All	of	these	findings	support	the	idea	that	both	across	and	within
populations,	high-fiber,	whole,	plant-based	foods	protect	against	diabetes,	and
high-fat,	high-protein,	animal-based	foods	promote	diabetes.CURING	THE	INCURABLE
All	of	the	research	cited	above	was	
observational
	and	an	observed
association,	even	if	frequently	seen,	may	only	be	an	incidental	association	that
masks	the	real	cause-effect	relationship	of	environment	(including	diet)	and
disease. There	is,	however,	also	research	of	the	“controlled”	or	intervention
variety. This	involves	changing	the	diets	of	people	who	already	have	either
full-blown	Type	1	or	Type	2	diabetes	or	mild	diabetic	symptoms	(impaired
glucose	tolerance). James	Anderson,	M.D.,	is	one	of	the	most	prominent	scientists	studying
diet	and	diabetes	today,	garnering	dramatic	results	using	dietary	means	alone. One	of	his	studies	examined	the	effects	of	a	high-fiber,	high-carbohydrate,
low-fat	diet	on	twenty-five	Type	1	diabetics	and	twenty-five	Type	2	diabetics
in	a	hospital	setting. 15
	None	of	his	fifty	patients	were	overweight	and	all	of
them	were	taking	insulin	shots	to	control	their	blood	sugar	levels. His	experimental	diet	consisted	mostly	of	whole	plant	foods	and	the
equivalent	of	only	a	cold	cut	or	two	of	meat	a	day. He	put	his	patients	on	the
conservative,	American-style	diet	recommended	by	the	American	
Diabetes
Association	for	one	week	and	then	switched	them	over	to	the	experimental
“veggie”	diet	for	three	weeks. He	measured	their	blood	sugar	levels,
cholesterol	levels,	weight	and	medication	requirements. The	results	were
impressive. Type	1	diabetics	cannot	produce	insulin. It	is	difficult	to	imagine	any
dietary	change	that	might	aid	their	predicament. But	after	just	three	weeks,	the
Type	1	diabetic	patients	were	able	to	lower	their	insulin	medication	by	an
average	of	40%! Their	blood	sugar	profiles	improved	dramatically. Just	as
importantly,	their	cholesterol	levels	dropped	by	30%! 15
	Remember,	one	of	the
dangers	of	being	diabetic	is	the	secondary	outcomes,	heart	disease	and	stroke. Lowering	risk	factors	for	those	secondary	outcomes	by	improving	the
cholesterol	profile	is	almost	as	important	as	treating	high	blood	sugar. Type	2	diabetics,	unlike	Type	1,	are	more	“treatable”	because	they	haven’t
incurred	such	extensive	damage	to	their	pancreas. So	when	Anderson’s	Type
2	patients	ate	the	high-fiber,	low-fat	diet,	the	results	were	even	more
impressive. Of	the	twenty-five	Type	2	patients,	twenty-four	were	able	to
discontinue	their	insulin	medication! Let	me	say	that	again. All	but	one	person
were	able	to	discontinue	their	insulin	medication	in	a	matter	of	weeks! 15
One	man	had	a	twenty-one-year	history	of	diabetes	and	was	taking	thirty-
five	units	of	insulin	a	day. After	three	weeks	of	intensive	dietary	treatment,
his	insulin	dosage	dropped	to	eight	units	a	day. After	eight	weeks	at	home,	hisneed	for	insulin	shots	vanished. 13
	
Chart	7.2
	shows	a	sample	of	patients	and
how	eating	a	plant-based	diet	lowered	their	insulin	medications. This	is	a
huge	effect. In	another	study	of	fourteen	lean	diabetic	patients,	Anderson	found	that
diet	alone	could	lower	total	cholesterol	levels	by	32%	
in	just	over	two
weeks
. 16
	Some	of	the	results	are	shown	in	
Chart	7.3
. These	benefits,	representing	a	decrease	in	blood	cholesterol	from	206
mg/dL	to	141	mg/dL,	are	astounding—especially	considering	the	speed	with
which	they	appear. Dr.	Anderson	also	found	no	evidence	that	this	cholesterol
decrease	was	temporary	as	long	as	people	continued	on	the	diet;	it	remained
low	for	four	years. 17
Another	group	of	scientists	at	the	Pritikin	Center	achieved	equally
spectacular	results	by	prescribing	a	low-fat,	plant-based	diet	and	exercise	to	a
group	of	diabetic	patients. Of	forty	patients	on	medication	at	the	start	of	the
program,	thirty-four	were	able	to	discontinue	all	medication	after	only
twenty-six	days. 18
	This	research	group	also	demonstrated	that	
the	benefits	of	a
plant-based	diet	will	last	for	years	if	the	same	diet	is	continued. 19
CHART	7.2:	INSULIN	DOSAGE	RESPONSE	TO	DIET
These	are	examples	of	some	very	dramatic	research,	but	they	only	scratch
the	surface	of	all	the	supporting	research	that	has	been	done. One	scientific
paper	reviewed	nine	publications	citing	the	use	of	high-carbohydrate,	high-
fiber	diets	and	two	more	standard-carbohydrate,	high-fiber	diets	to	treat
diabetic	patients. 20
	All	eleven	studies	resulted	in	improved	blood	sugar	and
cholesterol	levels. (Dietary	fiber	supplements,	by	the	way,	althoughbeneficial,	did	not	have	same	consistent	effects	as	a	change	to	a	plant-based,
whole	foods	diet.) 21THE	PERSISTENCE	OF	HABIT
As	you	can	see	by	these	findings,	we	can	beat	diabetes. Two	recent	studies
considered	a	combination	of	diet	and	exercise	effects	on	this	disease. 22,	23
	One
study	placed	3,234	non-diabetic	people	at	risk	for	diabetes	(elevated	blood
sugar)	into	three	different	groups. 22
	One	group,	the	control,	received	standard
dietary	information	and	a	drug	placebo	(no	effect),	one	received	the	standard
dietary	information	and	the	drug	metformin,	and	a	third	group	received
“intensive”	lifestyle	intervention,	which	included	a	moderately	low-fat	diet
and	exercise	plan	to	lose	at	least	7%	of	their	weight. After	almost	three	years,
the	lifestyle	group	had	
58%	fewer	cases	of	diabetes	than	the	control	group. The	drug	group	reduced	the	number	of	cases	only	by	31%. Compared	to	the
control,	both	treatments	worked,	but	clearly	a	lifestyle	change	is	much	more
powerful	and	safer	than	simply	taking	a	drug. Moreover,	the	lifestyle	change
would	be	effective	in	solving	other	health	problems,	whereas	the	drug	would
not. CHART	7.3:	BLOOD	CHOLESTEROL	ON	HIGH-CARBOHYDRATE,
HIGH-FIBER	DIET
The	second	study	also	found	that	the	rate	of	diabetes	could	be	reduced	by
58%	just	by	modest	lifestyle	changes,	including	exercise,	weight	loss	and	a
moderately	low-fat	diet. 23
	Imagine	what	would	happen	if	people	fully	adopted
the	healthiest	diet:	a	whole	foods,	plant-based	diet. I	strongly	suspect	that
virtually	all	Type	2	diabetes	cases	could	be	prevented. Unfortunately,	misinformation	and	ingrained	habits	are	wreaking	havoc	on
our	health. Our	habit	of	eating	hot	dogs,	hamburgers	and	French	fries	iskilling	us. Even	Dr.	James	Anderson,	who	achieved	profound	results	with
many	patients	by	prescribing	a	near-vegetarian	diet,	is	not	immune	to	habitual
health	advice. He	writes,	“Ideally,	diets	providing	70%	of	calories	as
carbohydrate	and	up	to	70	gm	fiber	daily	offer	the	greatest	health	benefits	for
individuals	with	diabetes. However,	these	diets	allow	only	one	to	two	ounces
of	meat	daily	and	are	impractical	for	home	use	for	many	individuals.”
20
	Why
does	Professor	Anderson,	a	very	
fine	researcher,	say	that	such	a	diet	is
“impractical”	and	thereby	prejudice	his	listeners	before	they	even	consider	the
evidence? Yes,	changing	your	lifestyle	may	seem	impractical. It	may	seem
impractical	to	give	up	meat	and	high-fat	foods,	but	I	wonder	how	practical	it
is	to	be	350	pounds	and	have	Type	2	diabetes	at	the	age	of	fifteen,	like	the	girl
mentioned	at	the	start	of	this	chapter. I	wonder	how	practical	it	is	to	have	a
lifelong	condition	that	can’t	be	cured	by	drugs	or	surgery;	a	condition	that
often	leads	to	heart	disease,	stroke,	blindness	or	amputation;	a	condition	that
might	require	you	to	inject	insulin	into	your	body	every	day	for	the	rest	of
your	life. Radically	changing	our	diets	may	be	“impractical,”	but	it	might	also	be
worth	it.8
Common	Cancers:	Breast,	Prostate,	Large
Bowel	(Colon	and	Rectal)
M
UCH	OF	MY	CAREER
	has	been	concentrated	on	the	study	of	cancer. My
laboratory	work	was	focused	on	several	cancers,	including	those	of	the	liver,
breast	and	pancreas,	and	some	of	the	most	impressive	data	from	China	were
related	to	cancer. For	this	lifetime	work,	the	American	Institute	for	Cancer
Research	kindly	presented	me	with	their	Research	Achievement	award	in
1998. An	exceptional	number	of	books	have	summarized	the	evidence	on	the
effects	of	nutrition	on	a	variety	of	cancers,	each	with	their	own	particularities. But	what	I’ve	found	is	that	the	nutritional	effects	on	the	cancers	I’ve	chosen
to	discuss	here	are	virtually	the	same	for	all	cancers,	regardless	of	whether
they	are	initiated	by	different	factors	or	are	located	in	different	parts	of	the
body. Using	this	principle,	I	can	limit	my	discussion	to	three	cancers,	which
will	allow	me	space	in	the	rest	of	the	book	to	address	diseases	other	than
cancer,	demonstrating	the	breadth	of	evidence	linking	food	to	many	health
concerns. I	have	chosen	to	comment	on	three	cancers	that	affect	hundreds	of
thousands	of	Americans	and	that	generally	represent	other	cancers	as	well:
two	reproductive	cancers	that	get	plenty	of	attention,	breast	and	
prostate,	and
one	digestive	cancer,	large	bowel—the	second	leading	cause	of	cancer	death,
behind	lung	cancer.BREAST	CANCER
It	was	spring	almost	ten	years	ago. I	was	in	my	office	at	Cornell	when	I	was
told	that	a	woman	with	a	question	regarding	breast	cancer	was	on	the	phone. “I	have	a	strong	history	of	breast	cancer	in	my	family,”	the	woman,	Betty,
said. “My	mother	and	grandmother	both	died	from	the	disease,	and	my	forty-
five-year-old	sister	was	recently	diagnosed	with	it. Given	this	family	problem,
I	can’t	help	but	be	afraid	for	my	nine-year-old	daughter. She’s	going	to	start
menstruating	soon	and	I	worry	about	her	risks	of	getting	breast	cancer.”	Her
fear	was	evident	in	her	voice. “I’ve	seen	a	lot	of	research	showing	that	family
history	is	important,	and	I’m	afraid	that	it’s	inevitable	that	my	daughter	will
get	breast	cancer. One	of	the	options	I’ve	been	thinking	about	is	a	mastectomy
for	my	daughter,	to	remove	both	breasts. Do	you	have	any	advice?”
