Because	of	this	the	two	groups	of	rats	were	starting	the	cancer
process	with	different	amounts	of	initiated,	cancerous	“seeds.”	Then,	during
the	promotion	phase,	we	fed	a	low-protein	diet	to	the	high-aflatoxin	dose
groups	and	a	high-protein	diet	to	the	low-aflatoxin	dose	group. We	wondered
whether	the	animals	that	start	with	lots	of	cancerous	seeds	are	able	to
overcome	their	predicament	by	eating	a	low-protein	diet. CHART	3.4:	DIETARY	PROTEIN	AND	FOCI	FORMATION
	CHART	3.5:	CARCINOGEN	DOSE	VERSUS	PROTEIN	INTAKE
Again,	the	results	were	remarkable	(
Chart	3.5
). Animals	starting	with	the
most	cancer	initiation	(high-aflatoxin	dose)	developed	
substantially	less	foci
when	fed	the	5%	protein	diet. In	contrast,	animals	initiated	with	a	low-
aflatoxin	dose	actually	produced	
substantially	more	foci
	when	subsequently
fed	the	20%	protein	diet. A	principle	was	being	established. Foci	development,	initially	determined
by	the	amount	of	the	carcinogen	exposure,	is	actually	controlled	far	more	by
dietary	protein	consumed	during	promotion. Protein	during	promotion	trumps
the	carcinogen,	regardless	of	initial	exposure. With	this	background	information	we	designed	a	much	more	substantial
experiment. Here	is	a	step-by-step	sequence	of	experiments,	carried	out	by
my	graduate	student	Linda	Youngman. 35
	All	animals	were	dosed	with	the
same	amount	of	carcinogen,	then	alternately	fed	either	5%	or	20%	dietary
protein	during	the	twelve-week	promotion	stage. We	divided	this	twelve-week
promotion	stage	into	four	periods	of	three	weeks	each. Period	1	represents
weeks	one	to	three,	period	2	represents	weeks	four	to	six,	and	so	on. When	animals	were	fed	the	20%	protein	diet	during	periods	1	and	2	(20-
20),	foci	continued	to	enlarge,	as	expected. But	when	animals	were	switched
to	the	low-protein	diet	at	the	beginning	of	period	3	(20-20-5),	there	was	a
sharp	decrease	in	foci	development. And,	when	animals	were	subsequently
switched	back	to	the	20%	protein	diet	during	period	4	(20-20-5-20),	foci
development	was	turned	on	once	again.In	another	experiment,	in	animals	fed	20%	dietary	protein	during	period	1
but	switched	to	5%	dietary	protein	during	period	2	(20-5),	foci	development
was	sharply	decreased. But	when	these	animals	were	returned	to	20%	dietary
protein	during	period	3	(20-5-20),	we	again	saw	the	dramatic	power	of	dietary
protein	to	promote	foci	development. These	several	experiments,	taken	together,	were	quite	profound. Foci
growth	could	be	reversed,	up	and	down,	by	switching	the	amount	of	protein
being	consumed,	and	at	all	stages	of	foci	development. These	experiments	also	demonstrated	that	the	body	could	“remember”
early	carcinogen	insults,
35,	36
	even	though	they	might	then	lie	dormant	with
low	protein	intake. That	is,	exposure	to	aflatoxin	left	a	genetic	“imprint”	that
remained	dormant	with	5%	dietary	protein	until	nine	weeks	later	when	this
imprint	reawakened	to	form	foci	with	20%	dietary	protein. In	simple	terms,
the	body	holds	a	grudge. It	suggests	that	if	we	are	exposed	in	the	past	to	a
carcinogen	that	initiates	a	bit	of	cancer	that	remains	dormant,	this	cancer	can
still	be	“reawakened”	by	bad	nutrition	some	time	later. These	studies	showed	that	cancer	development	is	modified	by	relatively
modest	changes	in	protein	consumption. But	how	much	protein	is	too	much	or
too	little? Using	rats,	we	investigated	a	range	of	4-24%	dietary	protein	(
Chart
3.6
37
). Foci	did	not	develop	with	up	to	about	10%	dietary	protein. Beyond
10%,	foci	development	increased	dramatically	with	increases	in	dietary
protein. The	results	were	later	repeated	a	second	time	in	my	laboratory	by	a
visiting	professor	from	Japan,	Fumiyiki	Horio. 38CHART	3.6:	FOCI	PROMOTION	BY	DIETARY	PROTEIN
The	most	significant	finding	of	this	experiment	was	this:	foci	developed
only	when	the	animals	met	or	exceeded	the	amount	of	dietary	protein	(12%)
needed	to	satisfy	their	body	growth	rate. 39
	That	is,	when	the	animals	met	and
surpassed	their	requirement	for	protein,	disease	onset	began. This	finding	may	have	considerable	relevance	for	humans	even	though
these	were	rat	studies. I	say	this	because	the	protein	required	for	growth	in
young	rats	and	humans	as	well	as	the	protein	required	to	maintain	health	for
adult	rats	and	humans	is	remarkably	similar. 40,	41
According	to	the	recommended	daily	allowance	(RDA)	for	protein
consumption,	we	humans	should	be	getting	about	10%	of	our	energy	from
protein. This	is	considerably	more	than	the	actual	amount	required. But
because	requirements	may	vary	from	individual	to	individual,	10%	dietary
protein	is	recommended	to	insure	adequate	intake	for	virtually	all	people. What	do	most	of	us	routinely	consume? Remarkably,	it	is	considerably	more
than	the	recommended	10%. The	average	American	consumes	15-16%
protein. Does	this	place	us	at	risk	for	getting	cancer? These	animal	studies
hint	that	it	does. Ten	percent	dietary	protein	is	equivalent	to	eating	about	50-60	grams	of
protein	per	day,	depending	on	body	weight	and	total	calorie	intake. Thenational	average	of	15-16%	is	about	70-100	grams	of	protein	per	day,	with
men	at	the	upper	part	of	the	range	and	women	at	the	lower	end. In	food	terms,
there	are	about	twelve	grams	of	protein	in	100	calories	of	spinach	(fifteen
ounces)	and	five	grams	of	protein	in	100	calories	of	raw	chick	peas	(just	over
two	tablespoons). There	are	about	thirteen	grams	of	protein	in	100	calories	of
porterhouse	steak	(just	over	one	and	a	half	ounces). Yet	another	question	was	whether	protein	intake	could	modify	the	all-
important	relationship	between	aflatoxin	dose	and	foci	formation. A	chemical
is	usually	not	considered	a	carcinogen	unless	higher	doses	yield	higher
incidences	of	cancer. For	example,	as	the	aflatoxin	dose	becomes	greater,	foci
and	tumor	growth	should	be	correspondingly	greater. If	an	increasing
response	is	not	observed	for	a	suspect	chemical	carcinogen,	serious	doubt
arises	whether	it	really	is	carcinogenic. To	investigate	this	dose-response	question,	ten	groups	of	rats	were
administered	increasing	doses	of	aflatoxin,	then	fed	either	regular	levels
(20%)	or	low	levels	(5-10%)	of	protein	during	the	promotion	period	(
Chart
3.7
34
). In	the	animals	fed	the	20%	level	of	protein,	foci	increased	in	number	and
size,	as	expected,	as	the	aflatoxin	dose	was	increased. The	dose-response
relationship	was	strong	and	clear. However,	in	the	animals	fed	5%	protein,	
the
dose-response	curve	completely	disappeared. There	was	no	foci	response,
even	when	animals	were	given	the	maximum	tolerated	aflatoxin	dose. This
was	yet	another	result	demonstrating	that	a	low-protein	diet	could	override	the
cancer-causing	effect	of	a	very	powerful	carcinogen,	aflatoxin. CHART	3.7:	AFLATOXIN	DOSE—FOCI	RESPONSE
Is	it	possible	that	chemical	carcinogens,	in	general,	do	not	cause	cancer
unless	the	nutritional	conditions	are	“right”? Is	it	possible	that,	for	much	of
our	lives,	we	are	being	exposed	to	small	amounts	of	cancer-causing
chemicals,	but	cancer	does	not	occur	unless	we	consume	foods	that	promoteand	nurture	tumor	development? Can	we	control	cancer	through	nutrition?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	pre-medical	student	doing	an	honors
degree	with	me,	David	Schulsinger,	did	the	study	(
Chart	3.8
42
). Gluten,	the
protein	of	wheat,	did	not	produce	the	same	result	as	casein,	even	when	fed	at
the	same	20%	level. CHART	3.8:	PROTEIN	TYPE	AND	FOCI	RESPONSE
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?ADDITIONAL	QUESTIONS
For	those	readers	who	want	to	know	somewhat	more,	I’ve	included	a	few
questions	in	
Appendix	A
.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. 36,	43
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. 36,	43
	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	0	score,	something	almost	never	seen
in	research	and	almost	identical	to	the	original	research	in	India. 16
In	this	same	experiment,
36
	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%-40%	less!) than	animals	fed	a	high-
protein	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.”
