2
	The	first	nine
comprise	97%	of	all	autoimmune	disease	cases. 2
	The	most	studied	are
multiple	sclerosis	(MS),	rheumatoid	arthritis,	lupus,	Type	1	diabetes	and
rheumatic	heart	disease. 2
	These	are	also	the	primary	autoimmune	diseases
that	have	been	studied	in	reference	to	diet. Others	not	listed	in	
Chart	9.1
	include	inflammatory	bowel	disease,
4
Crohn’s	disease,
4
	rheumatic	heart	disease
3
	and	(possibly)	Parkinson’s
disease. 5
Each	disease	name	may	sound	very	different,	but	as	one	recent	review
points	out,
2
	“…	it	is	important	to	consider…	these	disorders	as	a	group.”
They	show	similar	clinical	backgrounds,
3,	6,	7
	they	sometimes	occur	in	the
same	person	and	they	are	often	found	in	the	same	populations. 2
	MS	and	Type
1	diabetes,	for	example,	have	“near(ly)	identical	
ethnic	and	geographic
distribution.”
8
	Autoimmune	diseases	in	general	become	more	common	thegreater	the	distance	from	the	equator. This	phenomenon	has	been	known	since
1922. 9
	MS,	for	example,	is	over	a	hundred	times	more	prevalent	in	the	far
north	than	at	the	equator. 10
CHART	9.1:	COMMON	AUTOIMMUNE	DISEASES	(FROM
MOST	COMMON	TO	LEAST	COMMON)
1
. Graves’	disease	(Hyperthyroidism)
2
. Rheumatoid	arthritis
3
. Thyroiditis	(Hypothyroidism)
4
. Vitiligo
5
. Pernicious	anemia
6
. Glomerulonephritis
7
. Multiple	sclerosis
8
. Type	1	diabetes
9
. Systemic	lupus	erythematosus
10
. Sjogren’s	disease
11
. Myasthenia	gravis
12
. Polymyositis/dermatomyositis
13
. Addison’s	disease
14
. Scleroderma
15
. Primary	biliary	cirrhosis
16
. Uveitis
17
. Chronic	active	hepatitis
Because	of	some	of	these	common	features,	it	is	not	too	far-fetched	to
think	of	the	autoimmune	diseases	as	one	grand	disease	living	in	different
places	in	the	body	and	taking	on	different	names. We	refer	in	this	way	to
cancer,	which	is	specifically	named	depending	on	what	part	of	the	body	it
resides	in. All	autoimmune	diseases	are	the	result	of	one	group	of	mechanisms	gone
awry,	much	like	cancer. In	this	case,	the	mechanism	is	the	immune	system
mistakenly	attacking	cells	in	its	own	body. Whether	it	is	the	pancreas	as	in
Type	1	diabetes,	the	myelin	sheath	as	in	MS	or	joint	tissues	as	in	arthritis,	all
autoimmune	diseases	involve	an	immune	system	that	has	revolted. It	is	an
internal	mutiny	of	the	worst	kind,	one	in	which	our	body	becomes	its	own
worst	enemy.IMMUNITY	FROM	INVADERS
The	immune	system	is	astonishingly	complex. I	often	hear	people	speaking
about	this	system	as	if	it	were	an	identifiable	organ	like	a	lung. Nothing	could
be	further	from	the	truth. It	is	a	system,	not	an	organ. In	essence,	our	immune	system	is	like	a	military	network	designed	to
defend	against	foreign	invaders. The	“soldiers”	of	this	network	are	the	white
blood	cells,	which	are	comprised	of	many	different	sub-groups,	each	having
its	own	mission. These	sub-groups	are	analogous	to	a	navy,	army,	air	force
and	marines,	with	each	group	of	specialists	doing	highly	specialized	work. The	“recruitment	center”	for	the	system	is	in	the	marrow	of	our	bones. The
marrow	is	responsible	for	generating	specialized	cells	called	stem	cells. Some
of	these	cells	are	released	into	circulation	for	use	elsewhere	in	the	body;	these
are	called	B-cells	(for	bone). Other	cells	formed	in	the	bone	marrow	remain
immature,	or	unspecialized,	until	they	travel	to	the	thymus	(an	organ	in	the
chest	cavity	just	above	the	heart)	where	they	become	specialized;	these	are
called	T-cells	(for	thymus). These	“soldier”	cells,	along	with	other	specialized
cells,	team	up	to	create	intricate	defense	plans. They	meet	at	major
intersections	around	the	body,	including	the	spleen	(just	inside	the	left	lower
rib	cage)	and	the	lymph	nodes. These	meeting	points	are	like	command	and
control	centers,	where	the	“soldier	cells”	rearrange	themselves	into	teams	to
attack	foreign	invaders. These	cells	are	remarkably	adaptable	when	they	form	their	teams. They
are	able	to	respond	to	different	circumstances	and	different	foreign
substances,	even	those	they	have	never	before	seen. The	immune	response	to
these	strangers	is	an	incredibly	creative	process. It	is	one	of	the	true	wonders
of	nature. The	foreign	invaders	are	protein	molecules	called	antigens. These	foreign
cells	can	be	a	bacterium	or	a	virus	looking	to	corrupt	the	body’s	integrity. So
when	our	immune	system	notices	these	foreign	cells,	or	antigens,	it	destroys
them. Each	of	these	foreign	antigens	has	a	separate	identity,	which	is
determined	by	the	sequence	of	amino	acids	that	comprises	its	proteins. It	is
analogous	to	each	and	every	person	having	a	different	face. Because
numerous	amino	acids	are	available	for	creating	proteins,	there	are	infinite
varieties	of	distinctive	“faces.”
To	counter	these	antigens,	our	immune	system	must	customize	its	defense
to	each	attack. It	does	this	by	creating	a	“mirror	image”	protein	for	each
attacker. The	mirror	image	is	able	to	ht	perfectly	onto	the	antigen	and	destroy
it. Essentially,	the	immune	system	creates	a	mold	for	each	face	it	encounters. Every	time	it	sees	that	face	after	the	initial	encounter,	it	uses	the	custom-mademold	to	“capture”	the	invader	and	destroy	it. The	mold	may	be	a	B-cell
antibody	or	a	T-cell-based	receptor	protein. Remembering	each	defense	against	each	invader	is	what	immunization	is
all	about. An	initial	exposure	to	chicken	pox,	for	example,	is	a	difficult	battle,
but	the	second	time	you	encounter	that	virus	you	will	know	exactly	how	to
deal	with	it,	and	the	war	will	be	shorter,	less	painful	and	much	more
successful. You	may	not	even	get	sick.IMMUNITY	FROM	OURSELVES
Even	though	this	system	is	a	wonder	of	nature	when	it	is	defending	the	body
against	foreign	proteins,	it	is	also	capable	of	attacking	the	same	tissues	that	it
is	designed	to	protect. This	self-destructive	process	is	common	to	all
autoimmune	diseases. It	is	as	if	the	body	were	to	commit	suicide. One	of	the	fundamental	mechanisms	for	this	self-destructive	behavior	is
called	molecular	mimicry. It	so	happens	that	some	of	the	foreign	invaders	that
our	soldier	cells	seek	out	to	destroy	look	the	same	as	our	own	cells. The
immune	system	“molds”	that	ht	these	invaders	also	ht	our	own	cells. The
immune	system	then	destroys,	under	some	circumstances,	everything	that	fits
the	mold,	including	our	own	cells. This	is	an	extremely	complex	self-
destructive	process	involving	many	different	strategies	on	the	part	of	the
immune	system,	all	of	which	share	the	same	fatal	flaw	of	not	being	able	to
distinguish	“foreign”	invader	proteins	from	the	proteins	of	our	own	body. What	does	all	of	this	have	to	do	with	what	we	eat? It	so	happens	that	the
antigens	that	trick	our	bodies	into	attacking	our	own	cells	may	be	in	food. During	the	process	of	digestion,	for	example,	some	proteins	slip	into	our