This	woman	was	in	an	exceptionally	difficult	position. Does	she	let	her
daughter	grow	up	into	a	deathtrap,	or	grow	up	without	breasts? Although
extreme,	this	question	represents	a	variety	of	similar	questions	faced	every
day	by	thousands	of	women	around	the	world. These	questions	were	especially	encouraged	by	the	early	reports	on	the
discovery	of	the	breast	cancer	gene,	BRCA-1. Headline	articles	in	the	
New
York	Times
	and	other	newspapers	and	magazines	trumpeted	this	discovery	as
an	enormous	advance. The	hoopla	surrounding	BRCA-1,	which	now	also
includes	BRCA-2,	reinforced	the	idea	that	breast	cancer	was	due	to	genetic
misfortune. This	caused	great	fear	among	people	with	a	family	history	of
breast	cancer. It	also	generated	excitement	among	scientists	and
pharmaceutical	companies. The	possibility	was	high	that	new	technologies
would	be	able	to	assess	overall	breast	cancer	risk	in	women	by	doing	genetic
testing;	they	hoped	they	might	be	able	to	manipulate	this	new	gene	in	a	way
that	would	prevent	or	treat	breast	cancer. Journalists	busily	started	translating
selective	bits	of	this	information	for	the	public,	relying	heavily	on	the	genetic
fatalistic	attitude. No	doubt	this	contributed	to	the	concern	of	mothers	like
Betty. “Well,	let	me	first	tell	you	that	I	am	not	a	physician,”	I	said. “I	can’t	help
you	with	diagnosis	or	treatment	advice. That’s	for	your	physician	to	do. I	can
speak	about	the	current	research	in	a	more	general	way,	however,	if	that	is	of
any	help	to	you.”
“Yes,”	she	said,	“that’s	what	I	wanted.”
I	told	her	a	little	bit	about	the	China	Study	and	about	the	important	role	of
nutrition. I	told	her	that	just	because	a	person	has	the	gene	for	a	disease	does
not	mean	that	they	are	destined	to	get	the	cancer:	prominent	studies	reported
that	only	a	tiny	minority	of	cancers	can	be	solely	blamed	on	genes.I	was	surprised	at	how	little	she	knew	about	nutrition. She	thought
genetics	was	the	only	factor	that	determined	risk. She	didn’t	realize	that	food
was	an	important	factor	in	breast	cancer	as	well. We	talked	for	twenty	or	thirty	minutes,	a	brief	time	for	such	an	important
matter. By	the	end	of	the	conversation	I	had	the	feeling	that	she	was	not
satisfied	with	what	I	told	her. Perhaps	it	was	my	conservative,	scientific	way
of	talking,	or	my	reluctance	to	give	her	a	recommendation. Maybe,	I	thought,
she	had	already	made	up	her	mind	to	do	the	procedure. She	thanked	me	for	my	time	and	I	wished	her	well. I	remember	thinking
about	how	often	I	receive	questions	from	people	about	specific	health
situations,	and	that	this	was	one	of	the	most	unusual. But	Betty	wasn’t	alone. One	other	woman	also	talked	to	me	regarding	the
possibility	of	her	young	daughter	undergoing	surgery	to	remove	both	breasts. Other	women	who	already	had	one	breast	removed	wondered	whether	to	have
the	second	breast	removed	as	a	preventative	measure. It’s	clear	that	breast	cancer	is	an	important	concern	in	our	society. One	out
of	eight	American	women	will	be	diagnosed	with	this	disease	during	their
lifetimes—one	of	the	highest	rates	in	the	world. Breast	cancer	grassroots
organizations	are	widespread,	strong,	relatively	well	funded	and	exceptionally
active	compared	to	other	health	activist	organizations. This	disease,	perhaps
more	than	any	other,	incites	panic	and	fear	in	many	women. When	I	think	back	to	that	conversation	I	had	with	Betty,	I	now	feel	that	I
could	have	made	a	stronger	statement	about	the	role	nutrition	plays	in	breast
cancer. I	still	would	not	have	been	able	to	give	her	clinical	advice,	but	the
information	I	now	know	might	have	been	of	more	use	to	her. So	what	would	I
tell	her	now?RISK	FACTORS
There	are	at	least	four	important	breast	cancer	risk	factors	that	are	affected	by
nutrition,	as	shown	in	
Chart	8.1
. Many	of	these	relationships	were	confirmed
in	the	China	Study	after	being	well	established	in	other	research. CHART	8.1:	BREAST	CANCER	RISK	FACTORS	AND
NUTRITIONAL	INFLUENCE
Risk	of	breast	cancer	increases
when	a	woman	has…
A	diet	high	in	animal	foods	and
refined	carbohydrates…
…early	age	of	menarche	(first
menstruation)
…	lowers	the	age	of	menarche
…	late	age	of	menopause
…	raises	the	age	of	menopause
…	high	levels	of	female	hormones
in	the	blood
…	increases	female	hormone	levels
…	high	blood	cholesterol
…	increases	blood	cholesterol	levels
With	the	exception	of	blood	cholesterol,	these	risk	factors	are	variations	on
the	same	theme:	exposure	to	excess	amounts	of	female	hormones,	including
estrogen	and	progesterone,	leads	to	an	increased	risk	of	breast	cancer. Women
who	consume	a	diet	rich	in	animal-based	foods,	with	a	reduced	amount	of
whole,	plant-based	foods,	reach	puberty	earlier	and	menopause	later,	thus
extending	their	reproductive	lives. They	also	have	higher	levels	of	female
hormones	throughout	their	lifespan,	as	shown	in	
Chart	8.2
. According	to	our	China	Study	data,	lifetime	exposure	to	estrogen
1
	is	at
least	2.5–3.0	times	higher	among	Western	women	when	compared	with	rural
Chinese	women. This	is	a	huge	difference	for	such	a	critically	important
hormone. 2
	To	use	the	words	of	one	of	the	leading	breast	cancer	research
groups	in	the	world,
3
	“there	is	overwhelming	evidence	that	estrogen	levels	are
a	critical	determinant	of	breast	cancer	risk.”
4,	5
	Estrogen	directly	participates
in	the	cancer	process. 6,	7
	It	also	tends	to	indicate	the	presence	of	other	female
hormones
8–12
	that	play	a	role	in	breast	cancer	risk. 6,	7
	Increased	levels	of
estrogen	and	related	hormones	are	a	result	of	the	consumption	of	typical
Western	diets,	high	in	fat	and	animal	protein	and	low	in	dietary	fiber. 3,	13–18CHART	8.2:	DIETARY	INFLUENCE	ON	FEMALE	HORMONE
EXPOSURE	OVER	A	WOMAN’S	LIFETIME	(SCHEMATIC)
The	difference	in	estrogen	levels	between	rural	Chinese	women	and
Western	women
19
	is	all	the	more	remarkable	because	a	previous	report
20
found	that	a	mere	17%	decrease	in	estrogen	levels	could	account	for	a	huge
difference	in	breast	cancer	rates	when	comparing	different	countries. Imagine,
then,	what	26-63%	lower	blood	estrogen	levels	and	eight	to	nine	fewer
reproductive	years	of	blood	estrogen	exposure	could	mean,	as	we	found	in	the
China	Study. This	idea	that	breast	cancer	is	centered	on	estrogen	exposure
3,	21,	22
	is
profound	because	diet	plays	a	major	role	in	establishing	estrogen	exposure. This	suggests	that	the	risk	of	breast	cancer	is	preventable	if	we	eat	foods	that
will	keep	estrogen	levels	under	control. The	sad	truth	is	that	most	women
simply	are	not	aware	of	this	evidence. If	this	information	were	properly
reported	by	responsible	and	credible	public	health	agencies,	I	suspect	that
many	more	young	women	might	be	taking	very	real,	very	effective	steps	to
avoid	this	awful	disease.THE	COMMON	ISSUES
Genes
Understandably,	women	who	are	most	afraid	of	this	disease	have	a	family
history	of	breast	cancer. Family	history	implies	that	genes	do	play	a	role	in	the
development	of	breast	cancer. But	I	hear	too	many	people	say,	in	effect,	that
“it’s	all	in	the	family”	and	deny	that	they	can	do	anything	to	help	themselves. This	fatalistic	attitude	removes	a	sense	of	personal	responsibility	for	one’s
own	health	and	profoundly	limits	available	options. It	is	true	that	if	you	have	a	family	history	of	breast	cancer,	you	are	at	an
increased	risk	of	getting	the	disease. 23,	24
	However,	one	research	group	found
that	less	than	3%	of	all	breast	cancer	cases	can	be	attributed	to	family
history. 24
	Even	though	other	groups	have	estimated	that	a	higher	percentage
of	cases	are	due	to	family	history
25
	the	vast	majority	of	breast	
cancer	in
American	women	is	not	due	to	family	history	or	genes. But	genetic	fatalism
continues	to	define	the	nation’s	mindset. Among	the	genes	that	influence	breast	cancer	risk,	BRCA-1	and	BRCA-2
have	received	the	most	attention	since	their	discovery	in	1994. 26–29
	These
genes,	when	mutated,	confer	a	higher	risk	both	for	breast	and	ovarian
cancers. 30,	31
	These	mutated	genes	may	be	passed	on	from	generation	to
generation;	that	is,	they	are	inherited	genes. In	the	excitement	over	these	discoveries,	however,	other	information	has
been	ignored. First,	only	0.2%	of	individuals	in	the	general	population	(1	in
500)	carry	the	mutated	forms	of	these	genes. 25
	Because	of	the	rarity	of	these
genetic	aberrations,	only	a	few	percent	of	the	breast	cancer	cases	in	the
general	population	can	be	attributed	to	mutated	BRCA-1	or	BRCA-2	genes. 32,
33
	Second,	these	genes	are	not	the	only	genes	that	participate	in	the
development	of	this	disease
32
;	many	more	will	surely	be	discovered. Third,
the	mere	presence	of	BRCA-1,	BRCA-2	or	any	other	breast	cancer	gene	does
not	guarantee	disease	occurrence. Environmental	and	dietary	factors	play	a
central	role	in	determining	whether	these	genes	are	expressed. A	recent	paper
31
	reviewed	twenty-two	studies	that	assessed	the	risk	of
breast	(and	ovarian)	cancer	among	women	who	carried	mutated	BRCA-1	and
BRCA-2	genes. Overall,	disease	risk	was	65%	for	breast	cancer	and	39%	for
ovarian	cancer	by	age	seventy	for	BRCA-1	women,	and	45%	and	11%,
respectively,	for	BRCA-2	women. Women	with	these	genes	certainly	face
high	risks	for	breast	cancer. But	even	among	these	high-risk	women,	there	is
still	good	reason	to	believe	that	more	attention	to	diet	is	likely	to	payhandsome	rewards. About	half	of	the	women	who	carry	these	rare,	potent