CHART	3.9A:	TUMOR	DEVELOPMENT	AT	100	WEEKS
	CHART	3.9B:	EARLY	FOCI,	“LIFETIME”
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	(
Chart	3.9a
). 36,	43
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	(10-20%)	commonly	used	both	in	rodents	and
humans	makes	it	especially	tantalizing—and	provocative.OTHER	CANCERS,	OTHER	CARCINOGENS
Okay,	so	here’s	the	central	question:	how	does	this	research	apply	to	human
health	and	human	liver	cancer	in	particular? One	way	to	investigate	this
question	is	to	research	other	species,	other	carcinogens	and	other	organs. If
casein’s	effect	on	cancer	is	consistent	across	these	categories,	it	becomes
more	likely	that	humans	better	take	note. So	our	research	became	broader	in
scope,	to	see	whether	our	discoveries	would	hold	up. While	our	rat	studies	were	underway,	studies	were	published
44,	45
	claiming
that	chronic	infection	with	hepatitis	B	virus	(HBV)	was	the	major	risk	factor
for	human	liver	cancer. It	was	thought	that	people	who	remained	chronically
infected	with	HBV	had	twenty	to	forty	times	the	risk	of	getting	liver	cancer. Over	the	years,	considerable	research	had	been	done	on	how	this	virus
causes	liver	cancer. 46
	In	effect,	a	piece	of	the	virus	gene	inserts	itself	into	the
genetic	material	of	the	mouse	liver	where	it	initiates	liver	cancer. When	this	is
done	experimentally	the	animals	are	considered	
transgenic. Virtually	all	of	the	research	done	in	other	laboratories	on	HBV	transgenic
mice—and	there	was	a	lot	of	it—was	done	primarily	to	understand	the
molecular	mechanism	by	which	HBV	worked. No	attention	was	given	to
nutrition	and	its	effect	on	tumor	development. I	watched	with	some
amusement	for	several	years	how	one	community	of	researchers	argued	for
aflatoxin	as	the	key	cause	of	human	liver	cancer	and	another	
community
argued	for	HBV. No	one	in	either	community	dared	to	suggest	that	nutrition
had	anything	to	do	with	this	disease. We	wanted	to	know	about	the	effect	of	casein	on	HBV-induced	liver
cancer	in	mice. This	was	a	big	step. It	went	beyond	aflatoxin	as	a	carcinogen
and	rats	as	a	species. A	brilliant	young	graduate	student	from	China	in	my
group,	Jifan	Hu,	initiated	studies	to	answer	this	question	and	was	later	joined
by	Dr.	Zhiqiang	Cheng. We	needed	a	colony	of	these	transgenic	mice. There
were	two	such	“breeds”	of	mice,	one	living	in	La	Jolla,	California,	the	other
in	Rockville,	Maryland. Each	strain	had	a	different	piece	of	HBV	gene	stuck
in	the	genes	of	their	livers,	and	each	was	therefore	highly	prone	to	liver
cancer. I	contacted	the	responsible	researchers	and	inquired	about	their
helping	us	to	establish	our	own	mouse	colony. Both	research	groups	asked
what	we	wanted	to	do	and	both	were	inclined	to	think	that	studying	the
protein	effect	was	foolish. I	also	sought	a	research	grant	to	study	this	question
and	it	was	rejected. The	reviewers	did	not	take	kindly	to	the	idea	of	a
nutritional	effect	on	a	virus-induced	cancer,	especially	of	a	dietary	protein
effect. I	was	beginning	to	wonder:	was	I	now	being	too	explicit	in	questioning
the	mythical	health	value	of	protein? The	reviews	of	the	grant	proposalcertainly	indicated	this	possibility. We	eventually	obtained	funding,	did	the	study	on	both	strains	of	mice	
and
got	essentially	the	same	result	as	we	did	with	the
	rats. 47,	48
	You	can	see	the
results	for	yourself. The	adjoining	picture	(
Chart	3.10
47
)	shows	what	a	cross-
section	of	the	mouse	livers	looks	like	under	a	microscope. The	dark-colored
material	is	indicative	of	cancer	development	(ignore	the	“hole”;	that’s	only	a
cross-section	of	a	vein). There	is	intense	early	cancer	formation	in	the	22%
casein	animals	(D),	much	less	in	the	14%	casein	animals	(C),	and	none	in	the
6%	casein	animals	(B);	the	remaining	picture	(A)	shows	a	liver	having	no
virus	gene	(the	control). The	adjoining	graph	(
Chart	3.11
47
)	shows	the	expression	(activity)	of	two
HBV	genes	that	cause	cancer	inserted	in	the	mouse	liver. Both	the	picture	and
the	graph	show	the	same	thing:	the	22%	casein	diet	turned	on	expression	of
the	viral	gene	to	cause	cancer,	whereas	the	6%	casein	diet	showed	almost	no
such	activity. By	this	time,	we	had	more	than	enough	information	to	conclude	that
casein,	that	sacred	protein	of	cow’s	milk,	dramatically	promotes	liver	cancer
in:
rats	dosed	with	aflatoxin
mice	infected	with	HBVCHART	3.10:	DIETARY	PROTEIN	EFFECT	ON	GENETICALLY-
BASED	(HBV)	LIVER	CANCER	(MICE)
	
CHART	3.11:	DIETARY	PROTEIN	EFFECT	ON	GENE	EXPRESSION
(MICE)
Not	only	are	these	effects	substantial,	but	we	also	discovered	a	network	of
complementary	ways	by	which	they	worked.Next	question:	can	we	generalize	these	findings	to	other	cancers	and	to
other	carcinogens? At	the	University	of	Illinois	Medical	Center	in	Chicago,
another	research	group	was	working	with	mammary	(breast)	cancer	in	rats. 49–
51
	This	research	showed	that	increasing	intakes	of	casein	promoted	the
development	of	mammary	(breast)	cancer. They	found	that	higher	casein
intake:
promotes	breast	cancer	in	rats	dosed	with	two	experimental	carcinogens
(7,12-dimethybenz(a)anthracene	(DBMA)	and	N-nitroso-methylurea
(NMU))
operates	through	a	network	of	reactions	that	combine	to	increase	cancer
operates	through	the	same	female	hormone	system	that	operates	in
humansLARGER	IMPLICATIONS
An	impressively	consistent	pattern	was	beginning	to	emerge. For	two
different	organs,	four	different	carcinogens	and	two	different	species,	casein
promotes	cancer	growth	while	using	a	highly	integrated	system	of
mechanisms. It	is	a	powerful,	convincing	and	consistent	effect. For	example,
casein	affects	the	way	cells	interact	with	carcinogens,	the	way	DNA	reacts
with	carcinogens	and	the	way	cancerous	cells	grow. The	depth	and
consistency	of	these	findings	strongly	suggest	that	they	are	relevant	for
humans,	for	four	reasons. First,	rats	and	humans	have	an	almost	identical	need
for	protein. Second,	protein	operates	in	humans	virtually	the	same	way	it	does
in	rats. Third,	the	level	of	protein	intake	causing	tumor	growth	is	the	same
level	that	humans	consume. And	fourth,	in	both	rodents	and	humans	the
initiation	stage	is	far	less	important	than	the	promotion	stage	of	cancer. This	is
because	we	are	very	likely	“dosed”	with	a	certain	amount	of	carcinogens	in
our	everyday	lives,	but	whether	they	lead	to	full	tumors	depends	on	their
promotion,	or	lack	thereof. Even	though	I	became	convinced	that	increasing	casein	intake	promotes
cancer,	I	still	had	to	be	wary	of	generalizing	too	much. This	was	an
exceptionally	provocative	finding	that	drew	fierce	skepticism. But	these
findings	nonetheless	were	a	hint	of	things	to	come. I	wanted	to	broaden	my
evidence	still	more. What	effect	did	other	nutrients	have	on	
cancer,	and	how
did	they	interact	with	different	carcinogens	and	different	organs? Might	the
effects	of	other	nutrients,	carcinogens	or	organs	cancel	each	other,	or	might
there	be	consistency	of	effect	for	nutrients	within	certain	types	of	food? Would	promotion	continue	to	be	reversible? If	so,	cancer	might	be	readily
controlled,	even	reversed,	simply	by	decreasing	the	intakes	of	the	promoting
nutrients	and/or	increasing	the	intakes	of	the	anti-promoting	nutrients. We	initiated	more	studies	using	several	different	nutrients,	including	fish
protein,	dietary	fats	and	the	antioxidants	known	as	carotenoids. A	couple	of
excellent	graduate	students	of	mine,	Tom	O’Connor	and	Youping	He,
measured	the	ability	of	these	nutrients	to	affect	liver	and	pancreatic	cancer. The	results	of	these,	and	many	other	studies,	showed	nutrition	to	be	far	more
important	in	controlling	cancer	promotion	than	the	dose	of	the	initiating
carcinogen. The	idea	that	nutrients	primarily	affect	tumor	development	during
promotion	was	beginning	to	appear	to	be	a	general	property	of	nutrition	and
cancer	relationships. The	
Journal	of	the	National	Cancer	Institute,
	which	is
the	official	publication	of	the	U.S.	National	Cancer	Institute,	took	note	of
these	studies	and	featured	some	of	our	findings	on	its	cover. 52
Furthermore,	a	pattern	was	beginning	to	emerge:	
nutrients	from	animal-based	foods	increased	tumor	development	while	nutrients	from	plant-based
foods	decreased	tumor	development. In	our	large	lifetime	study	of	rats	with
aflatoxin-induced	tumors,	the	pattern	was	consistent. In	mice	with	hepatitis	B
virus-altered	genes,	the	pattern	was	consistent. In	studies	done	by	another
research	group,	with	breast	cancer	and	different	carcinogens,	the	pattern	was
consistent. In	studies	of	pancreatic	cancer	and	other	nutrients,	the	pattern	was
consistent. 52,	53
	In	studies	on	carotenoid	antioxidants	and	cancer	initiation,	the
pattern	was	consistent. 54,	55
	From	the	first	stage	of	cancer	initiation	to	the