bloodstream	from	the	intestine	without	being	fully	broken	down	into	their
amino	acid	parts. The	remnants	of	undigested	proteins	are	treated	as	foreign
invaders	by	our	immune	system,	which	sets	about	making	molds	to	destroy
them	and	sets	into	motion	the	self-destructive	autoimmune	process. 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
example
1
	of	the	exceptional	elegance	of	nature’s	ability	to	regulate	itself. The	immune	system	uses	a	very	delicate	process	to	decide	which	proteins
should	be	attacked	and	which	should	be	left	alone. 11
	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	todifferentiate	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	diabetes
12–14
	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’s	
milk	may
cause	one	of	the	most	devastating	diseases	that	can	befall	a	child
. For
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	consumedcow’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	this
13,	19
:	infants	or	very	young	children	of	a
certain	genetic	background,
20,	21
	who	are	weaned	from	the	breast	too	early
22
onto	cow’s	milk	and	who,	perhaps,	become	infected	
with	a	virus	that	may
corrupt	the	gut	immune	system,
19
	are	likely	to	have	a	high	risk	for	Type	1
diabetes. A	study	in	Chile
23
	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)	andpeople	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. 13,	20,	21,	25,	26
If	it	were	all	due	to	genes,	closer	to	100%	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. CHART	9.2:	RELATIVE	RISKS	OF	VARIOUS	FACTORS	ON
VARIOUS	DISEASE	OUTCOMES
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	countries
27
	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	1diabetes	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. 27
CHART	9.3:	ASSOCIATION	OF	COW’S	MILK	CONSUMPTION	AND
INCIDENCE	OF	TYPE	1	DIABETES	IN	DIFFERENT	COUNTRIES
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. 30–32
	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	any	one	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’smilk	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	researchers
19
	have	developed	prospective
studies—the	kind	that	follow	individuals	into	the	future—to	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	1980s
15
	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	second
35
	tells	us	that	cow’s	milk	increases	the
development	of	at	least	another	three	to	four	antibodies	
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	cow’s	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	review
38
	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	
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’tinclude	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	cow’s	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	unintentionally—they	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	
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	
and	controlled. This	is	because
the	insulating	cover	or	sheath	of	the	nerve	fibers,	the	myelin,	is	being
destroyed	by	an	autoimmune	reaction. Think	of	what	would	happen	to	your
household	wiring	if	the	electrical	insulation	became	thin	or	was	stripped	away
leaving	bare	wires. The	electrical	signals	would	be	short-circuited. That	is
what	happens	with	MS;	the	wayward	electrical	signals	may	destroy	cells	and
“burn”	patches	of	neighboring	tissue,	leaving	little	scars	or	bits	of	sclerotic
tissue. These	“burns”	can	become	serious	and	ultimately	destroy	the	body. The	initial	research	showing	an	effect	of	diet	on	MS	goes	back	more	than
half	a	century	to	the	research	of	Dr.	Roy	Swank,	who	began	his	work	in
Norway	and	at	the	Montreal	Neurological	Institute	during	the	1940s. Later,
Dr.	Swank	headed	the	Division	of	Neurology	at	the	University	of	Oregon
Medical	School. 43
Dr.	Swank	became	interested	in	the	dietary	connection	when	he	learnedthat	MS	appeared	to	be	more	common	in	the	northern	climates. 43
	There	is	a
huge	difference	in	MS	prevalence	as	one	moves	away	from	the	equator:	MS	is
over	100	times	more	prevalent	in	the	far	north	than	at	the	equator,
10
	and	seven
times	more	prevalent	in	south	Australia	(closer	to	the	South	Pole)	than	in
north	Australia. 44
	This	distribution	is	very	similar	to	the	distribution	of	other
autoimmune	diseases,	including	Type	1	diabetes	and	rheumatoid	arthritis. 43,	46
Although	some	scientists	speculated	that	magnetic	fields	might	be
responsible	for	the	disease,	Dr.	Swank	thought	it	was	diet,	especially	animal-
based	foods	high	in	saturated	fats. 43
	He	found	that	inland	dairy-consuming
areas	of	Norway	had	higher	rates	of	MS	than	coastal	fish-consuming	areas. Dr.	Swank	conducted	his	best-known	trial	on	144	MS	patients	recruited
from	the	Montreal	Neurological	Institute. He	kept	records	on	these	patients
for	the	next	thirty-four	years. 47
	He	advised	his	patients	to	consume	a	diet	low
in	saturated	fat,	most	of	whom	did,	but	many	of	whom	did	not. He	then
classified	them	as	good	dieters	or	poor	dieters,	based	on	whether	they
consumed	less	than	20	g/day	or	more	than	20	g/day	of	saturated	fat. (For
comparison,	a	bacon	cheeseburger	with	condiments	has	about	sixteen	grams
of	saturated	fat. One	small	frozen	chicken	pot	pie	has	almost	ten	grams	of
saturated	fat.) As	the	study	continued,	Dr.	Swank	found	that	progression	of	disease	was
greatly	reduced	by	the	low-saturated	fat	diet,	which	worked	even	for	people
with	initially	advanced	conditions. He	summarized	his	work	in	1990,
47
concluding	that	for	the	sub-group	of	patients	who	began	the	
low-saturated	fat
diet	during	the	earlier	stages	of	their	disease,	“about	95%…	remained	only
mildly	disabled	for	approximately	thirty	years.”	Only	5%	of	these	patients
died. In	contrast,	80%	of	the	patients	with	early-stage	MS	who	consumed	the
“
poor
”	
diet
	(
higher	saturated	fat
)	
died	of	MS
. The	results	from	all	144
patients,	including	those	who	started	the	diet	at	a	later	stage	of	disease,	are
shown	in	
Chart	9.4
.CHART	9.4:	MS	DEATH	RATE	AFTER	144	PATIENTS	DIETED	FOR
THIRTY-FOUR	YEARS
This	work	is	remarkable. To	follow	people	for	thirty-four	years	is	an
exceptional	demonstration	of	perseverance	and	dedication. Moreover,	if	this
were	a	study	testing	a	potential	drug,	these	findings	would	make	any
pharmaceutical	manufacturer	jingle	the	coins	in	his	or	her	pocket. Swank’s
first	results	were	published	more	than	a	half	century	ago,
48
	then	again
49
	and
again
50
	and	again
47
	for	the	next	forty	years. More	recently,	additional	studies
42,	51,	52
	have	confirmed	and	extended
Swanks	observations	and	gradually	have	begun	to	place	more	emphasis	on
cow’s	milk. These	new	studies	show	that	consuming	cow’s	milk	is	strongly
linked	to	MS	both	when	comparing	different	countries
52
	and	when	comparing
states	within	the	U.S.
