- Lid geworden
- 19 apr 2010
- Berichten
- 70
- Waardering
- 1
- Lengte
- 1m71
- Massa
- 60kg
- Vetpercentage
- 7%
Hey DBBers,
Ik heb een half jaar echt dedicated getraint en willekeurig gegeten (alles wat ik maar kon binnenkrijgen) Ik heb overal een laagje spieren gekregen en mijn kracht is echt flink tot soms wel 300% toegenomen. Ik ben van 57 naar 63 KG gegaan met een lengte van 171CM.
De maanden daarna, de afgelopen maanden dus heb ik heel wat literatuur gelezen (en een keer week getraint waar ik zin in had om in conditie te blijven) met als topic fitness en algemene voeding, het meest intressante boek vond ik "The China Study".
Dit boek suggereert dat alle niet genetische kankers gerelateerd zijn met dierlijke eiwitten. Alle ratten die meer dan 5% van hun eiwitconsumtie uit dierlijke producten haalde kregen allemaal ergens in hun leven een vorm van kanker.
Dit boek beschreef ook dat melk meer Calcium uit het lichaam ontrekt dan het eraan toevoegt en dat kinderen die koeienmelk gegeven word een aanzienlijk risico krijgen op diabetes type 1.
Ondersteunt met vele jaren durende onderzoeken.
Toen ik klaar was met dit boek dacht ik, je kan alleen maar flink groeien als je vlees eet, altans dat is online forum BBers algemeen denken en ik dus ook gewoon overgenomen had en daarbij als ik geen vlees at voelde ik me alsof ik geen avondeten gegeten had!
Toen dacht ik opeens een olifant kan duizende kilos wegen en die eet niets meer dan gras en boomschors. Een boom groeit ook tot 100 meter op zonlicht en water.
Dus waarom zou een mens niet kunnen groeien op niet dierlijke producten?
Versta me niet verkeerd, het intresseert me niets wat ik eet. Ik ben niet zo´n dood geen dieren hippie. Ik wil op de lange termein gezond blijven en dan maar geen "zekere" korte termein gains.
Ik kan nergens een serieuze ecto bodybuilder vinden op het internet die jarenlang vegan getraint heeft en succes heeft.
K= Kcal
E=Eiwit
KD= Koolydraten die niet uit suiker komen
OV= (Meervoudig) Onverzadigt vet
V = Vezels
800 gram Pinda´s in schaal K 6300, E 265G, KD 50G, OV 400G, V 58G
500 gram bio lijnzaad K 2225, E 125G, KD --. OV 140G, V 175G
1KG Vruchten müsli K 3310, E 90G, KD 413G, OV 30G, V 100G
2KG BioBananen K 1720, E 24G, KD --, OV --, V 40G
1 KG Spinazie K 160, E 20G, KD 20G, OV --, V 33G
200 gram walnoten K 1400 E 30G, KD 24G, OV 120G, V --
400 gram pistace noten K 2400, E 100G, KD 24G, OV 160G, V 24G
Dagelijks gemiddelde K 2500 E 94G KD 75G OV 121G, V 61G
Dit is puur de basis van wat ik eet, wat er elke week zeker ingaat. Hiernaast Broccoli, Chocolade, een pakje sardientjes uit blik voor omega3, andere soorten groenten en fruit voor afwisseling, studentenvoer als dat er naast al die andere noten nog ingaat, Vitamine B12 Supplement, en alles wat ik toevallig nog tegenkom, de basis is dus ongeveer 70% van wat ik eet.
22 jaar, lengte is 171CM en ik weeg ongeveer 60 Kilo. Het beetje vet dat ik had is wel weg, zit denk ik rond de 6 a 7 procent.
Mijn trainingschema voor de komende 7 maanden is
----------------------------
Weighted Chin Ups, Weighted Push ups, Weighted back Extentions, Dumbbell Shrug, Glute Ham Raise.
2 dagen pauze
Deadlift, Incline Bench Press, 1 Arm Dumbbell row, Standing Dumbbell Curl
2 dagen pauze
Squat, Close grip bench press, Pull up, Barbell Militairy Press.
1 Dag pauze en opnieuw.
1 set opwarmen en dan meteen max set. 5 tot 8 reps met een gewicht dat ik bij herhaling 9 niet verder kan uitvoeren door uitputting. Een set erna kan ik niet omdat ik dan al te afgezwakt ben. 2 dagen pauze is omdat ik gewoon niet vaker kan omdat mijn lichaam nog niet herstelt is.
----------------------------
Jongens, Gaat het lukken om met deze instelling over 2 jaar 75 Kilo te wegen? Ga ik bij deze voeding iedere week 2.5 Kilo aan de stang kunnen toevoegen? Hoe ziet dit er uit? Mensen met veganische ervaring? Mis ik nog iets?
Bron:
THE CHINA STUDY: THE MOST COMPREHENSIVE STUDY OF NUTRITION EVER CONDUCTED
Indian researchers had studied two groups
of rats. In one group, they administered the cancer-causing aflatoxin,
then fed a diet that was composed of 20% protein, a level near what
many of us consume in the West. In the other group, they administered
the same amount of aflatoxin, but then fed a diet that was only composed
of 5% protein. Incredibly, every Single animal that consumed the
20% protein diet had evidence of liver cancer, and every single animal
that consumed a 5% protein diet avoided liver cancer. It was a 100 to 0
score, leaving no doubt that nutrition trumped chemical carcinogens,
even very potent carcinogens, in controlling cancer.
This information countered everything I had been taught. It was
heretical to say that protein wasn't healthy, let alone say it promoted
cancer
--
What we found was shocking. Low-protein diets inhibited the initiation
of cancer by aflatoxin, regardless of how much of this carcinogen
was administered to these animals. After cancer initiation was completed,
low-protein diets also dramatically blocked subsequent cancer
growth. In other words, the cancer-producing effects of this highly carcinogenic
chemical were rendered insignificant by a low-protein diet. In
fact, dietary protein proved to be so powerful in its effect that we could tum
on and tum off cancer growth simply by changing the level consumed.
Furthermore, the amounts of protein being fed were those that we
humans routinely consume. We didn't use extraordinary levels, as is so
often the case in carcinogen studies.
---
But that's not all. We found that not all proteins had this effect. What
protein consistently and strongly promoted cancer? Casein, which
makes up 87% of cow's milk protein, promoted all stages of the cancer
process. What type of protein did not promote cancer, even at high levels
of intake? The safe proteins were from plants, including wheat and
soy. As this picture came into view, it began to challenge and then to
shatter some of my most cherished assumptions.
---
These experimental animal studies didn't end there. I went on to
direct the most comprehensive study of diet, lifestyle and disease ever
done with humans in the history of biomedical research. It was a massive
undertaking jointly arranged through Cornell University, Oxford
University and the Chinese Academy of Preventive Medicine. The New
York Times called it the "Grand Prix of Epidemiology." This project
surveyed a vast range of diseases and diet and lifestyle factors in rural
China and, more recently, in Taiwan. More commonly known as the
China Study, this project eventually produced more than 8,000 statistically
significant associations between various dietary factors and disease!
What made this project especially remarkable is that, among the
many associations that are relevant to diet and disease, so many pointed
to the same finding: people who ate the most animal-based foods got
the most chronic disease. Even relatively small intakes of animal-based
food were associated with adverse effects. People who ate the most
plant-based foods were the healthiest and tended to avoid chronic disease.