second	stage	of	cancer	promotion,	the	pattern	was	consistent. From	one
mechanism	to	another,	the	pattern	was	consistent. So	much	consistency	was	stunningly	impressive,	but	one	aspect	of	this
research	demanded	that	we	remain	cautious:	all	this	evidence	was	gathered	in
experimental	animal	studies. Although	there	are	strong	arguments	that	these
provocative	findings	are	
qualitatively
	relevant	to	human	health,	we	cannot
know	the	
quantitative
	relevance. In	other	words,	are	these	principles
regarding	animal	protein	and	cancer	critically	important	for	all	humans	in	all
situations,	or	are	they	merely	marginally	important	for	a	minority	of	people	in
fairly	unique	situations? Are	these	
principles	involved	in	one	thousand	human
cancers	every	year,	one	million	human	cancers	every	year,	or	more? We	need
direct	evidence	from	human	research. Ideally,	this	evidence	would	be
gathered	with	rigorous	methodology	and	would	investigate	dietary	patterns
comprehensively,	using	large	numbers	of	people	who	had	similar	lifestyles,
similar	genetic	backgrounds,	and	yet	had	widely	varying	incidences	of
disease. Having	the	opportunity	to	do	such	a	study	is	rare,	at	best,	but	by	incredibly
good	luck	we	were	given	exactly	the	opportunity	we	needed. In	1980	I	had
the	good	fortune	of	welcoming	in	my	laboratory	a	most	personable	and
professional	scientist	from	mainland	China,	Dr.	Junshi	Chen. With	this
remarkable	man,	opportunities	arose	to	search	for	some	larger	truths. We	were
given	the	chance	to	do	a	human	study	that	would	take	all	of	these	principles
we	had	begun	to	uncover	in	the	lab	to	the	next	level. It	was	time	to	study	the
role	of	nutrition,	lifestyle	and	disease	in	the	most	comprehensive	manner	ever
undertaken	in	the	history	of	medicine. We	were	on	to	the	China	Study.4
Lessons	from	China
	
	
	A	SNAPSHOT	IN	TIME
Have	you	ever	had	the	sensation	of	wanting	to	permanently	capture	a
moment? Such	moments	can	grip	you	in	a	way	you	will	never	forget. For
some	people,	those	moments	center	on	family	close	friends	or	related
activities;	for	others	those	moments	may	center	on	nature,	spirituality	or
religion. For	most	of	us,	I	suspect,	it	can	be	a	little	of	each. They	become	the
personal	moments,	both	happy	and	sad,	which	define	our	memories. It’s	these
moments	in	which	everything	just	“comes	together.”	They	are	the	snapshots
of	time	that	define	much	of	our	life	experience. The	value	of	a	snapshot	of	time	is	not	lost	on	researchers	either. We
construct	experiments,	hoping	to	preserve	and	analyze	the	specific	details	of	a
certain	moment	for	years	to	come. I	was	fortunate	enough	to	be	privy	to	such
an	opportunity	in	the	early	1980s,	after	a	distinguished	senior	scientist	from
China,	Dr.	Junshi	Chen,	came	to	Cornell	to	work	in	my	lab. He	was	deputy
director	of	China’s	premier	health	research	laboratory	and	one	of	the	first
handful	of	Chinese	scholars	to	visit	the	U.S.	following	the	establishment	of
relations	between	our	two	countries.THE	CANCER	ATLAS
In	the	early	1970s,	the	premier	of	China,	Chou	EnLai,	was	dying	of	cancer. In
the	grips	of	this	terminal	disease,	Premier	Chou	initiated	a	nationwide	survey
to	collect	information	about	a	disease	that	was	not	
well	understood. It	was	to
be	a	monumental	survey	of	death	rates	for	twelve	different	kinds	of	cancer	for
more	than	2,400	Chinese	counties	and	880	million	(96%)	of	their	citizens. The	survey	was	remarkable	in	many	ways. It	involved	650,000	workers,	the
most	ambitious	biomedical	research	project	ever	undertaken. The	end	result
of	the	survey	was	a	beautiful,	color-coded	atlas	showing	where	certain	types
of	cancer	were	high	and	where	they	were	almost	nonexistent. 1
CHART	4.1:	SAMPLE	CANCER	ATLAS	IN	CHINA
This	atlas	made	it	clear	that	in	China	cancer	was	geographically	localized. Some	cancers	were	much	more	common	in	some	places	than	in	others. Earlier
studies	had	set	the	stage	for	this	idea,	showing	that	cancer	incidence	also
varies	widely	between	different	countries. 2–4
	But	these	China	data	were	more
remarkable	because	the	geographic	variations	in	cancer	rates	were	much
greater	(
Chart	4.2
). They	also	occurred	in	a	country	where	87%	of	the
population	is	the	same	ethnic	group,	the	Han	people.CHART	4.2. RANGE	OF	CANCER	RATES	IN	CHINESE	COUNTIES
Cancer	Site
Males
Females
All	Cancers
35–721
35–491
Nasopharynx
0–75
0–26
Esophagus
1–435
0–286
Stomach
6–386
2–141
Liver
7–248
3–67
Colorectal
2–67
2–61
Lung
3–59
0–26
Breast
—
0–20
*	Age-adjusted	death	rates,	representing	#	cases/100,000	people/year
Why	was	there	such	a	massive	variation	in	cancer	rates	among	different
counties	when	genetic	backgrounds	were	similar	from	place	to	place? Might	it
be	possible	that	cancer	is	largely	due	to	environmental/lifestyle	factors,	and
not	genetics? A	few	prominent	scientists	had	already	reached	that	conclusion. The	authors	of	a	major	review	on	diet	and	cancer,	prepared	for	the	U.S.
Congress	in	1981,	estimated	that	genetics	only	determines	about	
2-3%	of	the
total	cancer	risk
. 4
The	data	behind	the	China	cancer	atlas	were	profound. The	counties	with
the	highest	rates	of	some	cancers	were	more	than	100	times	greater	than
counties	with	the	lowest	rates	of	these	cancers. These	are	truly	remarkable
figures. By	way	of	comparison,	we	in	the	U.S.	see,	at	most,	two	to	three	times
the	cancer	rates	from	one	part	of	the	country	to	another. In	fact,	very	small	and	relatively	unimportant	differences	in	cancer	rates
make	big	news,	big	money	and	big	politics. There	has	been	a	long-standing
story	in	my	state	of	New	York	about	the	increased	rates	of	breast	cancer	in
Long	Island. Large	amounts	of	money	(about	$30	million
3
)	and	years	and
years	of	work	have	been	spent	examining	the	issue. What	sorts	of	rates	were
causing	such	a	furor? Two	counties	in	Long	Island	had	rates	of	breast	cancer
only	10–20%	higher	than	the	state	average. This	difference	was	enough	to
make	front-page	news,	scare	people	and	move	politicians	to	action. Contrast
this	with	the	findings	in	China	where	some	parts	of	the	country	had	cancer
rates	100	times	(10,000%)	higher	than	others. Because	China	is	relatively	homogenous	genetically,	it	was	clear	that	these
differences	had	to	be	explained	by	environmental	causes. This	raised	a
number	of	critical	questions:
Why	was	cancer	so	high	in	some	rural	Chinese	counties	and	not	inothers? Why	were	these	differences	so	incredibly	large? Why	was	overall	cancer,	in	the	aggregate,	less	common	in	China	than	in
the	U.S.? The	more	Dr.	Chen	and	I	talked,	the	more	we	wished	that	we	had	a
snapshot	in	time	of	the	dietary	and	environmental	conditions	in	rural	China. If
only	we	could	look	into	these	people’s	lives,	note	what	they	eat,	how	they
live,	what	is	in	their	blood	and	their	urine	and	how	they	die. If	only	we	could
construct	a	picture	of	their	experience	with	unprecedented	clarity	and	detail	so
that	we	could	study	it	for	years	to	come. If	we	could	do	that,	we	might	be	able
to	offer	some	answers	to	our	“why”	questions. Occasionally	science,	politics	and	financing	come	together	in	a	way	that
allows	a	truly	extraordinary	study	to	take	place. This	happened	for	us,	and	we
got	the	opportunity	to	do	everything	we	wanted,	and	more. We	were	able	to
create	the	most	comprehensive	snapshot	of	diet,	lifestyle	and	disease	ever
taken.PULLING	IT	TOGETHER
We	assembled	a	world-class	scientific	team. There	was	Dr.	Chen,	who	was
the	deputy	director	of	the	most	significant	government	diet	and	health
research	laboratory	in	all	of	China. We	enlisted	Dr.	Junyao	Li,	one	of	the
authors	of	the	
Cancer	Atlas	Survey
	and	a	key	scientist	in	China’s	Academy	of
Medical	Sciences	in	the	Ministry	of	Health. The	third	member	was	Richard
Peto	of	Oxford	University. Considered	one	of	the	premier	epidemiologists	in
the	world,	Peto	has	since	been	knighted	and	has	received	several	awards	for
cancer	research. I	rounded	out	the	team	as	the	Project	Director. Everything	was	coming	together. It	was	to	be	the	first	major	research
project	between	China	and	the	United	States. We	cleared	the	necessary
funding	hurdles,	weathering	both	CIA	intrusiveness	and	Chinese	government
reticence. We	were	on	our	way. We	decided	to	make	the	study	as	comprehensive	as	possible. From	the
Cancer	Atlas,
	we	had	access	to	disease	mortality	rates	on	more	than	
four
dozen	different	kinds	of	disease,	including	individual	cancers,	heart	diseases
and	infectious	diseases. 6
	We	gathered	data	on	367	variables	and	then
compared	each	variable	with	every	other	variable. We	went	into	sixty-five
counties	across	China	and	administered	questionnaires	and	blood	tests	on
6,500	adults. We	took	urine	samples,	directly	measured	everything	families
ate	over	a	three-day	period	and	analyzed	food	samples	from	marketplaces