genes	do	not	get	breast	cancer. In	short,	although	the	discovery	of	BRCA-1	and	BRCA-2	added	an
important	dimension	to	the	breast	cancer	story,	the	excessive	emphasis	given
to	these	particular	genes	and	genetic	causation	in	general	is	not	warranted. I	do	not	mean	to	diminish	the	importance	of	knowing	all	there	is	to	know
about	these	genes	for	the	small	minority	of	women	who	carry	them. But	we
need	to	remind	ourselves	that	these	genes	need	to	be	“expressed”	in	order	for
them	to	participate	in	disease	formation,	and	nutrition	can	affect	this. We’ve
already	seen	in	chapter	three	how	a	diet	high	in	animal-based	protein	has	the
potential	to	control	genetic	expression.Screening	and	Non-Nutritional	Prevention
With	all	of	this	new	information	regarding	genetic	risk	and	family	history,
women	are	often	encouraged	to	get	screened	for	breast	cancer. Screening	is	a
reasonable	step,	especially	for	women	who	may	have	tested	positive	for	the
BRCA	genes. But	it’s	important	to	remember	that	doing	a	mammography	or
getting	a	genetic	test	to	see	if	you	harbor	BRCA	genes	does	not	constitute
prevention	of	breast	cancer. Screening	is	merely	an	observation	to	see	whether	the	disease	has
progressed	to	an	observable	state. Some	studies
34–36
	have	found	that	groups
of	women	who	undergo	frequent	mammography	have	slightly	lower	mortality
rates	than	groups	of	women	who	do	not	undergo	frequent	mammography. This	implies	that	our	cancer	treatments	are	more	likely	to	be	successful	if	the
cancer	is	found	at	an	earlier	stage. This	is	likely	to	be	true,	but	there	is	some
concern	over	the	way	statistics	are	used	in	this	debate. One	of	the	statistics	used	to	support	early	detection	and	the	ensuing
treatments	is	that	once	diagnosed	with	breast	cancer,	the	likelihood	of
surviving	for	at	least	five	years	is	higher	than	ever	before. 37
	What	this	really
means	is	that	with	the	aggressive	campaign	for	regular	screening,	many
women	are	discovering	their	breast	cancer	at	an	earlier	stage	of	disease. When
disease	is	discovered	at	an	earlier	stage	it	is	less	likely	to	lead	to	death	within
five	years,	
regardless	of	treatment. As	a	consequence,	we	may	have	an
improved	five-year	survival	rate	simply	because	women	find	out	that	they
have	breast	cancer	earlier	in	the	disease	progression,	not	because	our
treatments	have	improved	over	time. 38
Beyond	the	current	screening	methods,	there	are	other	non-nutritional
options	for	prevention	that	have	been	promoted. They	are	especially	of
interest	to	women	who	have	a	high	risk	of	breast	cancer	due	to	family	history
and/or	to	the	presence	of	the	BRCA	genes. These	options	include	taking	a
drug	such	as	tamoxifen	and/or	mastectomy. Tamoxifen	is	one	of	the	most	popular	drugs	taken	to	prevent	breast
cancer,
39,	40
	but	the	long-term	benefits	of	this	option	are	not	clear. One	major
U.S.	study	showed	that	tamoxifen	administered	over	a	period	of	four	years	to
women	at	increased	risk	of	breast	cancer	reduced	the	number	of	cases	by	an
impressive	49%. 41
	This	benefit,	however,	may	be	limited	to	women	whose
estrogen	levels	are	very	high. It	was	this	result	that	led	the	U.S.	Food	and
Drug	Administration	to	approve	use	of	tamoxifen	by	women	who	met	certain
criteria. 42
	Other	studies	suggest	that	the	enthusiasm	
for	this	drag	is	not
warranted. Two	less	substantial	European	trials
43,	44
	have	failed	to	show	anystatistically	significant	tamoxifen	benefit,	raising	some	doubt	about	how
dramatic	the	benefit	really	is. Moreover,	there	is	the	additional	concern	that
tamoxifen	raises	the	risks	for	stroke,	uterine	cancer,	cataracts,	deep	vein
thrombosis	and	pulmonary	embolism,	although	the	overall	benefits	of	breast
cancer	prevention	are	still	believed	to	outweigh	the	risks. 42
	Other	chemicals
have	also	been	investigated	as	alternatives	to	tamoxifen,	but	these	drags	are
encumbered	by	limited	effectiveness	and/or	some	of	the	same	troublesome
side	effects. 45,	46
Drugs	such	as	tamoxifen	and	its	newer	analogues	are	considered	
anti-
estrogen
	drugs. In	effect,	they	work	by	reducing	the	activity	of	estrogen,
which	is	known	to	be	associated	with	elevated	breast	cancer	risk. 4,	5
	My
question	is	quite	simple:	why	don’t	we	ask	why	estrogen	is	so	high	in	the	first
place,	and	once	we	recognize	its	nutritional	origin,	why	don’t	we	then	correct
that	cause? We	now	have	enough	information	to	show	that	a	diet	low	in
animal-based	protein,	low	in	fat	and	high	in	whole	plant	foods	will	reduce
estrogen	levels. Instead	of	suggesting	dietary	change	as	a	solution,	we	spend
hundreds	of	millions	of	dollars	developing	and	publicizing	a	drug	that	may	or
may	not	work	and	that	almost	certainly	will	have	unintended	side	effects. The	ability	of	dietary	factors	to	control	female	hormone	levels	has	long
been	known	in	the	research	community,	but	a	recent	study	was	particularly
impressive. 47
	Several	female	hormones,	which	increase	with	the	onset	of
puberty,	were	lowered	by	20–30%	(even	50%	lower	levels	for	progesterone!) simply	by	having	girls	eight	to	ten	years	of	age	consume	a	modestly	low-fat,
low	animal-based	food	diet	for	seven	years. 47
	These	results	are	extraordinary
because	they	were	obtained	with	a	modest	dietary	change	and	were	produced
during	a	critical	time	of	a	young	girl’s	life,	when	the	first	seeds	of	breast
cancer	were	being	sowed. These	girls	consumed	a	diet	of	no	more	than	28%
fat	and	less	than	150	mg	cholesterol/day:	a	moderate	plant-based	diet. I
believe	that	had	they	consumed	a	diet	devoid	of	animal-based	foods	and	had
they	started	this	diet	earlier	in	life,	they	would	have	seen	even	greater
benefits,	including	a	delay	in	puberty	and	an	even	lower	risk	of	breast	cancer
later	in	life. Women	at	high	risk	for	breast	cancer	are	given	three	options:	watch	and
wait,	take	tamoxifen	medication	for	the	remainder	of	their	lives	or	undergo
mastectomy. There	should	be	a	fourth	option:	consuming	a	diet	free	of
animal-based	foods	and	low	in	refined	carbohydrates,	aided	by	regular
monitoring	for	those	at	high	risk. I	stand	by	the	usefulness	
of	this	fourth
option	even	for	women	who	have	already	had	a	first	mastectomy. Using	diet
as	an	effective	treatment	of	already-diagnosed	disease	has	been	welldocumented	in	human	studies	with	advanced	heart	disease,
48,	49
	clinically
documented	Type	2	diabetes	(see	chapter	seven),	advanced	melanoma
50
	(a
deadly	skin	cancer)	and,	in	experimental	animal	studies,
51
	liver	cancer.Environmental	Chemicals
There	is	another	breast	cancer	conversation	that	has	been	taking	place	for
some	years	now. It	concerns	environmental	chemicals. These	widely
distributed	chemicals	have	been	shown	to	disrupt	hormones,	although	it	is	not
clear	which	hormones	in	humans	are	being	disrupted. These	chemicals	may
also	cause	reproductive	abnormalities,	birth	defects	and	Type	2	diabetes. There	are	many	different	types	of	offending	chemicals,	most	of	which	are
commonly	associated	with	industrial	pollution. One	group,	including	dioxins
and	PCBs,	persist	in	the	environment	because	they	are	not	metabolized	when
consumed. Thus	they	are	not	excreted	from	the	body. Because	of	this	lack	of
metabolism,	these	chemicals	accumulate	in	body	fat	and	breast	milk	of
lactating	mothers. Some	of	these	chemicals	are	known	to	promote	the	growth
of	cancer	cells,	although	humans	may	not	be	at	significant	risk	unless	one
consumes	excessive	quantities	of	meat,	milk	and	fish. Indeed,	90–95%	of	our
exposure	to	these	chemicals	comes	from	consuming	animal	products—yet
another	reason	why	consuming	animal-based	foods	can	be	risky. There	is	a	second	group	of	these	environmental	chemicals	that	are	also
commonly	perceived	to	be	significant	causes	of	breast
52
	and	other	cancers. They	are	called	PAHs	(Polycyclic	Aromatic	Hydrocarbons)	and	are	found	in
auto	exhaust,	factory	smoke	stacks,	petroleum	tar	products	and	tobacco
smoke,	among	other	processes	common	to	an	industrial	society	Unlike	the
PCBs	and	dioxins,	when	we	consume	PAHs	(in	food	and	water),	we	can
metabolize	and	excrete	them. But	there	is	a	snag:	when	the	PAHs	are
metabolized	within	the	body,	they	produce	intermediate	products	that	react
with	DNA	to	form	tightly	bound	complexes,	or	adducts	(see	chapter	three). This	is	the	first	step	in	causing	cancer. In	fact,	these	chemicals	have	recently
been	shown	to	adversely	affect	the	BRCA-1	and	BRCA-2	genes	of	breast
cancer	cells	grown	in	the	laboratory. 53
In	chapter	three,	I	described	studies	in	my	laboratory	showing	that	when	a
very	potent	carcinogen	is	put	into	the	body,	the	rate	at	which	
it	causes
problems	is	mostly	controlled	by	nutrition. Thus	the	rate	at	which	PAHs	are
metabolized	into	products	that	bind	to	DNA	is	very	much	controlled	by	what
we	eat. Very	simply	consuming	a	Western-type	diet	will	increase	the	rate	at
which	chemical	carcinogens	like	PAHs	bind	to	DNA	to	form	products	that
cause	cancer. So	when	a	recent	study	found	slightly	increased	levels	of	PAH-DNA
adducts	in	women	with	breast	cancer	in	Long	Island,	New	York,
54
	it	may	well
have	been	that	these	women	were	consuming	a	more	meaty	diet,	which
increased	the	binding	of	the	PAHs	to	DNA. It	is	entirely	possible	that	thequantity	of	PAHs	being	consumed	had	nothing	to	do	with	increasing	breast
cancer	risk. In	fact,	in	this	study,	the	number	of	PAH-DNA	adducts	in	these
women	seem	to	be	
unrelated
	to	PAH	exposure. 54