These results could not be ignored. From the initial experimental
animal studies on animal protein effects to this massive human study
on dietary patterns, the findings proved to be consistent. The health
implications of consuming either animal or plant-based nutrients were
remarkably different.
I could not, and did not, rest on the findings of our animal studies
and the massive human study in China, however impressive they may
have been. I sought out the findings of other researchers and clinicians.
The findings of these individuals have proved to be some of the most
exciting findings of the past fifty years.
---
Early scientists like Carl Voit (1831-1908), a prominent German
scientist, were staunch champions of protein. Voit found that "man"
needed only 48.5 grams per day, but nonetheless he recommended a
whopping 118 grams per day because of the cultural bias of the time.
Protein equaled meat, and everyone aspired to have meat on his or her
table, just as we aspire to have bigger houses and faster cars. Voit figured
you can't get too much of a good thing.
---
About eight amino acids ("colored beads") that are needed for making
our tissue proteins must be provided by the food we eat. They are
called "essential" because our bodies cannot make them. If, like our
string of beads, our food protein lacks enough of even one of these
eight "essential" amino acids, then the synthesis of the new proteins
will be slowed down or stopped. This is where the idea of protein quality
comes into play. Food proteins of the highest quality are, very simply,
those that provide, upon digestion, the right kinds and amounts of
amino acids needed to efficiently synthesize our new tissue proteins.
This is what that word "quality" really means: it is the ability of food
proteins to provide the right kinds and amounts of amino acids to make
our new proteins.
Can you guess what food we might eat to most efficiently provide
the building blocks for our replacement proteins? The answer is human
flesh. Its protein has just the right amount of the needed amino acids.
But while our fellow men and women are not for dinner, we do get
the next "best" protein by eating other animals. The proteins of other
animals are very similar to our proteins because they mostly have the
right amounts of each of the needed amino acids. These proteins can be
used very efficiently and therefore are called "high quality." Among animal
foods, the proteins of milk and eggs represent the best amino acid
matches for our proteins, and thus are considered the highest quality.
While the "lower quality" plant proteins may be lacking in one or more
of the essential amino acids, as a group they do contain all of them.
The concept of quality really means the efficiency with which food
proteins are used to promote growth. This would be well and good if the
greatest efficiency equaled the greatest health, but it doesn't, and that's
why the terms efficiency and quality are misleading. In fact, to give you
a taste of what's to come, there is a mountain of compelling research
showing that "low-quality" plant protein, which allows for slow but
steady synthesis of new proteins, is the healthiest type of protein. Slow
but steady wins the race. The quality of protein found in a specific food
is determined by seeing how fast animals would grow while consuming
it. Some foods, namely those from animals, emerge with a very high
protein efficiency ratio and value. 1
This focus on efficiency of body growth, as if it were good health, encourages
the consumption of protein with the highest "quality." As any
marketer will tell you, a product that is defined as being high quality
instantly earns the trust of consumers. For well over 100 years, we have
been captive to this misleading language and have oftentimes made the
unfortunate leap to thinking that more quality equals more health.
The basis for this concept of protein quality was not well known
among the public, but its impact was-and still is-highly significant.
People, for example, who choose to consume a plant-based diet will
often ask, even today, "Where do I get my protein?" as if plants don't
have protein. Even if it is known that plants have protein, there is still
the concern about its perceived poor quality: This has led people to
believe that they must meticulously combine proteins from different
plant sources during each meal so that they can mutually compensate
for each other's amino acid deficits. However, this is overstating the
case. We now know that through enormously complex metabolic systems,
the human body can derive all the essential amino acids from the
natural variety of plant proteins that we encounter every day. It doesn't
require eating higher quantities of plant protein or meticulously planning
every meal. Unfortunately, the enduring concept of protein quality
has greatly obscured this information.
---
NOT ALL PROTEINS ARE ALIKE
If you have followed the story so far, you have seen how provocative
these findings are. Controlling cancer through nutrition was, and still
is, a radical idea. But as if this weren't enough, one more issue would
yield explOSive information: did it make any difference what type of
protein was used in these experiments? For all of these experiments,
we were using casein, which makes up 87% of cow's milk protein. So
the next logical question was whether plant protein, tested in the same
way, has the same effect on cancer promotion as casein. The answer is
an astonishing "NO." In these experiments, plant protein did not promote
cancer growth, even at the higher levels of intake. An undergraduate premedical
student doing an honors degree with me, David Schulsinger,
did the study
We also examined whether soy protein had the same effect as casein
on foci development. Rats fed 20% soy protein diets did not form. early foci,
just like the 20% wheat protein diets. Suddenly protein, milk protein in this
case, wasn't looking so good. We had discovered that low protein intake
reduces cancer initiation and works in multiple synchronous ways. As if
that weren't enough, we were finding that high protein intake, in excess
of the amount needed for growth, promotes cancer after initiation. Like
flipping a light switch on and off, we could control cancer promotion
merely by changing levels of protein, regardless of initial carcinogen
exposure. But the cancer-promoting factor in this case was cow's milk
protein. It was difficult enough for my colleagues to accept the idea that
protein might help cancer grow, but cow's milk protein? Was I crazy?
---
THE GRAND FINALE
Thus far we had relied on experiments where we measured only the early
indicators of tumor development, the early cancer-like foci. Now, it
was time to do the big study, the one where we would measure complete
tumor formation. We organized a very large study of several hundred
rats and examined tumor formation over their lifetimes using several
different approaches.
The effects of protein feeding on tumor development were nothing
less than spectacular. Rats generally live for about two years, thus the
study was 100 weeks in length. All animals that were administered aflatoxin
and fed the regular 20% levels of casein either were dead or near
death from liver tumors at 100 weeks.
All animals administered the
same level of aflatoxin but fed the low 5% protein diet were alive, active
and thrifty, with sleek hair coats at 100 weeks. This was a virtual 100 to
o score, something almost never seen in research and almost identical
to the original research in India.
In this same experiment we switched the diets of some rats at either
forty or sixty weeks, to again investigate the reversibility of cancer promotion.
Animals switched from a high-protein to a low-protein diet had
significantly less tumor growth (35°tb-40% less!) than animals fed a highprotein
diet. Animals switched from a low-protein diet to a high-protein
diet halfway through their lifetime started growing tumors again. These
findings on full-blown tumors confirmed our earlier findings using foci.
Namely, nutritional manipulation can turn cancer "on" and "off."
We also measured early foci in these "lifetime" studies to see if their
response to dietary protein was similar to that for tumor response. The
correspondence between foci growth and tumor growth could not have
been greater
How much more did we need to find out? I would never have dreamed
that our results up to this point would be so incredibly consistent, biologically
plausible and statistically significant. We had fully confirmed the
original work from India and had done it in exceptional depth.
Let there be no doubt: cow's milk protein is an exceptionally potent
cancer promoter in rats dosed with aflatoxin. The fact that this promotion
effect occurs at dietary protein levels 00-20%) commonly used both in
rodents and humans makes it especially tantalizing-and provocative.
---
I doubt that a high-calcium diet, obtained through calcium supplements
or through calcium-rich cow's milk, has a beneficial effect on
colon cancer. In rural China where calcium consumption is modest and
almost no dairy food is consumed,87 colon cancer rates are not higher;
instead they are much lower than in the U.S. The parts of the world that
consume the most calcium, Europe and North America, have the highest
rates of colorectal cancer.
