of lipids in the myelin, and hence
jeopardizes the development of the brain and nervous system."
Zinc and the Brain
Relatively high levels of zinc are found in the brain, especially the
hippocampus. Zinc plays an important role in the transmission of the nerve
impulse between brain cells. Deficiency of zinc during pregnancy and
lactation has been shown to be related to many congenital abnormalities of
the nervous system in offspring. In children, "insufficient levels of zinc
have been associated with lowered learning ability, apathy, lethargy, and
mental retardation." [37]
The USDA references a study of 372 Chinese school children with very low
levels of zinc in their bodies. The children who received zinc supplements
had the most improved performance - especially in perception, memory,
reasoning, and psychomotor skills such as eye-hand coordination. Three
earlier studies with adults also showed that changes in zinc intake affected
cognitive function. [38]
New research has identified a specific contingent of neurons, called
"zinc-containing" neurons, which are found almost exclusively in the
forebrain, where in mammals they have evolved into a "complex and elaborate
associational network that interconnects most of the cerebral cortices and
limbic structures." This suggests the importance of zinc in the normal and
pathological processes of the cerebral cortex. [39] Furthermore, age-related
tissue zinc deficiency may contribute to brain cell death in Alzheimer's
dementia. [40]
Safe Soy
To produce soy milk, the beans are first soaked in an alkaline solution,
then heated to about 115 degrees C in order to remove as much of the trypsin
inhibitors as possible. Fallon says this method destroys most, but not all
of the anti-nutrients, however it has the "unhappy side effect of so
denaturing the proteins that they become very difficult to digest and much
reduced in effectiveness." Furthermore, phytates remain in soy milk to block
the uptake of essential minerals.
Only a long period of fermentation will significantly reduce the phytate
content of soybeans, as well as the trypsin inhibitors that interfere with
enzymes and amino acids. Therefore, fermented soy products such as tempeh
and miso (not tofu) provide nourishment that is easily assimilated.

"Richard Schulman" <ra.schulman-xyz@verizon.net> wrote in message
news:chc4jvo8paet3c2h0eapp6lnha0sen00gb@4ax.com...
> On Thu, 07 Aug 2003 05:47:54 GMT, molab@ww.co.nz (R Molony) wrote:
>
> >>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
> >>
> >Big problem Tofu contains other things besides soy.
> >Frequently aluminium sulphate or alum is illicitly included in the
> >coagulant used to gell the soy. The addition of aluminium helps to
> >give the tofu a much firmer texture.
> >
> >Surely this must complicate any statistical research demonstrating
> >neurotoxicity of Tofu products.
>
> This raises the question as to whether soy bean products generally may
> be tarnished by research findings that are properly applicable only to
> tofu. Certainly my initial reaction was to fall into that groove.
> ---
> Richard Schulman
> Remove antispamming "-xyz" for email reply

Another good presentation of issues against Soy.