51
	
Chart	9.5
,	published	by	French	researchers,	compares
the	consumption	of	cow’s	milk	with	MS	for	twenty-six	populations	in	twenty-
four	countries. 52
This	relationship,	which	is	virtually	identical	to	that	for	Type	1	diabetes,	is
remarkable,	and	it	is	not	due	to	variables	such	as	the	availability	of	medical
services	or	geographic	latitude. 51
	In	some	studies
52,	53
	researchers	suggest	this
strong	correlation	with	fresh	cow’s	milk	might	
be	due	to	the	presence	of	a
virus	in	the	milk. These	more	recent	studies	also	suggest	that	saturated	fat
alone	probably	was	not	fully	responsible	for	Swank’s	results. The
consumption	of	meat	high	in	saturated	fat,	like	milk,	was	also	associated	with
MS	in	these	multi-country	studies,
54
	while	the	consumption	of	fish,
containing	more	omega-3	fat,	was	associated	with	low	rates	of	disease. 55CHART	9.5:	ASSOCIATION	OF	COW’S	MILK	CONSUMPTION	AND
MULTIPLE	SCLEROSIS
The	association	of	cow’s	milk	with	MS,	shown	in	
Chart	9.5
,	may	be
impressive,	but	it	does	not	constitute	proof. For	example,	where	do	genes	and
viruses	come	into	play? Each	of	these,	in	theory,	might	account	for	the
unusual	geographic	distribution	of	this	disease. In	the	case	of	viruses,	no	definite	conclusions	are	yet	possible. A	variety	of
different	virus	types	have	been	suggested	and	a	variety	of	effects	on	the
immune	system	may	be	involved. However,	nothing	very	convincing	has	been
proven. Some	of	the	evidence	is	based	on	finding	more	viral	antibodies	in	MS
patients	than	in	controls,	some	is	based	on	sporadic	outbreaks	of	MS	among
isolated	communities,	and	some	is	based	on	finding	virus-like	genes	among
MS	cases. 13,	19,	56
With	regard	to	genes,	we	can	begin	to	puzzle	out	their	association	with	MS
by	asking	the	usual	question:	what	happens	to	people	who	migrate	from	one
population	to	another,	keeping	their	genes	the	same	
but	changing	their	diets
and	their	environment? The	answer	is	the	same	as	it	was	for	cancer,	heart
disease	and	Type	2	diabetes. People	acquire	the	risk	of	the	population	to
which	they	move,	especially	if	they	move	before	their	adolescent	years. 57,	58
This	tells	us	that	this	disease	is	more	strongly	related	to	environmental	factors
than	it	is	to	genes. 59
Specific	genes	have	been	identified	as	possible	candidates	for	causing	MS
but,	according	to	a	recent	report,
3
	there	may	be	as	many	as	twenty-five	genes
playing	such	a	role. Therefore,	it	will	undoubtedly	be	a	long	time	before	we
determine	with	any	precision	which	genes	or	combinations	of	genespredispose	someone	to	MS.	Genetic	predisposition	may	make	a	difference	as
to	who	gets	MS,	but	even	at	best,	genes	can	only	account	for	about	one-fourth
of	the	total	disease	risk. 60
Although	MS	and	Type	1	diabetes	share	some	of	the	same	unanswered
questions	on	the	exact	roles	of	viruses	and	genes	and	the	immune	system,
they	also	share	the	same	alarming	evidence	regarding	diet. For	both	diseases,
a	“Western”	diet	is	strongly	associated	with	disease	incidence. Despite	the
efforts	of	those	who	would	rather	dismiss	or	mire	these	observational	studies
in	controversy,	they	paint	a	consistent	picture. Intervention	studies	conducted
on	people	already	suffering	from	these	diseases	only	reinforce	the	findings	of
the	observational	studies. Dr.	Swank	did	brilliant	work	on	MS,	and	you	may
recall	from	chapter	seven	that	Dr.	James	Anderson	successfully	reduced	the
medication	requirements	for	Type	1	diabetics	using	diet	alone. It’s	important
to	note	that	both	of	these	doctors	used	a	diet	that	was	significantly	more
moderate	than	a	total	whole	foods,	plant-based	diet. I	wonder	what	would
happen	to	these	autoimmune	patients	if	the	ideal	diet	were	followed. I	would
bet	on	even	greater	success.THE	COMMONALITY	OF	AUTOIMMUNE
DISEASES
What	about	other	autoimmune	diseases? There	are	dozens	of	autoimmune
diseases	and	I	have	mentioned	only	two	of	the	more	prominent	ones. Can	we
say	anything	about	autoimmune	diseases	as	a	whole? To	answer	this	question,	we	need	to	identify	how	much	these	diseases
have	in	common. The	more	they	have	in	common,	the	greater	the	probability
that	they	also	will	share	a	common	cause	(or	causes). This	is	like	seeing	two
people	you	don’t	know,	both	of	whom	have	a	similar	body	type,	hair	color,
eye	color,	facial	features,	physical	and	vocal	mannerisms	and	age,	and
concluding	that	they	come	from	the	same	parents. Just	as	we	hypothesized
that	diseases	of	affluence	such	as	cancer	and	
heart	disease	have	common
causes	because	they	share	similar	geography	and	similar	biochemical
biomarkers	(chapter	four),	we	can	also	hypothesize	that	MS,	Type	1	diabetes,
rheumatoid	arthritis,	lupus	and	other	autoimmune	diseases	may	share	a
similar	cause	if	they	exhibit	similar	characteristics. First,	by	definition,	each	of	these	diseases	involves	an	immune	system	that
has	gone	awry	in	such	a	way	that	it	attacks	“self”	proteins	that	look	the	same
as	foreign	proteins. Second,	all	the	autoimmune	diseases	that	have	been	studied	have	been
found	to	be	more	common	at	the	higher	geographic	latitudes	where	there	is
less	constant	sunshine. 9,	10,	61
Third,	some	of	these	diseases	have	a	tendency	to	afflict	the	same	people. MS	and	Type	1	diabetes,	for	example,	have	been	shown	to	coexist	in	the	same
individuals. 62–65
	Parkinson’s	disease,	a	non-autoimmune	disease	with
autoimmune	characteristics,	is	often	found	with	MS,	both	within	the	same
geographic	regions
66
	and	within	the	same	individuals. 5
	MS	also	has	been
associated—either	geographically	or	within	the	same	individuals—with	other
autoimmune	diseases	like	lupus,	myasthenia	gravis,	Graves’	disease	and
eosinophilic	vasculitis. 63
	Juvenile	rheumatoid	arthritis,	another	autoimmune
disease,	has	been	shown	to	have	an	unusually	strong	association	with
Hashimoto	thyroiditis. 67
Fourth,	of	those	diseases	studied	in	relation	to	nutrition,	the	consumption
of	animal-based	foods—especially	cow’s	milk—is	associated	with	greater
disease	risk. Fifth,	there	is	evidence	that	a	virus	(or	viruses)	may	trigger	the	onset	of
several	of	these	diseases. A	sixth	and	most	important	characteristic	binding	together	these	diseasesis	the	evidence	that	their	“mechanisms	of	action”	have	much	in	common—
jargon	used	to	describe	the	“how	to”	of	disease	formation. As	we	consider
common	mechanisms	of	action,	we	might	start	with	sunlight	exposure,
because	this	somehow	seems	linked	to	the	autoimmune	diseases. Sunlight
exposure,	which	decreases	with	increasing	latitude,	could	be	important—but
clearly	there	are	other	factors. The	consumption	of	animal-based	foods,
especially	cow’s	milk,	also	increases	with	distance	from	the	equator. In	fact,
in	one	of	the	more	extensive	studies,	cow’s	milk	was	found	to	be	as	good	of	a
predictor	of	MS	as	latitude	(i.e.,	sunshine). 51
	In	Dr.	Swank’s	studies	in
Norway,	MS	was	less	common	near	the	coastal	areas	of	the	country	where
fish	intake	was	more	common. This	gave	rise	to	the	idea	that	the	omega-3	fats
common	
to	fish	might	have	a	protective	effect. What	is	almost	never
mentioned,	however,	is	that	dairy	consumption	(and	saturated	fat)	was	much
lower	in	the	fish-eating	areas. Is	it	possible	that	cow’s	milk	and	lack	of
sunshine	are	having	a	similar	effect	on	MS	and	other	autoimmune	diseases
because	they	operate	through	a	similar	mechanism? This	could	be	very
interesting,	if	true. As	it	turns	out,	the	idea	is	not	so	crazy. This	mechanism	involves,	once
again,	vitamin	D.	There	are	experimental	animal	models	of	lupus,	MS,
rheumatoid	arthritis	and	inflammatory	bowel	disease	(e.g.,	Crohn’s	disease,
ulcerative	colitis),	each	of	which	is	an	autoimmune	disease. 6,	7,	68
	Vitamin	D,
operating	through	a	similar	mechanism	in	each	case,	prevents	the
experimental	development	of	each	of	these	diseases. This	becomes	an	even
more	intriguing	story	when	we	think	about	the	effect	of	food	on	vitamin	D.
The	first	step	in	the	vitamin	D	process	occurs	when	you	go	outside	on	a
sunny	day. When	the	sunshine	hits	your	exposed	skin,	the	skin	produces
vitamin	D.	The	vitamin	D	then	must	be	activated	in	the	kidney	in	order	to
produce	a	form	that	helps	repress	the	development	of	autoimmune	diseases. As	we’ve	seen	before,	this	critically	important	activation	step	can	be	inhibited
by	foods	that	are	high	in	calcium	and	by	acid-producing	animal	proteins	like
cow’s	milk	(some	grains	also	produce	excess	acid). Under	experimental
conditions,	the	activated	vitamin	D	operates	in	two	ways:	it	inhibits	the
development	of	certain	T-cells	and	their	production	of	active	agents	(called
cytokines)	that	initiate	the	autoimmune	response,	and/or	it	encourages	the
production	of	other	T-cells	that	oppose	this	effect. 69,	70
	(An	abbreviated
schematic	of	this	vitamin	D	network	is	shown	in	
Appendix	C
.) This
mechanism	of	action	appears	to	be	a	strong	commonality	between	all
autoimmune	diseases	so	far	studied. Knowing	the	strength	of	the	evidence	against	animal	foods,	cow’s	milk	in
particular,	for	both	MS	and	Type	1	diabetes,	and	knowing	how	much	incommon	all	of	the	autoimmune	diseases	have,	it	is	reasonable	to	begin
thinking	about	food	and	its	relationship	to	a	much	broader	group	of
autoimmune	diseases. Obviously	caution	is	called	for;	more	research	is
needed	to	make	conclusive	statements	about	cross-autoimmune	disease
similarities. But	the	evidence	we	have	now	is	already	striking. Today	almost	no	indication	of	the	dietary	connection	to	these	diseases	has
reached	public	awareness. The	Web	site	of	the	Multiple	Sclerosis
International	Federation,	for	example,	reads,	“There	is	no	credible	
evidence
that	MS	is	due	to	poor	diet	or	dietary	deficiencies.”	They	warn	that	dietary
regimens	can	be	“expensive”	and	“can	alter	the	normal	nutritional	balance.”