	How	is	this	possible? Perhaps	all	of	the	women	in	this	Long	Island	study	consumed	a	relatively
uniform,	low	level	of	PAHs,	and	the	only	ones	who	subsequently	got	breast
cancer	were	the	ones	who	ate	a	diet	high	in	fat	and	animal	protein,	thus
causing	more	of	the	ingested	PAHs	to	bind	to	their	DNA. In	this	same	Long	Island	study,	breast	cancer	was	not	associated	with
PCBs	and	dioxins,	the	chemicals	that	can’t	be	metabolized. 55
	As	a	result	of
the	Long	Island	study,	the	hype	associating	environmental	chemicals	with
breast	cancer	has	been	somewhat	muted. This	and	other	findings	suggest	that
environmental	chemicals	seem	to	play	a	far	less	significant	role	for	breast
cancer	than	the	kind	of	foods	we	choose	to	eat.Hormone	Replacement	Therapy
I	must	briefly	mention	one	final	breast	cancer	issue:	whether	to	use	hormone
replacement	therapy	(HRT),	which	increases	breast	cancer	risk. HRT	is	taken
by	many	women	in	order	to	alleviate	unpleasant	effects	of	menopause,	protect
bone	health	and	prevent	coronary	heart	disease. 56
	However,	it	is	now
becoming	widely	acknowledged	that	HRT	is	not	as	beneficial	as	once	thought,
and	it	may	have	certain	severe	side	effects. So	what	are	the	facts? I	am	writing	this	commentary	at	an	opportune	time	because	the	results	of
some	large	trials	of	HRT	use	have	been	released	in	the	last	year. 56
	Of	special
interest	are	two	large	randomized	intervention	trials:	the	Women’s	Health
Initiative	(WHI)
57
	and	the	Heart	and	Estrogen/Progestin	Replacement	Study
(HERS). 58
	Among	women	who	take	HRT,	after	5.2	years	the	WHI	trial	is
showing	a	26%	
increase
	in	breast	cancer	
cases	while	the	HERS	study	is
seeing	an	even	greater	30%	increase. 59
	These	studies	are	consistent. It	appears
that	increased	exposure	to	female	hormones,	via	HRT,	does	indeed	lead	to
more	breast	cancer. It	has	been	thought	that	HRT	is	associated	with	lower	rates	of	coronary
heart	disease. 56
	However,	this	is	not	necessarily	true. In	the	large	WHI	trial,
for	every	10,000	healthy	postmenopausal	women	who	took	HRT,	there	were
seven	more	women	with	heart	disease,	eight	more	with	strokes	and	eight	more
with	pulmonary	embolism
57
—the	opposite	of	what	had	been	expected. HRT
may	
increase
	cardiovascular	disease	risk	after	all. On	the	other	hand,	HRT	did
have	a	beneficial	effect	on	colorectal	cancer	and	bone	fracture	rate. Among
every	10,000	women,	there	were	six	fewer	colorectal	cancers	and	five	fewer
bone	fractures. 57
So	how	do	you	make	a	decision	with	such	information? Just	by	adding	and
subtracting	the	numbers	we	can	see	that	HRT	may	well	be	the	cause	of	more
harm	than	good. We	can	tell	each	individual	woman	to	make	her	own	decision
depending	on	which	disease	and	which	unpleasantry	she	fears	the	most,	as
many	physicians	are	likely	to	do. But	this	can	be	a	tough	decision	for	women
who	are	having	a	difficult	time	with	menopause. These	women	must	choose
between	living	unaided	through	the	emotional	and	physical	symptoms	of
menopause	in	order	to	preserve	a	low	risk	of	breast	cancer,	or	taking	HRT	to
manage	their	menopause	discomforts	while	increasing	their	risk	of	breast
cancer	and,	possibly,	cardiovascular	disease. To	say	that	this	scenario	troubles
me	would	be	an	understatement. We	have	spent	well	over	a	billion	dollars	on
the	research	and	development	of	these	HRT	medical	preparations,	and	all	we
get	is	some	apparent	pluses	and	probably	even	more	minuses. Calling	thistroubling	doesn’t	begin	to	describe	it. Instead	of	relying	on	HRT,	I	suggest	that	there	is	a	better	way,	using	food. The	argument	goes	like	this:
During	the	reproductive	years,	hormone	levels	are	elevated,	although	the
levels	among	women	who	eat	plant-based	diets	are	not	as	elevated. When	women	reach	the	end	of	their	reproductive	years,	it	is	entirely
natural	for	reproductive	hormones	of	all	women	to	drop	to	a	low	“base”
level. As	reproductive	years	come	to	an	end,	the	lower	hormone	levels	among
plant	eaters	don’t	crash	as	hard	as	they	do	among	animal	eaters. Using
hypothetical	numbers	to	illustrate	the	concept,	the	
levels	of	plant	eaters
may	crash	from	forty	to	fifteen,	rather	than	sixty	to	fifteen	for	animal
eaters. These	abrupt	hormone	changes	in	the	body	are	what	cause	menopausal
symptoms. Therefore,	a	plant-based	diet	leads	to	less	severe	hormone	crash	and	a
gentler	menopause. This	argument	is	eminently	reasonable	based	on	what	we	know,	although
more	studies	would	be	helpful. But	even	if	future	studies	fail	to	confirm	these
details,	a	plant-based	diet	still	offers	the	lowest	risk	for	both	breast	cancer	and
heart	disease	for	other	reasons. It	might	just	be	the	best	of	all	worlds,
something	that	no	drug	can	offer. In	each	of	the	various	issues	involving	breast	cancer	risk	(tamoxifen	use,
HRT	use,	environmental	chemical	exposure,	preventive	mastectomy),	I	am
convinced	that	these	practices	are	distractions	that	prevent	us	from
considering	a	safer	and	far	more	useful	nutritional	strategy. It	is	critical	that
we	change	the	way	we	think	about	this	disease,	and	that	we	provide	this
information	to	the	women	who	need	it.LARGE	BOWEL	CANCER	(INCLUDING	COLON
AND	RECTUM)
At	the	end	of	June	2002,	George	W.	Bush	handed	the	presidency	over	to	Dick
Cheney	for	a	period	of	roughly	two	hours	while	he	underwent	a	colonoscopy. Because	of	the	implications	President	Bush’s	colonoscopy	had	for	world
politics,	the	story	made	national	news,	and	colon	and	rectal	screening	were
briefly	thrust	into	the	spotlight. Across	the	country,	whether	the	comedians
were	making	jokes	or	the	news	anchors	were	describing	the	drama,	everybody
was	suddenly,	briefly,	talking	about	this	thing	called	a	colonoscopy	and	what
it	was	for. It	was	a	rare	moment	in	which	the	country	turned	its	focus	to	some
of	the	most	prolific	killer	diseases,	colon	and	rectal	cancers. Because	colon	and	rectal	cancers	are	both	cancers	of	the	large	bowel,	and
because	of	their	other	similarities,	they	often	are	grouped	together	under	the
term	colorectal	cancer. Colorectal	cancer	is	the	fourth	most	common	cancer
worldwide,	in	terms	of	overall	mortality. 60
	It	is	the	second	most	common	in
the	United	States,	with	6%	of	Americans	getting	the	cancer	during	their
lifetime. 37
	Some	even	claim	that,	by	age	seventy,	one-half	of	the	population
of	“Westernized”	countries	will	develop	a	tumor	in	the	large	bowel	and	10%
of	these	cases	will	progress	to	a	malignancy. 61GEOGRAPHIC	DISPARITY
North	America,	Europe,	Australia	and	wealthier	Asian	countries	(Japan,
Singapore)	have	very	high	rates	of	colorectal	cancer,	while	Africa,	Asia	and
most	of	Central	and	South	America	have	very	low	rates	of	this	cancer. For
example,	the	Czech	Republic	has	a	death	rate	of	34.19	per	100,000	males,
while	Bangladesh	has	a	death	rate	of	0.63	per	100,000	males! 62,	63
	
Chart	8.3
shows	a	comparison	of	average	death	rates	between	more	developed	countries
and	less	developed	countries;	all	these	rates	are	age-adjusted. The	fact	that	rates	of	colorectal	cancer	vary	hugely	between	countries	has
been	known	for	decades. The	question	has	always	been	why. Are	the
differences	due	to	genetics,	or	to	environment? It	seems	that	environmental	factors,	including	diet,	play	the	most
important	roles	in	colorectal	cancer. Migrant	studies	have	shown	that	as
people	move	from	a	low-cancer	risk	area	to	a	high-cancer	risk	area,	they
assume	an	increased	risk	within	two	generations. 64
	This	suggests	that	diet	and
lifestyle	are	important	causes	of	this	cancer. Other	studies	have	also	found
that	rates	of	colorectal	cancer	change	rapidly	as	a	population’s	diet	or	lifestyle
changes. 64
	These	rapid	changes	in	cancer	rates	within	one	population	cannot
possibly	be	explained	by	changes	in	inherited	genes. In	the	context	of	human
society,	it	takes	thousands	of	years	to	get	widespread,	permanent	changes	in
the	inherited	genes	that	are	passed	from	one	generation	to	the	next. Clearly,
something	about	environment	or	lifestyle	is	either	preventing	or	enhancing
the	risk	of	getting	colorectal	cancer.CHART	8.3:	COLORECTAL	CANCER	DEATH	RATE	IN	“MORE
DEVELOPED”	COUNTRIES	AND	“LESS	DEVELOPED”
COUNTRIES
In	a	landmark	paper	published	almost	thirty	years	ago,	researchers
compared	environmental	factors	and	cancer	rates	in	thirty-two	countries
around	the	world. 65
	One	of	the	strongest	links	between	any	cancer	and	any
dietary	factor	was	between	colon	cancer	and	meat	intake. Chart	8.4
	shows	this
link	for	women	in	twenty-three	different	countries. In	this	report,	countries	where	more	meat,	more	animal	protein,	more
sugar	and	fewer	cereal	grains	were	consumed	had	far	higher	rates	of	colon
cancer. 65
	Another	researcher	whom	I	mentioned	in	chapter	four,	Denis
Burkitt,	hypothesized	that	intake	of	dietary	fiber	was	essential	for	digestive
health	in	general. He	compared	stool	samples	and	fiber	intakes	in	Africa	and
Europe	and	proposed	that	colorectal	cancers	were	largely	the	result	of	low
fiber	intake. 66
	Fiber,	remember,	is	only	found	in	plant	foods. It	is	the	part	of
the	plant	that	our	body	cannot	digest. Using	data	from	another	famous	study
that	compared	diets	in	seven	different	countries,	researchers	found	that	eating
an	additional	ten	grams	of	dietary	fiber	a	day	lowered	the	long-term	risk	of
colon	cancer	by	33%. 67
	There	are	ten	grams	of	fiber	in	one	cup	of	red
raspberries,	one	Asian	pear	or	one	cup	of	peas. A	cup	of	just	about	any	variety