Jack N Dalton

Newest Research On Why You Should Avoid Soy
by Sally Fallon email: SAFallon@aol.com & Mary G. Enig, PhD email:
MGEnig@aol.com
About the Authors:
Sally Fallon is the author of Nourishing Traditions: The Cookbook that
Challenges Politically Correct Nutrition and the Diet Dictocrats (1999, 2nd
edition, New Trends Publishing, tel +1 877 707 1776 or +1 219 268 2601) and
President of the Weston A. Price Foundation, Washington, DC
(www.WestonAPrice.org).
Each year, research on the health effects of soy and soybean components
seems to increase exponentially. Furthermore, research is not just expanding
in the primary areas under investigation, such as cancer, heart disease and
osteoporosis; new findings suggest that soy has potential benefits that may
be more extensive than previously thought.
So writes Mark Messina, PhD, General Chairperson of the Third International
Soy Symposium, held in Washington, DC, in November 1999.1 For four days,
well-funded scientists gathered in Washington made presentations to an
admiring press and to their sponsors - United Soybean Board, American
Soybean Association, Monsanto, Protein Technologies International, Central
Soya, Cargill Foods, Personal Products Company, SoyLife, Whitehall-Robins
Healthcare and the soybean councils of Illinois, Indiana, Kentucky,
Michigan, Minnesota, Nebraska, Ohio and South Dakota.
The symposium marked the apogee of a decade-long marketing campaign to gain
consumer acceptance of tofu, soy milk, soy ice cream, soy cheese, soy
sausage and soy derivatives, particularly soy isoflavones like genistein and
diadzen, the oestrogen-like compounds found in soybeans. It coincided with a
US Food and Drug Administration (FDA) decision, announced on October 25,
1999, to allow a health claim for products "low in saturated fat and
cholesterol" that contain 6.25 grams of soy protein per serving. Breakfast
cereals, baked goods, convenience food, smoothie mixes and meat substitutes
could now be sold with labels touting benefits to cardiovascular health, as
long as these products contained one heaping teaspoon of soy protein per
100-gram serving.
Marketing The Perfect Food
"Just imagine you could grow the perfect food. This food not only would
provide affordable nutrition, but also would be delicious and easy to
prepare in a variety of ways. It would be a healthful food, with no
saturated fat. In fact, you would be growing a virtual fountain of youth on
your back forty." The author is Dean Houghton, writing for The Furrow,2 a
magazine published in 12 languages by John Deere. "This ideal food would
help prevent, and perhaps reverse, some of the world's most dreaded
diseases. You could grow this miracle crop in a variety of soils and
climates. Its cultivation would build up, not deplete, the land...this
miracle food already exists... It's called soy."
Just imagine. Farmers have been imagining - and planting more soy. What was
once a minor crop, listed in the 1913 US Department of Agriculture (USDA)
handbook not as a food but as an industrial product, now covers 72 million
acres of American farmland. Much of this harvest will be used to feed
chickens, turkeys, pigs, cows and salmon. Another large fraction will be
squeezed to produce oil for margarine, shortenings and salad dressings.
Advances in technology make it possible to produce isolated soy protein from
what was once considered a waste product - the defatted, high-protein soy
chips - and then transform something that looks and smells terrible into
products that can be consumed by human beings. Flavorings, preservatives,
sweeteners, emulsifiers and synthetic nutrients have turned soy protein
isolate, the food processors' ugly duckling, into a New Age Cinderella.
The new fairy-tale food has been marketed not so much for her beauty but for
her virtues. Early on, products based on soy protein isolate were sold as
extenders and meat substitutes - a strategy that failed to produce the
requisite consumer demand. The industry changed its approach. "The quickest
way to gain product acceptability in the less affluent society," said an
industry spokesman, "is to have the product consumed on its own merit in a
more affluent society."3 So soy is now sold to the upscale consumer, not as
a cheap, poverty food but as a miracle substance that will prevent heart
disease and cancer, whisk away hot flushes, build strong bones and keep us
forever young. The competition - meat, milk, cheese, butter and eggs - has
been duly demonised by the appropriate government bodies. Soy serves as meat
and milk for a new generation of virtuous vegetarians.
Marketing costs money, especially when it needs to be bolstered with
"research", but there's plenty of funds available. All soybean producers pay
a mandatory assessment of one-half to one per cent of the net market price
of soybeans. The total - something like US$80 million annually4 - supports
United Soybean's program to "strengthen the position of soybeans in the
marketplace and maintain and expand domestic and foreign markets for uses
for soybeans and soybean products". State soybean councils from Maryland,
Nebraska, Delaware, Arkansas, Virginia, North Dakota and Michigan provide
another $2.5 million for "research".5 Private companies like Archer Daniels
Midland also contribute their share. ADM spent $4.7 million for advertising
on Meet the Press and $4.3 million on Face the Nation during the course of a
year.6 Public relations firms help convert research projects into newspaper
articles and advertising copy, and law firms lobby for favorable government
regulations. IMF money funds soy processing plants in foreign countries, and
free trade policies keep soybean abundance flowing to overseas destinations.
The push for more soy has been relentless and global in its reach. Soy
protein is now found in most supermarket breads. It is being used to
transform "the humble tortilla, Mexico's corn-based staple food, into a
protein-fortified 'super-tortilla' that would give a nutritional boost to
the nearly 20 million Mexicans who live in extreme poverty".7 Advertising
for a new soy-enriched loaf from Allied Bakeries in Britain targets
menopausal women seeking relief from hot flushes. Sales are running at a
quarter of a million loaves per week.8
The soy industry hired Norman Robert Associates, a public relations firm, to
"get more soy products onto school menus".9 The USDA responded with a
proposal to scrap the 30 per cent limit for soy in school lunches. The
NuMenu program would allow unlimited use of soy in student meals. With soy
added to hamburgers, tacos and lasagna, dieticians can get the total fat
content below 30 per cent of calories, thereby conforming to government
dictates. "With the soy-enhanced food items, students are receiving better
servings of nutrients and less cholesterol and fat."
Soy milk has posted the biggest gains, soaring from $2 million in 1980 to
$300 million in the US last year.10 Recent advances in processing have
transformed the gray, thin, bitter, beany-tasting Asian beverage into a
product that Western consumers will accept - one that tastes like a
milkshake, but without the guilt.
Processing miracles, good packaging, massive advertising and a marketing
strategy that stresses the products' possible health benefits account for
increasing sales to all age groups. For example, reports that soy helps
prevent prostate cancer have made soy milk acceptable to middle-aged men.
"You don't have to twist the arm of a 55- to 60-year-old guy to get him to
try soy milk," says Mark Messina. Michael Milken, former junk bond
financier, has helped the industry shed its hippie image with
well-publicized efforts to consume 40 grams of soy protein daily.
America today, tomorrow the world. Soy milk sales are rising in Canada, even
though soy milk there costs twice as much as cow's milk. Soybean milk
processing plants are sprouting up in places like Kenya.11 Even China, where
soy really is a poverty food and whose people want more meat, not tofu, has
opted to build Western-style soy factories rather than develop western
grasslands for grazing animals.12
Cinderella's Dark Side
The propaganda that has created the soy sales miracle is all the more
remarkable because, only a few decades ago, the soybean was considered unfit
to eat - even in Asia. During the Chou Dynasty (1134-246 BC) the soybean was
designated one of the five sacred grains, along with barley, wheat, millet
and rice. However, the pictograph for the soybean, which dates from earlier
times, indicates that it was not first used as a food; for whereas the
pictographs for the other four grains show the seed and stem structure of
the plant, the pictograph for the soybean emphasizes the root structure.
Agricultural literature of the period speaks frequently of the soybean and
its use in crop rotation. Apparently the soy plant was initially used as a
method of fixing nitrogen.13
The soybean did not serve as a food until the discovery of fermentation
techniques, some time during the Chou Dynasty. The first soy foods were
fermented products like tempeh, natto, miso and soy sauce. At a later date,
possibly in the 2nd century BC, Chinese scientists discovered that a pur�e
of cooked soybeans could be precipitated with calcium sulfate or magnesium
sulfate (plaster of Paris or Epsom salts) to make a smooth, pale curd - tofu
or bean curd. The use of fermented and precipitated soy products soon spread
to other parts of the Orient, notably Japan and Indonesia.
The Chinese did not eat unfermented soybeans as they did other legumes such
as lentils because the soybean contains large quantities of natural toxins
or "antinutrients". First among them are potent enzyme inhibitors that block
the action of trypsin and other enzymes needed for protein digestion. These
inhibitors are large, tightly folded proteins that are not completely
deactivated during ordinary cooking. They can produce serious gastric
distress, reduced protein digestion and chronic deficiencies in amino acid
uptake. In test animals, diets high in trypsin inhibitors cause enlargement
and pathological conditions of the pancreas, including cancer.14
Soybeans also contain haemagglutinin, a clot-promoting substance that causes
red blood cells to clump together.
Trypsin inhibitors and haemagglutinin are growth inhibitors. Weanling rats
fed soy containing these antinutrients fail to grow normally.
Growth-depressant compounds are deactivated during the process of
fermentation, so once the Chinese discovered how to ferment the soybean,
they began to incorporate soy foods into their diets. In precipitated
products, enzyme inhibitors concentrate in the soaking liquid rather than in
the curd. Thus, in tofu and bean curd, growth depressants are reduced in
quantity but not completely eliminated.
Soy also contains goitrogens - substances that depress thyroid function.
Soybeans are high in phytic acid, present in the bran or hulls of all seeds.
It's a substance that can block the uptake of essential minerals - calcium,
magnesium, copper, iron and especially zinc - in the intestinal tract.
Although not a household word, phytic acid has been extensively studied;
there are literally hundreds of articles on the effects of phytic acid in
the current scientific literature. Scientists are in general agreement that
grain- and legume-based diets high in phytates contribute to widespread
mineral deficiencies in third world countries.15 Analysis shows that
calcium, magnesium, iron and zinc are present in the plant foods eaten in
these areas, but the high phytate content of soy- and grain-based diets
prevents their absorption.
The soybean has one of the highest phytate levels of any grain or legume
that has been studied,16 and the phytates in soy are highly resistant to
normal phytate-reducing techniques such as long, slow cooking.17 Only a long
period of fermentation will significantly reduce the phytate content of
soybeans. When precipitated soy products like tofu are consumed with meat,
the mineral-blocking effects of the phytates are reduced.18 The Japanese
traditionally eat a small amount of tofu or miso as part of a mineral-rich
fish broth, followed by a serving of meat or fish.
Vegetarians who consume tofu and bean curd as a substitute for meat and
dairy products risk severe mineral deficiencies. The results of calcium,
magnesium and iron deficiency are well known; those of zinc are less so.
Zinc is called the intelligence mineral because it is needed for optimal
development and functioning of the brain and nervous system. It plays a role
in protein synthesis and collagen formation; it is involved in the
blood-sugar control mechanism and thus protects against diabetes; it is
needed for a healthy reproductive system. Zinc is a key component in
numerous vital enzymes and plays a role in the immune system. Phytates found
in soy products interfere with zinc absorption more completely than with
other minerals.19 Zinc deficiency can cause a "spacey" feeling that some
vegetarians may mistake for the "high" of spiritual enlightenment.
Milk drinking is given as the reason why second-generation Japanese in
America grow taller than their native ancestors. Some investigators
postulate that the reduced phytate content of the American diet - whatever
may be its other deficiencies - is the true explanation, pointing out that
both Asian and Western children who do not get enough meat and fish products
to counteract the effects of a high phytate diet, frequently suffer rickets,
stunting and other growth problems.20
Soy Protein Isolate: Not So Friendly
Soy processors have worked hard to get these antinutrients out of the
finished product, particularly soy protein isolate (SPI) which is the key
ingredient in most soy foods that imitate meat and dairy products, including
baby formulas and some brands of soy milk.
SPI is not something you can make in your own kitchen. Production takes
place in industrial factories where a slurry of soy beans is first mixed
with an alkaline solution to remove fiber, then precipitated and separated
using an acid wash and, finally, neutralized in an alkaline solution. Acid
washing in aluminum tanks leaches high levels of aluminum into the final
product. The resultant curds are spray- dried at high temperatures to
produce a high-protein powder. A final indignity to the original soybean is
high-temperature, high-pressure extrusion processing of soy protein isolate
to produce textured vegetable protein (TVP).
Much of the trypsin inhibitor content can be removed through
high-temperature processing, but not all. Trypsin inhibitor content of soy
protein isolate can vary as much as fivefold.21 (In rats, even low-level
trypsin inhibitor SPI feeding results in reduced weight gain compared to
controls.22) But high-temperature processing has the unfortunate side-effect
of so denaturing the other proteins in soy that they are rendered largely
ineffective.23 That's why animals on soy feed need lysine supplements for
normal growth.
Nitrites, which are potent carcinogens, are formed during spray-drying, and
a toxin called lysinoalanine is formed during alkaline processing.24
Numerous artificial flavorings, particularly MSG, are added to soy protein
isolate and textured vegetable protein products to mask their strong "beany"
taste and to impart the flavor of meat.25
In feeding experiments, the use of SPI increased requirements for vitamins
E, K, D and B12 and created deficiency symptoms of calcium, magnesium,
manganese, molybdenum, copper, iron and zinc.26 Phytic acid remaining in
these soy products greatly inhibits zinc and iron absorption; test animals
fed SPI develop enlarged organs, particularly the pancreas and thyroid
gland, and increased deposition of fatty acids in the liver.27
Yet soy protein isolate and textured vegetable protein are used extensively
in school lunch programs, commercial baked goods, diet beverages and fast
food products. They are heavily promoted in third world countries and form
the basis of many food giveaway programs.
In spite of poor results in animal feeding trials, the soy industry has
sponsored a number of studies designed to show that soy protein products can
be used in human diets as a replacement for traditional foods. An example is
"Nutritional Quality of Soy Bean Protein Isolates: Studies in Children of
Preschool Age", sponsored by the Ralston Purina Company.28 A group of
Central American children suffering from malnutrition was first stabilized
and brought into better health by feeding them native foods, including meat
and dairy products. Then, for a two-week period, these traditional foods
were replaced by a drink made of soy protein isolate and sugar. All nitrogen
taken in and all nitrogen excreted was measured in truly Orwellian fashion:
the children were weighed naked every morning, and all excrement and vomit
gathered up for analysis. The researchers found that the children retained
nitrogen and that their growth was "adequate", so the experiment was
declared a success.
Whether the children were actually healthy on such a diet, or could remain
so over a long period, is another matter. The researchers noted that the
children vomited "occasionally", usually after finishing a meal; that over
half suffered from periods of moderate diarrhea; that some had upper
respiratory infections; and that others suffered from rash and fever.
It should be noted that the researchers did not dare to use soy products to
help the children recover from malnutrition, and were obliged to supplement
the soy-sugar mixture with nutrients largely absent in soy products -
notably, vitamins A, D and B12, iron, iodine and zinc.
FDA Health Claim Challenged
The best marketing strategy for a product that is inherently unhealthy is,
of course, a health claim.
"The road to FDA approval," writes a soy apologist, "was long and demanding,
consisting of a detailed review of human clinical data collected from more
than 40 scientific studies conducted over the last 20 years. Soy protein was
found to be one of the rare foods that had sufficient scientific evidence
not only to qualify for an FDA health claim proposal but to ultimately pass
the rigorous approval process."29
The "long and demanding" road to FDA approval actually took a few unexpected
turns. The original petition, submitted by Protein Technology International,
requested a health claim for isoflavones, the estrogen-like compounds found
plentifully in soybeans, based on assertions that "only soy protein that has
been processed in a manner in which isoflavones are retained will result in
cholesterol lowering". In 1998, the FDA made the unprecedented move of
rewriting PTI's petition, removing any reference to the phyto-estrogens and
substituting a claim for soy protein - a move that was in direct
contradiction to the agency's regulations. The FDA is authorized to make
rulings only on substances presented by petition.
The abrupt change in direction was no doubt due to the fact that a number of
researchers, including scientists employed by the US Government, submitted
documents indicating that isoflavones are toxic.
The FDA had also received, early in 1998, the final British Government
report on phytoestrogens, which failed to find much evidence of benefit and
warned against potential adverse effects.30
Even with the change to soy protein isolate, FDA bureaucrats engaged in the
"rigorous approval process" were forced to deal nimbly with concerns about
mineral blocking effects, enzyme inhibitors, goitrogenicity, endocrine
disruption, reproductive problems and increased allergic reactions from
consumption of soy products.31
One of the strongest letters of protest came from Dr Dan Sheehan and Dr
Daniel Doerge, government researchers at the National Center for
Toxicological Research.32 Their pleas for warning labels were dismissed as
unwarranted.
"Sufficient scientific evidence" of soy's cholesterol-lowering properties is
drawn largely from a 1995 meta-analysis by Dr James Anderson, sponsored by
Protein Technologies International and published in the New England Journal
of Medicine.33
A meta-analysis is a review and summary of the results of many clinical
studies on the same subject. Use of meta-analyses to draw general
conclusions has come under sharp criticism by members of the scientific
community. "Researchers substituting meta-analysis for more rigorous trials
risk making faulty assumptions and indulging in creative accounting," says
Sir John Scott, President of the Royal Society of New Zealand. "Like is not
being lumped with like. Little lumps and big lumps of data are being
gathered together by various groups."34
There is the added temptation for researchers, particularly researchers
funded by a company like Protein Technologies International, to leave out
studies that would prevent the desired conclusions. Dr Anderson discarded
eight studies for various reasons, leaving a remainder of twenty-nine. The
published report suggested that individuals with cholesterol levels over 250
mg/dl would experience a "significant" reduction of 7 to 20 per cent in
levels of serum cholesterol if they substituted soy protein for animal
protein. Cholesterol reduction was insignificant for individuals whose
cholesterol was lower than 250 mg/dl.
In other words, for most of us, giving up steak and eating vegieburgers
instead will not bring down blood cholesterol levels. The health claim that
the FDA approved "after detailed review of human clinical data" fails to
inform the consumer about these important details.
Research that ties soy to positive effects on cholesterol levels is
"incredibly immature", said Ronald M. Krauss, MD, head of the Molecular
Medical Research Program and Lawrence Berkeley National Laboratory.35 He
might have added that studies in which cholesterol levels were lowered
through either diet or drugs have consistently resulted in a greater number
of deaths in the treatment groups than in controls - deaths from stroke,
cancer, intestinal disorders, accident and suicide.36 Cholesterol-lowering
measures in the US have fuelled a $60 billion per year cholesterol-lowering
industry, but have not saved us from the ravages of heart disease.
Soy And Cancer
The new FDA ruling does not allow any claims about cancer prevention on food
packages, but that has not restrained the industry and its marketers from
making them in their promotional literature.
"In addition to protecting the heart," says a vitamin company brochure, "soy
has demonstrated powerful anticancer benefits...the Japanese, who eat 30
times as much soy as North Americans, have a lower incidence of cancers of
the breast, uterus and prostate."37
Indeed they do. But the Japanese, and Asians in general, have much higher
rates of other types of cancer, particularly cancer of the esophagus,
stomach, pancreas and liver.38 Asians throughout the world also have high
rates of thyroid cancer.39 The logic that links low rates of reproductive
cancers to soy consumption requires attribution of high rates of thyroid and
digestive cancers to the same foods, particularly as soy causes these types
of cancers in laboratory rats.
Just how much soy do Asians eat? A 1998 survey found that the average daily
amount of soy protein consumed in Japan was about eight grams for men and
seven for women - less than two teaspoons.40 The famous Cornell China Study,
conducted by Colin T. Campbell, found that legume consumption in China
varied from 0 to 58 grams per day, with a mean of about twelve.41 Assuming
that two-thirds of legume consumption is soy, then the maximum consumption
is about 40 grams, or less than three tablespoons per day, with an average
consumption of about nine grams, or less than two teaspoons. A survey
conducted in the 1930s found that soy foods accounted for only 1.5 per cent
of calories in the Chinese diet, compared with 65 per cent of calories from
pork.42 (Asians traditionally cooked with lard, not vegetable oil!)
Traditionally fermented soy products make a delicious, natural seasoning
that may supply important nutritional factors in the Asian diet. But except
in times of famine, Asians consume soy products only in small amounts, as
condiments, and not as a replacement for animal foods - with one exception.
Celibate monks living in monasteries and leading a vegetarian lifestyle find
soy foods quite helpful because they dampen libido.
It was a 1994 meta-analysis by Mark Messina, published in Nutrition and
Cancer, that fuelled speculation on soy's anticarcinogenic properties.43
Messina noted that in 26 animal studies, 65 per cent reported protective
effects from soy. He conveniently neglected to include at least one study in
which soy feeding caused pancreatic cancer - the 1985 study by Rackis.44 In
the human studies he listed, the results were mixed. A few showed some
protective effect, but most showed no correlation at all between soy
consumption and cancer rates. He concluded that "the data in this review
cannot be used as a basis for claiming that soy intake decreases cancer
risk". Yet in his subsequent book, The Simple Soybean and Your Health,
Messina makes just such a claim, recommending one cup or 230 grams of soy
products per day in his "optimal" diet as a way to prevent cancer.
Thousands of women are now consuming soy in the belief that it protects them
against breast cancer. Yet, in 1996, researchers found that women consuming
soy protein isolate had an increased incidence of epithelial hyperplasia, a
condition that presages malignancies.45 A year later, dietary genistein was
found to stimulate breast cells to enter the cell cycle - a discovery that
led the study authors to conclude that women should not consume soy products
to prevent breast cancer.46
Phytoestrogens: Panacea Or Poison?
The male species of tropical birds carries the drab plumage of the female at
birth and 'colors up' at maturity, somewhere between nine and 24 months.
In 1991, Richard and Valerie James, bird breeders in Whangerai, New Zealand,
purchased a new kind of feed for their birds - one based largely on soy
protein.47 When soy-based feed was used, their birds 'colored up' after just
a few months. In fact, one bird-food manufacturer claimed that this early
development was an advantage imparted by the feed. A 1992 ad for Roudybush
feed formula showed a picture of the male crimson rosella, an Australian
parrot that acquires beautiful red plumage at 18 to 24 months, already
brightly colored at 11 weeks old.
Unfortunately, in the ensuing years, there was decreased fertility in the
birds, with precocious maturation, deformed, stunted and stillborn babies,