71
If	changing	your	diet	is	expensive,	I	don’t	know	what	they	would	say	about
being	bedridden	and	incapacitated. As	far	as	altering	the	“normal	nutritional
balance”	is	concerned,	what	is	normal? Does	this	mean	the	diet	that	we	now
eat	is	“normal”—the	diet	that	is	largely	responsible	for	diseases	that	cripple,
kill	and	make	profoundly	miserable	millions	of	Americans	every	year? Are
massive	rates	of	heart	disease,	cancer,	autoimmune	diseases,	obesity	and
diabetes	“normal”? If	this	is	normal,	I	propose	we	start	seriously	considering
the	abnormal. There	are	400,000	Americans	who	are	victims	of	multiple	sclerosis,	and
millions	more	with	other	autoimmune	diseases. While	statistics,	research
results	and	clinical	descriptions	form	the	basis	for	much	of	my	discussion	of
diet	and	disease,	the	importance	of	the	information	comes	down	to	the
intimate	experience	of	individual	people
. Any	one	of	these	serious	diseases
I’ve	talked	about	in	this	chapter	can	forever	alter	the	life	of	any	person—a
family	member,	a	friend,	a	neighbor,	a	coworker	or	you	yourself. It	is	time	to	sacrifice	our	sacred	cows. Reason	must	prevail. Professional
societies,	doctors	and	government	agencies	need	to	stand	up	and	do	their	duty,
so	that	children	being	born	today	do	not	face	tragedies	that	otherwise	could	be
prevented.10
Wide-Ranging	Effects:	Bone,	Kidney,	Eye
and	Brain	Diseases
O
NE	OF	THE	MOST	CONVINCING	ARGUMENTS
	for	a	plant-based	diet	is	the	fact	that
it	prevents	a	broad	range	of	diseases. If	I	have	a	conversation	with	someone
about	a	single	study	showing	the	protective	effect	of	fruits	and	vegetables	on
heart	disease,	they	may	agree	that	it’s	all	very	nice	for	fruits	and	vegetables,
but	they	will	probably	still	go	home	to	meatloaf	and	gravy. It	doesn’t	matter
how	big	the	study,	how	persuasive	the	results	or	how	respectable	the	scientists
who	conducted	the	investigation. The	fact	is	that	most	people	have	a	healthy
skepticism	about	one	study	standing	alone—as	well	they	should. But	if	I	tell	them	about	dozens	and	dozens	of	studies	showing	that	the
countries	with	low	rates	of	heart	disease	consume	low	amounts	of	animal-
based	foods,	and	dozens	and	dozens	of	studies	showing	that	individuals	who
eat	more	whole,	plant-based	foods	get	less	heart	disease,	and	I	go	on	to
document	still	more	studies	showing	that	a	diet	low	in	animal-based	foods
and	high	in	unprocessed	plant-based	foods	can	slow	or	reverse	heart	disease,
then	people	are	more	inclined	to	pay	some	attention. If	I	keep	talking	and	go	through	this	process	not	only	for	heart	disease,	but
obesity,	Type	2	diabetes,	breast	cancer,	colon	cancer,	prostate	
cancer,	multiple
sclerosis	and	other	autoimmune	diseases,	it’s	quite	possible	that	people	may
never	eat	meatloaf	and	gravy	again. What	has	become	so	convincing	about	the	effect	of	diet	on	health	is	the
breadth	of	the	evidence. While	a	single	study	might	be	found	to	support
almost	any	idea	under	the	sun,	what	are	the	chances	that	hundreds,	even
thousands,	of	different	studies	show	a	protective	benefit	of	plant-based	foods
and/or	harmful	effects	of	animal-based	foods	for	so	many	different	diseases?We	can’t	say	it’s	due	to	coincidence,	bad	data,	biased	research,	misinterpreted
statistics	or	“playing	with	numbers.”	This	has	got	to	be	the	real	deal. I	have	so	far	presented	only	a	small	sample	of	the	breadth	of	evidence	that
supports	plant-based	diets. To	show	you	just	how	broad	this	evidence	is,	I	will
cover	five	more	seemingly	unrelated	diseases	common	in	America:
osteoporosis,	kidney	stones,	blindness,	cognitive	dysfunction	and	Alzheimer’s
disease. These	disorders	are	not	often	fatal	and	are	often	regarded	as	the
inevitable	consequences	of	aging. Therefore,	we	don’t	think	it’s	unnatural
when	grandpa	gets	blurry	spots	in	his	vision,	can’t	remember	the	names	of	his
friends	or	needs	a	hip	replacement	operation. But,	as	we	shall	see,	even	these
diseases	have	a	dietary	link.OSTEOPOROSIS
Did	you	ever	have	an	elementary	school	teacher	tell	you	that	if	you	didn’t
have	bones,	you	would	just	be	a	shapeless	blob	on	the	floor? Or	maybe	you
learned	about	the	human	skeleton	from	that	popular	song,	“…	the	ankle	bone
is	connected	to	the	shin	bone,	the	shin	bone	is	connected	to	the	knee	bone,”
etc. At	that	same	time	in	your	life,	you	probably	were	told	to	drink	milk	to
build	strong	bones	and	teeth. Because	none	of	us	want	to	be	shapeless	blobs,
and	because	our	celebrities	have	been	paid	to	advertise	milk’s	presumed
benefits,	we	drank	it. Milk	is	to	bone	health	as	bees	are	to	honey. Americans	consume	more	cow’s	milk	and	its	products	per	person	than
most	populations	in	the	world. So	Americans	should	have	wonderfully	strong
bones,	right? Unfortunately	not. A	recent	study	showed	that	American	women
aged	fifty	and	older	have	one	of	the	highest	rates	of	hip	fractures	in	the
world. 1
	The	only	countries	with	higher	rates	are	in	Europe	and	in	the	south
Pacific	(Australia	and	New	Zealand)
1
	where	they	consume	even	more	milk
than	the	United	States. What’s	going	on? An	excess	rate	of	hip	fractures	is	often	used	as	a	reliable	indicator	of
osteoporosis,	a	bone	disease	that	especially	affects	women	after	menopause. It
is	often	claimed	to	be	due	to	an	inadequate	intake	of	calcium. Therefore,
health	policy	people	often	recommend	higher	calcium	consumption. Dairy
products	are	particularly	rich	in	calcium,	so	the	dairy	industry	eagerly
supports	efforts	to	boost	calcium	consumption. These	efforts	have	something
to	do	with	why	you	were	told	to	drink	your	milk	for	strong	bones—the
politics	of	which	are	discussed	in	
Part	IV
Something	is	amiss,	though,	because	those	countries	that	use	the	most
cow’s	milk	and	its	products	also	have	the	highest	fracture	rates	and	the	worst
bone	health. One	possible	explanation	is	found	in	a	report	showing	an
impressively	strong	association	between	animal	protein	intake	and	bone
fracture	rate	for	women	in	different	countries. 2
	Authored	in	1992	by
researchers	at	Yale	University	School	of	Medicine,	the	report	summarized
data	on	protein	intake	and	fracture	rates	taken	from	thirty-four	separate
surveys	in	sixteen	countries	that	were	published	in	twenty-nine	peer-reviewed
research	publications. All	the	subjects	in	these	surveys	were	women	fifty
years	and	older. It	found	that	a	very	impressive	70%	of	the	fracture	rate	was
attributable	to	the	consumption	of	animal	protein. These	researchers	explained	that	animal	protein,	unlike	plant	protein,
increases	the	acid	load	in	the	body. 3
	An	increased	acid	load	means	that	our
blood	and	tissues	become	more	acidic. The	body	does	not	like	this	acidicenvironment	and	begins	to	fight	it. In	order	to	neutralize	the	acid,	the	body
uses	calcium,	which	acts	as	a	very	effective	base. This	calcium,	however,
must	come	from	somewhere. It	ends	up	being	pulled	from	the	bones,	and	the
calcium	loss	weakens	them,	putting	them	at	greater	risk	for	fracture. We	have	had	evidence	for	well	over	a	hundred	years	that	animal	protein