---
One of the foods that supply many of the foreign proteins that mimic
our own body proteins is cow's milk. Most of the time, our immune
system is quite smart. Just like an army arranges for safeguards against
friendly fire, the immune system has safeguards to stop itself from attacking
the body it's supposed to protect. Even though an invading
antigen looks just like one of the cells in our own body, the system can
still distinguish our own cells from the invading antigen. In fact, the immune
system may use our own cells to practice making molds against
the invader antigen without actually destroying the friendly cell.
This is analogous to training camps in preparations for war. When our
immune system is working properly, we can use the cells in our body that
look like the antigens as a training exercise, without destroying them, to
prepare our soldier cells to repulse the invading antigens. It is one more
examplel of the exceptional elegance of nature's ability to regulate itself.
AUTOIMMUNE DISEASES 187
The immune system uses a very delicate process to decide which proteins
should be attacked and which should be left alone.ll The way this
process, which is incredibly complex, breaks down with autoimmune
diseases is not yet understood. We just know that the immune system
loses its ability to differentiate between the body's cells and the invading
antigen, and instead of using the body's cells for "training," it destroys
them along with the invaders.
TYPE 1 DIABETES
In the case of Type 1 diabetes, the immune system attacks the pancreas
cells responsible for producing insulin. This devastating, incurable
disease strikes children, creating a painful and difficult experience for
young families. What most people don't know, though, is that there is
strong evidence that this disease is linked to diet and, more specifically,
to dairy products. The ability of cow's milk protein to initiate Type 1
diabetes12
-
14 is well documented. The possible initiation of this disease
goes like this:
• A baby is not nursed long enough and is fed cow's milk protein,
perhaps in an infant formula.
• The milk reaches the small intestine, where it is digested down to
its amino acid parts.
• For some infants, cow's milk is not fully digested, and small amino
acid chains or fragments of the original protein remain in the intestine.
• These incompletely digested protein fragments may be absorbed
into the blood.
• The immune system recognizes these fragments as foreign invaders
and goes about destroying them.
• Unfortunately, some of the fragments look exactly the same as the
cells of the pancreas that are responsible for making insulin.
• The immune system loses its ability to distinguish between the
cow's milk protein fragments and the pancreatic cells, and destroys
them both, thereby eliminating the child's ability to produce insulin.
• The infant becomes a Type 1 diabetic, and remains so for the rest
of his or her life.
This process boils down to a truly remarkable statement: cow~ milk
may cause one of the most devastating diseases that can befall a child. For
188 THE CHINA STUDY
obvious reasons, this is one of the most contentious issues in nutrition
today.
One of the more remarkable reports on this cow's milk effect was
published over a decade ago, in 1992, in the New England Journal of
Medicine. 12 The researchers, from Finland, obtained blood from Type
1 diabetic children, aged four to twelve years. Then they measured the
levels of antibodies that had formed in the blood against an incompletely
digested protein of cow's milk called bovine serum albumin (BSA).
They did the same process with non-diabetic children and compared
the two groups (remember, an antibody is the mirror image, or "mold,"
of a foreign antigen) . Children who had antibodies to cow's milk protein
must have previously consumed cow's milk. It also means that undigested
protein fragments of the cow's milk proteins had to have entered
the infant's circulation in order to cause the formation of antibodies in
the first place.
The researchers discovered something truly remarkable. Of the 142
diabetic children measured, every Single one had antibody levels higher
than 3.55. Of the seventy-nine normal children measured, every single
one had antibody levels less than 3.55.
There is absolutely no overlap between antibodies of healthy and
diabetic children. All of the diabetic children had levels of cow's milk
antibodies that were higher than those of all of the non-diabetic children.
This implies two things: children with more antibodies consumed
more cow's milk, and second, increased antibodies may cause Type 1
diabetes.
These results sent shock waves through the research community. It
was the complete separation of antibody responses that made this study
so remarkable. This study,12 and others even earlier,15-17 initiated an avalanche
of additional studies over the next several years that continue to
this day. 13. 18. 19
Several studies have since investigated this effect of cow's milk on
BSA antibody levels. All but one showed that cow's milk increases BSA
antibodies in Type 1 diabetic children,18 although the responses were
quite variable in their magnitude.
Over the past decade, scientists have investigated far more than
just the BSA antibodies, and a more complete picture is coming into
view. Very briefly, it goes something like this13, 19: infants or very young
children of a certain genetic background,2o,21 who are weaned from the
breast too early22 onto cow's milk and who, perhaps, become infected
AUTOIMMUNE OISEASES 189
with a virus that may corrupt the gut immune system,l9 are likely to
have a high risk for Type 1 diabetes. A study in Chile23 considered the
first two factors, cow's milk and genes. Genetically susceptible children
weaned too early onto cow's milk-based formula had a risk of Type 1 diabetes
that was 13.1 times greater than children who did not have these
genes and who were breast-fed for at least three months (thus minimizing
their exposure to cow's milk). Another study in the U.S. showed that
genetically susceptible children fed cow's milk as infants had a risk of
disease that was 11.3 times greater than children who did not have these
genes and who were breast-fed for at least three months. 24 This eleven
to thirteen times greater risk is incredibly large (1,000-1,200%!); anything
over three to four times is usually considered very important. To
put this in perspective, smokers have approximately ten times greater
risk of getting lung cancer (still less than the eleven to thirteen times
risk here) and people with high blood pressure and cholesterol have a
2.5-3.0 times greater risk of heart disease (Chart 9.2) .18
So how much of the eleven to thirteen times increased risk of Type
1 diabetes is due to early exposure to cow's milk, and how much is due
to genes? These days, there is a popular opinion that Type 1 diabetes is
due to genetics, an opinion often shared by doctors as well. But genetics
alone cannot account for more than a very small fraction of cases of this
disease. Genes do not act in isolation; they need a trigger for their effects
to be produced. It has also been observed that after one member of
identical twin pairs gets Type 1 diabetes, there is only a 13-33% chance
of the second twin getting the disease, even though both twins have
the same genes. l3, 20, 21, 25. 26 If it were all due to genes, closer to lOO% of
the identical twins would get the disease. In addition, it is possible that
the 13-33% risk for the second twin is due to the sharing of a common
environment and diet, factors affecting both twins.
Consider, for example, the observation shown in Chart 9.3, which
highlights the link between one aspect of environment, cow's milk consumption,
and this disease. Cow's milk consumption by children zero
to fourteen years of age in twelve countries27 shows an almost perfect
correlation with Type 1 diabetes.28 The greater the consumption of
cow's milk, the greater the prevalence of Type 1 diabetes. In Finland,
Type 1 diabetes is thirty-six times more common than in Japan.29 Large
amounts of cow's milk products are consumed in Finland but very little
is consumed in Japan
As we have seen with other diseases of affluence, when people migrate
from areas of the world where disease incidence is low to areas of the
world where disease incidence is high, they quickly adopt the high incidence
rates as they change their diet and lifestyle.3O-32 This shows that even
though individuals may have the necessary gene(s), the disease will occur
only in response to certain dietary and/or environmental circumstances.
Disease trends over time show the same thing. The worldwide prevalence
of Type 1 diabetes is increasing at an alarming rate of 3% per year. 33
This increase is occurring for different populations even though there
may be substantial differences in disease rates. This relatively rapid increase
cannot be due to genetic susceptibility. The frequency of anyone
gene in a large population is relatively stable over time, unless there are
changing environmental pressures that allow one group to reproduce
more successfully than another group. For example, if all families with
Type 1 diabetic relatives had a dozen babies and all the families without
Type 1 diabetic relatives died off, then the gene or genes that may be
responsible for Type 1 diabetes would become much more common in
the population. This, of course, is not what is happening, and the fact
that Type 1 diabetes is increasing 3% every year is very strong evidence
that genes are not solely responsible for this disease.