and premature deaths, especially among females, with the result that the
total population in the aviaries went into steady decline. The birds
suffered beak and bone deformities, goiter, immune system disorders and
pathological, aggressive behavior. Autopsy revealed digestive organs in a
state of disintegration. The list of problems corresponded with many of the
problems the Jameses had encountered in their two children, who had been fed
soy-based infant formula.
Startled, aghast, angry, the Jameses hired toxicologist Mike Fitzpatrick.
PhD, to investigate further. Dr Fitzpatrick's literature review uncovered
evidence that soy consumption has been linked to numerous disorders,
including infertility, increased cancer and infantile leukemia; and, in
studies dating back to the 1950s,48 that genistein in soy causes endocrine
disruption in animals. Dr Fitzpatrick also analyzed the bird feed and found
that it contained high levels of phytoestrogens, especially genistein. When
the Jameses discontinued using soy-based feed, the flock gradually returned
to normal breeding habits and behavior.
The Jameses embarked on a private crusade to warn the public and government
officials about toxins in soy foods, particularly the endocrine-disrupting
isoflavones, genistein and diadzen. Protein Technology International
received their material in 1994.
In 1991, Japanese researchers reported that consumption of as little as 30
grams or two tablespoons of soybeans per day for only one month resulted in
a significant increase in thyroid-stimulating hormone.49 Diffuse goiter and
hypothyroidism appeared in some of the subjects and many complained of
constipation, fatigue and lethargy, even though their intake of iodine was
adequate. In 1997, researchers from the FDA's National Center for
Toxicological Research made the embarrassing discovery that the goitrogenic
components of soy were the very same isoflavones.50
Twenty-five grams of soy protein isolate, the minimum amount PTI claimed to
have cholesterol-lowering effects, contains from 50 to 70 mg of isoflavones.
It took only 45 mg of isoflavones in premenopausal women to exert
significant biological effects, including a reduction in hormones needed for
adequate thyroid function. These effects lingered for three months after soy
consumption was discontinued.51
One hundred grams of soy protein - the maximum suggested
cholesterol-lowering dose, and the amount recommended by Protein
Technologies International - can contain almost 600 mg of isoflavones,52 an
amount that is undeniably toxic. In 1992, the Swiss health service estimated
that 100 grams of soy protein provided the estrogenic equivalent of the
Pill.53
In vitro studies suggest that isoflavones inhibit synthesis of estradiol and
other steroid hormones.54 Reproductive problems, infertility, thyroid
disease and liver disease due to dietary intake of isoflavones have been
observed for several species of animals including mice, cheetah, quail,
pigs, rats, sturgeon and sheep.55
It is the isoflavones in soy that are said to have a favorable effect on
postmenopausal symptoms, including hot flushes, and protection from
osteoporosis. Quantification of discomfort from hot flushes is extremely
subjective, and most studies show that control subjects report reduction in
discomfort in amounts equal to subjects given soy.56 The claim that soy
prevents osteoporosis is extraordinary, given that soy foods block calcium
and cause vitamin D deficiencies. If Asians indeed have lower rates of
osteoporosis than Westerners, it is because their diet provides plenty of
vitamin D from shrimp, lard and seafood, and plenty of calcium from bone
broths. The reason that Westerners have such high rates of osteoporosis is
because they have substituted soy oil for butter, which is a traditional
source of vitamin D and other fat-soluble activators needed for calcium
absorption.
Birth Control Pills For Babies
But it was the isoflavones in infant formula that gave the Jameses the most
cause for concern. In 1998, investigators reported that the daily exposure
of infants to isoflavones in soy infant formula is 6 to11 times higher on a
body-weight basis than the dose that has hormonal effects in adults
consuming soy foods. Circulating concentrations of isoflavones in infants
fed soy-based formula were 13,000 to 22,000 times higher than plasma
estradiol concentrations in infants on cow's milk formula.57
Approximately 25 per cent of bottle-fed children in the US receive soy-based
formula - a much higher percentage than in other parts of the Western world.
Fitzpatrick estimated that an infant exclusively fed soy formula receives
the estrogenic equivalent (based on body weight) of at least five birth
control pills per day.58 By contrast, almost no phytoestrogens have been
detected in dairy-based infant formula or in human milk, even when the
mother consumes soy products.
Scientists have known for years that soy-based formula can cause thyroid
problems in babies. But what are the effects of soy products on the hormonal
development of the infant, both male and female?
Male infants undergo a "testosterone surge" during the first few months of
life, when testosterone levels may be as high as those of an adult male.
During this period, the infant is programmed to express male characteristics
after puberty, not only in the development of his sexual organs and other
masculine physical traits, but also in setting patterns in the brain
characteristic of male behavior. In monkeys, deficiency of male hormones
impairs the development of spatial perception (which, in humans, is normally
more acute in men than in women), of learning ability and of visual
discrimination tasks (such as would be required for reading).59 It goes
without saying that future patterns of sexual orientation may also be
influenced by the early hormonal environment. Male children exposed during
gestation to diethylstilbestrol (DES), a synthetic estrogen that has effects
on animals similar to those of phytoestrogens from soy, had testes smaller
than normal on manturation.60
Learning disabilities, especially in male children, have reached epidemic
proportions. Soy infant feeding - which began in earnest in the early
1970s - cannot be ignored as a probable cause for these tragic developments.
As for girls, an alarming number are entering puberty much earlier than
normal, according to a recent study reported in the journal Pediatrics.61
Investigators found that one per cent of all girls now show signs of
puberty, such as breast development or pubic hair, before the age of three;
by age eight, 14.7 per cent of white girls and almost 50 per cent of
African-American girls have one or both of these characteristics.
New data indicate that environmental estrogens such as PCBs and DDE (a
breakdown product of DDT) may cause early sexual development in girls.62 In
the 1986 Puerto Rico Premature Thelarche study, the most significant dietary
association with premature sexual development was not chicken - as reported
in the press - but soy infant formula.63
The consequences of this truncated childhood are tragic. Young girls with
mature bodies must cope with feelings and urges that most children are not
well-equipped to handle. And early maturation in girls is frequently a
harbinger for problems with the reproductive system later in life, including
failure to menstruate, infertility and breast cancer.
Parents who have contacted the Jameses recount other problems associated
with children of both sexes who were fed soy-based formula, including
extreme emotional behavior, asthma, immune system problems, pituitary
insufficiency, thyroid disorders and irritable bowel syndrome - the same
endocrine and digestive havoc that afflicted the Jameses' parrots.
Dissension In The Ranks
Organizers of the Third International Soy Symposium would be hard-pressed to
call the conference an unqualified success. On the second day of the
symposium, the London-based Food Commission and the Weston A. Price
Foundation of Washington, DC, held a joint press conference, in the same
hotel as the symposium, to present concerns about soy infant formula.
Industry representatives sat stony-faced through the recitation of potential
dangers and a plea from concerned scientists and parents to pull soy-based
infant formula from the market. Under pressure from the Jameses, the New
Zealand Government had issued a health warning about soy infant formula in
1998; it was time for the American government to do the same.
On the last day of the symposium, presentations on new findings related to
toxicity sent a well-oxygenated chill through the giddy helium hype. Dr Lon
White reported on a study of Japanese Americans living in Hawaii, that
showed a significant statistical relationship between two or more servings
of tofu a week and "accelerated brain aging".64 Those participants who
consumed tofu in mid-life had lower cognitive function in late life and a
greater incidence of Alzheimer's disease and dementia. "What's more," said
Dr White, "those who ate a lot of tofu, by the time they were 75 or 80
looked five years older".65 White and his colleagues blamed the negative
effects on isoflavones - a finding that supports an earlier study in which
postmenopausal women with higher levels of circulating estrogen experienced
greater cognitive decline.66
Scientists Daniel Sheehan and Daniel Doerge, from the National Center for
Toxicological Research, ruined PTI's day by presenting findings from rat
feeding studies, indicating that genistein in soy foods causes irreversible
damage to enzymes that synthesise thyroid hormones.67 "The association
between soybean consumption and goiter in animals and humans has a long
history," wrote Dr Doerge. "Current evidence for the beneficial effects of
soy requires a full understanding of potential adverse effects as well."
Dr Claude Hughes reported that rats born to mothers that were fed genistein
had decreased birth weights compared to controls, and onset of puberty
occurred earlier in male offspring.68 His research suggested that the
effects observed in rats "...will be at least somewhat predictive of what
occurs in humans. There is no reason to assume that there will be gross
malformations of fetuses but there may be subtle changes, such as
neurobehavioral attributes, immune function and sex hormone levels." The
results, he said, "could be nothing or could be something of great
concern...if mom is eating something that can act like sex hormones, it is
logical to wonder if that could change the baby's development".69
A study of babies born to vegetarian mothers, published in January 2000,
indicated just what those changes in baby's development might be. Mothers
who ate a vegetarian diet during pregnancy had a fivefold greater risk of
delivering a boy with hypospadias, a birth defect of the penis.70 The
authors of the study suggested that the cause was greater exposure to
phytoestrogens in soy foods popular with vegetarians. Problems with female
offspring of vegetarian mothers are more likely to show up later in life.
While soy's estrogenic effect is less than that of diethylstilbestrol (DES),
the dose is likely to be higher because it's consumed as a food, not taken
as a drug. Daughters of women who took DES during pregnancy suffered from
infertility and cancer when they reached their twenties.
Question Marks Over Gras Status
Lurking in the background of industry hype for soy is the nagging question
of whether it's even legal to add soy protein isolate to food. All food
additives not in common use prior to 1958, including casein protein from
milk, must have GRAS (Generally Recognized As Safe) status. In 1972, the
Nixon administration directed a re-examination of substances believed to be
GRAS, in the light of any scientific information then available. This
re-examination included casein protein that became codified as GRAS in 1978.
In 1974, the FDA obtained a literature review of soy protein because, as soy
protein had not been used in food until 1959 and was not even in common use
in the early 1970s, it was not eligible to have its GRAS status
grandfathered under the provisions of the Food, Drug and Cosmetic Act.71
The scientific literature up to 1974 recognized many antinutrients in
factory-made soy protein, including trypsin inhibitors, phytic acid and
genistein. But the FDA literature review dismissed discussion of adverse
impacts, with the statement that it was important for "adequate processing"
to remove them. Genistein could be removed with an alcohol wash, but it was
an expensive procedure that processors avoided. Later studies determined
that trypsin inhibitor content could be removed only with long periods of
heat and pressure, but the FDA has imposed no requirements for manufacturers
to do so.
The FDA was more concerned with toxins formed during processing,
specifically nitrites and lysinoalanine.72 Even at low levels of
consumption - averaging one-third of a gram per day at the time - the
presence of these carcinogens was considered too great a threat to public
health to allow GRAS status.
Soy protein did have approval for use as a binder in cardboard boxes, and
this approval was allowed to continue, as researchers considered that
migration of nitrites from the box into the food contents would be too small
to constitute a cancer risk. FDA officials called for safety specifications
and monitoring procedures before granting of GRAS status for food. These
were never performed. To this day, use of soy protein is codified as GRAS
only for this limited industrial use as a cardboard binder. This means that
soy protein must be subject to premarket approval procedures each time
manufacturers intend to use it as a food or add it to a food.
Soy protein was introduced into infant formula in the early 1960s. It was a
new product with no history of any use at all. As soy protein did not have
GRAS status, premarket approval was required. This was not and still has not
been granted. The key ingredient of soy infant formula is not recognized as
safe.
The Next Asbestos?
"Against the backdrop of widespread praise...there is growing suspicion that
soy - despite its undisputed benefits - may pose some health hazards,"
writes Marian Burros, a leading food writer for the New York Times. More
than any other writer, Ms Burros's endorsement of a low-fat, largely
vegetarian diet has herded Americans into supermarket aisles featuring soy
foods. Yet her January 26, 2000 article, "Doubts Cloud Rosy News on Soy",
contains the following alarming statement: "Not one of the 18 scientists
interviewed for this column was willing to say that taking isoflavones was
risk free." Ms Burros did not enumerate the risks, nor did she mention that
the recommended 25 daily grams of soy protein contain enough isoflavones to
cause problems in sensitive individuals, but it was evident that the
industry had recognized the need to cover itself.
Because the industry is extremely exposed...contingency lawyers will soon
discover that the number of potential plaintiffs can be counted in the
millions and the pockets are very, very deep. Juries will hear something
like the following: "The industry has known for years that soy contains many
toxins. At first they told the public that the toxins were removed by
processing. When it became apparent that processing could not get rid of
them, they claimed that these substances were beneficial. Your government
granted a health claim to a substance that is poisonous, and the industry
lied to the public to sell more soy."
The "industry" includes merchants, manufacturers, scientists, publicists,
bureaucrats, former bond financiers, food writers, vitamin companies and
retail stores. Farmers will probably escape because they were duped like the
rest of us. But they need to find something else to grow before the soy
bubble bursts and the market collapses: grass-fed livestock, designer
vegetables...or hemp to make paper for thousands and thousands of legal
briefs.
Extracted from Nexus Magazine, Volume 7, Number 3 (April-May 2000)
COMMENT: Sally Fallon and Dr. Enig are to be highly commended for this much
needed soy update. Together they have compiled the most definitive document
to date on why one should avoid soy. This is a MAJOR work and I am hoping to
promote it for the national media attention that it deserves.
ENDNOTES:
1. Program for the Third International Symposium on the Role of Soy in
Preventing and Treating Chronic Disease, Sunday, October 31, through
Wednesday, November 3, 1999, Omni Shoreham Hotel, Washington, DC.
2. Houghton, Dean, "Healthful Harvest", The Furrow, January 2000, pp. 10-13.
3. Coleman, Richard J., "Vegetable Protein - A Delayed Birth?" Journal of
the American Oil Chemists' Society 52:238A, April 1975.
4. See www/unitedsoybean.org.
5. These are listed in www.soyonlineservice.co.nz.
6. Wall Street Journal, October 27, 1995.
7. Smith, James F., "Healthier tortillas could lead to healthier Mexico",
Denver Post, August 22, 1999, p. 26A.
8. "Bakery says new loaf can help reduce hot flushes", Reuters, September
15, 1997.
9. "Beefing Up Burgers with Soy Products at School", Nutrition Week,
Community Nutrition Institute, Washington, DC, June 5, 1998, p. 2.
10. Urquhart, John, "A Health Food Hits Big Time", Wall Street Journal,
August 3, 1999, p. B1
11. "Soyabean Milk Plant in Kenya", Africa News Service, September 1998.
12. Simoons, Frederick J., Food in China: A Cultural and Historical Inquiry,
CRC Press, Boca Raton, 1991, p. 64.
13. Katz, Solomon H., "Food and Biocultural Evolution: A Model for the
Investigation of Modern Nutritional Problems", Nutritional Anthropology,
Alan R. Liss Inc., 1987, p. 50.
14. Rackis, Joseph J. et al., "The USDA trypsin inhibitor study. I.
Background, objectives and procedural details", Qualification of Plant Foods
in Human Nutrition, vol. 35, 1985.
15. Van Rensburg et al., "Nutritional status of African populations
predisposed to esophageal cancer", Nutrition and Cancer, vol. 4, 1983, pp.
206-216; Moser, P.B. et al., "Copper, iron, zinc and selenium dietary intake
and status of Nepalese lactating women and their breastfed infants",
American Journal of Clinical Nutrition 47:729-734, April 1988; Harland, B.F.
et al., "Nutritional status and phytate: zinc and phytate X calcium: zinc
dietary molar ratios of lacto-ovovegetarian Trappist monks: 10 years later",
Journal of the American Dietetic Association 88:1562-1566, December 1988.
16. El Tiney, A.H., "Proximate Composition and Mineral and Phytate Contents
of Legumes Grown in Sudan", Journal of Food Composition and Analysis (1989)
2:6778.
17. Ologhobo, A.D. et al., "Distribution of phosphorus and phytate in some
Nigerian varieties of legumes and some effects of processing", Journal of
Food Science 49(1):199-201, January/February 1984.
18. Sandstrom, B. et al., "Effect of protein level and protein source on
zinc absorption in humans", Journal of Nutrition 119(1):48-53, January 1989;
Tait, Susan et al., "The availability of minerals in food, with particular
reference to iron", Journal of Research in Society and Health 103(2):74-77,
April 1983.
19. Phytate reduction of zinc absorption has been demonstrated in numerous
studies. These results are summarised in Leviton, Richard, Tofu, Tempeh,
Miso and Other Soyfoods: The 'Food of the Future' - How to Enjoy Its
Spectacular Health Benefits, Keats Publishing, Inc., New Canaan, CT, USA,
1982, p. 1415.
20. Mellanby, Edward, "Experimental rickets: The effect of cereals and their
interaction with other factors of diet and environment in producing
rickets", Journal of the Medical Research Council 93:265, March 1925; Wills,
M.R. et al., "Phytic Acid and Nutritional Rickets in Immigrants", The
Lancet, April 8,1972, pp. 771-773.
21. Rackis et al., ibid.
22. Rackis et al., ibid., p. 232.
23. Wallace, G.M., "Studies on the Processing and Properties of Soymilk",
Journal of Science and Food Agriculture 22:526-535, October 1971.
24. Rackis, et al., ibid., p. 22; "Evaluation of the Health Aspects of Soy
Protein Isolates as Food Ingredients", prepared for FDA by Life Sciences
Research Office, Federation of American Societies for Experimental Biology
(9650 Rockville Pike, Bethesda, MD 20014), USA, Contract No. FDA
223-75-2004, 1979.
25. See www/truthinlabeling.org.
26. Rackis, Joseph, J., "Biological and Physiological Factors in Soybeans",
Journal of the American Oil Chemists' Society 51:161A-170A, January 1974.
27. Rackis, Joseph J. et al., "The USDA trypsin inhibitor study", ibid.
28. Torum, Benjamin, "Nutritional Quality of Soybean Protein Isolates:
Studies in Children of Preschool Age", in Soy Protein and Human Nutrition,
Harold L Wilcke et al. (eds), Academic Press, New York, 1979.
29. Zreik, Marwin, CCN, "The Great Soy Protein Awakening", Total Health
32(1), February 2000.
30. IEH Assessment on Phytoestrogens in the Human Diet, Final Report to the
Ministry of Agriculture, Fisheries and Food, UK, November 1997, p. 11.
31. Food Labeling: Health Claims: Soy Protein and Coronary Heart Disease,
Food and Drug Administration 21 CFR, Part 101 (Docket No. 98P-0683).
32. Sheegan, Daniel M. and Daniel R Doerge, Letter to Dockets Management
Branch (HFA-305), February 18, 1999.
33. Anderson, James W. et al., "Meta-analysis of the Effects of Soy Protein
Intake on Serum Lipids", New England Journal of Medicine (1995)
333:(5):276-282.
34. Guy, Camille, "Doctors warned against magic, quackery", New Zealand
Herald, September 9, 1995, section 8, p. 5.
35. Sander, Kate and Hilary Wilson, "FDA approves new health claim for soy,
but litte fallout expected for dairy", Cheese Market News, October 22, 1999,
p. 24.
36. Enig, Mary G. and Sally Fallon, "The Oiling of America", NEXUS Magazine,
December 1998-January 1999 and February-March 1999; also available at
www.WestonAPrice.org.
37. Natural Medicine News (L & H Vitamins, 32-33 47th Avenue, Long Island
City, NY 11101), USA, January/February 2000, p. 8.
38. Harras, Angela (ed.), Cancer Rates and Risks, National Institutes of
Health, National Cancer Institute, 1996, 4th edition.
39. Searle, Charles E. (ed.), Chemical Carcinogens, ACS Monograph 173,
American Chemical Society, Washington, DC, 1976.
40. Nagata, C. et al., Journal of Nutrition (1998) 128:209-213.
41. Campbell, Colin T. et al., The Cornell Project in China.
42. Chang, K.C. (ed.), Food in Chinese Culture: Anthropological and
Historical Perspectives, New Haven, 1977.
43. Messina, Mark J. et al., "Soy Intake and Cancer Risk: A Review of the In
Vitro and In Vivo Data", Nutrition and Cancer (1994) 21(2):113-131.
44. Rackis et al, "The USDA trypsin inhibitor study", ibid.
45. Petrakis, N.L. et al., "Stimulatory influence of soy protein isolate on
breast secretion in pre- and post-menopausal women", Cancer Epid. Bio. Prev.
(1996) 5:785-794.
46. Dees, C. et al., "Dietary estrogens stimulate human breast cells to
enter the cell cycle", Environmental Health Perspectives (1997) 105(Suppl.
3):633-636.
47. Woodhams, D.J., "Phytoestrogens and parrots: The anatomy of an
investigation", Proceedings of the Nutrition Society of New Zealand (1995)
20:22-30.
48. Matrone, G. et al., "Effect of Genistin on Growth and Development of the
Male Mouse", Journal of Nutrition (1956) 235-240.
49. Ishizuki, Y. et al., "The effects on the thyroid gland of soybeans
administered experimentally in healthy subjects", Nippon Naibunpi Gakkai
Zasshi (1991) 767:622-629.
50. Divi, R.L. et al., "Anti-thyroid isoflavones from the soybean",
Biochemical Pharmacology (1997) 54:1087-1096.
51. Cassidy, A. et al., "Biological Effects of a Diet of Soy Protein Rich in
Isoflavones on the Menstrual Cycle of Premenopausal Women", American Journal
of Clinical Nutrition (1994) 60:333-340.
52. Murphy, P.A., "Phytoestrogen Content of Processed Soybean Foods", Food
Technology, January 1982, pp. 60-64.
53. Bulletin de L'Office F�d�ral de la Sant� Publique, no. 28, July 20,
1992.
54. Keung, W.M., "Dietary oestrogenic isoflavones are potent inhibitors of
B-hydroxysteroid dehydrogenase of P. testosteronii", Biochemical and
Biophysical Research Committee (1995) 215:1137-1144; Makela, S.I. et al.,
"Estrogen-specific 12 B-hydroxysteroid oxidoreductase type 1 (E.C. 1.1.1.62)
as a possible target for the action of phytoestrogens", PSEBM (1995)
208:51-59.
55. Setchell, K.D.R. et al., "Dietary oestrogens - a probable cause of
infertility and liver disease in captive cheetahs", Gastroenterology (1987)
93:225-233; Leopald, A.S., "Phytoestrogens: Adverse effects on reproduction
in California Quail," Science (1976) 191:98-100; Drane, H.M. et al.,
"Oestrogenic activity of soya-bean products", Food, Cosmetics and Technology
(1980) 18:425-427; Kimura, S. et al., "Development of malignant goiter by
defatted soybean with iodine-free diet in rats", Gann. (1976) 67:763-765;
Pelissero, C. et al., "Oestrogenic effect of dietary soybean meal on
vitellogenesis in cultured Siberian Sturgeon Acipenser baeri", Gen. Comp.
End. (1991) 83:447-457; Braden et al., "The oestrogenic activity and
metabolism of certain isoflavones in sheep", Australian J. Agricultural
Research (1967) 18:335-348.
56. Ginsburg, Jean and Giordana M. Prelevic, "Is there a proven place for
phytoestrogens in the menopause?", Climacteric (1999) 2:75-78.
57. Setchell, K.D. et al., "Isoflavone content of infant formulas and the
metabolic fate of these early phytoestrogens in early life", American
Journal of Clinical Nutrition, December 1998 Supplement, 1453S-1461S.
58. Irvine, C. et al., "The Potential Adverse Effects of Soybean
Phytoestrogens in Infant Feeding", New Zealand Medical Journal May 24, 1995,
p. 318.
59. Hagger, C. and J. Bachevalier, "Visual habit formation in 3-month-old
monkeys (Macaca mulatta): reversal of sex difference following neonatal
manipulations of androgen", Behavior and Brain Research (1991) 45:57-63.
60. Ross, R.K. et al., "Effect of in-utero exposure to diethylstilbestrol on
age at onset of puberty and on post-pubertal hormone levels in boys",
Canadian Medical Association Journal 128(10):1197-8, May 15, 1983.
61. Herman-Giddens, Marcia E. et al., "Secondary Sexual Characteristics and
Menses in Young Girls Seen in Office Practice: A Study from the Pediatric
Research in Office Settings Network", Pediatrics 99(4):505-512, April 1997.
62. Rachel's Environment & Health Weekly 263, "The Wingspread Statement",
Part 1, December 11, 1991; Colborn, Theo, Dianne Dumanoski and John Peterson
Myers, Our Stolen Future, Little, Brown & Company, London, 1996.
63. Freni-Titulaer, L.W., "Premature Thelarch in Puerto Rico: A search for
environmental factors", American Journal of Diseases of Children