decreases	bone	health. The	explanation	of	animal	protein	causing	excess
metabolic	acid,	for	example,	was	first	suggested	in	the	1880s
4
	and	was
documented	as	long	ago	as	1920. 5
	We	also	have	known	that	animal	protein	is
more	effective	than	plant	protein	at	increasing	the	metabolic	acid	load	in	the
body. 6,	7,	8
When	animal	protein	increases	metabolic	acid	and	draws	calcium	from	the
bones,	the	amount	of	calcium	in	the	urine	is	increased. This	effect	has	been
established	for	over	eighty	years
5
	and	has	been	studied	in	some	detail	since
the	1970s. Summaries	of	these	studies	were	published	in	1974,
9
	1981
10
	and
1990. 11
	Each	of	these	summaries	clearly	shows	that	the	amount	of	animal
protein	consumed	by	many	of	us	on	a	daily	basis	is	capable	of	causing
substantial	increases	in	urinary	calcium. Chart	10.1
	is	taken	from	the	1981
publication. 10
	Doubling	protein	intake	(mostly	animal-based)	from	35–78
g/day	causes	an	alarming	50%	increase	in	urinary	calcium. This	effect	occurs
well	within	the	range	of	protein	intake	that	most	of	us	consume;	average
American	intake	is	around	70–100	g/day. Incidentally	as	mentioned	in	chapter
four,	a	six-month	study	funded	by	the	Atkins	Center	found	that	those	people
who	adopted	the	Atkins	Diet	excreted	50%	more	calcium	in	their	urine	after
six	months	on	the	diet. 12CHART	10.1:	ASSOCIATION	OF	URINARY	CALCIUM	EXCRETION
WITH	DIETARY	PROTEIN	INTAKE
The	initial	observations	on	the	association	between	animal	protein
consumption	and	bone	fracture	rates	are	very	impressive,	and	now	we	have	a
plausible	explanation	as	to	how	the	association	might	work,	a	mechanism	of
action. Disease	processes	are	rarely	as	simple	as	“one	mechanism	does	it	all,”	but
the	work	being	done	in	this	held	makes	a	strong	argument. A	more	recent
study,	published	in	2000,	comes	from	the	Department	of	Medicine	at	the
University	of	California	at	San	Francisco. Using	eighty-seven	surveys	in
thirty-three	countries,	it	compared	the	ratio	of	vegetable	to	animal	protein
consumption	to	the	rate	of	bone	fractures	(
Chart	10.2
). 1
	A	high	ratio	of
vegetable	to	animal	protein	consumption	was	found	to	be	impressively
associated	with	a	virtual	disappearance	of	bone	fractures. These	studies	are	compelling	for	several	reasons. They	were	published	in
leading	research	journals,	the	authors	were	careful	in	their	analyses	and
interpretation	of	data,	they	included	a	large	number	of	individual	research
reports,	and	the	statistical	significance	of	the	association	of	animal	protein
with	bone	fracture	rates	is	truly	exceptional. They	cannot	be	dismissed	as	just
another	couple	of	studies;	the	most	recent	study	represents	a	summary	of
eighty-seven	separate	surveys!CHART	10.2:	ASSOCIATION	OF	ANIMAL	VERSUS	PLANT
PROTEIN	INTAKE	AND	BONE	FRACTURE	RATES	FOR
DIFFERENT	COUNTRIES
The	Study	of	Osteoporotic	Fractures	Research	Group	at	the	University	of
California	at	San	Francisco	published	yet	another	study
13
	of	over	1,000
women	aged	sixty-five	and	up. Like	the	multi-country	study,	researchers
characterized	women’s	diets	by	the	proportions	of	animal	and	plant	protein. After	seven	years	of	observations,	the	women	with	the	highest	ratio	of	animal
protein	to	plant	protein	had	3.7	times	more	bone	fractures	than	the	women
with	the	lowest	ratio. Also	during	this	time	the	women	with	the	high	ratio	lost
bone	almost	four	times	as	fast	as	the	women	with	the	lowest	ratio. Experimentally,	this	study	is	high	quality	because	it	compared	protein
consumption,	bone	loss	and	broken	bones	for	the	same	subjects. This	3.7-fold
effect	is	substantial,	and	is	very	important	because	the	
women	with	the	lowest
bone	fracture	rates	still	consumed,	on	average,	about	half	of	their	total	protein
from	animal	sources. I	can’t	help	but	wonder	how	much	greater	the	difference
might	have	been	had	they	consumed	not	50%	but	0–10%	of	their	total	protein
from	animal	sources. In	our	rural	China	study,	where	the	animal	to	plant	ratio
was	about	10%,	the	fracture	rate	is	only	one-fifth	that	of	the	U.S.	Nigeria
shows	an	animal-to-plant	protein	ratio	only	about	10%	that	of	Germany,	and
the	hip	fracture	incidence	is	lower	by	over	99%. 1
These	observations	raise	a	serious	question	about	the	widely	advertisedclaim	that	protein-rich	dairy	foods	protect	our	bones. And	yet	we	still	are
warned	almost	daily	about	our	need	for	dairy	foods	to	provide	calcium	for
strong	bones. An	avalanche	of	commentary	warns	that	most	of	us	are	not
meeting	our	calcium	requirements,	especially	pregnant	and	lactating	women. This	calcium	bonanza,	however,	is	not	justified. In	one	study	of	ten
countries,
14
	a	higher	consumption	of	calcium	was	associated	with	a	higher—
not	lower—risk	of	bone	fracture	(
Chart	10.3
). Much	of	the	calcium	intake
shown	in	this	chart,	especially	in	high	consumption	countries,	is	due	to	dairy
foods,	rather	than	calcium	supplements	or	non-dairy	food	sources	of	calcium. Mark	Hegsted,	who	produced	the	results	in	
Chart	10.3
,	was	a	longtime
Harvard	professor. He	worked	on	the	calcium	issue	beginning	in	the	early
1950s,	was	a	principal	architect	of	the	nation’s	first	dietary	guidelines	in	1980
and	in	1986	published	this	graph. Professor	Hegsted	believes	that	excessively
high	intakes	of	calcium	consumed	over	a	long	time	impair	the	body’s	ability
to	control	how	much	calcium	it	uses	and	when. Under	healthy	conditions,	the
body	uses	an	activated	form	of	vitamin	D,	calcitriol,	to	adjust	how	much
calcium	it	absorbs	from	food	and	how	much	it	excretes	and	distributes	in	the
bone. Calcitriol	is	considered	a	hormone;	when	more	calcium	is	needed,	it
enhances	calcium	absorption	and	restricts	calcium	excretion. If	too	much
calcium	is	consumed	over	a	long	period	of	time,	the	body	may	lose	its	ability
to	regulate	calcitriol,	permanently	or	temporarily	disrupting	the	regulation	of
calcium	absorption	and	excretion. Ruining	the	regulatory	mechanism	in	this
way	is	a	recipe	for	osteoporosis	in	menopausal	and	post-menopausal	women. Women	at	this	stage	of	life	must	be	able	to	enhance	their	utilization	of
calcium	in	a	timely	manner,	especially	if	they	continue	to	consume	a	diet	high
in	animal	protein. The	fact	that	the	body	loses	its	ability	to	control	finely
tuned	mechanisms	when	they	are	subjected	to	continuous	abuse	is	a	well-
established	phenomenon	in	biology.CHART	10.3:	ASSOCIATION	OF	RATES	OF	HIP	FRACTURES	WITH
CALCIUM	INTAKE	FOR	DIFFERENT	COUNTRIES
Given	these	findings,	it	seems	perfectly	plausible	that	animal	protein	and
even	calcium—when	consumed	at	excessive	levels—are	capable	of
increasing	the	risk	of	osteoporosis. Dairy,	unfortunately,	is	the	only	food	that
is	rich	in	both	of	these	nutrients. Hegsted,	backed	by	his	exceptional
experience	in	calcium	research,	said	in	his	1986	paper,	“…hip	fractures	are
more	frequent	in	populations	where	dairy	products	are	commonly	consumed
and	calcium	intakes	are	relatively	high.”