It seems to me that we now have impressive evidence shOWing that
cow's milk is likely to be an important cause of Type 1 diabetes. When
the results of all these studies are combined (both genetically susceptible
and not susceptible), we find that children weaned too early and
fed cow's milk have, on average, a 50-60% higher risk of Type 1 diabetes
(1.5-1.6 times increased risk).34
The earlier information on diet and Type 1 diabetes was impressive
enough to cause two Significant developments. The American Academy
of Pediatrics in 1994 "strongly encouraged" that infants in families
where diabetes is more common not be fed cow's milk supplements for
their first two years of life. Second, many researchers19 have developed
prospective studies-the kind that follow individuals into the futureto
see if a careful monitoring of diet and lifestyle could explain the onset
of Type 1 diabetes.
Two of the better known of these studies have been underway in Finland,
one starting in the late 1980S15 and the other in the mid-1990s.35
One has shown that cow's milk consumption increases the risk of Type
1 diabetes five- to sixfold,36 while the second35 tells us that cow's milk
increases the development of at least another three to four antibodies
192 THE CHINA STUDY
in addition to those presented previously (p. 190). In a separate study,
antibodies to beta-casein, another cow's milk protein, were significantly
elevated in bottle-fed infants compared to breast-fed infants; children
with Type 1 diabetes also had higher levels of these antibodies.37 In
short, of the studies that have reported results, the findings strongly
confirm the danger of cows milk, especially for genetically susceptible
children.
THE CONTROVERSY OF CONTROVERSY
Imagine looking at the front page of the newspaper and finding the
following headline: "Cow's Milk the Likely Cause of Lethal Type 1
Diabetes." Because the reaction would be so strong, and the economic
impact monumental, this headline won't be written anytime soon,
regardless of the scientific evidence. Stifling this headline is accomplished
under the powerful label of "controversy." With so much at
stake, and so much information understood by so few people, it is easy
to generate and sustain controversy. Controversies are a natural part
of science. Too often, however, controversy is not the result of legitimate
scientific debate, but instead reflects the perceived need to delay
and distort research results. For example, if I say cigarettes are bad for
you and provide a mountain of evidence to support my contention,
the tobacco companies might come along and pick out one unsolved
detail and then claim that the whole idea of cigarettes being unhealthy
is mired in controversy, thereby nullifying all my conclusions. This is
easy to do, because there will always be unsolved details; this is the
nature of science. Some groups use controversy to stifle certain ideas,
impede constructive research, confuse the public and turn public
policy into babble rather than substance. Sustaining controversy as a
means of discrediting findings that cause economic or social discomfort
is one of the greatest sins in science.
It can be difficult for the layperson to assess the legitimacy of a highly
technical controversy such as that regarding cow's milk and Type 1 diabetes.
This is true even if the layperson is interested in reading scientific
articles.
Take a recent scientific review38 of the cow's milk-Type 1 diabetes
association. In ten human studies (all case-control) summarized in a
paper published as part of a "controversial topics series,"38 the authors
concluded that five of the ten studies showed a statistically Significant
positive association between cow's milk and Type 1 diabetes and five did
L
AUTOIMMUNE DISEASES 193
not. Obviously, this at first seems to demonstrate considerable uncertainty,
going a long way to discredit the hypothesis.
However, the five studies that were counted as "negative" did not
show that cow's milk decreased Type 1 diabetes. These five studies
showed no statistically significant effect either way. In contrast, there
are a total of five statistically significant studies and all five showed the
same result: early cow's milk consumption is associated with increased
risk of Type 1 diabetes. There is only one chance in sixty-four that this
was a random or chance result.
There are many, many reasons, some seen and some unseen, why an
experiment would find no statistically significant relationship between
two factors, even when a relationship really exists. Perhaps the study
didn't include enough people, and statistical certainty was unattainable.
Perhaps most of the subjects had very similar feeding practices, limiting
detection of the relationship you might otherwise see. Maybe trying to
measure infant feeding practices from years ago was inaccurate enough
that it obscured the relationship that does exist. Perhaps the researchers
were studying the wrong period of time in an infant's life.
The point is, if five of the ten studies did find a statistically significant
relationship, and all five showed that cow's milk consumption is linked
to increasing Type 1 diabetes, and none show that cow's milk consumption
is linked to decreasing Type 1 diabetes, I could hardly justify saying,
as the authors of this review did, that the hypothesis "has become
quite murky with inconsistencies in the literature. "38
In this same review,38 the authors summarized additional studies that
indirectly compared breast-feeding practices associated with cow's milk
consumption and Type 1 diabetes. This compilation involved fifty-two
possible comparisons, twenty of which were statistically significant. Of
these twenty significant findings, nineteen favored an association of cows
milk with disease, and only one did not. Again the odds heavily favored the
hypotheSized association, something that the authors failed to note.
I cite this example not only to support the evidence showing a cow's
milk effect on Type 1 diabetes, but also to illustrate one tactic that is
often used to make something controversial when it is not. This practice
is more common than it should be and is a source of unnecessary confusion.
When researchers do this-even if they do it unintentionallythey
often have a serious prejudice against the hypothesis in the first
place. Indeed, shortly after I wrote this, I heard a brief National Public
Radio interview on the Type 1 diabetes problem with the senior author
194 THE CHINA STUDY
of this review paper.38 Suffice it to say, the author did not acknowledge
the evidence for the cow's milk hypothesis.
Because this issue has mammoth financial implications for American
agriculture, and because so many people have such intense personal
biases against it, it is unlikely that this diabetes research will reach the
American media anytime soon. However, the depth and breadth of evidence
now implicating cow's milk as a cause of Type 1 diabetes is overwhelming,
even though the very complex mechanistic details are not
yet fully understood. We not only have evidence of the danger of cow's
milk, we also have considerable evidence showing that the association
between diabetes and cow's milk is biologically plausible. Human breast
milk is the perfect food for an infant, and one of the most damaging
things a mother can do is to substitute the milk of a cow for her own.
MULTIPLE SCLEROSIS
AND OTHER AUTOIMMUNE DISEASES
Multiple sclerosis (MS) is a particularly difficult autoimmune disease,
both for those who have it and for those who care for its victims. It is a
lifelong battle involving a variety of unpredictable and serious disabilities.
MS patients often pass through episodes of acute attacks while gradually
losing their ability to walk or to see. After ten to fifteen years, they often
are confined to a wheelchair, and then to a bed for the rest of their lives.
About 400,000 people in the u.s. alone have the disease, according
to the National Multiple Sclerosis Society.39 It is a disease that is initially
diagnosed between twenty and forty years of age and strikes women
about three times more often than men.
Even though there is widespread medical and scientific interest in
this disease, most authorities claim to know very little about causes
or cures. Major multiple sclerosis Internet Web sites all claim that the
disease is an enigma. They generally list genetics, viruses and environmental
factors as possibly playing roles in the development of this disease
but pay almost no heed to a possible role for diet. This is peculiar
considering the wealth of intriguing information on the effects of food
that is available from reputable research reports.40--42 Once again cow's
milk appears to play an important role.