"Richard Schulman" <ra.schulman-xyz@verizon.net> wrote in message
news:chc4jvo8paet3c2h0eapp6lnha0sen00gb@4ax.com...
> On Thu, 07 Aug 2003 05:47:54 GMT, molab@ww.co.nz (R Molony) wrote:
>
> >>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
> >>
> >Big problem Tofu contains other things besides soy.
> >Frequently aluminium sulphate or alum is illicitly included in the
> >coagulant used to gell the soy. The addition of aluminium helps to
> >give the tofu a much firmer texture.
> >
> >Surely this must complicate any statistical research demonstrating
> >neurotoxicity of Tofu products.
>
> This raises the question as to whether soy bean products generally may
> be tarnished by research findings that are properly applicable only to
> tofu. Certainly my initial reaction was to fall into that groove.
> ---
> Richard Schulman
> Remove antispamming "-xyz" for email reply


However I still believe the following is correct about soy-derived
phosphatidylserine benefits. I take the GNC PS 100 Phosphatidyl serine
complex but must add that the bottle does not indicate Soy as source.

Jack N Dalton

1: Nutr Neurosci  2002 Oct;5(5):337-43

Safety of soy-derived phosphatidylserine in elderly people.

Jorissen BL, Brouns F, Van Boxtel MP, Riedel WJ.
Department of Psychiatry and Neuropsychology, Brain and Behaviour Institute,
Universiteit Maastricht, The Netherlands.

Phosphatidylserine (PS) is a phospholipid which has been claimed to enhance
neuronal membrane function, and can be derived from several sources. Earlier
studies used brain cortex derived PS, of which the human tolerability of
300mg daily in 130 patients has been shown. The human tolerability of PS
derived from soybean has not been reported, although it is widely sold as a
nutritional supplement which may improve cognitive function in the elderly.
We report the results of a study of the safety of two dosages of
soy-phosphatidylserine (S-PS) in elderly. Subjects were 120 elderly of both
sexes who fulfilled the more stringent criteria for age-associated memory
impairment; some also fulfilled the criteria for age-associated cognitive
decline. Subjects were allocated at random to one of the three treatment
groups: placebo, 300 or 600 mg S-PS daily.  Standard biochemical and
hematological safety parameters, blood pressure, heart rate and adverse
events were assessed at baseline, after 6 and 12 weeks of treatment. No
significant differences were found in any of the outcome variables between
the treatment groups after Bonferonni-Holme correction. In conclusion, soy
derived PS is a safe nutritional supplement for older persons if taken up to
a dosage of 200 mg three times daily.

PMID: 12385596 [PubMed - in process]

<snip>

How common is this problem in Japan?

Tofu and miso are two staples of that land, so if there is a problem it
should be evident in that country.


--
to email me
Please remove "all your clothes"

Doug

Ian Goddard <igoddard@erols.mom> wrote in message news:<0v53jvsnc8c06r4jbe8030jfo6ostlegvg@4ax.com>...
> FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
[...]

also check this out: 

http://www.mercola.com/2000/oct/8/soy_crisis.htm

Dr. Joseph Mercola in the above article refers to reason for high
Aluminium in soy as follows:

"In addition, soy milk is high in aluminium. That's because the soy
protein isolate it's made from is acid-washed in aluminium tanks. No
wonder it tastes bad. "

-Anatoly

molab@ww.co.nz (R Molony) wrote:

>Ian Goddard <igoddard@erols.mom> wrote:
>>
>>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>>
>Big problem Tofu contains other things besides soy.
>Frequently aluminium sulphate or alum is illicitly included in the
>coagulant used to gell the soy. The addition of aluminium helps to
>give the tofu a much firmer texture.
>
>Surely this must complicate any statistical research demonstrating
>neurotoxicity of Tofu products.


  IAN: I doubt it. William Harris explored the question of
  aluminum's possible role in the findings of White et al:
  http://www.vegsource.com/harris/brain_aging.htm

  He had 16 soy products assayed for Al. Sure enough tofu
  was on the high side, at 15.99 parts per million. However,
  in the big picture that is not very remarkable. That's 
  16 micrograms of Al per gram of tofu. Estimates of daily 
  dietary Al intake range from 1.53 to 160 mg per person:
  http://www.inchem.org/documents/jecfa/jecmono/v12je04.htm

  So you'd have to eat about 2.2 lbs tofu/day to match the 
  high-end estimate of normal daily Al intake. Given that 
  White et al defined the high-end of tofu intake as two 
  or more servings per week, that would be below 2 lbs/day!
  And most likely "servings" among this Japanese American 
  cohort probably means meals wherein tofu is a component.

  That's not to say Al may not play a role in neurological 
  degeneration. I've posted a lot of evidence that it does:
http://www.google.com/groups?selm=gq8havshkhetd6s78ctbgvc8iev0gtma1n%404ax.com

  But given that there are many foods with as much or more 
  Al content than tofu as measured by Harris, and that 
  White et al tested ALL foods reported by the cohort and 
  only tofu produced a loud & clear statistically significant
  correlation to indicators of cognitive impairment and brain 
  atrophy, it stands to reason Al not producing that signal. 

  http://IanGoddard.net/journal.htm

  "To lengthen thy life, lessen thy meals." Ben Franklin

  Ongoing CR-monkey-study update: "In the monkeys...those on
  reduced feeding since the study started are dying at a rate 
  that is about half that of the monkeys receiving a full food
  ration." Associated Press: Eating less may extend human life.
  August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=- 

 

"Doug" <doug_adam@allyourclothesglobal.net.au> wrote:

><snip>
>
>How common is this problem in Japan?
>
>Tofu and miso are two staples of that land, so if there is a problem it
>should be evident in that country.