Years	later,	the	dairy	industry	still	suggests	that	we	should	be	consuming
more	of	its	products	to	build	strong	bones	and	teeth. The	confusion,	conflict
and	controversy	rampant	in	this	area	of	research	allow	anybody	to	say	just
about	anything. And	of	course,	huge	amounts	of	money	are	at	stake	as	well. One	of	the	most	cited	osteoporosis	experts—one	funded	by	the	dairy	industry
—angrily	wrote	in	a	prominent	editorial
15
	that	the	findings	favoring	a	diet
with	a	higher	ratio	of	plant-to-animal	protein	cited	above	could	have	been
“influenced	to	some	extent	by	currents	in	
the	larger	society.”	The	“currents”
he	was	referring	to	were	the	animal	rights	activists	opposed	to	the	use	of	dairy
foods. Much	of	the	debate	regarding	osteoporosis,	whether	it	is	conducted	withintegrity	or	otherwise,	resides	in	the	research	concerning	the	details. As	you
shall	see,	the	devil	lurks	in	the	details,	the	primary	detail	being	that	of	bone
mineral	density	(BMD). Many	scientists	have	investigated	how	various	diet	and	lifestyle	factors
affect	BMD. BMD	is	a	measure	of	bone	density	that	is	often	used	to	diagnose
bone	health. If	your	bone	density	falls	below	a	certain	level,	you	may	be	at
risk	for	osteoporosis. In	practical	terms,	this	means	that	if	you	have	a	low
BMD,	you	are	at	a	higher	risk	for	a	fracture. 16–18
	But	there	are	some
devilishly	contradictory	and	confusing	details	in	this	great	circus	of
osteoporosis	research. To	name	a	few:
A	high	BMD	increases	the	risk	of	osteoarthritis. 19
A	high	BMD	has	been	linked	to	a	higher	risk	of	breast	cancer. 20,	21
Although	high	BMD	is	linked	both	to	increased	breast	cancer	risk	and
decreased	osteoporotic	risk,	breast	cancer	and	osteoporosis	nonetheless
cluster	together	in	the	same	areas	of	the	world	and	even	in	the	same
individuals. 22
Rate	of	bone	loss	matters	just	as	much	as	overall	BMD. 23
There	are	places	where	overall	bone	mass,	bone	mineral	density	or	bone
mineral	content	measurements	are	lower	than	they	are	in	“Western”
countries,	but	the	fracture	rate	also	is	lower,	defying	accepted	logic	of
how	we	define	“big,	strong	bones.”
24–26
Being	fat	is	linked	to	greater	BMD,
24,	27
	even	though	areas	of	the	world
that	have	higher	rates	of	obesity	also	have	higher	rates	of	osteoporosis. Something	is	wrong	with	the	idea	that	BMD	reliably	represents
osteoporosis	and,	by	inference,	indicates	the	kind	of	diet	that	would	lower
fracture	rates. In	contrast,	an	alternative,	but	much	better,	predictor	of
osteoporosis	is	the	dietary	ratio	of	animal-to-plant	protein. 1,	13
	The	higher	the
ratio,	the	higher	the	risk	of	disease. And	guess	what? BMD	is	not	significantly
associated	with	this	ratio. 13
Clearly	the	conventional	recommendations	regarding	animal	foods,	dairy
and	bone	mineral	density,	which	are	influenced	and	advertised	by	the	dairy
industry,	are	besieged	by	serious	doubts	in	the	literature. Here	is	what	I	would
recommend	you	do,	based	on	the	research,	to	minimize	your	risk	of
osteoporosis:
Stay	physically	active. Take	the	stairs	instead	of	the	elevator,	go	for
walks,	jogs,	bicycle	rides. Swim,	do	yoga	or	aerobics	every	couple	of
days	and	don’t	be	afraid	to	buy	barbells	to	use	once	in	a	while. Play	asport	or	join	a	social	group	that	incorporates	exercise. The	possibilities
are	endless,	and	they	can	be	fun. You’ll	feel	better,	and	your	bones	will
be	much	healthier	for	the	effort. Eat	a	variety	of	whole	plant	foods,	and	avoid	animal	foods,	including
dairy. Plenty	of	calcium	is	available	in	a	wide	range	of	plant	foods,
including	beans	and	leafy	vegetables. As	long	as	you	stay	away	from
refined	carbohydrates,	like	sugary	cereals,	candies,	plain	pastas	and
white	breads,	you	should	have	no	problem	with	calcium	deficiency. Keep	your	salt	intake	to	a	minimum. Avoid	highly	processed	and
packaged	foods,	which	contain	excess	salt. There	is	some	evidence	that
excessive	salt	intake	can	be	a	problem.KIDNEYS
At	the	Web	site	for	the	UCLA	Kidney	Stone	Treatment	Center,
28
	you	will
discover	that	kidney	stones	may	cause	the	following	symptoms:
Nausea,	vomiting
Restlessness	(trying	to	find	comfortable	position	to	ease	the	pain)
Dull	pain	(ill-defined,	lumbar,	abdominal,	intermittent	pain)
Urgency	(urge	to	empty	the	bladder)
Frequency	(frequent	urination)
Bloody	urine	with	pain	(gross	hematuria)
Fever	(when	complicated	by	infection)
Acute	renal	colic	(severe	colicky	flank	pain	radiating	to	groin,	scrotum,
labia)
Acute	renal	colic	deserves	some	explanation. This	agonizing	symptom	is
the	result	of	a	crystallized	stone	trying	to	pass	through	the	thin	tube	in	your
body	(ureter)	that	transports	urine	from	the	kidney	to	the	bladder. In
describing	the	pain	involved,	the	Web	site	states,	“This	is	probably	one	of	the
worst	pains	humans	experience. Those	who	have	had	it	will	never	forget	it…. The	severe	pain	of	renal	colic	needs	to	be	controlled	by	potent	pain	killers. Don’t	expect	an	aspirin	to	do	the	trick. Get	yourself	to	a	doctor	or	an
emergency	room.”
28
I	don’t	know	about	you,	but	just	thinking	about	these	things	gives	me	
a
shiver. Unfortunately,	up	to	15%	of	Americans,	more	men	than	women,	will
be	diagnosed	with	having	a	kidney	stone	in	their	lifetime. 29
There	are	several	kinds	of	kidney	stones. Although	one	is	a	genetically
rare	type
30
	and	another	is	related	to	urinary	infection,	the	majority	involve
stones	made	of	calcium	and	oxalate. These	calcium	oxalate	stones	are
relatively	common	in	developed	countries	and	relatively	rare	in	developing
countries. 31
	Again,	this	illness	falls	into	the	same	global	patterns	as	all	the
other	Western	diseases. I	first	was	made	aware	of	the	dietary	connection	with	this	disease	at	the
Faculty	of	Medicine	of	the	University	of	Toronto. I	was	invited	to	give	a
seminar	on	our	China	Study	findings	and	while	there	I	met	Professor	W.	G.
Robertson	from	the	Medical	Research	Council	in	Leeds,	England. This
chance	encounter	was	extremely	rewarding. Dr.	Robertson,	as	I	have	come	to
learn,	is	one	of	the	world’s	foremost	experts	on	diet	and	kidney	stones. Dr.