around	the	country. The	sixty-five	counties	selected	for	the	study	were	located	in	rural	to	semi-
rural	parts	of	China. This	was	intentionally	done	because	we	wanted	to	study
people	who	mostly	lived	and	ate	food	in	the	same	area	for	most	of	their	lives. This	was	a	successful	strategy,	as	we	were	to	learn	than	an	average	of	90-94%
of	the	adult	subjects	in	each	county	still	lived	in	the	same	county	where	they
were	born. When	we	were	done	we	had	
more	than	8,000	statistically	significant
associations
	between	lifestyle,	diet	and	disease	variables. We	had	a	study	that
was	unmatched	in	terms	of	comprehensiveness,	quality	and	uniqueness. We
had	what	the	
New	York	Times
	termed	“the	Grand	Prix	of	epidemiology.”	In
short,	we	had	created	that	revealing	snapshot	of	time	that	we	had	originally
envisioned. This	was	the	perfect	opportunity	to	test	the	principles	that	we	discovered
in	the	animal	experiments. Were	the	findings	in	the	lab	going	to	be	consistent
with	the	human	experience	in	the	real	world? Were	our	discoveries	on
aflatoxin-induced	liver	cancer	in	rats	going	to	apply	to	other	types	of	cancer
and	other	types	of	diseases	in	humans?FOR	MORE	INFORMATION
We	take	great	pride	in	the	comprehensiveness	and	quality	of	the	China
Study. To	see	why,	read	
Appendix	B	on	page	353
. You’ll	find	a	more
complete	discussion	of	the	basic	design	and	characteristics	of	the	study.THE	CHINESE	DIETARY	EXPERIENCE
Critical	to	the	importance	of	the	China	Study	was	the	nature	of	the	diet
consumed	in	rural	China. It	was	a	rare	opportunity	to	study	health-related
effects	of	a	mostly	plant-based	diet. In	America,	15-16%	of	our	total	calories	comes	from	protein	and	upwards
of	80%	of	this	amount	comes	from	animal-based	foods. But	in	
rural	China
only	9-10%	of	total	calories	comes	from	protein	and	only	10%	of	the	protein
comes	from	animal-based	foods. This	means	that	there	are	major	nutritional
differences	in	the	Chinese	and	American	diets,	as	shown	in	
Chart	4.3
. CHART	4.3. CHINESE	AND	AMERICAN	DIETARY	INTAKES
Nutrient
China
United	States
Calories	(kcal/day)
7
2641
1989
Total	fat	(%	of	calories)
14.5
34–38
Dietary	fiber	(g/day)
33
12
Total	protein	(g/day)
64
91
Animal	protein	(%	of	calories)
0.8
10–11
Total	iron	(mg/day)
34
18
The	findings	shown	in	
Chart	4.3
	are	standardized	for	a	body	weight	of
sixty-five	kilograms	(143	pounds). This	is	the	standard	way	that	Chinese
authorities	record	such	information	and	it	allows	us	to	easily	compare
different	populations. (For	an	American	adult	male	of	seventy-seven
kilograms,	calorie	intake	will	be	about	2,400	calories	per	day. For	an	average
rural	Chinese	adult	male	of	seventy-seven	kilograms,	calorie	intake	will	be
about	3,000	calories	per	day.) In	every	category	seen	above,	there	are	massive	dietary	differences
between	the	Chinese	and	American	experiences:	much	higher	overall	calorie
intake,	less	fat,	less	protein,	much	less	animal	foods,	more	fiber	and	much
more	iron	are	consumed	in	China. These	dietary	differences	are	supremely
important. While	the	eating	pattern	in	China	is	far	different	from	that	of	the	United
States,	there	is	still	a	lot	of	variation	within	China. Experimental	variation
(i.e.,	a	range	of	values)	is	essential	when	we	investigate	diet	and	health
associations. Fortunately,	in	the	China	Study	considerable	variation	existed
for	most	of	the	measured	factors. There	was	exceptional	variation	in	disease
rates	(
Chart	4.2
)	and	more	than	adequate	variation	for	clinical	measurementsand	food	intakes. For	example,	blood	cholesterol	ranged—as	county	averages
—from	highest	to	lowest	almost	twofold,	blood	beta-carotene	about	ninefold,
blood	lipids	about	threefold,	fat	intake	about	sixfold	and	fiber	intake	about
fivefold. This	was	
crucial,	as	we	primarily	were	concerned	with	comparing
each	county	in	China	with	every	other	county. Ours	was	the	first	large	study	that	investigated	this	particular	range	of
dietary	experience	and	its	health	consequences. In	effect,	we	are	comparing,
within	the	Chinese	range,	diets	rich	in	plant-based	foods	to	diets	very	rich	in
plant-based	foods. In	almost	all	other	studies,	all	of	which	are	Western,
scientists	are	comparing	diets	rich	in	animal-based	foods	to	diets	very	rich	in
animal-based	foods. The	difference	between	rural	Chinese	diets	and	Western
diets,	and	the	ensuing	disease	patterns,	is	enormous. It	was	this	distinction,	as
much	as	any	other,	that	made	this	study	so	important. The	media	called	the	China	Study	a	“landmark	study.”	An	article	in	the
Saturday	Evening	Post
	said	the	project	“should	shake	up	medical	and
nutrition	researchers	everywhere.”
8
	Some	in	the	medical	establishment	said
another	study	like	this	could	never	be	done. What	I	knew	was	that	our	study
offered	an	opportunity	to	investigate	many	of	the	most	contentious	ideas	that	I
was	forming	about	food	and	health. Now,	I	want	to	show	you	what	we	learned	from	this	study	and	how	twenty
more	years	of	research,	thought	and	experience	have	changed	not	only	the
way	I	think	about	the	connection	between	nutrition	and	health,	but	the	way
my	family	and	I	eat	as	well.DISEASES	OF	POVERTY	AND	AFFLUENCE
It	doesn’t	take	a	scientist	to	figure	out	that	the	possibility	of	death	has	been
holding	pretty	steady	at	100%	for	quite	some	time. There’s	only	one	thing	that
we	have	to	do	in	life,	and	that	is	to	die. I	have	often	met	people	who	use	this
fact	to	justify	their	ambivalence	toward	health	information. But	I	take	a
different	view. I	have	never	pursued	health	hoping	for	immortality. Good
health	is	about	being	able	to	fully	enjoy	the	time	we	do	have. It	is	about	being
as	functional	as	possible	throughout	our	entire	lives	and	avoiding	crippling,
painful	and	lengthy	battles	with	disease. There	are	many	better	ways	to	die,
and	to	live. Because	the	China	
Cancer	Atlas
	had	mortality	rates	for	more	than	four
dozen	different	kinds	of	disease,	we	had	a	rare	opportunity	to	study	the	many
ways	that	people	die. We	wondered:	do	certain	diseases	tend	to	group	together
in	certain	areas	of	the	country? For	example,	did	colon	cancer	occur	in	the
same	regions	as	diabetes? If	this	proved	to	be	the	case,	we	could	assume	that
diabetes	and	colon	cancer	(or	other	diseases	that	grouped	together)	shared
common	causes. These	causes	
could	include	a	variety	of	possibilities,	ranging
from	the	geographic	and	environmental	to	the	biological. However,	because
all	diseases	are	biological	processes	(gone	awry),	we	can	assume	that
whatever	“causes”	are	observed,	they	will	eventually	operate	through
biological	events. When	these	diseases	were	cross-listed	in	a	way	that	allowed	every	disease
rate	to	be	compared	with	every	other	disease	rate,
9
	two	groups	of	diseases
emerged:	those	typically	found	in	more	economically	developed	areas
(diseases	of	affluence)	and	those	typically	found	in	rural	agricultural	areas
(diseases	of	poverty)
10
	(
Chart	4.4
). CHART	4.4. DISEASE	GROUPINGS	OBSERVED	IN	RURAL	CHINA
Diseases	of
Affluence
(Nutritional
Extravagance)
Cancer	(colon,	lung,	breast,	leukemia,	childhood	brain,
stomach,	liver),	diabetes,	coronary	heart	disease
Diseases	of
Poverty
(Nutritional
inadequacy	and
poor	sanitation)
Pneumonia,	intestinal	obstruction,	peptic	ulcer,	digestive
disease,	pulmonary	tuberculosis,	parasitic	disease,
rheumatic	heart	disease,	metabolic	and	endocrine	disease
other	than	diabetes,	diseases	of	pregnancy	and	many	othersChart	4.4
	shows	that	each	disease,	in	either	list,	tends	to	associate	with
diseases	in	its	own	list	but	not	in	the	opposite	list. A	region	in	rural	China	that
has	a	high	rate	of	pneumonia,	for	example,	will	not	have	a	high	rate	of	breast
cancer,	but	will	have	a	high	rate	of	a	parasitic	disease. The	disease	that	kills
most	Westerners,	coronary	heart	disease,	is	more	common	in	areas	where
breast	cancer	also	is	more	common. Coronary	heart	disease,	by	the	way,	is
relatively	uncommon	in	many	developing	societies	of	the	world. This	is	not
because	people	die	at	a	younger	age,	thus	avoiding	these	Western	diseases. These	comparisons	are	age-standardized	rates,	meaning	that	people	of	the
same	age	are	being	compared. Disease	associations	of	this	kind	have	been	known	for	quite	some	time. What	the	China	Study	added,	however,	was	an	unsurpassed	amount	of	data	on
death	rates	for	many	different	diseases	and	a	unique	range	of	dietary
experience. As	expected,	certain	diseases	do	cluster	together	in	the	same
geographic	areas,	implying	that	they	have	shared	causes. These	two	disease	groups	have	usually	been	referred	to	as	diseases	of
affluence	and	diseases	of	poverty. As	a	developing	population	accumulates
wealth,	people	change	their	eating	habits,	lifestyles	and	sanitation	systems. As