  IAN: But tofu isn't a Japanese "staple." According
  to Dr Mercola: "the Japanese don't eat that much soy: 
  a 1998 study showed that a Japanese man typically eats 
  about 8g (2 tsp) a day, nothing like the 220g (8oz) that 
  a Westerner could put away by eating a big chunk of tofu 
  and two glasses of soy milk." Link posted by Anatoly:
  http://www.mercola.com/2000/oct/8/soy_crisis.htm 

  While Alzheimer's disease is more common and vascular 
  dementia less common among Japanese Americans than among 
  native Japanese, [*] that doesn't tell us anything about 
  tofu's relationship to dementia. You'd have to examine the 
  relationship between dementia and tofu (soy) consumption
  in Japan, controlling for various facts as White et al 
  did in the Japanese American cohort they examined. 

[*]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8805729&dopt=Abstract

  http://IanGoddard.net/journal.htm

  "Our greatest illusion is to believe that we are what 
   we think ourselves to be." Henri Amiel (1821-1881)

  

wiretransfers@yahoo.com (Anatoly) wrote:

>Ian Goddard <igoddard@erols.mom> wrote in message news:<0v53jvsnc8c06r4jbe8030jfo6ostlegvg@4ax.com>...
>> FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>[...]
>
>also check this out: 
>
>http://www.mercola.com/2000/oct/8/soy_crisis.htm
>
>Dr. Joseph Mercola in the above article refers to reason for high
>Aluminium in soy as follows:
>
>"In addition, soy milk is high in aluminium. That's because the soy
>protein isolate it's made from is acid-washed in aluminium tanks. No
>wonder it tastes bad. "

It's made in food-grade STAINLESS STEEL tanks.  Mercola is a
clueless fool. 



Tsu

--
To doubt everything or to believe everything
are two equally convenient solutions; both
dispense with the necessity of reflection.
- Jules Henri Poincar�

Tsu Dho Nimh <tsudhonimh@lumbercartel.com> wrote:

>wiretransfers@yahoo.com (Anatoly) wrote:
>
>>Ian Goddard <igoddard@erols.mom> wrote in message news:<0v53jvsnc8c06r4jbe8030jfo6ostlegvg@4ax.com>...
>>> FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>>[...]
>>
>>also check this out: 
>>
>>http://www.mercola.com/2000/oct/8/soy_crisis.htm
>>
>>Dr. Joseph Mercola in the above article refers to reason for high
>>Aluminium in soy as follows:
>>
>>"In addition, soy milk is high in aluminium. That's because the soy
>>protein isolate it's made from is acid-washed in aluminium tanks. No
>>wonder it tastes bad. "
>
>It's made in food-grade STAINLESS STEEL tanks.  Mercola is a
>clueless fool. 

But it's still METAL, and an even heavier metal than aluminium. It
must be bad, especially if it gets into the mouth, where no metals
should go.

--
Peter Bowditch peterb@ratbags.com
The Millenium Project    http://www.ratbags.com/rsoles
The Green Light          http://www.ratbags.com/greenlight
I'm a Bright. Are you?

Jack, the two articles you posted

>The Trouble With Tofu: Soy and the Brain
>By John D. MacArthur

and 

>Newest Research On Why You Should Avoid Soy
>by Sally Fallon email: SAFallon@aol.com & Mary G. Enig, PhD email:
>MGEnig@aol.com

are truly astonishing, not only for their scientific interest and
relevance but also as political scandals and likely fodder for the
plaintiff bar.

One of the first things I'm going to do in the wake of reading these
two pieces is to contact our school district to inquire what soy
products are currently being used in the district's lunch programs.

---
Richard Schulman
Remove antispamming "-xyz" for email reply

On Fri, 08 Aug 2003 04:50:53 GMT, Richard Schulman
<ra.schulman-xyz@verizon.net> wrote:

>Jack, the two articles you posted
>
>>The Trouble With Tofu: Soy and the Brain
>>By John D. MacArthur
>
>and 
>
>>Newest Research On Why You Should Avoid Soy
>>by Sally Fallon email: SAFallon@aol.com & Mary G. Enig, PhD email:
>>MGEnig@aol.com
>
>are truly astonishing, not only for their scientific interest and
>relevance but also as political scandals and likely fodder for the
>plaintiff bar.
>
>One of the first things I'm going to do in the wake of reading these
>two pieces is to contact our school district to inquire what soy
>products are currently being used in the district's lunch programs.
>
>---
>Richard Schulman
>Remove antispamming "-xyz" for email reply

Not me.  I'm going to go into a health food store and show the
research to some hippies and laugh in their face.  Maybe I'll show up
with a bag full of McDonald's burgers in case they want to try a
healthier substitute for tofu.

Charlie

>FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>
>(c) 08/06/03 - Ian Williams Goddard
>
>In April 2000, Lon White and others reported a dose-dependent positive
>correlation between tofu consumption and brain atrophy in a large
>sample of men over several decades. [1] 

  White et al: http://www.jacn.org/cgi/content/full/19/2/242

  Posted this elsewhere (CR means caloric restriction):

  IAN: Here's a rebuttle to White et al followed by their 
  responce: http://www.jacn.org/cgi/content/full/19/4/467

  As I've noted, laboratory findings are also relevent. The 
  soy phytoestrogen genistein inhibits DNA synthesis in rat  
  cerebral cortex and suppresses a range of neurotrophic 
  (neuroprotective) factor functions. An important example:

  J Neurochem (Oct 1995): "The ability of the neurotrophic 
  factors to suppress glutamate toxicity and glutamate-induced
  peroxide accumulation [in hippocampal neurons] was attenuated 
  by the tyrosine kinase inhibitor genistein, indicating the
  requirement for tyrosine phosphorylation in the neuro-
  protective signal transduction mechanism."

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7561872&dopt=Abstract

  "Attenuated" of course means "reduced." Genistein reduced a 
  critical antiaging function. In fact, it's well-known that the 
  chemical class to which genistein is a member, tyrosine kinase
  inhibitors, interfere with neurotrophic (neuroprotective) 
  factors as a class trait. If CR is neuroprotective because it 
  raises neurotrophic factors, the same logic suggests that soy 
  could be neurotoxic for inducing the opposite (even if only in
  males). In short, the known effects of soy phytochemicals point
  to a prediction of brain atrophy. In my view, that adds weight 
  to the soy-dementia correlation reported by White et al.

  http://IanGoddard.net

  "To lengthen thy life, lessen thy meals." Ben Franklin

"Ian Goddard" <igoddard@erols.mom> wrote in message
news:0v53jvsnc8c06r4jbe8030jfo6ostlegvg@4ax.com...
>
> FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MALES
>
> (c) 08/06/03 - Ian Williams Goddard
>
> In April 2000, Lon White and others reported a dose-dependent positive
> correlation between tofu consumption and brain atrophy in a large
> sample of men over several decades. [1] While correlation does not
> prove causation, study size and duration along with the robust
> dose-dependent relationship caused me, even as a vegetarian, to avoid
> tofu and other soy products.

This is a nagging question for me also. I'm a vegetarian
also, and I used to regard soy beans and products made
from soy beans as ideal legumes and products made
from legumes. (Soy beans have a large amount of iron,
protein, and fiber per calorie.) I have largely eliminated
tofu, but I still consume soy milk, tempeh, and soy beans.
Perhaps I should stop consuming these foods also. This
thread may help me make that decision.

> Correlation-based hypotheses should be tested against the availability
> of possible causal mechanisms. In addition to possible causal
> mechanisms previously cited by this author, [2] recent findings
> significantly increase the case for a causal mechanism of soy-induced
> brain atrophy.
>
> Pro-Atrophy Pharmacology Indicated
>
> Brain-derived neurotrophic factor (BDNF) facilitates the survival and
> genesis of brain cells. [3-4] The neuroprotective effects of caloric
> restriction are attributed in part to increased BDNF. [5] On the other
> hand, reduced BDNF is known to cause brain-cell atrophy and is
> associated with Alzheimer's disease. [6-7] Now, a study in
> "Neuroscience Letters" reports that soy significantly reduced BDNF in
> the hippocampus and cerebral cortex of male rats. [8] Since reduced
> BDNF can cause neural atrophy, these findings appear to provide
> compelling evidence for a causal mechanism that might explain the
> positive correlation between tofu (soy) consumption and brain atrophy
> demonstrated by White et al. [1]

Is it correct to equate tofu and other soy products (beans
and tempeh, for example)? What form of soy was used in
the rat study you cite?

> Bad For Boys, Good For Girls?

I think I recall that the wives of the men studied
in Hawaii also experienced dose-dependent cog-
nitive slippage. (That study used tofu).

> While soy appears to reduce BDNF in male rats, it has also been shown
> to increase BDNF in female rats. [9] In fact, soy appears to affect
> neurological parameters in a sex-defined fashion wherein females
> benefit and males suffer. [10-13] There is little doubt among
> researchers that this is because soy is high in phytoestrogens, which
> are plant-derived substances that act like the female hormone
> estrogen.
>
> However, that sex-defined difference fails to explain the findings
> regarding the wives of male subjects in White et al, who reported: "A
> similar association of midlife tofu intake with poor late life
> cognitive test scores was also observed among wives of cohort members,
> using the husband's answers to food frequency questions as proxy for
> the wife's consumption." [1] White et al proposed that long-term
> consumption of weaker soy estrogens may displace the body's own
> stronger estrogen along with its benefits.

Yes, this is what I referred to above.

> Evidence Against Soy-Dementia Hypothesis?
>
> A possible signal contrary to a soy-dementia link is the low
> prevalence of dementia [14] and high consumption of soy in Okinawa,
> Japan. [15] However, that negative correlation, like any correlation,
> does not prove causation. For example, perhaps soy does cause dementia
> but other factors in Okinawa offset the effect.
>
> Also, White et al explored correlations of a range of foods to
> neurological parameters, whereas this Okinawa analysis is a sweeping
> generalization of only tofu to all of Okinawa. In other words, it
> stands to reason that the study by White et al finding a positive
> tofu-dementia correlation has the greater likelihood of providing the
> more accurate picture. Nevertheless, in my view this Okinawa data
> warrants further examination as a possible route to falsifying the
> soy-dementia hypotheses.
>
> In closing, the findings of soy-induced BDNF reduction in male rat
> brain regions that are central to the onset of dementia, in addition
> to previous findings, [2] appear to provide compelling evidence of a
> possible causal mechanism that might explain the soy-dementia
> correlation reported by White et al. [1] Obviously further research is
> necessary before a clear picture emerges regarding the effects of
> long-term soy consumption on the brain. But in the meantime, my
> inclination is to play it safe and avoid soy.

Could it be (I have my fingers crossed) that the
problem lies in the tofu process rather than the bean?

George


_______________________________________________________________________
> [1] White et al: "In this population, higher midlife tofu consumption
> was independently associated with indicators of cognitive impairment
> and brain atrophy in late life."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10763906&dopt=Abstract
>
> [2] Goddard (scroll to): "Is There Reason to Believe Tofu May Cause
> Brain Atrophy?" http://iangoddard.net/soy.htm
>
> [3] Exp Neurol (Sep 2002): "Neurotrophic factors have long been known
> to promote neuronal survival and differentiation."
> http://www.neuro.mpg.de/research/csn/bdnf_ltp
>
> [4] J Neurochem (Sep 2002): "These findings suggest that BDNF plays an
> important role in the regulation of the basal level of neurogenesis in
> dentate gyrus of adult mice [...]."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12354284&dopt=Abstract
>
> [5] Endocrinology (Jun 2003): "Recent studies have shown that DR
> [dietary restriction] stimulates the production of brain-derived
> neurotrophic factor (BDNF) in brain cells, which may mediate
> neuroprotective and neurogenic actions of DR."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12746306&dopt=Abstract
>
> [6] Arch Gen Psychiatry (Jul 1997): "stress can decrease the
> expression of brain-derived neurotrophic factor and lead to atrophy of
> these same populations of stress-vulnerable hippocampal neurons."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9236543&dopt=Abstract
>
> [7] Brain Res Mol Brain Res (Oct 3, 1997): "a reduction in BDNF mRNA
> expression has been observed in human post-mortem Alzheimer's disease
> hippocampi. [...] These results support and extend previous findings
> that BDNF mRNA is reduced in the human Alzheimer's disease hippocampus
> and temporal cortex, and suggest that loss of BDNF may contribute to
> the progressive atrophy of neurons in Alzheimer's disease."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9387865&dopt=Abstract
>
> [8] Neurosci Lett (Feb 27, 2003): "significant reductions were found
> in brain-derived neurotrophic factor (BDNF) mRNA expression in the CA3
> and CA4 region of the hippocampus and in the cerebral cortex in the
> [male] rats fed the diet containing phytoestrogens, compared with
> those on the soya-free diet."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12566171&dopt=Abstract
>
> [9] Neurosci Lett (Feb 1999): "soy phytoestrogens significantly
> increased the mRNA levels of BDNF [...in] female rats."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10081916&dopt=Abstract
>
> [10] Neurotoxicol Teratol (Jan-Feb 2002): "when learning and memory
> parameters were examined in a radial arm maze testing visual-spatial
> memory (VSM), the diet treatments significantly changed the typical
> sexually dimorphic pattern of VSM. Specifically, adult Phyto-rich fed
> females outperformed Phyto-free fed females, while in males on the
> same diets, the opposite pattern of maze performance was observed."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11836067&dopt=Abstract
>
> [11] BMC Neurosci (2001 2(1):20): "Female rats receiving lifelong
> exposure to a high-phytoestrogen containing diet (Phyto-600) acquired
> the maze faster than females fed a phytoestrogen-free diet
> (Phyto-free); in males the opposite diet effect was identified. [...]
> These findings suggest that dietary soy derived phytoestrogens can
> influence learning and memory and alter the expression of proteins
> involved in neural protection and inflammation in rats."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11801187&dopt=Abstract
>
> [12] BMC Neurosis (2001 2(1):21): "When a diet change was initiated in
> adulthood, control phytoestrogen-rich fed females outperformed control
> females switched to a phytoestrogen-free diet. Whereas, in control
> males the opposite diet effect was identified. "
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11801188&dopt=Abstract
>
> [13] Neurosci Lett (May 15, 2003): "This study is the first to show
> that lifelong consumption of dietary phytoestrogens alters the HPA
> stress response in male rats."
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12727319&dopt=Abstract
>
> [14] Dementia: http://okinawaprogram.com/images/dem.gif
>
> [15] Soy intake: http://okinawaprogram.com/images/ment.gif
>
> Some alternative views on soy:
> http://www.soyonlineservice.co.nz
> http://www.healingcrow.com/soy/soy.html
>
>
>  http://IanGoddard.net/journal.htm
>
>  "To lengthen thy life, lessen thy meals." Ben Franklin
>
>  Ongoing CR-monkey-study update: "In the monkeys...those on
>  reduced feeding since the study started are dying at a rate
>  that is about half that of the monkeys receiving a full food
>  ration." Associated Press: Eating less may extend human life.
>  August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=-
>
>