Robertson’s	research	group	has	investigated	the	relationship	between	food
and	kidney	stones	with	great	depth	and	breadth,	both	in	theory	and	in	practice.Their	work	began	more	than	thirty	years	ago	and	continues	to	the	present	day. A	search	of	the	scientific	publications	authored	or	co-authored	by	Robertson
shows	at	least	100	papers	published	since	the	mid-1960s. One	of	Robertson’s	charts	depicts	a	stunning	relationship	between	animal
protein	consumption	and	the	formation	of	kidney	stones	(
Chart	10.4
). 32
	It
shows	that	consuming	animal	protein	at	levels	above	twenty-one	grams	per
person	per	day	(slightly	less	than	one	ounce)	for	the	United	Kingdom	for	the
years	of	1958	to	1973	is	closely	correlated	with	a	high	number	of	kidney
stones	formed	per	10,000	individuals	per	year. This	is	an	impressive
relationship. Few	researchers	have	worked	out	the	details	of	a	research	question	more
thoroughly	than	Robertson	and	his	colleagues. They	have	developed	a	model
for	estimating	the	risk	of	stone	formation	with	remarkable	accuracy. 33
Although	they	have	identified	six	risk	factors	for	kidney	stones,
34,	35
	animal
protein	consumption	was	the	major	culprit. Consumption	of	animal	protein	at
levels	commonly	seen	in	affluent	countries	leads	to	the	development	of	four
of	the	six	risk	factors. 34,	35
Not	only	is	animal	protein	linked	to	risk	factors	for	future	formation	of
stones,	but	it	affects	recurring	stones	as	well. Robertson	published	findings
showing	that,	among	the	patients	who	had	recurrent	kidney	stones,	he	was
able	to	resolve	their	problem	simply	by	shifting	their	diet	away	from	animal
protein	foods. 36
CHART	10.4:	ASSOCIATION	BETWEEN	ANIMAL	PROTEIN
INTAKE	AND	FORMATION	OF	URINARY	CALCULI
How	does	this	work? When	enough	animal	protein-containing	foods	are
consumed,	the	concentrations	of	calcium	and	oxalate	in	the	urine	increasesharply,	usually	within	hours. Chart	10.5
	shows	these	impressive	changes,
published	by	Robertson’s	group. 35
The	individuals	in	this	study	consumed	only	fifty-five	grams	per	day	of
animal	protein,	to	which	was	added	another	thirty-four	grams	per	day	of
animal	protein	in	the	form	of	tuna	fish. This	amount	of	animal	protein
consumption	is	well	within	the	levels	most	Americans	regularly	eat. Men
consume	around	90–100	grams	of	total	protein	per	day,	the	majority	of	which
comes	from	animal	foods;	women	consume	about	70–90	grams	per	day. When	the	kidney	is	under	a	persistent,	long-term	assault	from	increased
calcium	and	oxalate,	kidney	stones	may	result. 35
	The	following,	excerpted
from	a	1987	review	by	Robertson,
37
	emphasizes	the	role	of	diet,	especially
foods	containing	animal	proteins:
Urolithiasis	[kidney	stone	formation]	is	a	worldwide	problem	which
appears	to	be	aggravated	by	the	high	dairy-produce,	highly	energy-rich
and	low-fibre	diets	consumed	in	most	industrialized	countries…. Evidence	points,	in	particular,	to	a	high-meat	protein	intake	as	being
the	dominant	factor…. On	the	basis	of	epidemiological	and
biochemical	studies	a	move	toward	a	more	vegetarian,	less	energy-rich
diet	would	be	predicted	to	reduce	the	risk	of	stone	in	the	population. CHART	10.5:	EFFECT	OF	ANIMAL	PROTEIN	INTAKE	ON
CALCIUM	AND	OXALATE	IN	THE	URINE
A	substantial	and	convincing	effect	on	stone	formation	has	been
demonstrated	for	animal-based	foods. Recent	research	also	shows	that	kidneystone	formation	can	be	initiated	by	the	activity	of	free	radicals,
38
	and	may
thus	be	prevented	by	consumption	of	antioxidant-containing	plant-based
foods	(see	chapter	four). For	yet	another	organ	and	another	disease,	we	see
opposing	effects	(in	this	case	on	stone	formation)	by	animal-	and	plant-based
foods.EYE	PROBLEMS
People	who	can	see	well	often	take	vision	for	granted. We	treat	our	eyes	more
as	little	bits	of	technology	than	as	living	parts	of	the	body,	and	are	all	too
willing	to	believe	that	lasers	are	the	best	course	of	action	for	maintaining
healthy	eyes. But	during	the	past	couple	of	decades,	research	has	shown	that
these	bits	of	“technology”	are	actually	greatly	affected	by	the	foods	we	eat. Our	breakfasts,	lunches	and	dinners	have	a	particular	effect	on	two	common
eye	diseases,	cataracts	and	macular	degeneration—diseases	which	afflict
millions	of	older	Americans. Yes,	that’s	right. I’m	about	to	tell	you	that	if	you	eat	animal	foods	instead
of	plant	foods,	you	just	might	go	blind. Macular	degeneration	is	the	leading	cause	of	irreversible	blindness	
among
people	over	age	sixty-five. Over	1.6	million	Americans	suffer	from	this
disease,	many	of	whom	become	blind. 39
	As	the	name	implies,	this	condition
involves	destruction	of	the	macula,	which	is	the	biochemical	intersection	in
the	eye—where	the	energy	of	the	light	coming	in	is	transformed	into	a	nerve
signal. The	macula	occupies	center	stage,	so	to	speak,	and	it	must	be
functional	for	sight	to	occur. Around	the	macula	there	are	fatty	acids	that	can	react	with	incoming	light
to	produce	a	low	level	of	highly	reactive	free	radicals. 40
	These	free	radicals
(see	chapter	four)	can	destroy,	or	degenerate,	neighboring	tissue,	including	the
macula. But	fortunately	for	us,	free	radical	damage	can	be	repressed	thanks	to
the	antioxidants	in	vegetables	and	fruits. Two	studies,	each	involving	a	team	of	experienced	researchers	at
prestigious	institutions,	provide	compelling	evidence	that	food	can	protect
against	macular	degeneration. Both	studies	were	published	a	decade	ago. One
evaluated	diet
41
	and	the	other	assessed	nutrients	in	blood. 42
	The	findings	of
these	two	studies	suggested	that	as	much	as	70–88%	of	blindness	caused	by
macular	degeneration	could	be	prevented	if	the	right	foods	are	eaten. The	study	on	dietary	intakes
41
	compared	356	individuals	fifty-five	to
eighty	years	of	age	who	were	diagnosed	with	advanced	macular	degeneration
(cases)	with	520	individuals	with	other	eye	diseases	(controls). Five
ophthalmology	medical	centers	collaborated	on	the	study. Researchers	found	that	a	higher	intake	of	total	carotenoids	was	associated
with	a	lower	frequency	of	macular	degeneration. Carotenoids	are	a	group	of
antioxidants	found	in	the	colored	parts	of	fruits	and	vegetables. When
carotenoid	intakes	were	ranked,	those	individuals	who	consumed	the	most
had	43%	less	disease	than	those	who	consumed	the	least. Not	surprisingly,five	out	of	six	plant-based	foods	measured	also	were	associated	with	lower
rates	of	macular	degeneration	(broccoli,	carrots,	spinach	or	collard	greens,
winter	squash	and	sweet	potato).