The "multiple" symptoms of this disease represent a nervous system
gone awry. The electrical signals carrying messages to and from the
central nervous system (brain and spinal cord) and out through the peripheral
nervous system to the rest of the body are not well coordinated
Ik heb een half jaar echt dedicated getraint en willekeurig gegeten (alles wat ik maar kon binnenkrijgen) Ik heb overal een laagje spieren gekregen en mijn kracht is echt flink tot soms wel 300% toegenomen. Ik ben van 57 naar 63 KG gegaan met een lengte van 171CM.
De maanden daarna, de afgelopen maanden dus heb ik heel wat literatuur gelezen (en een keer week getraint waar ik zin in had om in conditie te blijven) met als topic fitness en algemene voeding, het meest intressante boek vond ik "The China Study".
Dit boek suggereert dat alle niet genetische kankers gerelateerd zijn met dierlijke eiwitten. Alle ratten die meer dan 5% van hun eiwitconsumtie uit dierlijke producten haalde kregen allemaal ergens in hun leven een vorm van kanker.
Dit boek beschreef ook dat melk meer Calcium uit het lichaam ontrekt dan het eraan toevoegt en dat kinderen die koeienmelk gegeven word een aanzienlijk risico krijgen op diabetes type 1.
Ondersteunt met vele jaren durende onderzoeken.
Toen ik klaar was met dit boek dacht ik, je kan alleen maar flink groeien als je vlees eet, altans dat is online forum BBers algemeen denken en ik dus ook gewoon overgenomen had en daarbij als ik geen vlees at voelde ik me alsof ik geen avondeten gegeten had!
Toen dacht ik opeens een olifant kan duizende kilos wegen en die eet niets meer dan gras en boomschors. Een boom groeit ook tot 100 meter op zonlicht en water.
Dus waarom zou een mens niet kunnen groeien op niet dierlijke producten?
Versta me niet verkeerd, het intresseert me niets wat ik eet. Ik ben niet zo´n dood geen dieren hippie. Ik wil op de lange termein gezond blijven en dan maar geen "zekere" korte termein gains.
Ik kan nergens een serieuze ecto bodybuilder vinden op het internet die jarenlang vegan getraint heeft en succes heeft.
K= Kcal
E=Eiwit
KD= Koolydraten die niet uit suiker komen
OV= (Meervoudig) Onverzadigt vet
V = Vezels
800 gram Pinda´s in schaal K 6300, E 265G, KD 50G, OV 400G, V 58G
500 gram bio lijnzaad K 2225, E 125G, KD --. OV 140G, V 175G
1KG Vruchten müsli K 3310, E 90G, KD 413G, OV 30G, V 100G
2KG BioBananen K 1720, E 24G, KD --, OV --, V 40G
1 KG Spinazie K 160, E 20G, KD 20G, OV --, V 33G
200 gram walnoten K 1400 E 30G, KD 24G, OV 120G, V --
400 gram pistace noten K 2400, E 100G, KD 24G, OV 160G, V 24G
Dagelijks gemiddelde K 2500 E 94G KD 75G OV 121G, V 61G
Dit is puur de basis van wat ik eet, wat er elke week zeker ingaat. Hiernaast Broccoli, Chocolade, een pakje sardientjes uit blik voor omega3, andere soorten groenten en fruit voor afwisseling, studentenvoer als dat er naast al die andere noten nog ingaat, Vitamine B12 Supplement, en alles wat ik toevallig nog tegenkom, de basis is dus ongeveer 70% van wat ik eet.
22 jaar, lengte is 171CM en ik weeg ongeveer 60 Kilo. Het beetje vet dat ik had is wel weg, zit denk ik rond de 6 a 7 procent.
Mijn trainingschema voor de komende 7 maanden is
----------------------------
Weighted Chin Ups, Weighted Push ups, Weighted back Extentions, Dumbbell Shrug, Glute Ham Raise.
2 dagen pauze
Deadlift, Incline Bench Press, 1 Arm Dumbbell row, Standing Dumbbell Curl
2 dagen pauze
Squat, Close grip bench press, Pull up, Barbell Militairy Press.
1 Dag pauze en opnieuw.
1 set opwarmen en dan meteen max set. 5 tot 8 reps met een gewicht dat ik bij herhaling 9 niet verder kan uitvoeren door uitputting. Een set erna kan ik niet omdat ik dan al te afgezwakt ben. 2 dagen pauze is omdat ik gewoon niet vaker kan omdat mijn lichaam nog niet herstelt is.
----------------------------
Jongens, Gaat het lukken om met deze instelling over 2 jaar 75 Kilo te wegen? Ga ik bij deze voeding iedere week 2.5 Kilo aan de stang kunnen toevoegen? Hoe ziet dit er uit? Mensen met veganische ervaring? Mis ik nog iets?
Bron:
THE CHINA STUDY: THE MOST COMPREHENSIVE STUDY OF NUTRITION EVER CONDUCTED
Indian researchers had studied two groups
of rats. In one group, they administered the cancer-causing aflatoxin,
then fed a diet that was composed of 20% protein, a level near what
many of us consume in the West. In the other group, they administered
the same amount of aflatoxin, but then fed a diet that was only composed
of 5% protein. Incredibly, every Single animal that consumed the
20% protein diet had evidence of liver cancer, and every single animal
that consumed a 5% protein diet avoided liver cancer. It was a 100 to 0
score, leaving no doubt that nutrition trumped chemical carcinogens,
even very potent carcinogens, in controlling cancer.
This information countered everything I had been taught. It was
heretical to say that protein wasn't healthy, let alone say it promoted
cancer
--
What we found was shocking. Low-protein diets inhibited the initiation
of cancer by aflatoxin, regardless of how much of this carcinogen
was administered to these animals. After cancer initiation was completed,
low-protein diets also dramatically blocked subsequent cancer
growth. In other words, the cancer-producing effects of this highly carcinogenic
chemical were rendered insignificant by a low-protein diet. In
fact, dietary protein proved to be so powerful in its effect that we could tum
on and tum off cancer growth simply by changing the level consumed.
Furthermore, the amounts of protein being fed were those that we
humans routinely consume. We didn't use extraordinary levels, as is so
often the case in carcinogen studies.
---
But that's not all. We found that not all proteins had this effect. What
protein consistently and strongly promoted cancer? Casein, which
makes up 87% of cow's milk protein, promoted all stages of the cancer
process. What type of protein did not promote cancer, even at high levels
of intake? The safe proteins were from plants, including wheat and
soy. As this picture came into view, it began to challenge and then to
shatter some of my most cherished assumptions.
---
These experimental animal studies didn't end there. I went on to
direct the most comprehensive study of diet, lifestyle and disease ever
done with humans in the history of biomedical research. It was a massive
undertaking jointly arranged through Cornell University, Oxford
University and the Chinese Academy of Preventive Medicine. The New
York Times called it the "Grand Prix of Epidemiology." This project
surveyed a vast range of diseases and diet and lifestyle factors in rural
China and, more recently, in Taiwan. More commonly known as the
China Study, this project eventually produced more than 8,000 statistically
significant associations between various dietary factors and disease!
What made this project especially remarkable is that, among the
many associations that are relevant to diet and disease, so many pointed
to the same finding: people who ate the most animal-based foods got
the most chronic disease. Even relatively small intakes of animal-based
food were associated with adverse effects. People who ate the most
plant-based foods were the healthiest and tended to avoid chronic disease.
These results could not be ignored. From the initial experimental
animal studies on animal protein effects to this massive human study
on dietary patterns, the findings proved to be consistent. The health
implications of consuming either animal or plant-based nutrients were
remarkably different.