Hi Ian,
      Your well researched recent additions to this question of soy
consumption add to the slowly growing picture. I look forward to your
future updates. While in vitro and animal studies may suggest caution,
human studies must dominate the question when available. The HAAS
study which you posted has been widely misinterpreted by the popular
press, peer reviewers, and the authors themselves. I'm disappointed at
the lack of competency shown by the authors and their peer reviewers,
but take heart in the many good studies being done at an ever
increasing rate. Here is my critique.
      As of late it seems to have fallen my lot to criticize several
large observational and randomized trials. IMO the discrepancies I've
seen in the papers are due to a marked bias on the part of the
investigators against natural dietary supplements. The HAAS study that
Ian posted doesn't seem to follow the pattern, never the less the
rudimentary nature of the mistakes suggests to me some psychological
pressure rather than plain incompetency, perhaps the desire to be
published or to splash louder with the publication is the cause of the
large number of serious mistakes.
      I first read the paper with a sense of doubt that the long
standing custom of tofu consumption could display enough negative
power to stand out against such a cacophony of variables. Table 1
first caught my eye because of the small size of the low tofu
consumption group and the astounding fact that the authors had ignored
the second dietary survey, basing the table on the results of only the
first. In the absence of an explanation this surely smacks of
"doctoring" data. At the very bottom of the table they give scores of
the intelligence test. (CASI) It turns out that the failures of the
low consumption group are only 2.0%. This is an impossible number
since the denominator of the calculation is 38, the group size. If
unadjusted it must clearly be zero, or some multiple of 2.6%,
corresponding to failures of 1,2, 3 individuals etc. divided by 38.
The paper says these values were adjusted for age, and education, (why
only these factors among the many available?) but such an adjustment
would leave the values at zero or raise them to some value higher than
2.6%, probably, judging from similar adjustments in the study to about
four or five, which would take away almost all of the impact of tofu
consumption. "Mistakes" like this are almost always indicative of data
doctoring IMO.
       The hypothesis of the authors is not that the tofu consumption
in the cohort is associated with lifelong lower intelligence, but with
"accelerated brain aging". Figure two clearly shows them wrong on both
counts. The median age at testing was 80, putting the first two bar
graphs below the medium, and the last three above. A quick glance
shows that the younger members of the hi-hi tofu group failed at about
four times the rate of the low-low tofu group. As the members get
older this failure rate is gradually reduced to near equality.
Comparisons of the other two groups show the same trend but not as
significantly. ACCORDING TO THIS STUDY TOFU ATTENUATES BRAIN AGING
BETWEEN AGE 71 AND 93. Why were the hi tofu eaters so much less
intelligent at age 71-75 than the low group? They went to grade school
in Japan. People always (groups, not individuals) demonstrate a
relative lack of intelligence when dealing with written or oral tests
in a second language. A most pertinent example of this is the wives of
the cohort. Those who went to grade school in Japan failed the CASI
test at a rate of 2.7 times those who didn't (table 4). THIS HUGE
MULTIVARIENT FACTOR WAS NOT APPLIED TO HUSBANDS. Had it been, it would
have eliminated the difference in the CASI scores of the husbands at
age 71, and would have destroyed the thesis of the paper. A much
milder factor of 1.04 based on childhood years in Japan was applied to
them. Why was such a different factor used? All I know is there would
not have been a story without it. Why were the hi tofu eaters of about
equal intelligence at near age 90? Perhaps, because they ate tofu. No
other reason is apparent to me. This was the dependent variable after
adjusting for all others in the study. The stratification of the group
into two smaller groups (over 80 and under 80) would have reduced the
P values by about half leaving results only of marginal significance,
but still indicating with a probability of about ten to one that tofu
consumption attenuates brain aging from ages 71 to 93.
    Table 2 gives the heart of the papers results, the OR for the
failure rate in the CASI test of 1.0 (reference), 1.42, 1.74, and 1.62
for the low-low, the low, the hi, and the hi-hi groups respectively.
The difference for these rates is miniscule and totally insignificant
for all groups except the low-low one. The difference for the failure
rate between the low-low group and the low group is significant, but
the difference in tofu consumption is little more than answering once
last week instead of zero times last week in the second dietary survey
ALONE. That one serving per week of tofu can increase your failure
rate in a test by 42% is just not believable especially in the face of
such a small dose response and the many errors made by the authors.
Speaking of which they have more of the wives going to school in Japan
than were born there. (table 3), and they put the OR for going to
grade school in Japan at an unbelievably low 1.04, they may have meant
to add per year. These mistakes led to the apparent failure to adjust
properly for the all important lack of schooling in English. The data
are especially unconvincing since we are asked to believe that tofu
consumption until age 71 accelerates brain aging and then begins to
attenuate it after that age.
      Apart from the fatal mathematical and procedural mistakes listed
above. The authors made two fundamental mistakes in logic. First they
did not use the average CASI score, but rather the percentage of
failures. This would have been the appropriate dependent variable only
if their hypothesis were "tofu accelerates brain aging of those who
are of low mentality, but not those of normal or hi mentality." And
second their assumption that they had listed all the reasons for a
lower apparent intelligence of the hi tofu groups at age 71 was based
only on the logic that since that's all we can think of, there are no
more. I can easily think of several quite probable ones.
      Contrary to the CASI data the relationship with brain size was
most pronounced in the hi-hi group, being totally insignificant
between the other three groups. I would guess that this was caused by
lower growth due to the fact that soy protein is lacking in
methionine, a deficiency of which is known to slow growth rates, but
only at hi levels of deficiency.  The high-high group, which show
lowered growth would have been deficient to at least some extent in
this amino acid, the restriction of which is also shown to extend
lifespan.
       Buried in the small print is the important datum that tofu was
related to a lifespan extension of the autopsied members of about a
year and a half.
       In summary the data of the experiment, in contradiction to the
author's claims indicate that tofu consumption in men extends life
span and protects the aging brain from dementia, and further that the
vaunted peer reviewing of world class medical journals has room for
improvement.

Thomas

Richard Schulman <ra.schulman-xyz@verizon.net> schreef in 
berichtnieuws...news:v5b6jvsj0nc0fbgkv0upi8hia6cbdob0gf@4ax.com:

> One of the first things I'm going to do in the wake of reading these
> two pieces is to contact our school district to inquire what soy
> products are currently being used in the district's lunch programs.
> 

This is off-the-wall perhaps, but I wonder if there's any correlation 
between soy infant formula and the epidemic of autism?! 

> 
> Is it correct to equate tofu and other soy products (beans
> and tempeh, for example)? What form of soy was used in
> the rat study you cite?
>

Dr. Michael Lam, MD, www.drlam.com, himself an Asian, has long
recommended against all soy except for fermented soy products, tempeh
and miso.  Dr. Dean Ornish has recently sent an advisory suggesting
that males following his diet structure may wish to eliminate soy from
the diet and Dr Andrew Weil, has recently pulled back from an
enthusiastic endorsement of all soy products to cautious "one cup of
soy milk should be OK".

I have a possible pre-cancerous condition of the prostate (3-clean
biopsies in the last 8 years)that I think my substitution of soy (meat
substitutes and milk)has helped me with.  As I exersize hard, I find I
must have a good protein source.  Vitamin Shoppes has a non-soy
protein powder, but the problem with this is that it is expensive, 
$14/lb., and that much of its protein is derived from legumes, which
may replicate the soy problems. Misos may all be too salty  and tempeh
has a taste problem for me.  Perhaps egg-whites and a return to some
milk are what I must do.  It isn't easy.

"Rob" <robwid3000@hotmail.com> wrote in message
news:250fb761.0308101155.1c6fc039@posting.google.com...
> >
> > Is it correct to equate tofu and other soy products (beans
> > and tempeh, for example)? What form of soy was used in
> > the rat study you cite?
> >
>
> Dr. Michael Lam, MD, www.drlam.com, himself an Asian, has long
> recommended against all soy except for fermented soy products, tempeh
> and miso.  Dr. Dean Ornish has recently sent an advisory suggesting
> that males following his diet structure may wish to eliminate soy from
> the diet and Dr Andrew Weil, has recently pulled back from an
> enthusiastic endorsement of all soy products to cautious "one cup of
> soy milk should be OK".
>
> I have a possible pre-cancerous condition of the prostate (3-clean
> biopsies in the last 8 years)that I think my substitution of soy (meat
> substitutes and milk)has helped me with.  As I exersize hard, I find I
> must have a good protein source.  Vitamin Shoppes has a non-soy
> protein powder, but the problem with this is that it is expensive,
> $14/lb., and that much of its protein is derived from legumes, which
> may replicate the soy problems. Misos may all be too salty  and tempeh
> has a taste problem for me.  Perhaps egg-whites and a return to some
> milk are what I must do.  It isn't easy.

Have you given whey protein isolate a try?  While I don't use it
exclusively, I've been using it to increase my protein intake without some
of the problems possibly associated with increasing other sources of
protein.  It doesn't taste bad, isn't really high in calories, & doesn't
cost an arm & a leg.

Michele
I ENJOY being a cranky bitch.

tcarter2@elp.rr.com (Thomas Carter) wrote:

>      I first read the paper with a sense of doubt that the long
>standing custom of tofu consumption could display enough negative
>power to stand out against such a cacophony of variables. 

  IAN: Well, your conclusions certainly supported your bias.


>Table 1 first caught my eye because of the small size of the low tofu
>consumption group and the astounding fact that the authors had ignored
>the second dietary survey, basing the table on the results of only the
>first. In the absence of an explanation this surely smacks of
>"doctoring" data. 


  IAN: This is the Table 1 title: "Characteristics at Baseline and 
  at the Time of Cognitive Assessment, according to Response at 
  Baseline to the Question: 'How Often do You Eat Tofu?'" 
  http://www.jacn.org/cgi/content/full/19/2/242/T1


>At the very bottom of the table they give scores of
>the intelligence test. (CASI) It turns out that the failures of the
>low consumption group are only 2.0%. This is an impossible number
>since the denominator of the calculation is 38, the group size. If
>unadjusted it must clearly be zero, or some multiple of 2.6%,
>corresponding to failures of 1,2, 3 individuals etc. divided by 38.
>The paper says these values were adjusted for age, and education, (why
>only these factors among the many available?) but such an adjustment
>would leave the values at zero or raise them to some value higher than
>2.6%, probably, judging from similar adjustments in the study to about
>four or five, which would take away almost all of the impact of tofu
>consumption. "Mistakes" like this are almost always indicative of data
>doctoring IMO.


  IAN: It says, "CASI score adjusted for age (single year) and 
  years of schooling completed." As such, it need NOT be 2.6%.
  So you base the charge of "data doctoring" on your assumption 
  that the figure "probably" should have adjusted to some number 
  other than 2%. What a flimsy basis for such a harsh accusation!



>       The hypothesis of the authors is not that the tofu consumption
>in the cohort is associated with lifelong lower intelligence, but with
>"accelerated brain aging". Figure two clearly shows them wrong on both
>counts. The median age at testing was 80, putting the first two bar
>graphs below the medium, and the last three above. A quick glance


  IAN: Frankly, I don't believe your "quick glance" supercedes 
  the expertise of eight professional epidemeologists who spent
  years examining all the data. Frankly, that you believe you  
  can debunk these experts in a few moments speaks for itself.
  Moreover, that in a few moments you feel qualified to accuse
  these professionals of "data doctoring" because some numbers
  are "probably" not what you think they should be is outrageous.



>shows that the younger members of the hi-hi tofu group failed at about
>four times the rate of the low-low tofu group. As the members get
>older this failure rate is gradually reduced to near equality.
>Comparisons of the other two groups show the same trend but not as
>significantly. ACCORDING TO THIS STUDY TOFU ATTENUATES BRAIN AGING
>BETWEEN AGE 71 AND 93. 


  IAN: That's a cross-sectional, not longitudinal, analysis,
  so you can't really say, "As the members get older this 
  failure rate is gradually reduced," since each stratified
  group represents a different set of people. The important 
  point is the sixth grouping showing the overall relation:

  http://www.jacn.org/cgi/content/full/19/2/242/F2


>Why were the hi tofu eaters so much less
>intelligent at age 71-75 than the low group? They went to grade school
>in Japan. People always (groups, not individuals) demonstrate a
>relative lack of intelligence when dealing with written or oral tests
>in a second language. 


  IAN: But the study states: "The CASI has been validated as 
  a screening instrument for dementia in the United States 
  and Japan, in both English and Japanese languages. [...] 
  participants selected either Japanese or English for testing, 
  depending on the language with which they were most comfortable."