of	bean	would	provide	significantly	more	than	ten	grams	of	fiber.CHART	8.4:	FEMALE	COLON	CANCER	INCIDENCE	AND	DAILY
MEAT	CONSUMPTION
From	all	this	research,	it	seems	clear	that	something	can	be	said	for	the
importance	of	diet	in	colorectal	cancer. But	what	exactly	stops	colon	and
rectal	cancer? Is	it	fiber? Is	it	fruits	and	vegetables? Is	it	carbohydrates? Is	it
milk? Each	of	these	foods	or	nutrients	has	been	suggested	to	play	a	role. The
debate	has	raged,	and	solid	answers	are	seldom	agreed	upon.THE	SPECIFIC	CURE
Most	of	the	debate	over	the	past	twenty-five	years	on	dietary	fiber	and	its	link
to	large	bowel	cancer	began	with	Burkitt’s	work	in	Africa. Because	of
Burkitt’s	prominence,	many	people	have	believed	that	fiber	is	the	source	of
colorectal	health. Perhaps	you	have	already	heard	that	fiber	is	good	for
preventing	colon	cancer. At	least	you	probably	have	heard	that	fiber	“keeps
things	running	well.”	Isn’t	that	what	prunes	are	known	for? Yet	nobody	has	ever	been	able	to	prove	that	fiber	is	the	magic	bullet	for
preventing	colorectal	cancer. There	are	important	technical	reasons	why	a
definitive	conclusion	regarding	fiber	is	difficult	to	make. 68
	Each	of	these
reasons	is	related	either	directly	or	indirectly	to	the	fact	that	dietary	fiber	is
not	a	single,	simple	substance	producing	a	single,	simple	benefit. Fiber
represents	hundreds	of	substances,	and	“its”	benefits	operate	through	an
exceptionally	complex	series	of	biochemical	and	physiological	events. Each
time	researchers	assess	the	consumption	of	dietary	fiber,	they	must	decide
which	of	the	hundreds	of	fiber	sub-fractions	to	measure	and	which	methods	to
use. It	is	nearly	impossible	to	establish	a	standard	procedure	because	it	is
virtually	impossible	to	know	what	each	fiber	sub-fraction	does	in	the	body. The	uncertainty	of	having	a	standard	procedure	prompted	us	to	measure
fiber	in	more	than	a	dozen	ways	in	our	China	Study. As	summarized	in
chapter	four,	as	consumption	of	almost	all	of	these	fiber	types	went	up,	colon
and	rectal	cancer	rates	went	down. 69
	But	we	could	make	no	clear
interpretations
70
	as	to	which	type	of	fiber	was	especially	important. Despite	the	uncertainties,	I	continue	to	believe	that	Burkitt’s
66
	initial
hypothesis	that	
fiber-containing	diets
	prevent	colorectal	cancers	is	correct	and
that	some	of	this	effect	is	due	to	the	aggregate	effect	of	all	the	fiber	types. In
fact,	the	hypothesis	that	dietary	fiber	prevents	large	
bowel	cancers	has
become	even	more	convincing. In	1990,	a	group	of	researchers	reviewed	sixty
different	studies	that	had	been	done	on	fiber	and	colon	cancer. 71
	They	found
that	most	of	the	studies	supported	the	idea	that	fiber	protects	against	colon
cancer. They	noted	that	the	combined	results	showed	that	the	people	who
consumed	the	most	fiber	had	a	43%	lower	risk	of	colon	cancer	than	the
people	who	consumed	the	least	fiber. 71
	Those	who	consume	the	most
vegetables	had	a	52%	lower	risk	than	those	who	consume	the	least
vegetables. 71
	But	even	in	this	large	review	of	the	evidence,	researchers	noted,
“the	data	do	not	permit	discrimination	between	effects	due	to	fiber	and	non-
fiber	effects	due	to	vegetables.”
71
	So	is	fiber,	all	by	itself,	the	magic	bullet
we’ve	been	looking	for? We	still,	in	1990,	didn’t	know.Two	years	later,	in	1992,	a	different	group	of	researchers	reviewed	thirteen
studies	that	had	compared	people	with	and	without	colorectal	cancer	(case-
control	design). 72
	They	found	that	those	who	had	consumed	the	most	fiber
had	a	47%	lower	risk	of	colorectal	cancer	than	those	who	consumed	the
least. 72
	In	fact,	they	found	that	if	Americans	ate	an	additional	thirteen	grams
of	fiber	a	day	
from	food	sources
	(not	as	supplements),	about	a	third	of	all
colorectal	cancer	cases	in	the	U.S.	could	be	avoided. 72
	If	you’ll	remember,
thirteen	grams,	in	real	world	terms,	is	the	amount	found	in	about	a	cup	of	any
variety	of	beans. More	recently,	a	mammoth	study	called	the	EPIC	study	collected	data	on
fiber	intake	and	colorectal	cancer	in	519,000	people	across	Europe. 73
	They
found	that	the	20%	of	people	who	consumed	the	most	fiber	in	their	diet,	about
thirty-four	grams	per	day,	had	a	42%	lower	risk	of	colorectal	cancer	than	the
20%	who	consumed	the	least	fiber	in	their	diet,	about	thirteen	grams	per
day. 73
	It’s	important	to	note	once	again	that,	as	with	all	of	these	studies,
dietary	fiber	was	obtained	in	food,	not	as	supplements. So	all	we	can	say	is
“fiber-containing	diets”	seem	to	significantly	reduce	the	risk	of	colorectal
cancer. We	still	can’t	say	anything	definitive	about	isolated	fiber	itself. This
means	that	attempts	to	add	isolated	fiber	to	foods	may	not	produce	benefits. But	consuming	plant	foods	naturally	high	in	fiber	is	clearly	beneficial. These
foods	include	vegetables	(the	non-root	parts),	fruits	and	whole	grains. In	reality,	we	can’t	even	be	sure	how	much	of	the	prevention	of	colorectal
cancer	is	due	to	fiber-containing	foods,	because	as	people	eat	more	of	these
foods	they	usually	consume	less	animal-based	foods. In	other	words,	are
fruits,	vegetables	and	whole	grains	protective,	or	is	meat	dangerous? Or	is	it
both? A	recent	study	in	South	Africa	helped	
to	answer	these	questions. White
South	Africans	have	seventeen	times	more	large	bowel	cancer	than	black
South	Africans,	and	this	was	first	thought	to	be	due	to	the	much	higher
consumption	of	dietary	fiber	among	black	South	Africans	provided	by
unrefined	maize. 74
	However,	in	more	recent	years,	black	South	Africans	have
been	increasingly	consuming	commercially	
refined
	maize-meal—maize
minus	its	fiber. They	now	eat	even	less	fiber	than	the	white	South	Africans. Yet,	colon	cancer	rates	among	blacks	remain	at	a	low	level,
75
	which	calls	into
question	how	much	of	the	cancer-protective	effect	is	due	to	dietary	fiber
alone. A	more	recent	study
76
	showed	that	the	higher	colon	cancer	rates	among
white	South	Africans	could	well	be	due	to	their	elevated	consumption	of
animal	protein	(77	vs.	25	g/day),	total	fat	(115	vs.	71	g/day)	and	cholesterol
(408	vs.	211	mg/day),	as	seen	in	
Chart	8.5
. The	researchers	suggested	that	the
much	higher	colon	cancer	rates	among	white	South	Africans	may	be	morerelated	to	the	quantity	of	animal	protein	and	fat	in	their	diets	than	their
lacking	the	protective	factor	of	dietary	fiber. 76
CHART	8.5:	INTAKE	OF	ANIMAL	PROTEIN,	TOTAL	FAT	AND
CHOLESTEROL	AMONG	BLACK	AND	WHITE	SOUTH	AFRICANS
What	is	clear	is	that	diets	naturally	high	in	fiber	and	low	in	animal-based
foods	can	prevent	colorectal	cancer. Even	in	the	absence	of	more	specific
details,	we	can	still	make	important	public	health	recommendations. The	data
clearly	show	that	a	whole	foods,	plant-based	diet	can	dramatically	lower
colorectal	cancer	rates. We	don’t	need	to	know	which	fiber	is	responsible,
what	mechanism	is	involved	or	even	how	much	of	the	effect	is	independently
due	to	fiber.OTHER	FACTORS
It	has	been	recently	noted	that	the	same	risk	factors	that	promote	colorectal
cancer,	a	diet	low	in	fruits	and	vegetables	and	high	in	animal	foods	and
refined	carbohydrates,	can	also	promote	insulin	resistance	syndrome. 77–79
From	there,	scientists	have	hypothesized	that	insulin	resistance	may	be
responsible	for	colon	cancer. 77–82
	Insulin	resistance	was	described	in	chapter
six	as	a	diabetic	condition. And	what’s	good	for	keeping	insulin	resistance
under	control	is	also	good	for	colon	cancer:	a	diet	of	whole,	plant-based
foods. This	diet	happens	to	be	very	high	in	carbohydrates,	which	have	recently
been	under	assault	in	the	marketplace. Because	carbohydrate-confusion
persists,	let	me	remind	you	that	there	are	two	different	types	of	carbohydrates:
refined	carbohydrates	and	complex	carbohydrates. Refined	carbohydrates	are
the	starches	and	sugars	obtained	from	plants	by	mechanically	stripping	off
their	outer	layers,	which	contain	most	of	the	plant’s	vitamins,	minerals,
protein	and	fiber. This	“food”	(regular	sugar,	white	flour,	etc.) has	very	little
nutritional	value. Foods	such	as	pastas	made	from	refined	flour,	sugary
cereals,	white	bread,	candies	and	sugar-laden	soft	drinks	should	be	avoided	as
much	as	possible. But	do	eat	whole,	complex	carbohydrate-containing	foods
such	as	unprocessed	fresh	fruits	and	vegetables,	and	whole	grain	products	like
brown	rice	and	oatmeal. These	unprocessed	carbohydrates,	especially	from
fruits	and	vegetables,	are	exceptionally	health-promoting. You	also	may	have	heard	that	calcium	is	beneficial	in	fighting	colon
cancer. This,	of	course,	gets	extended	to	the	argument	that	cow’s	milk	fights
colon	cancer. It	has	been	hypothesized	that	high-calcium	diets	prevent	colon
cancer	in	two	ways:	first,	it	inhibits	the	growth	of	critical	cells	in	the	colon,
83,
84
	and	second,	it	binds	up	intestinal	bile	acids. These	bile	acids	arise	in	the
liver,	move	to	the	intestine	and	are	thought	to	get	
into	the	large	bowel	and
promote	colon	cancer	development. By	binding	these	bile	acids,	calcium	is
said	to	prevent	colon	cancer. One	research	group	demonstrated	that	high-calcium	diets—generally
meaning	diets	high	in	dairy	foods—inhibit	the	growth	of	certain	cells	in	the
colon,
84
	
but	this	effect	was	not	entirely	consistent	for	the	various	indicators	of
cell	growth. Furthermore,	it	is	not	clear	whether	these	presumably	favorable
biochemical	effects	really	lead	to	less	cancer	growth