wealth	accumulates,	more	and	more	people	die	from	“rich”	diseases	of
affluence	than	“poor”	diseases	of	poverty. Because	these	diseases	of	affluence
are	so	tightly	linked	to	eating	habits,	diseases	of	affluence	might	be	better
named	“diseases	of	nutritional	extravagance.”	The	vast	majority	of	people	in
the	United	States	and	other	Western	countries	die	from	diseases	of	affluence. For	this	reason,	these	diseases	are	often	referred	to	as	“Western”	diseases. Some	rural	counties	had	few	diseases	of	affluence	while	other	counties	had
far	more	of	these	diseases. The	core	question	of	the	China	Study	was	this:	is	it
because	of	differences	in	dietary	habits? STATISTICAL	SIGNIFICANCE
As	I	go	through	this	chapter,	I	will	indicate	the	statistical	significance	of
various	observations. Roman	numeral	one	(
I
)	means	95+%	certainty;
roman	numeral	two	(
II
)	means	99+%	certainty;	and	roman	numeral	three
(
III
)	means	99.9+%	certainty. No	roman	numeral	means	that	the	association
is	something	less	than	95%	certainty. 11
	These	probabilities	also	can	be
described	as	the	probability	that	an	observation	is	real. A	95%	certainty
means	a	19	in	20	probability	that	the	observation	is	real;	a	99%	certainty
means	a	99	in	100	probability	that	the	observation	is	real;	and	a	99.9%
certainty	means	a	999	in	1,000	probability	that	the	observation	is	real.BLOOD	CHOLESTEROL	AND	DISEASE
We	compared	the	prevalence	of	Western	diseases	in	each	county	with	diet	and
lifestyle	variables	and,	to	our	surprise,	we	found	that	one	of	the	strongest
predictors	of	Western	diseases	was	blood	cholesterol. IIIIN	YOUR	FOOD—IN	YOUR	BLOOD
There	are	two	main	categories	of	cholesterol. Dietary	cholesterol
	is	present	in
the	food	we	eat. It	is	a	component	of	food,	much	like	sugar,	fat,	protein,
vitamins	and	minerals. This	cholesterol	is	found	only	in	animal-based	food
and	is	the	one	we	find	on	food	labels. How	much	dietary	cholesterol	you
consume	is	
not
	something	your	doctor	can	know	when	he	or	she	checks	your
cholesterol	levels. The	doctor	can’t	
measure	dietary	cholesterol	any	more	than
he	or	she	can	measure	how	many	hot	dogs	and	chicken	breasts	you’ve	been
eating. Instead,	the	doctor	measures	the	amount	of	cholesterol	present	in	your
blood. This	second	type	of	cholesterol,	
blood	cholesterol,
	is	made	in	the	liver. Blood	cholesterol	and	dietary	cholesterol,	although	chemically	identical,	do
not	represent	the	same	thing. A	similar	situation	occurs	with	fat. Dietary	fat	is
the	stuff	you	eat:	the	grease	on	your	French	fries,	for	example. Body	fat,	on
the	other	hand,	is	the	stuff	made	by	your	body	and	is	very	different	from	the
fat	that	you	spread	on	your	toast	in	the	morning	(butter	or	margarine). Dietary
fats	and	cholesterol	don’t	necessarily	turn	into	body	fat	and	blood	cholesterol. The	way	the	body	makes	body	fat	and	blood	cholesterol	is	extremely
complex,	involving	hundreds	of	different	chemical	reactions	and	dozens	of
nutrients. Because	of	this	complexity,	the	health	effects	of	eating	dietary	fat
and	dietary	cholesterol	may	be	very	different	from	the	health	effects	of	having
high	blood	cholesterol	(what	your	doctor	measures)	or	having	too	much	body
fat. As	blood	cholesterol	levels	in	rural	China	rose	in	certain	counties,	the
incidence	of	“Western”	diseases	also	increased. What	made	this	so	surprising
was	that	Chinese	levels	were	far	lower	than	we	had	expected. The	average
level	of	blood	cholesterol	was	only	127	mg/dL,	which	is	almost	100	points
less	than	the	American	average	(215	mg/dL)! 12
	Some	counties	had	average
levels	as	low	as	94	mg/dL. For	two	groups	of	about	twenty-five	women	in	the
inner	part	of	China,	average	blood	cholesterol	was	at	the	amazingly	low	level
of	80	mg/dL. If	you	know	your	own	cholesterol	levels,	you’ll	appreciate	how	low	these
values	really	are. In	the	U.S.,	our	range	is	around	170-290	mg/dL. Our	low
values	are	near	the	high	values	for	rural	China. Indeed,	in	the	U.S.,	there	was
a	myth	that	there	might	be	health	problems	if	cholesterol	levels	were	below
150	mg/dL. If	we	followed	that	line	of	thinking,	about	85%	of	the	rural
Chinese	would	appear	to	be	in	trouble. But	the	truth	is	quite	different. Lower
blood	cholesterol	levels	are	linked	to	lower	rates	of	heart	disease,	cancer	and
other	Western	diseases,	even	at	levels	far	below	those	considered	“safe”	in
the	West.At	the	outset	of	the	China	Study,	no	one	could	or	would	have	predicted
that	there	would	be	a	relationship	between	cholesterol	and	any	of	the	disease
rates. What	a	surprise	we	got! As	blood	cholesterol	levels	decreased	from	170
mg/dL	to	90	mg/dL,	cancers	of	the	liver,
II
	rectum,
I
	colon,
II
	male	lung,
I
	female
lung,	breast,	childhood	leukemia,	
adult	leukemia,
I
	childhood	brain,	adult
brain,
I
	stomach	and	esophagus	(throat)	decreased. As	you	can	see,	this	is	a
sizable	list. Most	Americans	know	that	if	you	have	high	cholesterol,	you
should	worry	about	your	heart,	but	they	don’t	know	that	you	might	want	to
worry	about	cancer	as	well. There	are	several	types	of	blood	cholesterol,	including	LDL	and	HDL
cholesterol. LDL	is	the	“bad”	kind	and	HDL	is	the	“good”	kind. In	the	China
Study	higher	levels	of	the	bad	LDL	cholesterol	also	were	associated	with
Western	diseases. Keep	in	mind	that	these	diseases,	by	Western	standards,	were	relatively
rare	in	China	and	that	blood	cholesterol	levels	were	quite	low	by	Western
standards. Our	findings	made	a	convincing	case	that	many	Chinese	had	an
advantage	at	the	lower	cholesterol	levels,	even	below	170	mg/dL. Now
imagine	a	country	where	the	inhabitants	had	blood	cholesterol	levels	far
higher	than	the	Chinese	average. You	might	expect	that	these	relatively	rare
diseases,	such	as	heart	disease	and	some	cancers,	would	be	prevelant,	perhaps
even	the	leading	killers! Of	course,	this	is	exactly	the	case	in	the	West. To	give	a	couple	of
examples	at	the	time	of	our	study,	the	death	rate	from	coronary	heart	disease
was	
seventeen	times	higher
	among	American	men	than	rural	Chinese	men. 13
The	American	death	rate	from	breast	cancer	was	
five	times	higher
	than	the
rural	Chinese	rate. Even	more	remarkable	were	the	extraordinarily	low	rates	of	coronary	heart
disease	(CHD)	in	the	southwestern	Chinese	provinces	of	Sichuan	and
Guizhou. During	a	three-year	observation	period	(1973–1975),	there	was	not
one	single	person	who	died	of	CHD	before	the	age	of	sixty-four,	among
246,000	men	in	a	Guizhou	county	and	181,000	women	in	a	Sichuan	county! 14
After	these	low	cholesterol	data	were	made	public,	I	learned	from	three
very	prominent	heart	disease	researchers	and	physicians,	Drs. Bill	Castelli,
Bill	Roberts	and	Caldwell	Esselstyn,	Jr.,	that	in	their	long	careers	they	had
never	seen	a	heart	disease	fatality	among	their	patients	who	had	blood
cholesterol	levels	below	150	mg/dL. Dr.	Castelli	was	the	long-time	director	of
the	famous	Framingham	Heart	Study	of	NIH;	Dr.	Esselstyn	was	a	renowned
surgeon	at	the	Cleveland	Clinic	who	did	a	remarkable	study	reversing	heart
disease	(chapter	five);	Dr.	Roberts	has	long	been	editor	of	the	prestigiousmedical	journal	
Cardiology.BLOOD	CHOLESTEROL	AND	DIET
Blood	cholesterol	is	clearly	an	important	indicator	of	disease	risk. The	big
question	is:	how	will	food	affect	blood	cholesterol? In	brief,	animal-based
foods	were	correlated	with	
increasing
	blood	cholesterol	(
Chart	4.5
). With
almost	no	exceptions,	nutrients	from	plant-based	foods	were	associated	with
decreasing
	levels	of	blood	cholesterol. Several	studies	have	now	shown,	in	both	experimental	animals	and	in
humans,	that	consuming	animal-based	protein	increases	blood	cholesterol
levels. 15–18
	Saturated	fat	and	dietary	cholesterol	also	raise	blood	cholesterol,
although	these	nutrients	are	not	as	effective	at	doing	this	as	is	animal	protein. In	contrast,	plant-based	foods	contain	no	cholesterol	and,	in	various	other
ways,	help	to	decrease	the	amount	of	cholesterol	made	by	the	body. All	of	this
was	consistent	with	the	findings	from	the	China	Study. CHART	4.5. FOODS	ASSOCIATED	WITH	BLOOD	CHOLESTEROL
As	intakes	of	meat,
I
	milk,	eggs,	fish,
I–II
	fat
I
	and	animal	protein
go	up…
Blood
Cholesterol
goes	up. As	intakes	of	plant-based	foods	and	nutrients	(including	plant
protein,
I
	dietary	fiber,”	cellulose,”	hemicellulose,
I
	soluble
carbohydrate,
II
	B-vitamins	of	plants	(carotenes,	B
2
,	B
3
),
I
legumes,	light	colored	vegetables,	fruit,	carrots,	potatoes	and
several	cereal	grains)	go	up…
Blood
Cholesterol
goes	down. These	disease	associations	with	blood	cholesterol	were	remarkable,
because	blood	cholesterol	and	animal-based	food	consumption	both	were	so
low	by	American	standards. In	rural	China,	animal	protein	intake	(for	the
same	individual)	averages	only	7.1	g/day	whereas	Americans	average	a