  So your conclusion that scores were biased by native education
  stands in direct opposition to information provided in the study.


>A most pertinent example of this is the wives of
>the cohort. Those who went to grade school in Japan failed the CASI
>test at a rate of 2.7 times those who didn't (table 4). 


  IAN: That's irrelevant due to your oversight noted above. 


>THIS HUGE
>MULTIVARIENT FACTOR WAS NOT APPLIED TO HUSBANDS. Had it been, it would
>have eliminated the difference in the CASI scores of the husbands at
>age 71, and would have destroyed the thesis of the paper. 


  IAN: That's a false assumption based on your oversight above. 

  Frankly, I just don't have time to respond point-by-point. 
  Given that you're asking us to believe your personal analysis 
  and thereby doubt eight expert epidemiologists and their peer-
  reviewers, it's fair to ask: exactly what are your credentials?
  I don't care for appeals to authority, but regarding complex
  statistical data analyses, expertise really means something.

  One last comment:


>      Contrary to the CASI data the relationship with brain size was
>most pronounced in the hi-hi group, being totally insignificant
>between the other three groups. I would guess that this was caused by
>lower growth due to the fact that soy protein is lacking in
>methionine, a deficiency of which is known to slow growth rates, but
>only at hi levels of deficiency.  The high-high group, which show
>lowered growth would have been deficient to at least some extent in
>this amino acid, the restriction of which is also shown to extend
>lifespan.


  IAN: So there IS a relation to smaller brain size and tofu 
  (which was the primary focus of my post), but alas you've 
  determined that it is a result of methionine deficiency. 
  http://www.jacn.org/cgi/content/full/19/2/242/F3  You know,
  you could broach your comments as hypotheses and questions,
  rather than, as you have, accusations of "data doctoring" and 
  firm conclusions of "fatal mistakes" and such by the authors
  that you use to caste sweeping aspersion on peer-review per se.
  Moreover, you should locate and ask the authors directly before
  posting public accusations against their expertise and honor. 

  http://IanGoddard.net/journal.htm

  "Our greatest illusion is to believe that we are what 
   we think ourselves to be." Henri Amiel (1821-1881)

  

Thomas 
Hi Ian,
       Foremost allow me to apologize if I upset you. I know how
easily we humans can be irritated by opposing opinions, and I try to
avoid it. But I guess I'll have to try harder. I'd like to continue
our discussion in a dispassionate, scientific manner. If you can't,
feel free to cuss away. I have a thick skin, and a short memory for
such things. :>) And I believe I understand the emotions involved. I
also invite others to weigh in. After all we are discussing a study
which shows a rare life extension of about a year and a half by a
common food, in a cohort of reasonable size, (290) as well as
attenuation of brain aging after age 71, but is suspected of
accelerating brain aging. Or in other words a matter of some import. I
will snip freely, repost anything you wish.


Thomas wrote:

> >At the very bottom of the table they give scores of
> >the intelligence test. (CASI) It turns out that the failures of the
> >low consumption group are only 2.0%. This is an impossible number
> >since the denominator of the calculation is 38, the group size. If
> >unadjusted it must clearly be zero, or some multiple of 2.6%,
> >corresponding to failures of 1,2, 3 individuals etc. divided by 38.
> >The paper says these values were adjusted for age, and education, (why
> >only these factors among the many available?) but such an adjustment
> >would leave the values at zero or raise them to some value higher than
> >2.6%, probably, judging from similar adjustments in the study to about
> >four or five, which would take away almost all of the impact of tofu
> >consumption. "Mistakes" like this are almost always indicative of data
> >doctoring IMO.
> 
> 
>   IAN: It says, "CASI score adjusted for age (single year) and 
>   years of schooling completed." As such, it need NOT be 2.6%.
>   So you base the charge of "data doctoring" on your assumption 
>   that the figure "probably" should have adjusted to some number 
>   other than 2%.

No, I did not say improbable, I said impossible. This is matter that
can be resolved by simple math and need not be disputed among
intelligent people. 1/38=2.6%. The low cohort of 38 was younger, and
had more education, so the stated adjustments could only have raised
the 2.6%, as I stated.

 What a flimsy basis for such a harsh accusation!

If you call the accusation harsh, what you call the actual deed? 
       
Thomas wrote: 
> >       The hypothesis of the authors is not that the tofu consumption
> >in the cohort is associated with lifelong lower intelligence, but with
> >"accelerated brain aging". Figure two clearly shows them wrong on both
> >counts. The median age at testing was 80, putting the first two bar
> >graphs below the medium, and the last three above. A quick glance
> >shows that the younger members of the hi-hi tofu group failed at about
> >four times the rate of the low-low tofu group. As the members get
> >older this failure rate is gradually reduced to near equality.
> >Comparisons of the other two groups show the same trend but not as
> >significantly. ACCORDING TO THIS STUDY TOFU ATTENUATES BRAIN AGING
> >BETWEEN AGE 71 AND 93. 
> 
> 
>   IAN: That's a cross-sectional, not longitudinal, analysis,
>   so you can't really say, "As the members get older this 
>   failure rate is gradually reduced," since each stratified
>   group represents a different set of people. The important 
>   point is the sixth grouping showing the overall relation:
> 
>   http://www.jacn.org/cgi/content/full/19/2/242/F2

     Are you quibbling about my syntax? I will restate it for you more
formally, but the conclusion is the same. The low-low group members
who died just after age 71 failed at one fourth the rate of the hi-hi
group members who died just after age 71. BUT the low-low group
members who died just after age 90 failed at nearly the same rate as
the hi-hi members who died just after age 90. The obvious presumption
is that at age 71 the low-low group members were more intelligent, but
those low-low members who survived to age 90 were only of equal
intelligence with the hi-hi group members. Thus between the ages of 71
and 90 the intelligence of the longer lived low-low members declined
relative to the intelligence of the hi-hi members.
This suggests that tofu attenuated brain aging. 
 
 
> >Why were the hi tofu eaters so much less
> >intelligent at age 71-75 than the low group? They went to grade school
> >in Japan. People always (groups, not individuals) demonstrate a
> >relative lack of intelligence when dealing with written or oral tests
> >in a second language. 
> 
> 
>   IAN: But the study states: "The CASI has been validated as 
>   a screening instrument for dementia in the United States 
>   and Japan, in both English and Japanese languages. [...] 
>   participants selected either Japanese or English for testing, 
>   depending on the language with which they were most comfortable."
> 
>   So your conclusion that scores were biased by native education
>   stands in direct opposition to information provided in the study.
> 
No, people who switch from one language to another are less
comfortable in either language, but both my point and yours are
irrelevant to the question. The relevant point is that table 4 shows
that the wives who went to grade school in Japan failed at a rate of
270% higher than those who didn't. The fact that they had their choice
of languages for the test can not negate (and in fact doesn't even
relate to) this OVERWHELMINGLY  large factor which was not applied to
the men.

> >A most pertinent example of this is the wives of
> >the cohort. Those who went to grade school in Japan failed the CASI
> >test at a rate of 2.7 times those who didn't (table 4). 
> 
> 
>   IAN: That's irrelevant due to your oversight noted above. 
No, Ian, the relevance is that if the wives failed at a rate of 270%
because of their schooling, we should expect the husbands who went to
grade school in Japan to also fail at somewhere near the same
percentage because of their own schooling.
> 
> >THIS HUGE
> >MULTIVARIENT FACTOR WAS NOT APPLIED TO HUSBANDS. Had it been, it would
> >have eliminated the difference in the CASI scores of the husbands at
> >age 71, and would have destroyed the thesis of the paper. 
> 
> 
>   IAN: That's a false assumption based on your oversight above. 

About 20% more of the hi-hi group compared to the low-low group went
to grade school in Japan. If these men failed at just 200% the rate,
this would have tripled one fifth of the failings due to schooling in
Japan which would have added 60% to the total number of failings and
all but wiped out the 62% advantage of the low-low group in table 2
relative to the hi-hi group.

>   Frankly, I just don't have time to respond point-by-point. 
>   Given that you're asking us to believe your personal analysis 
>   and thereby doubt eight expert epidemiologists and their peer-
>   reviewers, it's fair to ask: exactly what are your credentials?
>   I don't care for appeals to authority, but regarding complex
>   statistical data analyses, expertise really means something.

No, I'm asking you and others to read, and follow my math and logic. I
don't think it's too complex for many of the group with a bit of
effort.
 
>   One last comment:
> 
> 
> >      Contrary to the CASI data the relationship with brain size was
> >most pronounced in the hi-hi group, being totally insignificant
> >between the other three groups. I would guess that this was caused by
> >lower growth due to the fact that soy protein is lacking in
> >methionine, a deficiency of which is known to slow growth rates, but
> >only at hi levels of deficiency.  The high-high group, which show
> >lowered growth would have been deficient to at least some extent in
> >this amino acid, the restriction of which is also shown to extend
> >lifespan.
> 
> 
>   IAN: So there IS a relation to smaller brain size and tofu 
>   (which was the primary focus of my post), but alas you've 
>   determined that it is a result of methionine deficiency. 

But not brain atrophy, nor accelerated brain aging. At least not shown
by this paper. Some of the animal and in vitro data is quite
suggestive.
 
>   http://www.jacn.org/cgi/content/full/19/2/242/F3  You know,
>   you could broach your comments as hypotheses and questions,
>   rather than, as you have, accusations of "data doctoring" and 
>   firm conclusions of "fatal mistakes" and such by the authors
>   that you use to caste sweeping aspersion on peer-review per se.
>   Moreover, you should locate and ask the authors directly before
>   posting public accusations against their expertise and honor. 

Actually I've always emailed a copy to any author who has a currently
valid address in their Pubmed listing. Most don't, and none have
replied. All humans, including myself, have a difficult time accepting
and dealing logically with unsettling facts. We can all profit by
recognizing and dealing with this "design flaw" to the best of our
ability.

Thomas

tcarter2@elp.rr.com (Thomas Carter) wrote:

>Hi Ian,
>       Foremost allow me to apologize if I upset you. I know how
>easily we humans can be irritated by opposing opinions, and I try to
>avoid it. But I guess I'll have to try harder. I'd like to continue
>our discussion in a dispassionate, scientific manner. If you can't,
>feel free to cuss away. I have a thick skin, and a short memory for
>such things. :>) 


 IAN: Tom, it's important to accurately represent another's response.
 You represent my response as "cussing away." "Cuss" means to curse,
 and curse means "a profane word or phrase." A review of my reply 
 to you will not find the profanity that you imply exists therein:

http://www.google.com/groups?selm=fdpfjvs4ss628n4oqojjqbpjneelodk7rp%404ax.com

 As I said there: "you could broach your comments as hypotheses and
 questions, rather than, as you have, accusations of 'data doctoring'
 and firm conclusions of 'fatal mistakes' and such by the authors that
 you use to caste sweeping aspersion on peer-review per se." Yet once
 again in this response you're back declaring that your quick-glance 
 conclusions are inherently accurate prior to consultation with the 
 authors regarding what are really questions, not clear conclusions. 



>>   IAN: It says, "CASI score adjusted for age (single year) and 
>>   years of schooling completed." As such, it need NOT be 2.6%.
>>   So you base the charge of "data doctoring" on your assumption 
>>   that the figure "probably" should have adjusted to some number 
>>   other than 2%.
>
>No, I did not say improbable, I said impossible. This is matter that
>can be resolved by simple math and need not be disputed among
>intelligent people. 1/38=2.6%. The low cohort of 38 was younger, and
>had more education, so the stated adjustments could only have raised
>the 2.6%, as I stated.


  IAN: That the unajusted figure must at least be 2.6% is obvious,
  which is why I said the adjusted figure need not be 2.6%. Your 
  point is it MUST be higher. I don't know what it should be so
  I sent an email to Lon White asking him why the figure is 2%.



>>   IAN: That's a cross-sectional, not longitudinal, analysis,
>>   so you can't really say, "As the members get older this 
>>   failure rate is gradually reduced," since each stratified
>>   group represents a different set of people. The important 
>>   point is the sixth grouping showing the overall relation:
>> 
>>   http://www.jacn.org/cgi/content/full/19/2/242/F2
>
>     Are you quibbling about my syntax? I will restate it for you more
>formally, but the conclusion is the same. The low-low group members
>who died just after age 71 failed at one fourth the rate of the hi-hi
>group members who died just after age 71. BUT the low-low group
>members who died just after age 90 failed at nearly the same rate as
>the hi-hi members who died just after age 90. The obvious presumption
>is that at age 71 the low-low group members were more intelligent, but
>those low-low members who survived to age 90 were only of equal
>intelligence with the hi-hi group members. Thus between the ages of 71
>and 90 the intelligence of the longer lived low-low members declined
>relative to the intelligence of the hi-hi members.
>This suggests that tofu attenuated brain aging. 


  IAN: Well, I still think my reply above holds--some subgroups 
  could easily stand outside the overall trend, but that does not
  refute the overall trend. I raised your argument an email to White. 



>> >Why were the hi tofu eaters so much less
>> >intelligent at age 71-75 than the low group? They went to grade school
>> >in Japan. People always (groups, not individuals) demonstrate a
>> >relative lack of intelligence when dealing with written or oral tests
>> >in a second language. 
>> 
>> 
>>   IAN: But the study states: "The CASI has been validated as 
>>   a screening instrument for dementia in the United States 
>>   and Japan, in both English and Japanese languages. [...] 
>>   participants selected either Japanese or English for testing, 
>>   depending on the language with which they were most comfortable."
>> 
>>   So your conclusion that scores were biased by native education
>>   stands in direct opposition to information provided in the study.
>> 
>No, people who switch from one language to another are less
>comfortable in either language, 


  IAN: Well, that's not what you said before. The study seems to 
  have delt any language problem as effectively as possible, and...