. 83,	85
	Another	research
group	demonstrated	that	calcium	does	reduce	the	presumably	dangerous	bile
acids,	but	also	observed	that	
a	high-wheat	diet	did	an	even	better	job	of
reducing	the	bile	acids
. 86
	But—and	this	is	the	really	odd	part—when	acombination	high-calcium	and	high-wheat	diet	was	consumed,	the	binding
effect	on	bile	acids	was	weaker	than	for	each	individual	supplement	taken
alone. 86
	It	just	goes	to	show	that	when	individually-observed	nutrient	effects
are	combined,	as	in	a	dietary	situation,	the	expected	may	become	the
unexpected. I	doubt	that	a	high-calcium	diet,	obtained	through	calcium	supplements	or
through	calcium-rich	cow’s	milk,	has	a	beneficial	effect	on	colon	cancer. In
rural	China	where	calcium	consumption	is	modest	and	almost	no	dairy	food	is
consumed,
87
	colon	cancer	rates	are	not	higher;	instead	they	are	much	lower
than	in	the	U.S. The	parts	of	the	world	that	consume	the	most	calcium,
Europe	and	North	America,	have	the	highest	rates	of	colorectal	cancer. Another	lifestyle	choice	that	is	clearly	important	for	this	disease	is
exercise. Increased	exercise	is	convincingly	associated	with	less	colorectal
cancer. In	one	summary	from	the	World	Cancer	Research	Fund	and	the
American	Institute	for	Cancer	Research,	seventeen	out	of	twenty	studies
found	that	exercise	protected	against	colon	cancer. 64
	Unfortunately,	there
seems	to	be	no	convincing	evidence	as	to	why	or	how	this	occurs.SCREENING	FOR	TROUBLE
The	benefits	of	exercise	bring	me	back	to	President	George	W.	Bush. He	is
known	to	enjoy	staying	physically	fit	with	a	regular	running	routine,	and	that
is	undoubtedly	one	of	the	reasons	why	he	received	a	clean	bill	of	health	when
he	had	a	colonoscopy. But	what	is	a	colonoscopy	anyway,	and	is	it	really
worth	the	effort	to	get	checked? When	people	go	to	the	doctor	to	get	a
colonoscopy,	the	doctor	inspects	the	large	bowel	using	a	rectal	probe	and
looks	for	abnormal	tissue	growth. The	most	commonly	found	abnormality	is	a
polyp. Although	it	is	not	yet	clear	exactly	how	tumors	
are	related	to	polyps,
most	scientists	would	agree
88,	89
	that	they	share	similar	dietary	associations
and	genetic	characteristics. Those	people	who	have	noncancerous	problems	in
the	large	bowel,	such	as	polyps,	often	are	the	same	people	who	later	develop
cancerous	tumors. So	getting	screened	for	polyps	or	other	problems	is	a	reasonable	way	to
establish	risk	for	large	bowel	cancer	in	the	future. But	what	if	you	have	a
polyp? What	is	the	best	thing	to	do? Will	surgical	removal	of	the	polyp	lessen
colon	cancer	risk? A	nationwide	study	has	shown	that,	when	polyps	were
removed,	there	was	a	76–90%	decrease	in	the	expected	cases	of	colon
cancer. 89,	90
	This	certainly	supports	the	idea	of	routine	screening. 89,	91
	It	is
commonly	recommended	that	people	get	a	colonoscopy	once	every	ten	years
starting	at	the	age	of	fifty. If	you	have	a	higher	risk	of	colorectal	cancer,	it	is
recommended	that	you	start	at	the	age	of	forty	and	screen	more	frequently. How	do	you	know	if	you	are	at	a	higher	risk	for	colorectal	cancer? We	can
very	roughly	assess	our	personal	genetic	risk	in	several	ways. We	can
consider	the	probability	of	our	getting	colon	cancer	based	on	the	number	of
immediate	family	members	who	already	have	the	disease,	we	can	screen	for
the	presence	of	polyps,	and	we	now	can	clinically	test	for	the	presence	of
suspect	genes. 92
This	is	an	excellent	example	of	how	genetic	research	can	lead	to	a	better
understanding	of	complex	diseases. However,	in	the	enthusiasm	for	studying
the	genetic	basis	for	this	cancer,	two	things	often	get	overlooked. First,	the
proportion	of	colon	cancer	cases	attributed	to	known	inherited	genes	is	only
about	1–3%. 89
	Another	10–30%
89
	tend	to	occur	in	some	families	more	than
others	(called	familial	clustering),	an	effect	possibly	reflective	of	a	significant
genetic	contribution. These	numbers,	however,	exaggerate	the	number	of
cancers	that	are	solely	“due	to	genes.”
Except	for	the	very	few	people	whose	colon	cancer	risk	is	largely
determined	by	known	inherited	genes	(1–3%),	most	of	the	family-connectedcolon	cancer	cases	(i.e,	the	additional	10–30%)	are	still	largely	determined	by
environmental	and	dietary	factors. After	all,	place	of	residence	and	diet	are
often	shared	experiences	within	families. Even	if	you	have	a	high	genetic	risk,	a	healthy	plant-based	diet	is	capable
of	negating	most,	if	not	all,	of	that	risk	by	controlling	the	expression	of	these
genes. Because	a	high-fiber	diet	can	only	prevent	colon	cancer—extra	fiber
won’t	ever	
promote
	colon	cancer—dietary	recommendations	should	be	the
same	regardless	of	one’s	genetic	risk.PROSTATE	CANCER
I	suspect	that	most	people	do	not	know	exactly	what	a	prostate	is,	even
though	prostate	cancer	is	commonly	discussed. The	prostate	is	a	male
reproductive	organ	about	the	size	of	a	walnut,	located	between	the	bladder
and	the	colon. It	is	responsible	for	producing	some	of	the	fluid	that	helps
sperm	on	its	quest	to	fertilize	the	female’s	egg. For	such	a	little	thing,	it	sure	can	cause	a	lot	of	problems. Several	of	my
friends	now	have	prostate	cancer	or	closely	related	conditions,	and	they	aren’t
alone. As	one	recent	report	pointed	out,	“Prostate	cancer	is	one	of	the	most
commonly	diagnosed	cancers	among	men	in	the	United	States,	representing
about	25%	of	all	tumors…,”
93
	As	many	as	half	of	all	men	seventy	years	and
older	have	latent	prostate	cancer,
94
	a	silent	form	of	the	cancer	which	is	not	yet
causing	discomfort. Prostate	cancer	is	not	only	extremely	prevalent,	but	also
slow-growing. Only	7%	of	diagnosed	prostate	cancer	victims	die	within	five
years. 95
	This	makes	it	difficult	to	know	how	and	if	the	cancer	should	be
treated. The	main	question	for	the	patient	and	doctor	is:	will	this	cancer
become	life	threatening	before	death	comes	from	other	causes? One	of	the	markers	used	to	determine	the	likelihood	of	prostate	cancer
becoming	life	threatening	is	the	blood	level	of	prostate	specific	antigen
(PSA). Men	are	diagnosed	as	having	prostate	problems	when	their	PSA	levels
are	above	four. But	this	test	alone	is	hardly	a	firm	diagnosis	of	cancer,
especially	if	the	PSA	level	is	barely	above	four. The	ambiguity	of	this	test
leads	to	some	very	difficult	decision-making. Occasionally	my	friends	ask	for
my	opinion. Should	they	have	a	little	surgery	or	a	lot? Is	a	PSA	value	of	6.0	a
serious	problem	or	just	a	wake-up	call? If	it’s	a	wake-up	call,	then	what	must
they	do	to	reduce	such	a	number? While	I	cannot	speak	to	the	clinical
condition	of	an	individual,	I	can	speak	to	the	research,	and	of	the	research	I
have	seen,	there	is	no	doubt	that	diet	plays	a	key	role	in	this	disease. Although	there	is	debate	regarding	the	specifics	of	diet	and	this	cancer,
let’s	start	with	some	very	safe	assumptions	that	have	long	been	accepted	in
the	research	community:
Prostate	cancer	rates	vary	widely	between	different	countries,	even	more
than	breast	cancer. High	prostate	cancer	rates	primarily	exist	in	societies	with	“Western”
diets	and	lifestyles. In	developing	countries,	men	who	adopt	Western	eating	practices	or
move	to	Western	countries	suffer	more	prostate	cancer.These	disease	patterns	are	similar	to	those	of	other	diseases	of	affluence. Mostly	this	tells	us	that	although	prostate	cancer	certainly	has	a	genetic
component,	environmental	factors	play	the	dominant	role. So	what
environmental	factors	are	important? You	can	guess	that	I’m	going	to	say
plant-based	foods	are	good	and	animal-based	foods	are	bad,	but	do	we	know
anything	more	specific? Surprisingly,	one	of	the	most	consistent,	specific
links	between	diet	and	prostate	cancer	has	been	dairy	consumption. A	2001	Harvard	review	of	the	research	could	hardly	be	more
convincing
96
:
…	twelve	of	…	fourteen	case-control	studies	and	seven	of	…	nine
cohort	studies	[have]	observed	a	positive	association	for	some	measure
of	dairy	products	and	prostate	cancer;	
this	is	one	of	the	most	consistent
dietary	predictors	for	prostate	cancer	in	the	published	literature
	[my
emphasis]. In	these	studies,	men	with	the	highest	dairy	intakes	had
approximately	double	the	risk	of	total	prostate	cancer,	and	up	to	a
fourfold	increase	in	risk	of	metastatic	or	fatal	prostate	cancer	relative	to
low	consumers. 96
Let’s	consider	that	again:	dairy	intake	is	“one	of	the	most	consistent
dietary	predictors	for	prostate	cancer	in	the	published	literature,”	and	those
who	consume	the	most	dairy	have	double	to	quadruple	the	risk. Another	review	of	published	literature	done	in	1998	reached	a	similar
conclusion:
In	ecologic	data,	correlations	exist	between	per	capita	meat	and	dairy
consumption	and	prostate	cancer	mortality	rate	[one	study	cited]. In
case	control	and	prospective	studies,	the	major	contributors	of	animal
protein,	meats,	dairy	products	and	eggs	have	frequently	been	associated
with	a	higher	risk	of	prostate	cancer…	[twenty-three	studies	cited]. Of
note,	numerous	studies	have	found	an	association	primarily	in	older
men	[six	studies	cited]	though	not	all	[one	study	cited]…. The
consistent	associations	with	dairy	products	could	result	from,	at	least	in
part,	their	calcium	and	phosphorous	content. 97
In	other	words,	an	enormous	body	of	evidence	shows	that	animal-based
foods	are	associated	with	prostate	cancer. In	the	case	of	dairy,	the	high	intake