whopping	70	g/day. To	put	this	into	perspective,	seven	grams	of	animal
protein	is	found	in	about	three	chicken	nuggets	from	McDonald’s. We
expected	that	when	animal	protein	consumption	and	blood	cholesterol	levels
were	as	low	as	they	are	in	rural	China,	there	would	be	no	further	association
with	the	Western	diseases. But	we	were	wrong. Even	these	small	amounts	of
animal-based	food	in	rural	China	raised	the	risk	for	Western	diseases. We	studied	dietary	effects	on	the	different	types	of	blood	cholesterol. The
same	dramatic	effects	were	seen. Animal	protein	consumption	by	
men	was
associated	with	increasing	levels	of	“bad”	blood	cholesterol
III
	whereas	plant
protein	consumption	was	associated	with	decreasing	levels	of	this	samecholesterol. II
Walk	into	almost	any	doctor’s	office	and	ask	which	dietary	factors	affect
blood	cholesterol	levels	and	he	or	she	will	likely	mention	saturated	fat	and
dietary	cholesterol. In	more	recent	decades,	some	might	also	mention	the
cholesterol-lowering	effect	of	soy	or	high-fiber	bran	products,	but	few	will
say	that	animal	protein	has	anything	to	do	with	blood	cholesterol	levels. It	has	always	been	this	way. While	on	sabbatical	at	the	University	of
Oxford,	I	attended	lectures	given	to	medical	students	on	the	dietary	causes	of
heart	disease	by	one	of	their	prominent	professors	of	medicine. He	went	on
and	on	about	the	adverse	effects	of	saturated	fat	and	cholesterol	intakes	on
coronary	heart	disease	as	if	these	were	the	only	dietary	factors	that	were
important. He	was	unwilling	to	concede	that	animal	protein	consumption	had
anything	to	do	with	blood	cholesterol	levels,	even	though	the	evidence	at	that
time	made	it	abundantly	clear	that	animal	protein	was	more	strongly
correlated	with	blood	cholesterol	levels	than	saturated	fat	and	dietary
cholesterol. 15
	Like	too	many	others,	his	blind	faith	in	the	status	quo	left	him
unwilling	to	be	open-minded. As	these	findings	poured	in,	I	was	beginning	to
discover	that	being	open-minded	was	not	a	luxury,	but	a	necessity.FAT	AND	BREAST	CANCER
If	there	were	some	sort	of	nutrition	parade,	and	each	nutrient	had	a	float,	by
far	the	biggest	would	belong	to	fat. So	many	people,	from	researchers	to
educators,	from	government	policy	makers	to	industry	representatives,	have
investigated	or	made	pronouncements	on	fat	for	so	long. People	from	a	huge
number	of	different	communities	have	been	constructing	this	behemoth	for
over	half	a	century. As	this	strange	parade	got	started	on	Main	Street,	USA,	the	attention	of
everyone	sitting	on	the	sidewalks	would	inevitably	be	drawn	to	the	fat	float. Most	people	might	see	the	fat	float	and	say,	“I	should	stay	away	from	that,”
and	then	eat	a	hefty	piece	of	it. Others	would	climb	on	the	unsaturated	half	of
the	float	and	say	that	these	fats	are	healthy	and	only	saturated	fats	are	bad. Many	scientists	would	point	fingers	at	the	fat	float	and	claim	that	the	heart
disease	and	cancer	clowns	are	hiding	inside. Meanwhile,	some	self-
proclaimed	diet	gurus,	like	the	late	Dr.	Robert	Atkins,	might	set	up	shop	on
the	float	and	start	selling	books. At	the	
end	of	the	day	the	average	person	who
gorged	on	the	float	would	be	left	scratching	his	head	and	feeling	queasy,
wondering	what	he	should	have	done	and	why. There’s	good	reason	for	the	average	consumer	to	be	confused. The
unanswered	questions	on	fat	remain	unanswered,	as	they	have	for	the	past
forty	years. How	much	fat	can	we	have	in	our	diets? What	kind	of	fat? Is
polyunsaturated	fat	better	than	saturated	fat? Is	monounsaturated	fat	better
than	either? What	about	those	special	fats	like	omega-3,	omega-6,	trans	fats
and	DHA? Should	we	avoid	coconut	fat? What	about	fish	oil? Is	there
something	special	about	flaxseed	oil? What’s	a	high-fat	diet	anyway? A	low-
fat	diet? This	can	be	confusing,	even	for	trained	scientists. The	details	that	underlie
these	questions,	
when	considered	in	isolation,
	are	very	misleading. As	you
shall	see,	considering	how	networks	of	chemicals	behave	instead	of	isolated
single	chemicals	is	far	more	meaningful. In	some	ways,	however,	it	is	this	foolish	mania	regarding	isolated	aspects
of	fat	consumption	that	teaches	us	the	best	lessons. Therefore,	let’s	look	a
little	more	closely	at	this	story	of	fat	as	it	has	emerged	during	the	past	forty
years. It	illustrates	why	the	public	is	so	confused	both	about	fat	and	about	diet
in	general. On	average,	we	consume	35-40%	of	our	total	calories	as	fat. 19
	We	have
been	consuming	high-fat	diets	like	this	since	the	late	nineteenth	century,	at	the
onset	of	our	industrial	revolution. Because	we	had	more	money,	we	began
consuming	more	meat	and	dairy,	which	are	relatively	high	in	fat. We	weredemonstrating	our	affluence	by	consuming	such	foods. Then	came	the	mid	to	late	twentieth	century	when	scientists	began	to
question	the	advisability	of	consuming	diets	so	high	in	fat. National	and
international	dietary	recommendations
20–23
	emerged	to	suggest	that	we	should
decrease	our	fat	intake	below	30%	of	calories. That	lasted	for	a	couple
decades,	but	now,	the	fears	surrounding	high-fat	diets	are	abating. Some
authors	of	popular	books	even	advocate	increased	fat	intake! Some
experienced	researchers	have	suggested	that	it	is	not	necessary	to	go	below
30%	fat,	as	long	as	we	consume	the	right	kind	of	fat. The	level	of	30%	fat	has	become	a	benchmark,	even	though	there	is	no
evidence	to	suggest	that	this	is	a	vital	threshold. Let’s	get	some	perspective	on
this	figure	by	considering	the	fat	contents	of	a	few	foods,	as	seen	in	
Chart	4.6
. CHART	4.6:	FAT	CONTENT	OF	SAMPLE	FOODS
Food
Percent	of	calories	derived	from	fat
Butter
100%
McDonald’s	Double	Cheeseburger
67%
Whole	Cow’s	Milk
64%
Ham
61%
Hotdog
54%
Soybeans
42%
“Low-Fat”	(or	2%)	Milk
35%
Chicken
26%
Spinach
14%
Wheaties	Breakfast	Cereal
8%
Skim	Milk
5%
Peas
5%
Carrots
4%
Green	Beans
3.5%
Whole	Baked	Potatoes
1%
With	a	few	exceptions,	animal-based	foods	contain	considerably	more	fat
than	plant-based	foods. 24
	This	is	well	illustrated	by	comparing	the	amount	of
fat	in	the	diets	of	different	countries. The	correlation	between	fat	intake	and
animal	protein	intake	is	more	than	90%. 25
	This	means	that	fat	intake	increases
in	parallel	with	animal	protein	intake. In	other	words,	dietary	fat	is	an
indicator	of	how	much	animal-based	food	is	in	the	diet. It	is	almost	a	perfectmatch.FAT	AND	A	FOCUS	ON	CANCER
The	1982	National	Academy	of	Sciences	(NAS)	report	on	Diet,	Nutrition	and
Cancer,	of	which	I	was	a	co-author,	was	the	first	expert	panel	report	that
deliberated	on	the	association	of	dietary	fat	with	cancer. This	report	was	the
first	to	recommend	a	maximum	fat	intake	of	30%	of	calories	for	cancer
prevention. Previously,	the	U.S.	Senate	Select	Committee	on	Nutrition
chaired	by	Senator	George	McGovern
26
	held	widely	publicized	hearings	on
diet	and	heart	disease	and	recommended	a	maximum	intake	of	30%	dietary
fat. Although	the	McGovern	report	
generated	a	public	discourse	on	diet	and
disease,	it	was	the	1982	NAS	report	that	gave	momentum	to	this	debate. Its
focus	on	cancer,	as	opposed	to	heart	disease,	increased	public	interest	and
concern. It	spurred	additional	research	activity	and	public	awareness	of	the
importance	of	diet	in	disease	prevention. Many	of	the	reports	at	the	time
20,	27,	28
	were	centered	on	the	question	of
how	much	dietary	fat	was	appropriate	for	good	health. The	unique	attention
given	to	fat	was	motivated	by	international	studies	showing	that	the	amount
of	dietary	fat	consumed	was	closely	associated	with	the	incidence	of	breast
cancer,	large	bowel	cancer	and	heart	disease. These	were	the	diseases	that	kill
the	majority	of	people	in	Western	countries	before	their	time. Clearly,	this
correlation	was	destined	to	attract	great	public	attention. The	China	Study	was
begun	in	the	midst	of	this	environment. The	best	known	study,
29
	in	my	view,	was	that	of	the	late	Ken	Carroll,
professor	at	the	University	of	Western	Ontario	in	Canada. His	findings
showed	a	very	impressive	relationship	between	dietary	fat	and	breast	cancer
(
Chart	4.7
).CHART	4.7:	TOTAL	FAT	INTAKE	AND	BREAST	CANCER
This	finding,	which	corresponded	to	the	earlier	reports	of	others,
3,	30
became	especially	intriguing	when	compared	with	migrant	studies. 31,	32
	These
studies	showed	that	people	who	migrated	from	one	area	to	another	and	who
started	eating	the	typical	diet	of	their	new	residency	assumed	the	disease	risk
of	the	area	to	which	they	moved. This	strongly	
implied	that	diet	and	lifestyle
were	the	principle	causes	of	these	diseases. It	also	suggested	that	genes	are
not	necessarily	that	important. As	noted	earlier,	a	very	prominent	report	by	Sir
Richard	Doll	and	Sir	Richard	Peto	of	the	University	of	Oxford	(U.K.)