I could not, and did not, rest on the findings of our animal studies
and the massive human study in China, however impressive they may
have been. I sought out the findings of other researchers and clinicians.
The findings of these individuals have proved to be some of the most
exciting findings of the past fifty years.
---
Early scientists like Carl Voit (1831-1908), a prominent German
scientist, were staunch champions of protein. Voit found that "man"
needed only 48.5 grams per day, but nonetheless he recommended a
whopping 118 grams per day because of the cultural bias of the time.
Protein equaled meat, and everyone aspired to have meat on his or her
table, just as we aspire to have bigger houses and faster cars. Voit figured
you can't get too much of a good thing.
---
About eight amino acids ("colored beads") that are needed for making
our tissue proteins must be provided by the food we eat. They are
called "essential" because our bodies cannot make them. If, like our
string of beads, our food protein lacks enough of even one of these
eight "essential" amino acids, then the synthesis of the new proteins
will be slowed down or stopped. This is where the idea of protein quality
comes into play. Food proteins of the highest quality are, very simply,
those that provide, upon digestion, the right kinds and amounts of
amino acids needed to efficiently synthesize our new tissue proteins.
This is what that word "quality" really means: it is the ability of food
proteins to provide the right kinds and amounts of amino acids to make
our new proteins.
Can you guess what food we might eat to most efficiently provide
the building blocks for our replacement proteins? The answer is human
flesh. Its protein has just the right amount of the needed amino acids.
But while our fellow men and women are not for dinner, we do get
the next "best" protein by eating other animals. The proteins of other
animals are very similar to our proteins because they mostly have the
right amounts of each of the needed amino acids. These proteins can be
used very efficiently and therefore are called "high quality." Among animal
foods, the proteins of milk and eggs represent the best amino acid
matches for our proteins, and thus are considered the highest quality.
While the "lower quality" plant proteins may be lacking in one or more
of the essential amino acids, as a group they do contain all of them.
The concept of quality really means the efficiency with which food
proteins are used to promote growth. This would be well and good if the
greatest efficiency equaled the greatest health, but it doesn't, and that's
why the terms efficiency and quality are misleading. In fact, to give you
a taste of what's to come, there is a mountain of compelling research
showing that "low-quality" plant protein, which allows for slow but
steady synthesis of new proteins, is the healthiest type of protein. Slow
but steady wins the race. The quality of protein found in a specific food
is determined by seeing how fast animals would grow while consuming
it. Some foods, namely those from animals, emerge with a very high
protein efficiency ratio and value. 1
This focus on efficiency of body growth, as if it were good health, encourages
the consumption of protein with the highest "quality." As any
marketer will tell you, a product that is defined as being high quality
instantly earns the trust of consumers. For well over 100 years, we have
been captive to this misleading language and have oftentimes made the
unfortunate leap to thinking that more quality equals more health.
The basis for this concept of protein quality was not well known
among the public, but its impact was-and still is-highly significant.
People, for example, who choose to consume a plant-based diet will
often ask, even today, "Where do I get my protein?" as if plants don't
have protein. Even if it is known that plants have protein, there is still
the concern about its perceived poor quality: This has led people to
believe that they must meticulously combine proteins from different
plant sources during each meal so that they can mutually compensate
for each other's amino acid deficits. However, this is overstating the
case. We now know that through enormously complex metabolic systems,
the human body can derive all the essential amino acids from the
natural variety of plant proteins that we encounter every day. It doesn't
require eating higher quantities of plant protein or meticulously planning
every meal. Unfortunately, the enduring concept of protein quality
has greatly obscured this information.
---
NOT ALL PROTEINS ARE ALIKE
If you have followed the story so far, you have seen how provocative
these findings are. Controlling cancer through nutrition was, and still
is, a radical idea. But as if this weren't enough, one more issue would
yield explOSive information: did it make any difference what type of
protein was used in these experiments? For all of these experiments,
we were using casein, which makes up 87% of cow's milk protein. So
the next logical question was whether plant protein, tested in the same
way, has the same effect on cancer promotion as casein. The answer is
an astonishing "NO." In these experiments, plant protein did not promote
cancer growth, even at the higher levels of intake. An undergraduate premedical
student doing an honors degree with me, David Schulsinger,
did the study
We also examined whether soy protein had the same effect as casein
on foci development. Rats fed 20% soy protein diets did not form. early foci,
just like the 20% wheat protein diets. Suddenly protein, milk protein in this
case, wasn't looking so good. We had discovered that low protein intake
reduces cancer initiation and works in multiple synchronous ways. As if
that weren't enough, we were finding that high protein intake, in excess
of the amount needed for growth, promotes cancer after initiation. Like
flipping a light switch on and off, we could control cancer promotion
merely by changing levels of protein, regardless of initial carcinogen
exposure. But the cancer-promoting factor in this case was cow's milk
protein. It was difficult enough for my colleagues to accept the idea that
protein might help cancer grow, but cow's milk protein? Was I crazy?
---
THE GRAND FINALE
Thus far we had relied on experiments where we measured only the early
indicators of tumor development, the early cancer-like foci. Now, it
was time to do the big study, the one where we would measure complete
tumor formation. We organized a very large study of several hundred
rats and examined tumor formation over their lifetimes using several
different approaches.
The effects of protein feeding on tumor development were nothing
less than spectacular. Rats generally live for about two years, thus the
study was 100 weeks in length. All animals that were administered aflatoxin
and fed the regular 20% levels of casein either were dead or near
death from liver tumors at 100 weeks.
All animals administered the
same level of aflatoxin but fed the low 5% protein diet were alive, active
and thrifty, with sleek hair coats at 100 weeks. This was a virtual 100 to
o score, something almost never seen in research and almost identical
to the original research in India.
In this same experiment we switched the diets of some rats at either
forty or sixty weeks, to again investigate the reversibility of cancer promotion.
Animals switched from a high-protein to a low-protein diet had
significantly less tumor growth (35°tb-40% less!) than animals fed a highprotein
diet. Animals switched from a low-protein diet to a high-protein
diet halfway through their lifetime started growing tumors again. These
findings on full-blown tumors confirmed our earlier findings using foci.
Namely, nutritional manipulation can turn cancer "on" and "off."
We also measured early foci in these "lifetime" studies to see if their
response to dietary protein was similar to that for tumor response. The
correspondence between foci growth and tumor growth could not have
been greater
How much more did we need to find out? I would never have dreamed
that our results up to this point would be so incredibly consistent, biologically
plausible and statistically significant. We had fully confirmed the
original work from India and had done it in exceptional depth.
Let there be no doubt: cow's milk protein is an exceptionally potent
cancer promoter in rats dosed with aflatoxin. The fact that this promotion
effect occurs at dietary protein levels 00-20%) commonly used both in
rodents and humans makes it especially tantalizing-and provocative.
---
I doubt that a high-calcium diet, obtained through calcium supplements
or through calcium-rich cow's milk, has a beneficial effect on
colon cancer. In rural China where calcium consumption is modest and
almost no dairy food is consumed,87 colon cancer rates are not higher;
instead they are much lower than in the U.S. The parts of the world that
consume the most calcium, Europe and North America, have the highest
rates of colorectal cancer.