of	calcium	and	phosphorus	also	could	be	partly	responsible	for	this	effect. This	research	leaves	little	room	for	dissent;	each	of	the	above	studies
represents	analyses	of	over	a	dozen	individual	studies,	providing	animpressive	bulk	of	convincing	literature.THE	MECHANISMS
As	we	have	seen	with	other	forms	of	cancer,	large-scale	observational	studies
show	a	link	between	prostate	cancer	and	an	animal-based	diet,	particularly
one	based	heavily	on	dairy. Understanding	the	mechanisms	behind	the
observed	link	between	prostate	cancer	and	dairy	clinches	the	argument. The	first	mechanism	concerns	a	hormone	that	increases	cancer	cell
growth,	a	hormone	that	our	bodies	make,	as	needed. This	growth	hormone,
Insulin-like	Growth	Factor	1	(IGF-1),	is	turning	out	to	be	a	predictor	of
cancer	just	as	cholesterol	is	a	predictor	for	heart	disease. Under	normal
conditions,	this	hormone	efficiently	manages	the	rates	at	which	cells
“grow”—that	is,	how	they	reproduce	themselves	and	how	they	discard	old
cells,	all	in	the	name	of	good	health. Under	unhealthy	conditions,	however,	IGF-1	becomes	more	active,
increasing	the	birth	and	growth	of	new	cells	while	simultaneously	inhibiting
the	removal	of	old	cells,	both	of	which	favor	the	development	of	cancer
[seven	studies	cited
98
]. So	what	does	this	have	to	do	with	the	food	we	eat? It
turns	out	that	consuming	animal-based	foods	increases	the	blood	levels	of	this
growth	hormone,	IGF-1. 99–101
With	regard	to	prostate	cancer,	people	with	higher	than	normal	blood
levels	of	IGF-I	have	been	shown	to	have	5.1	times	the	risk	of	advanced-stage
prostate	cancer. 98
	There’s	more:	when	men	also	have	low	blood	levels	of	a
protein	that	binds	and	inactivates	IGF-I,
102
	they	will	have	
9.5	times	the	risk	of
advanced-stage	prostate	cancer
,
98
	Let’s	put	a	few	stars	by	these	numbers. They	are	big	and	impressive—and	fundamental	to	this	finding	is	the	fact	that
we	make	more	IGF-I	when	we	consume	animal-based	foods	like	meat	and
dairy. 99–101
The	second	mechanism	relates	to	vitamin	D	metabolism. This	“vitamin”	is
not	a	nutrient	that	we	need	to	consume. Our	body	can	make	all	that	we	need
simply	by	being	in	sunlight	fifteen	to	thirty	minutes	every	couple	of	days. In
addition	to	the	production	of	vitamin	D	being	
affected	by	sunlight,	it	is	also
affected	by	the	food	that	we	eat. The	formation	of	the	most	active	form	of
vitamin	D	is	a	process	that	is	closely	monitored	and	controlled	by	our	bodies. This	process	is	a	great	example	of	our	bodies’	natural	balancing	act,	affecting
not	only	prostate	cancer,	but	breast	cancer,	colon	cancer,	osteoporosis	and
autoimmune	diseases	like	Type	1	diabetes. Because	of	its	importance	for
multiple	diseases,	and	because	of	the	complexity	involved	in	explaining	how
it	all	works,	I	have	provided	in	
Appendix	C
	an	abbreviated	scheme,	just
enough	to	illustrate	my	point. This	web	of	reactions	illustrates	many	similarand	highly	integrated	reaction	networks	showing	how	food	controls	health. The	main	component	of	this	process	is	an	active	form	of	vitamin	D
produced	in	the	body	from	the	vitamin	D	that	we	get	from	food	or	sunshine. This	active	or	“supercharged”	D	produces	many	benefits	throughout	the	body,
including	the	prevention	of	cancer,	autoimmune	diseases	and	diseases	like
osteoporosis. This	all-important	supercharged	D	is	not	something	that	you	get
from	food	or	from	a	drug. A	drug	composed	of	isolated	supercharged	D
would	be	far	too	powerful	and	far	too	dangerous	for	medical	use. Your	body
uses	a	carefully	composed	series	of	controls	and	sensors	to	produce	just	the
right	amount	of	supercharged	D	for	each	task	at	exactly	the	right	time. As	it	turns	out,	our	diet	can	determine	how	much	of	this	supercharged	D	is
produced	and	how	it	works	once	it	is	produced. Animal	protein	that	we
consume	has	the	tendency	to	block	the	production	of	supercharged	D,	leaving
the	body	with	low	levels	of	this	vitamin	D	in	the	blood. If	these	low	levels
persist,	prostate	cancer	can	result. Also,	persistently	high	intakes	of	calcium
create	an	environment	where	supercharged	D	declines,	thus	adding	to	the
problem. So	what	food	substance	has	both	animal	protein	and	large	amounts	of
calcium? Milk	and	other	dairy	foods. This	fits	in	perfectly	with	the	evidence
that	links	dairy	consumption	with	prostate	cancer. This	information	provides
what	we	call	biological	plausibility	and	shows	how	the	observational	data	fit
together. To	review	the	mechanisms:
Animal	protein	causes	the	body	to	produce	more	IGF-1,	which	in	turn
throws	cell	growth	and	removal	out	of	whack,	stimulating	cancer
development. Animal	protein	suppresses	the	production	of	“supercharged”	D.
Excessive	calcium,	as	found	in	milk,	also	suppresses	the	production	of
“supercharged”	D.
“Supercharged”	D	is	responsible	for	creating	a	wide	variety	of	health
benefits	in	the	body. Persistently	low	levels	of	supercharged	D	create	an
inviting	environment	for	different	cancers,	autoimmune	diseases,
osteoporosis	and	other	diseases. The	important	story	here	is	how	the	effects	of	food—both	good	and	bad—
operate	through	a	symphony	of	coordinated	reactions	to	prevent	diseases	like
prostate	cancer. In	discovering	the	existence	of	these	networks,	we	sometimes
wonder	which	specific	function	comes	first	and	which	comes	next. We	tend	to
think	of	these	reactions	within	the	network	as	independent. But	this	surely
misses	the	point. What	impresses	me	is	the	multitude	of	reactions	working
together	in	so	many	ways	to	produce	the	same	effect:	in	this	case,	to	preventdisease. There	is	no	single	“mechanism”	that	fully	explains	what	causes	diseases
such	as	cancer. Indeed,	it	would	be	foolish	to	even	think	along	these	lines. But
what	I	do	know	is	this:	the	totality	and	breadth	of	the	evidence,	operating
through	highly	coordinated	networks,	supports	the	conclusions	that
consuming	dairy	and	meat	are	serious	risk	factors	for	prostate	cancer.BRINGING	IT	TOGETHER
Roughly	half	a	million	Americans	this	year	will	go	to	the	doctor’s	office	and
be	told	that	they	have	cancer	of	the	breast,	prostate	or	large	bowel. People
who	get	one	of	these	cancers	represent	40%	of	all	new	cancer	patients. These
three	cancers	devastate	the	lives	of	not	only	the	victims	themselves,	but	also
their	family	and	friends. When	my	mother-in-law	died	of	colon	cancer	at	the	age	of	fifty-one,	none
of	us	knew	that	much	about	nutrition	or	what	it	meant	for	health. It	wasn’t
that	we	didn’t	care	about	the	health	of	our	loved	ones—of	course	we	did. We
just	didn’t	have	the	information. Yet,	over	thirty	years	later,	not	much	has
changed. Of	the	people	you	know	who	have	cancer,	or	are	at	risk	of	having
cancer,	how	many	of	them	have	considered	the	possibility	of	adopting	a
whole	foods,	plant-based	diet	to	improve	their	chances? I’m	guessing	very
few	of	them	have	done	so. Probably	they,	too,	don’t	have	the	information. Our	institutions	and	information	providers	are	failing	us. Even	cancer
organizations,	at	both	the	national	and	local	level,	are	reluctant	to	discuss	or
even	believe	this	evidence. Food	as	a	key	to	health	represents	a	powerful
challenge	to	conventional	medicine,	which	is	fundamentally	built	on	
drugs
and	surgery	(see	
Part	IV
). The	widespread	communities	of	nutrition
professionals,	researchers	and	doctors	are,	as	a	whole,	either	unaware	of	this
evidence	or	reluctant	to	share	it. Because	of	these	failings,	Americans	are
being	cheated	out	of	information	that	could	save	their	lives. There	is	enough	evidence	now	that	doctors	should	be	discussing	the	option
of	pursuing	dietary	change	as	a	potential	path	to	cancer	prevention	and
treatment. There	is	enough	evidence	now	that	the	U.S.	government	should	be
discussing	the	idea	that	the	toxicity	of	our	diet	is	the	single	biggest	cause	of
cancer. There	is	enough	evidence	now	that	local	breast	cancer	alliances,	and
prostate	and	colon	cancer	institutions,	should	be	discussing	the	possibility	of
providing	information	to	Americans	everywhere	on	how	a	whole	foods,	plant-
based	diet	may	be	an	incredibly	effective	anti-cancer	medicine. If	these	discussions	were	to	happen,	it	is	possible	that,	next	year,	fewer
than	500,000	people	would	go	to	the	doctor’s	office	and	be	told	they	have
cancer	of	the	breast,	prostate	or	large	bowel. The	year	after	that,	even	fewer
friends,	coworkers	and	family	members	would	be	given	the	most	dreaded	of
all	diagnoses. And	the	following	year,	even	fewer. The	possibility	that	this	future	could	be	our	reality	is	real,	and	as	long	as
this	future	holds	such	promise	for	the	health	of	people	everywhere,	it	is	a
future	worth	working	for.9
Autoimmune	Diseases
N
O	GROUP	OF	DISEASES
	is	more	insidious	than	autoimmune	diseases. They	are
difficult	to	treat,	and	progressive	loss	of	physical	and	mental	function	is	a
common	outcome. Unlike	heart	disease,	cancer,	obesity	and	Type	2	diabetes,
with	autoimmune	diseases	the	body	systematically	attacks	itself. The	afflicted
patient	is	almost	guaranteed	to	lose. A	quarter	million	people	in	the	U.S.	are	diagnosed	with	one	of	the	forty
separate	autoimmune	diseases	each	year. 1,	2
	Women	are	2.7	times	more	likely
to	be	afflicted	than	are	men. About	3%	of	Americans	(one	in	every	thirty-one
people)	have	an	autoimmune	disease,	a	staggering	total	of	8.5	million	people;
some	people	put	the	total	at	as	many	as	12–13	million	people. 3
The	more	common	of	these	diseases	are	listed	in	
Chart	9.1
.