>The relevant point is that table 4 shows
>that the wives who went to grade school in Japan failed at a rate of
>270% higher than those who didn't. The fact that they had their choice
>of languages for the test can not negate (and in fact doesn't even
>relate to) this OVERWHELMINGLY  large factor which was not applied to
>the men.
[...]
>No, Ian, the relevance is that if the wives failed at a rate of 270%
>because of their schooling, we should expect the husbands who went to
>grade school in Japan to also fail at somewhere near the same
>percentage because of their own schooling.
[...]
>About 20% more of the hi-hi group compared to the low-low group went
>to grade school in Japan. If these men failed at just 200% the rate,
>this would have tripled one fifth of the failings due to schooling in
>Japan which would have added 60% to the total number of failings and
>all but wiped out the 62% advantage of the low-low group in table 2
>relative to the hi-hi group.


  IAN: The study (http://www.jacn.org/cgi/content/full/19/2/242) says:

"To investigate alternative explanations for the association of high 
mid-life tofu intake with poorer cognition in late life, analyses were
conducted to identify possible confounding factors [...] Thirty-one 
factors were examined [...] birth in Japan, years of childhood lived 
in Japan [...] When the 933 subjects who had lived one or more years 
of their childhood in Japan were excluded from the analysis, the 
corresponding values were beta=-1.69, p=0.01 for 1965�67 tofu intake; 
beta=-0.65, p=0.01 for 1971�74 tofu intake, and beta=-0.72, p=0.015 
for the composite tofu intake index." 

  So even when the subgroup you claim biased the results was excluded,
  a statistically significant relationship to tofu intake remained. 



>>   Frankly, I just don't have time to respond point-by-point. 
>>   Given that you're asking us to believe your personal analysis 
>>   and thereby doubt eight expert epidemiologists and their peer-
>>   reviewers, it's fair to ask: exactly what are your credentials?
>>   I don't care for appeals to authority, but regarding complex
>>   statistical data analyses, expertise really means something.
>
>No, I'm asking you and others to read, and follow my math and logic. I
>don't think it's too complex for many of the group with a bit of
>effort.
> 
>>   One last comment:
>> 
>> 
>> >      Contrary to the CASI data the relationship with brain size was
>> >most pronounced in the hi-hi group, being totally insignificant
>> >between the other three groups. I would guess that this was caused by
>> >lower growth due to the fact that soy protein is lacking in
>> >methionine, a deficiency of which is known to slow growth rates, but
>> >only at hi levels of deficiency.  The high-high group, which show
>> >lowered growth would have been deficient to at least some extent in
>> >this amino acid, the restriction of which is also shown to extend
>> >lifespan.
>> 
>> 
>>   IAN: So there IS a relation to smaller brain size and tofu 
>>   (which was the primary focus of my post), but alas you've 
>>   determined that it is a result of methionine deficiency. 
>
>But not brain atrophy, nor accelerated brain aging. At least not shown
>by this paper. Some of the animal and in vitro data is quite
>suggestive.
> 
>>   http://www.jacn.org/cgi/content/full/19/2/242/F3  You know,
>>   you could broach your comments as hypotheses and questions,
>>   rather than, as you have, accusations of "data doctoring" and 
>>   firm conclusions of "fatal mistakes" and such by the authors
>>   that you use to caste sweeping aspersion on peer-review per se.
>>   Moreover, you should locate and ask the authors directly before
>>   posting public accusations against their expertise and honor. 
>
>Actually I've always emailed a copy to any author who has a currently
>valid address in their Pubmed listing. Most don't, and none have
>replied. All humans, including myself, have a difficult time accepting
>and dealing logically with unsettling facts. We can all profit by
>recognizing and dealing with this "design flaw" to the best of our
>ability.
>
>Thomas

Ian Goddard <igoddard@erols.mon> wrote in message news:<fkfljvcdcvj3csi0v12p6tp8foutmst2r2@4ax.com>...
> tcarter2@elp.rr.com (Thomas Carter) wrote:
> 
> >Hi Ian,
> >       Foremost allow me to apologize if I upset you. I know how
> >easily we humans can be irritated by opposing opinions, and I try to
> >avoid it. But I guess I'll have to try harder. I'd like to continue
> >our discussion in a dispassionate, scientific manner. If you can't,
> >feel free to cuss away. I have a thick skin, and a short memory for
> >such things. :>) 
> 
> 
>  IAN: Tom, it's important to accurately represent another's response.
>  You represent my response as "cussing away." "Cuss" means to curse,
>  and curse means "a profane word or phrase." A review of my reply 
>  to you will not find the profanity that you imply exists therein:
 
Hi Ian,
     It never occured to me that the remark could be taken that way.
Even so the remark was unappropeiate and I apoligize, and hope that
you too, have a short memory for such things.

> 
>  As I said there: "you could broach your comments as hypotheses and
>  questions, rather than, as you have, accusations of 'data doctoring'
>  and firm conclusions of 'fatal mistakes' and such by the authors that
>  you use to caste sweeping aspersion on peer-review per se." Yet once
>  again in this response you're back declaring that your quick-glance 
>  conclusions are inherently accurate prior to consultation with the 
>  authors regarding what are really questions, not clear conclusions. 
 
Yes I could have, but they are my conclusions, not questions nor
hypotheses.
 
> 
> 
>   IAN: The study (http://www.jacn.org/cgi/content/full/19/2/242) says:
> 
> "To investigate alternative explanations for the association of high 
> mid-life tofu intake with poorer cognition in late life, analyses were
> conducted to identify possible confounding factors [...] Thirty-one 
> factors were examined [...] birth in Japan, years of childhood lived 
> in Japan [...] When the 933 subjects who had lived one or more years 
> of their childhood in Japan were excluded from the analysis, the 
> corresponding values were beta=-1.69, p=0.01 for 1965?67 tofu intake; 
> beta=-0.65, p=0.01 for 1971?74 tofu intake, and beta=-0.72, p=0.015 
> for the composite tofu intake index." 
> 
>   So even when the subgroup you claim biased the results was excluded,
>   a statistically significant relationship to tofu intake remained. 

    A statistically significant relationship between tofu and what?
I'm glad you brought that up. It's another example of data doctoring
that I had missed.
    Thruout the article the authors based the cognitive differences on
the FAILURE rate in the CASI score.  Which was about 1000 out of 7000.
After adjusting for the confounding factors they wished to, (leaving
out grade school in Japan among others) they managed to get an Odds
Ratio for failure rate of 1.62 for the hi-hi group against the low-low
group with a significant p value of .03. I will now show that had they
left out the 933 men born in Japan the p value would have most likely
been over .12, a mathematically insignificant value and would IMO have
likey made the report unpublishable for lack of interest.
     Below I post the full paragraph of the partial quote Ian posted
just above. It shows that when the 933 men born in Japan were left out
for the average CASI scores the p value rose by over a factor of four,
from .0025 to .015, showing that the scores of the men born in Japan
were dragging down the the scores of the hi-hi group. The obvious
conclusion is that the p value for the falure rate in the CASI test
would have risen by about the same, or from .03 to .12. The average
CASI scores for the two groups are never given in the report. Only the
p values are given which are significant because they are the averages
of 7000 men, not the falures of only 1000. My estimate is that the
difference in the CASI average scores would have been less than three
points, a very uninteresting figure and that's why the authors used
the failure rate instead carefully concealing the fact that the
average scores were quite similar.
     In a scientific paper reporting on the differenc in intelligence
of a group of men twice placed in a low tofu group with that of
another group twice placed in a hi tofu group the actual test scores
of the groups are concealed.  Furthermore the data that are spoonfed
to us are selected to exagerate the difference in test performance.
When they wish to titalate us with large differences, they use failure
rates. When they wish to assure us with low p values, they use average
scores. When they wish to persuade us with doctored statistics, they
leave out key factors.
      Here is the paragraph from which I based my estimate.      
 
"Initial multivariate analyses were done using linear regression
modeling with the participant's CASI score as the dependent variable.
Controlling covariates included all of the candidate confounders and
predictors of CASI score mentioned above, together with midlife FEV-1
(a pulmonary function indicator previously reported to predict CASI
scores) and midlife BMI (a predictor of brain weight in subsequent
analyses). In a model using the 1965�1967 tofu intake question as the
primary predictor variable, while controlling for all other
independent variables, there was a significant inverse association
with CASI score (beta=-1.4, p < .006). Similar associations were seen
with the 1971�1974 tofu intake variable (beta=-0.74, p=.0005), and
with the composite variable (beta=-0.86, p=.0025). When the 933
subjects who had lived one or more years of their childhood in Japan
were excluded from the analysis, the corresponding values were
beta=-1.69, p=0.01 for 1965�67 tofu intake; beta=-0.65, p=0.01 for
1971�74 tofu intake, and beta=-0.72, p=0.015 for the composite tofu
intake index. There was no evidence of interaction between
apolipoprotein E genotype and tofu in their associations with
cognitive test performance."

Thomas

tcarter2@elp.rr.com (Thomas Carter) wrote:

>> >Hi Ian,
>> >       Foremost allow me to apologize if I upset you. I know how
>> >easily we humans can be irritated by opposing opinions, and I try to
>> >avoid it. But I guess I'll have to try harder. I'd like to continue
>> >our discussion in a dispassionate, scientific manner. If you can't,
>> >feel free to cuss away. I have a thick skin, and a short memory for
>> >such things. :>) 
>> 
>> 
>>  IAN: Tom, it's important to accurately represent another's response.
>>  You represent my response as "cussing away." "Cuss" means to curse,
>>  and curse means "a profane word or phrase." A review of my reply 
>>  to you will not find the profanity that you imply exists therein:
> 
>Hi Ian,
>     It never occured to me that the remark could be taken that way.


  IAN: Well, it's always good to keep a dictionary on hand. :)



>Even so the remark was unappropeiate and I apoligize, and hope that
>you too, have a short memory for such things.


  IAN: But regarding my previous comments, I hope you have a
  long memory for such things. I really think it's extremely 
  inappropriate to accuse researchers of "data doctoring," 
  especially when your claim is based on assumptions about 
  data that you do not have. Assumptions are highly fallible. 

  For example, your primary argument was that adjustment for 
  education should have increased the percentage of the "almost
  never" tofu-eating group (n=38) above 2.6%, since 1/38 = 2.6% 
  (see: http://www.jacn.org/cgi/content/full/19/2/242/T1). But
  doesn't that ASSUME that the lowest number of those scoring 
  below 50 must be 1?  If ZERO people scored below 50, then 
  the listed 2.0% could be the upward adjustment. Or have I 
  missed some statement that says one person scored below 50?


 
>>  As I said there: "you could broach your comments as hypotheses and
>>  questions, rather than, as you have, accusations of 'data doctoring'
>>  and firm conclusions of 'fatal mistakes' and such by the authors that
>>  you use to caste sweeping aspersion on peer-review per se." Yet once
>>  again in this response you're back declaring that your quick-glance 
>>  conclusions are inherently accurate prior to consultation with the 
>>  authors regarding what are really questions, not clear conclusions. 
> 
>Yes I could have, but they are my conclusions, not questions nor
>hypotheses.


  IAN: But anytime you read a study and suspect the researchers 
  have doctored the data, that suspicion is just a hypothesis, 
  and thus should not be stated as more than that. Moreover, in 
  most cases like this it should not even be mentioned unless 
  you have ALL the data and knew what was going on in the minds 
  of the researchers, which virtually excludes ever mentioning it.

  We benefit by having and encouraging professionals to post in 
  these fora, but what professional should want to risk their 
  their long-and-hard-won reputation in places where charges of 
  professional fraud are so easily thrown about? Knock it off!
  You have made many excellent contributions to our inquiries 
  here, which is why I'm aghast at your raising such accusations.



>>   IAN: The study (http://www.jacn.org/cgi/content/full/19/2/242) says:
>> 
>> "To investigate alternative explanations for the association of high 
>> mid-life tofu intake with poorer cognition in late life, analyses were
>> conducted to identify possible confounding factors [...] Thirty-one 
>> factors were examined [...] birth in Japan, years of childhood lived 
>> in Japan [...] When the 933 subjects who had lived one or more years 
>> of their childhood in Japan were excluded from the analysis, the 
>> corresponding values were beta=-1.69, p=0.01 for 1965?67 tofu intake; 
>> beta=-0.65, p=0.01 for 1971?74 tofu intake, and beta=-0.72, p=0.015 
>> for the composite tofu intake index." 
>> 
>>   So even when the subgroup you claim biased the results was excluded,
>>   a statistically significant relationship to tofu intake remained. 
>
>    A statistically significant relationship between tofu and what?
>I'm glad you brought that up. It's another example of data doctoring
>that I had missed.
>    Thruout the article the authors based the cognitive differences on
>the FAILURE rate in the CASI score.  Which was about 1000 out of 7000.
>After adjusting for the confounding factors they wished to, (leaving
>out grade school in Japan among others) they managed to get an Odds
>Ratio for failure rate of 1.62 for the hi-hi group against the low-low
>group with a significant p value of .03. I will now show that had they
>left out the 933 men born in Japan the p value would have most likely
>been over .12, a mathematically insignificant value and would IMO have
>likey made the report unpublishable for lack of interest.


  IAN: Tom, you are doing it again. You argue that "another example of
  data doctoring" is data that "would have most likely been over .12."
  By saying "most likely" you concede you are making an ASSUMPTION, 
  yet that does not stop you from stating with full certitude that 
  "another example of data doctoring" has been discovered. It seems 
  only too clear that your answer for anything you run into that you 
  don't immediately understand is that you've found "data doctoring."
  It suggests to me that you approach this study hoping to find such.

  Other than these observations, I just don't have any further time to
  weed through your arguments and measure them against the study; and
  frankly, I don't have confidence based on what I have reviewed of 
  your responses that doing so will result some meaningful insight.

  http://IanGoddard.net/philo.htm 

  "Zen wants absolute freedom, even from God." T.D. Suzuki