_OceanofPDF.com_The_China_Study__The_Most_Comprehensive_St_-_T_Colin_Campbell.txt
Summarize the following text section accurately and concisely. Maintain specific details and numerical information, and use anti-repetition mechanisms:

        2
	The	first	nine
comprise	97%	of	all	autoimmune	disease	cases. 2
	The	most	studied	are
multiple	sclerosis	(MS),	rheumatoid	arthritis,	lupus,	Type	1	diabetes	and
rheumatic	heart	disease. 2
	These	are	also	the	primary	autoimmune	diseases
that	have	been	studied	in	reference	to	diet. Others	not	listed	in	
Chart	9. 1
	include	inflammatory	bowel	disease,
4
Crohn’s	disease,
4
	rheumatic	heart	disease
3
	and	(possibly)	Parkinson’s
disease. 5
Each	disease	name	may	sound	very	different,	but	as	one	recent	review
points	out,
2
	“…	it	is	important	to	consider…	these	disorders	as	a	group. ”
They	show	similar	clinical	backgrounds,
3,	6,	7
	they	sometimes	occur	in	the
same	person	and	they	are	often	found	in	the	same	populations. 2
	MS	and	Type
1	diabetes,	for	example,	have	“near(ly)	identical	
ethnic	and	geographic
distribution. ”
8
	Autoimmune	diseases	in	general	become	more	common	thegreater	the	distance	from	the	equator. This	phenomenon	has	been	known	since
1922. 9
	MS,	for	example,	is	over	a	hundred	times	more	prevalent	in	the	far
north	than	at	the	equator. 10
CHART	9. 1:	COMMON	AUTOIMMUNE	DISEASES	(FROM
MOST	COMMON	TO	LEAST	COMMON)
1. Graves’	disease	(Hyperthyroidism)
2. Rheumatoid	arthritis
3. Thyroiditis	(Hypothyroidism)
4. Vitiligo
5. Pernicious	anemia
6. Glomerulonephritis
7. Multiple	sclerosis
8. Type	1	diabetes
9. Systemic	lupus	erythematosus
10. Sjogren’s	disease
11. Myasthenia	gravis
12. Polymyositis/dermatomyositis
13. Addison’s	disease
14. Scleroderma
15. Primary	biliary	cirrhosis
16. Uveitis
17. Chronic	active	hepatitis
Because	of	some	of	these	common	features,	it	is	not	too	far-fetched	to
think	of	the	autoimmune	diseases	as	one	grand	disease	living	in	different
places	in	the	body	and	taking	on	different	names. We	refer	in	this	way	to
cancer,	which	is	specifically	named	depending	on	what	part	of	the	body	it
resides	in. All	autoimmune	diseases	are	the	result	of	one	group	of	mechanisms	gone
awry,	much	like	cancer. In	this	case,	the	mechanism	is	the	immune	system
mistakenly	attacking	cells	in	its	own	body. Whether	it	is	the	pancreas	as	in
Type	1	diabetes,	the	myelin	sheath	as	in	MS	or	joint	tissues	as	in	arthritis,	all
autoimmune	diseases	involve	an	immune	system	that	has	revolted. It	is	an
internal	mutiny	of	the	worst	kind,	one	in	which	our	body	becomes	its	own
worst	enemy. IMMUNITY	FROM	INVADERS
The	immune	system	is	astonishingly	complex. I	often	hear	people	speaking
about	this	system	as	if	it	were	an	identifiable	organ	like	a	lung. Nothing	could
be	further	from	the	truth. It	is	a	system,	not	an	organ. In	essence,	our	immune	system	is	like	a	military	network	designed	to
defend	against	foreign	invaders. The	“soldiers”	of	this	network	are	the	white
blood	cells,	which	are	comprised	of	many	different	sub-groups,	each	having
its	own	mission. These	sub-groups	are	analogous	to	a	navy,	army,	air	force
and	marines,	with	each	group	of	specialists	doing	highly	specialized	work. The	“recruitment	center”	for	the	system	is	in	the	marrow	of	our	bones. The
marrow	is	responsible	for	generating	specialized	cells	called	stem	cells. Some
of	these	cells	are	released	into	circulation	for	use	elsewhere	in	the	body;	these
are	called	B-cells	(for	bone). Other	cells	formed	in	the	bone	marrow	remain
immature,	or	unspecialized,	until	they	travel	to	the	thymus	(an	organ	in	the
chest	cavity	just	above	the	heart)	where	they	become	specialized;	these	are
called	T-cells	(for	thymus). These	“soldier”	cells,	along	with	other	specialized
cells,	team	up	to	create	intricate	defense	plans. They	meet	at	major
intersections	around	the	body,	including	the	spleen	(just	inside	the	left	lower
rib	cage)	and	the	lymph	nodes. These	meeting	points	are	like	command	and
control	centers,	where	the	“soldier	cells”	rearrange	themselves	into	teams	to
attack	foreign	invaders. These	cells	are	remarkably	adaptable	when	they	form	their	teams. They
are	able	to	respond	to	different	circumstances	and	different	foreign
substances,	even	those	they	have	never	before	seen. The	immune	response	to
these	strangers	is	an	incredibly	creative	process. It	is	one	of	the	true	wonders
of	nature. The	foreign	invaders	are	protein	molecules	called	antigens. These	foreign
cells	can	be	a	bacterium	or	a	virus	looking	to	corrupt	the	body’s	integrity. So
when	our	immune	system	notices	these	foreign	cells,	or	antigens,	it	destroys
them. Each	of	these	foreign	antigens	has	a	separate	identity,	which	is
determined	by	the	sequence	of	amino	acids	that	comprises	its	proteins. It	is
analogous	to	each	and	every	person	having	a	different	face. Because
numerous	amino	acids	are	available	for	creating	proteins,	there	are	infinite
varieties	of	distinctive	“faces. ”
To	counter	these	antigens,	our	immune	system	must	customize	its	defense
to	each	attack. It	does	this	by	creating	a	“mirror	image”	protein	for	each
attacker. The	mirror	image	is	able	to	ht	perfectly	onto	the	antigen	and	destroy
it. Essentially,	the	immune	system	creates	a	mold	for	each	face	it	encounters. Every	time	it	sees	that	face	after	the	initial	encounter,	it	uses	the	custom-mademold	to	“capture”	the	invader	and	destroy	it. The	mold	may	be	a	B-cell
antibody	or	a	T-cell-based	receptor	protein. Remembering	each	defense	against	each	invader	is	what	immunization	is
all	about. An	initial	exposure	to	chicken	pox,	for	example,	is	a	difficult	battle,
but	the	second	time	you	encounter	that	virus	you	will	know	exactly	how	to
deal	with	it,	and	the	war	will	be	shorter,	less	painful	and	much	more
successful. You	may	not	even	get	sick. IMMUNITY	FROM	OURSELVES
Even	though	this	system	is	a	wonder	of	nature	when	it	is	defending	the	body
against	foreign	proteins,	it	is	also	capable	of	attacking	the	same	tissues	that	it
is	designed	to	protect. This	self-destructive	process	is	common	to	all
autoimmune	diseases. It	is	as	if	the	body	were	to	commit	suicide. One	of	the	fundamental	mechanisms	for	this	self-destructive	behavior	is
called	molecular	mimicry. It	so	happens	that	some	of	the	foreign	invaders	that
our	soldier	cells	seek	out	to	destroy	look	the	same	as	our	own	cells. The
immune	system	“molds”	that	ht	these	invaders	also	ht	our	own	cells. The
immune	system	then	destroys,	under	some	circumstances,	everything	that	fits
the	mold,	including	our	own	cells. This	is	an	extremely	complex	self-
destructive	process	involving	many	different	strategies	on	the	part	of	the
immune	system,	all	of	which	share	the	same	fatal	flaw	of	not	being	able	to
distinguish	“foreign”	invader	proteins	from	the	proteins	of	our	own	body. What	does	all	of	this	have	to	do	with	what	we	eat. It	so	happens	that	the
antigens	that	trick	our	bodies	into	attacking	our	own	cells	may	be	in	food. During	the	process	of	digestion,	for	example,	some	proteins	slip	into	our
bloodstream	from	the	intestine	without	being	fully	broken	down	into	their
amino	acid	parts. The	remnants	of	undigested	proteins	are	treated	as	foreign
invaders	by	our	immune	system,	which	sets	about	making	molds	to	destroy
them	and	sets	into	motion	the	self-destructive	autoimmune	process. 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
example
1
	of	the	exceptional	elegance	of	nature’s	ability	to	regulate	itself. The	immune	system	uses	a	very	delicate	process	to	decide	which	proteins
should	be	attacked	and	which	should	be	left	alone. 11
	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	todifferentiate	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	diabetes
12–14
	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’s	
milk	may
cause	one	of	the	most	devastating	diseases	that	can	befall	a	child. For
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	consumedcow’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.
97%
What percentage of autoimmune disease cases are caused by the first nine diseases mentioned in the text?
Multiple sclerosis, rheumatoid arthritis, lupus, Type 1 diabetes, and rheumatic heart disease
According to the text, which autoimmune diseases are the most studied?
The text suggests that there is a strong link between the two, with the risk increasing with the consumption of cow's milk, especially in early childhood.
What is the relationship between cow's milk consumption and the risk of Type 1 diabetes?
The text states that they all have similar clinical backgrounds, often occur in the same person, and are found in the same populations.
What is the commonality among all autoimmune diseases?
The study found that the risk of developing MS increased with the consumption of cow's milk, with a 5-6 fold increase.
What is the conclusion of the study that found an association between cow's milk consumption and the risk of developing multiple sclerosis?