submitted	to	the	U.S.	Congress	summarized	many	of	these	studies	and
concluded	that	only	2-3%	of	all	cancers	could	be	attributed	to	genes. 4
Do	the	data	from	these	international	and	migrant	studies	mean	that	we	can
lower	our	rate	of	breast	cancer	to	almost	zero	if	we	make	perfect	lifestyle
choices? The	information	certainly	suggests	that	this	could	be	the	case. Concerning	the	evidence	in	
Chart	4.7
,	the	solution	seems	obvious:	if	we	eat
less	fat,	then	we’ll	lower	our	breast	cancer	risk. Most	scientists	made	this
conclusion	and	some	surmised	that	dietary	fat	caused	breast	cancer. But	that
interpretation	was	too	simple. Other	charts	prepared	by	Professor	Carroll	were
largely,	almost	totally,	ignored	(
Charts	4.8
	and	
4.9
). They	show	that	breast
cancer	was	associated	with	animal	fat	intake	but	not	with	plant	fat. In	rural	China,	dietary	fat	intake	(at	the	time	of	the	survey	in	1983)	was
very	different	from	the	United	States	in	two	ways. First,	fat	was	only	14.5%
of	calorie	intake	in	China,	compared	with	about	36%	in	the	U.S.	Second,	the
amount	of	fat	in	the	diets	of	rural	China	depended	almost	entirely	on	theamount	of	animal-based	food	in	the	diet,	just	like	the	
findings	in	
Chart	4.7
. The	correlation	between	dietary	fat	and	animal	protein	in	rural	China	was
very	high,	at	70-84%,
33
	similar	to	the	93%	seen	when	comparing	different
countries. 23
CHART	4.8:	ANIMAL	FAT	INTAKE	AND	BREAST	CANCER
	CHART	4.9:	PLANT	FAT	INTAKE	AND	BREAST	CANCER
This	is	important	because	in	China	and	the	international	studies,	fat
consumption	was	only	an	indication	of	
animal-based	food
	consumption. Thus,	the	association	between	fat	and	breast	cancer	might	really	be	telling	us
that	as	consumption	of	
animal-based	foods
	goes	up,	so	does	breast	cancer. This	is	not	the	case	in	the	U.S.,	where	we	selectively	add	or	remove	fat	from
our	foods	and	our	diets. We	get	as	much	or	more	fat	from	plant-based	food
(potato	chips,	French	fries)	as	we	get	from	processed	animal-based	foods
(skim	milk,	lean	cuts	of	meat). China	does	not	tinker	with	fat	in	their	food
supply	as	we	do	here. At	this	very	low	range	of	dietary	fat	in	China,	from	6%-24%,	I	initially
thought	that	dietary	fat	would	not	be	linked	with	diseases	like	heart	disease	or
the	various	cancers,	as	it	is	in	the	West. Some	people	in	the	U.S.—like	many
of	my	colleagues	in	science	and	medicine—call	a	30%	fat	diet	a	“low-fat”
diet. Therefore,	a	low-fat	diet	containing	only	
25-30%	fat	was	thought	to	be
low	enough	to	obtain	the	maximum	amount	of	health	benefits. This	implied
that	going	lower	provided	no	further	benefit. Surprise! Findings	from	rural	China	showed	that	reducing	dietary	fat	from	24%	to
6%	was	associated	with	lower	breast	cancer	risk. However,	lower	dietary	fat
in	rural	China	meant	less	consumption	not	only	of	fat	but,	more	importantly,
of	animal-based	food. This	connection	of	breast	cancer	with	dietary	fat,	thus	with	animal-basedfoods,	brought	into	consideration	other	factors	that	also	place	a	woman	at	risk
for	breast	cancer:
Early	age	of	menarche	(age	of	first	menstruation)
High	blood	cholesterol
Late	menopause
High	exposure	to	female	hormones
What	does	the	China	Study	show	regarding	these	risk	factors? Higher
dietary	fat	is	associated	with	higher	blood	cholesterol
I
	and	both	of	these
factors,	along	with	higher	female	hormone	levels,	are	associated,	in	turn,	with
more	breast	cancer
I
	and	earlier	age	of	menarche. I
The	much	later	age	of	menarche	in	rural	China	is	remarkable. Twenty-five
women	in	each	of	the	130	villages	in	the	survey	were	asked	when	they	had
their	first	menstrual	period. The	range	of	village	averages	was	fifteen	to
nineteen	years,	with	an	average	of	seventeen	years. The	U.S.	average	is
roughly	eleven	years! Many	studies	have	shown	that	earlier	menarche	leads	to	higher	risk	for
breast	cancer. 34
	Menarche	is	triggered	by	the	growth	rate	of	the	girl;	the	faster
the	growth,	the	earlier	the	age	of	onset. It	also	is	well	established	that	rapid
growth	of	young	girls	often	leads	to	greater	adult	body	height	and	more	body
weight	and	body	fatness,	each	of	which	is	associated	with	higher	breast
cancer	risk. Early	age	of	menarche,	both	in	Chinese	and	in	Western	women,
also	leads	to	higher	levels	of	blood	hormones	such	as	estrogen. These
hormone	levels	remain	high	throughout	the	reproductive	years	if	consumption
of	a	diet	rich	in	animal-based	food	is	maintained. Under	these	conditions,	age
of	menopause	is	deferred	by	three	to	four	years,
I
	thus	extending	the
reproductive	life	from	beginning	to	end	by	about	nine	to	ten	years	and	greatly
increasing	lifetime	exposure	to	female	hormones. Other	studies	have	shown
that	an	increase	in	years	of	reproductive	life	is	associated	with	increased
breast	cancer	risk. 35,	36
This	network	of	relationships	becomes	still	more	impressive. Higher	
fat
consumption	is	associated	with	higher	blood	levels	of	estrogen	during	the
critical	years	of	thirty-five	to	forty-four	years
III
	and	higher	blood	levels	of	the
female	hormone	prolactin	during	the	later	years	of	fifty-five	to	sixty-four
years. III
	These	hormones	are	highly	correlated	with	animal	protein	intake
III
and	milk
III
	and	meat. II
	Unfortunately	we	could	not	demonstrate	whether	these
hormone	levels	were	directly	related	to	breast	cancer	risk	in	China	because
the	rate	of	disease	is	so	low. 37
Nonetheless,	when	hormone	levels	among	Chinese	women	were	comparedwith	those	of	British	women,
38
	Chinese	estrogen	levels	were	only	about	one-
half	those	of	the	British	women,	who	have	an	equivalent	hormone	profile	to
that	of	American	women. Because	the	length	of	the	reproductive	life	of	a
Chinese	woman	is	only	about	75%	of	that	of	the	British	(or	American)
woman,	this	means	that	with	lower	estrogen	levels,	the	Chinese	woman	only
experiences	about	35-40%	of	the	lifetime	estrogen	exposure	of	British	(and
American)	women. This	corresponds	to	Chinese	breast	cancer	rates	that	are
only	one-fifth	of	those	of	Western	women. The	strong	association	of	a	high-animal	protein,	high-fat	diet	with
reproductive	hormones	and	early	age	of	menarche,	both	of	which	raise	the
risk	of	breast	cancer,	is	an	important	observation. It	makes	clear	that	we
should	not	have	our	children	consume	diets	high	in	animal-based	foods. If
you	are	a	woman,	would	you	ever	have	imagined	that	eating	diets	higher	in
animal-based	foods	would	expand	your	reproductive	life	by	about	nine	to	ten
years? As	an	aside,	an	interesting	implication	of	this	observation,	as	noted	by
Ms.	magazine	founder	Gloria	Steinem,	is	that	eating	the	right	foods	could
reduce	teenage	pregnancy	by	delaying	the	age	of	menarche. Beyond	the	hormone	findings,	is	there	a	way	to	show	that	animal-based
food	intake	relates	to	overall	cancer	rates? This	is	somewhat	difficult,	but	one
of	the	factors	we	measured	was	how	much	cancer	there	was	in	each	family. Animal	protein	intake	was	convincingly	associated	in	the	China	Study	with
the	prevalence	of	cancer	in	families. III
	This	association	is	an	impressive	and
significant	observation,	considering	the	unusually	low	intake	of	animal
protein. Diet	and	disease	factors	such	as	animal	protein	consumption	or	breast
cancer	incidence	lead	to	changes	in	the	concentrations	of	certain	chemicals	in
our	blood. These	chemicals	are	called	biomarkers. As	an	example,	blood
cholesterol	is	a	biomarker	for	heart	disease. We	measured	six	blood
biomarkers	that	are	associated	with	animal	protein	intake. 39
	Do	they	confirm
the	finding	that	animal	protein	intake	is	
associated	with	cancer	in	families? Absolutely. Every	single	animal	protein-related	blood	biomarker	is
significantly	associated	with	the	amount	of	cancer	in	a	family. II–III
In	this	case,	multiple	observations,	tightly	networked	into	a	web,	show	that
animal-based	foods	are	strongly	linked	to	breast	cancer. What	makes	this
conclusion	especially	compelling	are	two	kinds	of	evidence. First,	the
individual	parts	of	this	web	were	consistently	correlated	and,	in	most	cases,
were	statistically	significant. Second,	this	effect	occurred	
at	unusually	low
intakes	of	animal-based	foods. Our	investigation	of	breast	cancer	(detailed	further	in	chapter	seven)	is	aperfect	example	of	what	makes	the	China	Study	so	convincing. Rather	than	a
single,	simple	association	of	fat	and	breast	cancer,
1
	we	were	able	to	construct
a	much	more	expansive	web	of	information	about	how	diet	affects	breast
cancer	risk. We	were	able	to	examine	in	multiple	ways	the	role	of	diet	and
cholesterol,	age	of	menarche	and	female	hormone	levels,	all	of	which	are
known	risk	factors	for	breast	cancer. When	each	new	finding	pointed	in	the
same	direction,	we	were	able	to	see	a	picture	that	was	convincing,	consistent
and	biologically	plausible.THE	IMPORTANCE	OF	FIBER
The	late	Professor	Denis	Burkitt,	of	Trinity	College,	Dublin,	was	unusually
articulate. His	common	sense,	scientific	credibility	and	sense	of	humor	made
quite	an	impression	on	me	when	I	first	met	him	at	a	Cornell	seminar. The
subject	of	his	work	was	dietary	fiber. He	had	traveled	10,000	miles	in	a	jeep
over	rugged	countryside	to	study	the	dietary	habits	of	Africans. He	asserted	that	even	though	fiber	was	not	digested,	it	was	vital	for	good
health. Fiber	was	able	to	pull	water	from	the	body	into	the	intestines	to	keep
things	moving	along. These	undigested	fibers,	like	stick-um	paper,	also	gather
up	nasty	chemicals	that	find	their	way	into	our	intestines	and	that	might	be
carcinogenic. If	we	don’t	consume	enough	fiber,	we	are	susceptible	to
constipation-based	diseases. According	to	Burkitt,	these	include	large	bowel
cancer,	diverticulosis,	hemorrhoids	and	varicose	veins. In	1993,	Dr.	Burkitt	was	awarded	the	prestigious	Bower	Award,	the	richest
award	in	the	world	next	to	the	Nobel	Prize. He	invited	me	to	speak	at	his
award	ceremony	at	the	Franklin	Institute	in	Philadelphia,	only	two	months
before	his	unfortunate	passing. He	offered	his	opinion	that	our	China	Study
was	the	most	significant	work	on	diet	and	health	in	the	world	at	that	time. Dietary	fiber	is	exclusively	found	in	plant-based	foods. This	material,
which	gives	rigidity	to	the	cell	walls	of	plants,	comes	in	thousands	of
different	chemical	variations. It	is	mostly	made	of	highly	complex
carbohydrate	molecules. We	digest	very	little	or	no	fiber. Nonetheless,	fiber,
having	few	or	no	calories	itself,	helps	dilute	the	caloric	density	of	our	diets,
creates	a	sense	of	fullness	and	helps	to	shut	down	appetite,	among	other
things. In	doing	so,	it	satisfies	our	hunger	and	minimizes	the	overconsumption
of	calories. Average	fiber	intake	(
Chart	4.10
)	is	about	three	times	higher	in	China	than
in	the	U.S.