---
One of the foods that supply many of the foreign proteins that mimic
our own body proteins is cow's milk. Most of the time, our immune
system is quite smart. Just like an army arranges for safeguards against
friendly fire, the immune system has safeguards to stop itself from attacking
the body it's supposed to protect. Even though an invading
antigen looks just like one of the cells in our own body, the system can
still distinguish our own cells from the invading antigen. In fact, the immune
system may use our own cells to practice making molds against
the invader antigen without actually destroying the friendly cell.
This is analogous to training camps in preparations for war. When our
immune system is working properly, we can use the cells in our body that
look like the antigens as a training exercise, without destroying them, to
prepare our soldier cells to repulse the invading antigens. It is one more
examplel of the exceptional elegance of nature's ability to regulate itself.
AUTOIMMUNE DISEASES 187
The immune system uses a very delicate process to decide which proteins
should be attacked and which should be left alone.ll The way this
process, which is incredibly complex, breaks down with autoimmune
diseases is not yet understood. We just know that the immune system
loses its ability to differentiate between the body's cells and the invading
antigen, and instead of using the body's cells for "training," it destroys
them along with the invaders.
TYPE 1 DIABETES
In the case of Type 1 diabetes, the immune system attacks the pancreas
cells responsible for producing insulin. This devastating, incurable
disease strikes children, creating a painful and difficult experience for
young families. What most people don't know, though, is that there is
strong evidence that this disease is linked to diet and, more specifically,
to dairy products. The ability of cow's milk protein to initiate Type 1
diabetes12
-
14 is well documented. The possible initiation of this disease
goes like this:
• A baby is not nursed long enough and is fed cow's milk protein,
perhaps in an infant formula.
• The milk reaches the small intestine, where it is digested down to
its amino acid parts.
• For some infants, cow's milk is not fully digested, and small amino
acid chains or fragments of the original protein remain in the intestine.
• These incompletely digested protein fragments may be absorbed
into the blood.
• The immune system recognizes these fragments as foreign invaders
and goes about destroying them.
• Unfortunately, some of the fragments look exactly the same as the
cells of the pancreas that are responsible for making insulin.
• The immune system loses its ability to distinguish between the
cow's milk protein fragments and the pancreatic cells, and destroys
them both, thereby eliminating the child's ability to produce insulin.
• The infant becomes a Type 1 diabetic, and remains so for the rest
of his or her life.
This process boils down to a truly remarkable statement: cow~ milk
may cause one of the most devastating diseases that can befall a child. For
188 THE CHINA STUDY
obvious reasons, this is one of the most contentious issues in nutrition
today.
One of the more remarkable reports on this cow's milk effect was
published over a decade ago, in 1992, in the New England Journal of
Medicine. 12 The researchers, from Finland, obtained blood from Type
1 diabetic children, aged four to twelve years. Then they measured the
levels of antibodies that had formed in the blood against an incompletely
digested protein of cow's milk called bovine serum albumin (BSA).
They did the same process with non-diabetic children and compared
the two groups (remember, an antibody is the mirror image, or "mold,"
of a foreign antigen) . Children who had antibodies to cow's milk protein
must have previously consumed cow's milk. It also means that undigested
protein fragments of the cow's milk proteins had to have entered
the infant's circulation in order to cause the formation of antibodies in
the first place.
The researchers discovered something truly remarkable. Of the 142
diabetic children measured, every Single one had antibody levels higher
than 3.55. Of the seventy-nine normal children measured, every single
one had antibody levels less than 3.55.
There is absolutely no overlap between antibodies of healthy and
diabetic children. All of the diabetic children had levels of cow's milk
antibodies that were higher than those of all of the non-diabetic children.
This implies two things: children with more antibodies consumed
more cow's milk, and second, increased antibodies may cause Type 1
diabetes.
These results sent shock waves through the research community. It
was the complete separation of antibody responses that made this study
so remarkable. This study,12 and others even earlier,15-17 initiated an avalanche
of additional studies over the next several years that continue to
this day. 13. 18. 19
Several studies have since investigated this effect of cow's milk on
BSA antibody levels. All but one showed that cow's milk increases BSA
antibodies in Type 1 diabetic children,18 although the responses were
quite variable in their magnitude.
Over the past decade, scientists have investigated far more than
just the BSA antibodies, and a more complete picture is coming into
view. Very briefly, it goes something like this13, 19: infants or very young
children of a certain genetic background,2o,21 who are weaned from the
breast too early22 onto cow's milk and who, perhaps, become infected
AUTOIMMUNE OISEASES 189
with a virus that may corrupt the gut immune system,l9 are likely to
have a high risk for Type 1 diabetes. A study in Chile23 considered the
first two factors, cow's milk and genes. Genetically susceptible children
weaned too early onto cow's milk-based formula had a risk of Type 1 diabetes
that was 13.1 times greater than children who did not have these
genes and who were breast-fed for at least three months (thus minimizing
their exposure to cow's milk). Another study in the U.S. showed that
genetically susceptible children fed cow's milk as infants had a risk of
disease that was 11.3 times greater than children who did not have these
genes and who were breast-fed for at least three months. 24 This eleven
to thirteen times greater risk is incredibly large (1,000-1,200%!); anything
over three to four times is usually considered very important. To
put this in perspective, smokers have approximately ten times greater
risk of getting lung cancer (still less than the eleven to thirteen times
risk here) and people with high blood pressure and cholesterol have a
2.5-3.0 times greater risk of heart disease (Chart 9.2) .18
So how much of the eleven to thirteen times increased risk of Type
1 diabetes is due to early exposure to cow's milk, and how much is due
to genes? These days, there is a popular opinion that Type 1 diabetes is
due to genetics, an opinion often shared by doctors as well. But genetics
alone cannot account for more than a very small fraction of cases of this
disease. Genes do not act in isolation; they need a trigger for their effects
to be produced. It has also been observed that after one member of
identical twin pairs gets Type 1 diabetes, there is only a 13-33% chance
of the second twin getting the disease, even though both twins have
the same genes. l3, 20, 21, 25. 26 If it were all due to genes, closer to lOO% of
the identical twins would get the disease. In addition, it is possible that
the 13-33% risk for the second twin is due to the sharing of a common
environment and diet, factors affecting both twins.
Consider, for example, the observation shown in Chart 9.3, which
highlights the link between one aspect of environment, cow's milk consumption,
and this disease. Cow's milk consumption by children zero
to fourteen years of age in twelve countries27 shows an almost perfect
correlation with Type 1 diabetes.28 The greater the consumption of
cow's milk, the greater the prevalence of Type 1 diabetes. In Finland,
Type 1 diabetes is thirty-six times more common than in Japan.29 Large
amounts of cow's milk products are consumed in Finland but very little
is consumed in Japan
As we have seen with other diseases of affluence, when people migrate
from areas of the world where disease incidence is low to areas of the
world where disease incidence is high, they quickly adopt the high incidence
rates as they change their diet and lifestyle.3O-32 This shows that even
though individuals may have the necessary gene(s), the disease will occur
only in response to certain dietary and/or environmental circumstances.
Disease trends over time show the same thing. The worldwide prevalence
of Type 1 diabetes is increasing at an alarming rate of 3% per year. 33
This increase is occurring for different populations even though there
may be substantial differences in disease rates. This relatively rapid increase
cannot be due to genetic susceptibility. The frequency of anyone
gene in a large population is relatively stable over time, unless there are
changing environmental pressures that allow one group to reproduce
more successfully than another group. For example, if all families with
Type 1 diabetic relatives had a dozen babies and all the families without
Type 1 diabetic relatives died off, then the gene or genes that may be
responsible for Type 1 diabetes would become much more common in
the population. This, of course, is not what is happening, and the fact
that Type 1 diabetes is increasing 3% every year is very strong evidence
that genes are not solely responsible for this disease.