40
	These	differences	are	exceptional,	especially	considering	the	fact
that	many	county	averages	were	even	much	higher. But	according	to	some	“experts”	in	the	U.S.,	there	is	a	dark	side	to	dietary
fiber. They	contend	that	if	fiber	intake	is	too	high	our	bodies	are	not	able	to
absorb	as	much	iron	and	related	minerals,	which	are	essential	for	health.
_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:

        Because	of	this	the	two	groups	of	rats	were	starting	the	cancer
process	with	different	amounts	of	initiated,	cancerous	“seeds. ”	Then,	during
the	promotion	phase,	we	fed	a	low-protein	diet	to	the	high-aflatoxin	dose
groups	and	a	high-protein	diet	to	the	low-aflatoxin	dose	group. We	wondered
whether	the	animals	that	start	with	lots	of	cancerous	seeds	are	able	to
overcome	their	predicament	by	eating	a	low-protein	diet. CHART	3. 4:	DIETARY	PROTEIN	AND	FOCI	FORMATION
	CHART	3. 5:	CARCINOGEN	DOSE	VERSUS	PROTEIN	INTAKE
Again,	the	results	were	remarkable	(
Chart	3. 5
). Animals	starting	with	the
most	cancer	initiation	(high-aflatoxin	dose)	developed	
substantially	less	foci
when	fed	the	5%	protein	diet. In	contrast,	animals	initiated	with	a	low-
aflatoxin	dose	actually	produced	
substantially	more	foci
	when	subsequently
fed	the	20%	protein	diet. A	principle	was	being	established. Foci	development,	initially	determined
by	the	amount	of	the	carcinogen	exposure,	is	actually	controlled	far	more	by
dietary	protein	consumed	during	promotion. Protein	during	promotion	trumps
the	carcinogen,	regardless	of	initial	exposure. With	this	background	information	we	designed	a	much	more	substantial
experiment. Here	is	a	step-by-step	sequence	of	experiments,	carried	out	by
my	graduate	student	Linda	Youngman. 35
	All	animals	were	dosed	with	the
same	amount	of	carcinogen,	then	alternately	fed	either	5%	or	20%	dietary
protein	during	the	twelve-week	promotion	stage. We	divided	this	twelve-week
promotion	stage	into	four	periods	of	three	weeks	each. Period	1	represents
weeks	one	to	three,	period	2	represents	weeks	four	to	six,	and	so	on. When	animals	were	fed	the	20%	protein	diet	during	periods	1	and	2	(20-
20),	foci	continued	to	enlarge,	as	expected. But	when	animals	were	switched
to	the	low-protein	diet	at	the	beginning	of	period	3	(20-20-5),	there	was	a
sharp	decrease	in	foci	development. And,	when	animals	were	subsequently
switched	back	to	the	20%	protein	diet	during	period	4	(20-20-5-20),	foci
development	was	turned	on	once	again. In	another	experiment,	in	animals	fed	20%	dietary	protein	during	period	1
but	switched	to	5%	dietary	protein	during	period	2	(20-5),	foci	development
was	sharply	decreased. But	when	these	animals	were	returned	to	20%	dietary
protein	during	period	3	(20-5-20),	we	again	saw	the	dramatic	power	of	dietary
protein	to	promote	foci	development. These	several	experiments,	taken	together,	were	quite	profound. Foci
growth	could	be	reversed,	up	and	down,	by	switching	the	amount	of	protein
being	consumed,	and	at	all	stages	of	foci	development. These	experiments	also	demonstrated	that	the	body	could	“remember”
early	carcinogen	insults,
35,	36
	even	though	they	might	then	lie	dormant	with
low	protein	intake. That	is,	exposure	to	aflatoxin	left	a	genetic	“imprint”	that
remained	dormant	with	5%	dietary	protein	until	nine	weeks	later	when	this
imprint	reawakened	to	form	foci	with	20%	dietary	protein. In	simple	terms,
the	body	holds	a	grudge. It	suggests	that	if	we	are	exposed	in	the	past	to	a
carcinogen	that	initiates	a	bit	of	cancer	that	remains	dormant,	this	cancer	can
still	be	“reawakened”	by	bad	nutrition	some	time	later. These	studies	showed	that	cancer	development	is	modified	by	relatively
modest	changes	in	protein	consumption. But	how	much	protein	is	too	much	or
too	little. Using	rats,	we	investigated	a	range	of	4-24%	dietary	protein	(
Chart
3. 6
37
). Foci	did	not	develop	with	up	to	about	10%	dietary	protein. Beyond
10%,	foci	development	increased	dramatically	with	increases	in	dietary
protein. The	results	were	later	repeated	a	second	time	in	my	laboratory	by	a
visiting	professor	from	Japan,	Fumiyiki	Horio. 38CHART	3. 6:	FOCI	PROMOTION	BY	DIETARY	PROTEIN
The	most	significant	finding	of	this	experiment	was	this:	foci	developed
only	when	the	animals	met	or	exceeded	the	amount	of	dietary	protein	(12%)
needed	to	satisfy	their	body	growth	rate. 39
	That	is,	when	the	animals	met	and
surpassed	their	requirement	for	protein,	disease	onset	began. This	finding	may	have	considerable	relevance	for	humans	even	though
these	were	rat	studies. I	say	this	because	the	protein	required	for	growth	in
young	rats	and	humans	as	well	as	the	protein	required	to	maintain	health	for
adult	rats	and	humans	is	remarkably	similar. 40,	41
According	to	the	recommended	daily	allowance	(RDA)	for	protein
consumption,	we	humans	should	be	getting	about	10%	of	our	energy	from
protein. This	is	considerably	more	than	the	actual	amount	required. But
because	requirements	may	vary	from	individual	to	individual,	10%	dietary
protein	is	recommended	to	insure	adequate	intake	for	virtually	all	people. What	do	most	of	us	routinely	consume. Remarkably,	it	is	considerably	more
than	the	recommended	10%. The	average	American	consumes	15-16%
protein. Does	this	place	us	at	risk	for	getting	cancer. These	animal	studies
hint	that	it	does. Ten	percent	dietary	protein	is	equivalent	to	eating	about	50-60	grams	of
protein	per	day,	depending	on	body	weight	and	total	calorie	intake. Thenational	average	of	15-16%	is	about	70-100	grams	of	protein	per	day,	with
men	at	the	upper	part	of	the	range	and	women	at	the	lower	end. In	food	terms,
there	are	about	twelve	grams	of	protein	in	100	calories	of	spinach	(fifteen
ounces)	and	five	grams	of	protein	in	100	calories	of	raw	chick	peas	(just	over
two	tablespoons). There	are	about	thirteen	grams	of	protein	in	100	calories	of
porterhouse	steak	(just	over	one	and	a	half	ounces). Yet	another	question	was	whether	protein	intake	could	modify	the	all-
important	relationship	between	aflatoxin	dose	and	foci	formation. A	chemical
is	usually	not	considered	a	carcinogen	unless	higher	doses	yield	higher
incidences	of	cancer. For	example,	as	the	aflatoxin	dose	becomes	greater,	foci
and	tumor	growth	should	be	correspondingly	greater. If	an	increasing
response	is	not	observed	for	a	suspect	chemical	carcinogen,	serious	doubt
arises	whether	it	really	is	carcinogenic. To	investigate	this	dose-response	question,	ten	groups	of	rats	were
administered	increasing	doses	of	aflatoxin,	then	fed	either	regular	levels
(20%)	or	low	levels	(5-10%)	of	protein	during	the	promotion	period	(
Chart
3. 7
34
). In	the	animals	fed	the	20%	level	of	protein,	foci	increased	in	number	and
size,	as	expected,	as	the	aflatoxin	dose	was	increased. The	dose-response
relationship	was	strong	and	clear. However,	in	the	animals	fed	5%	protein,	
the
dose-response	curve	completely	disappeared. There	was	no	foci	response,
even	when	animals	were	given	the	maximum	tolerated	aflatoxin	dose. This
was	yet	another	result	demonstrating	that	a	low-protein	diet	could	override	the
cancer-causing	effect	of	a	very	powerful	carcinogen,	aflatoxin.
The purpose of the experiment was to investigate whether the animals that started with a lot of cancerous "seeds" could overcome their predicament by eating a low-protein diet.
What was the purpose of the experiment where rats were fed different levels of protein during the promotion stage?
The study showed that plant-based protein did not promote cancer growth, even at higher levels of intake.
What did the study on plant-based protein and cancer show?
The study found that higher levels of fat consumption were associated with higher blood cholesterol levels, which in turn was associated with a higher risk of breast cancer.
What was the conclusion of the study on the relationship between blood cholesterol and the risk of breast cancer?
The study found that animal-based foods were strongly correlated with higher blood cholesterol levels.
What did the China Study reveal about the relationship between animal-based foods and blood cholesterol?
The study showed that high fiber intake was associated with a lower risk of certain diseases, including breast cancer.
What did the study on the relationship between fiber intake and disease risk show?