It seems to me that we now have impressive evidence shOWing that
cow's milk is likely to be an important cause of Type 1 diabetes. When
the results of all these studies are combined (both genetically susceptible
and not susceptible), we find that children weaned too early and
fed cow's milk have, on average, a 50-60% higher risk of Type 1 diabetes
(1.5-1.6 times increased risk).34
The earlier information on diet and Type 1 diabetes was impressive
enough to cause two Significant developments. The American Academy
of Pediatrics in 1994 "strongly encouraged" that infants in families
where diabetes is more common not be fed cow's milk supplements for
their first two years of life. Second, many researchers19 have developed
prospective studies-the kind that follow individuals into the futureto
see if a careful monitoring of diet and lifestyle could explain the onset
of Type 1 diabetes.
Two of the better known of these studies have been underway in Finland,
one starting in the late 1980S15 and the other in the mid-1990s.35
One has shown that cow's milk consumption increases the risk of Type
1 diabetes five- to sixfold,36 while the second35 tells us that cow's milk
increases the development of at least another three to four antibodies
192 THE CHINA STUDY
in addition to those presented previously (p. 190). In a separate study,
antibodies to beta-casein, another cow's milk protein, were significantly
elevated in bottle-fed infants compared to breast-fed infants; children
with Type 1 diabetes also had higher levels of these antibodies.37 In
short, of the studies that have reported results, the findings strongly
confirm the danger of cows milk, especially for genetically susceptible
children.
THE CONTROVERSY OF CONTROVERSY
Imagine looking at the front page of the newspaper and finding the
following headline: "Cow's Milk the Likely Cause of Lethal Type 1
Diabetes." Because the reaction would be so strong, and the economic
impact monumental, this headline won't be written anytime soon,
regardless of the scientific evidence. Stifling this headline is accomplished
under the powerful label of "controversy." With so much at
stake, and so much information understood by so few people, it is easy
to generate and sustain controversy. Controversies are a natural part
of science. Too often, however, controversy is not the result of legitimate
scientific debate, but instead reflects the perceived need to delay
and distort research results. For example, if I say cigarettes are bad for
you and provide a mountain of evidence to support my contention,
the tobacco companies might come along and pick out one unsolved
detail and then claim that the whole idea of cigarettes being unhealthy
is mired in controversy, thereby nullifying all my conclusions. This is
easy to do, because there will always be unsolved details; this is the
nature of science. Some groups use controversy to stifle certain ideas,
impede constructive research, confuse the public and turn public
policy into babble rather than substance. Sustaining controversy as a
means of discrediting findings that cause economic or social discomfort
is one of the greatest sins in science.
It can be difficult for the layperson to assess the legitimacy of a highly
technical controversy such as that regarding cow's milk and Type 1 diabetes.
This is true even if the layperson is interested in reading scientific
articles.
Take a recent scientific review38 of the cow's milk-Type 1 diabetes
association. In ten human studies (all case-control) summarized in a
paper published as part of a "controversial topics series,"38 the authors
concluded that five of the ten studies showed a statistically Significant
positive association between cow's milk and Type 1 diabetes and five did
L
AUTOIMMUNE DISEASES 193
not. Obviously, this at first seems to demonstrate considerable uncertainty,
going a long way to discredit the hypothesis.
However, the five studies that were counted as "negative" did not
show that cow's milk decreased Type 1 diabetes. These five studies
showed no statistically significant effect either way. In contrast, there
are a total of five statistically significant studies and all five showed the
same result: early cow's milk consumption is associated with increased
risk of Type 1 diabetes. There is only one chance in sixty-four that this
was a random or chance result.
There are many, many reasons, some seen and some unseen, why an
experiment would find no statistically significant relationship between
two factors, even when a relationship really exists. Perhaps the study
didn't include enough people, and statistical certainty was unattainable.
Perhaps most of the subjects had very similar feeding practices, limiting
detection of the relationship you might otherwise see. Maybe trying to
measure infant feeding practices from years ago was inaccurate enough
that it obscured the relationship that does exist. Perhaps the researchers
were studying the wrong period of time in an infant's life.
The point is, if five of the ten studies did find a statistically significant
relationship, and all five showed that cow's milk consumption is linked
to increasing Type 1 diabetes, and none show that cow's milk consumption
is linked to decreasing Type 1 diabetes, I could hardly justify saying,
as the authors of this review did, that the hypothesis "has become
quite murky with inconsistencies in the literature. "38
In this same review,38 the authors summarized additional studies that
indirectly compared breast-feeding practices associated with cow's milk
consumption and Type 1 diabetes. This compilation involved fifty-two
possible comparisons, twenty of which were statistically significant. Of
these twenty significant findings, nineteen favored an association of cows
milk with disease, and only one did not. Again the odds heavily favored the
hypotheSized association, something that the authors failed to note.
I cite this example not only to support the evidence showing a cow's
milk effect on Type 1 diabetes, but also to illustrate one tactic that is
often used to make something controversial when it is not. This practice
is more common than it should be and is a source of unnecessary confusion.
When researchers do this-even if they do it unintentionallythey
often have a serious prejudice against the hypothesis in the first
place. Indeed, shortly after I wrote this, I heard a brief National Public
Radio interview on the Type 1 diabetes problem with the senior author
194 THE CHINA STUDY
of this review paper.38 Suffice it to say, the author did not acknowledge
the evidence for the cow's milk hypothesis.
Because this issue has mammoth financial implications for American
agriculture, and because so many people have such intense personal
biases against it, it is unlikely that this diabetes research will reach the
American media anytime soon. However, the depth and breadth of evidence
now implicating cow's milk as a cause of Type 1 diabetes is overwhelming,
even though the very complex mechanistic details are not
yet fully understood. We not only have evidence of the danger of cow's
milk, we also have considerable evidence showing that the association
between diabetes and cow's milk is biologically plausible. Human breast
milk is the perfect food for an infant, and one of the most damaging
things a mother can do is to substitute the milk of a cow for her own.
MULTIPLE SCLEROSIS
AND OTHER AUTOIMMUNE DISEASES
Multiple sclerosis (MS) is a particularly difficult autoimmune disease,
both for those who have it and for those who care for its victims. It is a
lifelong battle involving a variety of unpredictable and serious disabilities.
MS patients often pass through episodes of acute attacks while gradually
losing their ability to walk or to see. After ten to fifteen years, they often
are confined to a wheelchair, and then to a bed for the rest of their lives.
About 400,000 people in the u.s. alone have the disease, according
to the National Multiple Sclerosis Society.39 It is a disease that is initially
diagnosed between twenty and forty years of age and strikes women
about three times more often than men.
Even though there is widespread medical and scientific interest in
this disease, most authorities claim to know very little about causes
or cures. Major multiple sclerosis Internet Web sites all claim that the
disease is an enigma. They generally list genetics, viruses and environmental
factors as possibly playing roles in the development of this disease
but pay almost no heed to a possible role for diet. This is peculiar
considering the wealth of intriguing information on the effects of food
that is available from reputable research reports.40--42 Once again cow's
milk appears to play an important role.
The "multiple" symptoms of this disease represent a nervous system
gone awry. The electrical signals carrying messages to and from the
central nervous system (brain and spinal cord) and out through the peripheral
nervous system to the rest of the body are not well coordinated
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