_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:

        All	of	these	findings	support	the	idea	that	both	across	and	within
populations,	high-fiber,	whole,	plant-based	foods	protect	against	diabetes,	and
high-fat,	high-protein,	animal-based	foods	promote	diabetes. CURING	THE	INCURABLE
All	of	the	research	cited	above	was	
observational
	and	an	observed
association,	even	if	frequently	seen,	may	only	be	an	incidental	association	that
masks	the	real	cause-effect	relationship	of	environment	(including	diet)	and
disease. There	is,	however,	also	research	of	the	“controlled”	or	intervention
variety. This	involves	changing	the	diets	of	people	who	already	have	either
full-blown	Type	1	or	Type	2	diabetes	or	mild	diabetic	symptoms	(impaired
glucose	tolerance). James	Anderson,	M. D. ,	is	one	of	the	most	prominent	scientists	studying
diet	and	diabetes	today,	garnering	dramatic	results	using	dietary	means	alone. One	of	his	studies	examined	the	effects	of	a	high-fiber,	high-carbohydrate,
low-fat	diet	on	twenty-five	Type	1	diabetics	and	twenty-five	Type	2	diabetics
in	a	hospital	setting. 15
	None	of	his	fifty	patients	were	overweight	and	all	of
them	were	taking	insulin	shots	to	control	their	blood	sugar	levels. His	experimental	diet	consisted	mostly	of	whole	plant	foods	and	the
equivalent	of	only	a	cold	cut	or	two	of	meat	a	day. He	put	his	patients	on	the
conservative,	American-style	diet	recommended	by	the	American	
Diabetes
Association	for	one	week	and	then	switched	them	over	to	the	experimental
“veggie”	diet	for	three	weeks. He	measured	their	blood	sugar	levels,
cholesterol	levels,	weight	and	medication	requirements. The	results	were
impressive. Type	1	diabetics	cannot	produce	insulin. It	is	difficult	to	imagine	any
dietary	change	that	might	aid	their	predicament. But	after	just	three	weeks,	the
Type	1	diabetic	patients	were	able	to	lower	their	insulin	medication	by	an
average	of	40%. Their	blood	sugar	profiles	improved	dramatically. Just	as
importantly,	their	cholesterol	levels	dropped	by	30%. 15
	Remember,	one	of	the
dangers	of	being	diabetic	is	the	secondary	outcomes,	heart	disease	and	stroke. Lowering	risk	factors	for	those	secondary	outcomes	by	improving	the
cholesterol	profile	is	almost	as	important	as	treating	high	blood	sugar. Type	2	diabetics,	unlike	Type	1,	are	more	“treatable”	because	they	haven’t
incurred	such	extensive	damage	to	their	pancreas. So	when	Anderson’s	Type
2	patients	ate	the	high-fiber,	low-fat	diet,	the	results	were	even	more
impressive. Of	the	twenty-five	Type	2	patients,	twenty-four	were	able	to
discontinue	their	insulin	medication. Let	me	say	that	again. All	but	one	person
were	able	to	discontinue	their	insulin	medication	in	a	matter	of	weeks. 15
One	man	had	a	twenty-one-year	history	of	diabetes	and	was	taking	thirty-
five	units	of	insulin	a	day. After	three	weeks	of	intensive	dietary	treatment,
his	insulin	dosage	dropped	to	eight	units	a	day. After	eight	weeks	at	home,	hisneed	for	insulin	shots	vanished. 13
	
Chart	7. 2
	shows	a	sample	of	patients	and
how	eating	a	plant-based	diet	lowered	their	insulin	medications. This	is	a
huge	effect. In	another	study	of	fourteen	lean	diabetic	patients,	Anderson	found	that
diet	alone	could	lower	total	cholesterol	levels	by	32%	
in	just	over	two
weeks. 16
	Some	of	the	results	are	shown	in	
Chart	7. 3. These	benefits,	representing	a	decrease	in	blood	cholesterol	from	206
mg/dL	to	141	mg/dL,	are	astounding—especially	considering	the	speed	with
which	they	appear. Dr. Anderson	also	found	no	evidence	that	this	cholesterol
decrease	was	temporary	as	long	as	people	continued	on	the	diet;	it	remained
low	for	four	years. 17
Another	group	of	scientists	at	the	Pritikin	Center	achieved	equally
spectacular	results	by	prescribing	a	low-fat,	plant-based	diet	and	exercise	to	a
group	of	diabetic	patients. Of	forty	patients	on	medication	at	the	start	of	the
program,	thirty-four	were	able	to	discontinue	all	medication	after	only
twenty-six	days. 18
	This	research	group	also	demonstrated	that	
the	benefits	of	a
plant-based	diet	will	last	for	years	if	the	same	diet	is	continued. 19
CHART	7. 2:	INSULIN	DOSAGE	RESPONSE	TO	DIET
These	are	examples	of	some	very	dramatic	research,	but	they	only	scratch
the	surface	of	all	the	supporting	research	that	has	been	done. One	scientific
paper	reviewed	nine	publications	citing	the	use	of	high-carbohydrate,	high-
fiber	diets	and	two	more	standard-carbohydrate,	high-fiber	diets	to	treat
diabetic	patients. 20
	All	eleven	studies	resulted	in	improved	blood	sugar	and
cholesterol	levels. (Dietary	fiber	supplements,	by	the	way,	althoughbeneficial,	did	not	have	same	consistent	effects	as	a	change	to	a	plant-based,
whole	foods	diet. ) 21THE	PERSISTENCE	OF	HABIT
As	you	can	see	by	these	findings,	we	can	beat	diabetes. Two	recent	studies
considered	a	combination	of	diet	and	exercise	effects	on	this	disease. 22,	23
	One
study	placed	3,234	non-diabetic	people	at	risk	for	diabetes	(elevated	blood
sugar)	into	three	different	groups. 22
	One	group,	the	control,	received	standard
dietary	information	and	a	drug	placebo	(no	effect),	one	received	the	standard
dietary	information	and	the	drug	metformin,	and	a	third	group	received
“intensive”	lifestyle	intervention,	which	included	a	moderately	low-fat	diet
and	exercise	plan	to	lose	at	least	7%	of	their	weight. After	almost	three	years,
the	lifestyle	group	had	
58%	fewer	cases	of	diabetes	than	the	control	group. The	drug	group	reduced	the	number	of	cases	only	by	31%. Compared	to	the
control,	both	treatments	worked,	but	clearly	a	lifestyle	change	is	much	more
powerful	and	safer	than	simply	taking	a	drug. Moreover,	the	lifestyle	change
would	be	effective	in	solving	other	health	problems,	whereas	the	drug	would
not. CHART	7. 3:	BLOOD	CHOLESTEROL	ON	HIGH-CARBOHYDRATE,
HIGH-FIBER	DIET
The	second	study	also	found	that	the	rate	of	diabetes	could	be	reduced	by
58%	just	by	modest	lifestyle	changes,	including	exercise,	weight	loss	and	a
moderately	low-fat	diet. 23
	Imagine	what	would	happen	if	people	fully	adopted
the	healthiest	diet:	a	whole	foods,	plant-based	diet. I	strongly	suspect	that
virtually	all	Type	2	diabetes	cases	could	be	prevented. Unfortunately,	misinformation	and	ingrained	habits	are	wreaking	havoc	on
our	health. Our	habit	of	eating	hot	dogs,	hamburgers	and	French	fries	iskilling	us. Even	Dr. James	Anderson,	who	achieved	profound	results	with
many	patients	by	prescribing	a	near-vegetarian	diet,	is	not	immune	to	habitual
health	advice. He	writes,	“Ideally,	diets	providing	70%	of	calories	as
carbohydrate	and	up	to	70	gm	fiber	daily	offer	the	greatest	health	benefits	for
individuals	with	diabetes. However,	these	diets	allow	only	one	to	two	ounces
of	meat	daily	and	are	impractical	for	home	use	for	many	individuals. ”
20
	Why
does	Professor	Anderson,	a	very	
fine	researcher,	say	that	such	a	diet	is
“impractical”	and	thereby	prejudice	his	listeners	before	they	even	consider	the
evidence. Yes,	changing	your	lifestyle	may	seem	impractical. It	may	seem
impractical	to	give	up	meat	and	high-fat	foods,	but	I	wonder	how	practical	it
is	to	be	350	pounds	and	have	Type	2	diabetes	at	the	age	of	fifteen,	like	the	girl
mentioned	at	the	start	of	this	chapter. I	wonder	how	practical	it	is	to	have	a
lifelong	condition	that	can’t	be	cured	by	drugs	or	surgery;	a	condition	that
often	leads	to	heart	disease,	stroke,	blindness	or	amputation;	a	condition	that
might	require	you	to	inject	insulin	into	your	body	every	day	for	the	rest	of
your	life. Radically	changing	our	diets	may	be	“impractical,”	but	it	might	also	be
worth	it. 8
Common	Cancers:	Breast,	Prostate,	Large
Bowel	(Colon	and	Rectal)
M
UCH	OF	MY	CAREER
	has	been	concentrated	on	the	study	of	cancer. My
laboratory	work	was	focused	on	several	cancers,	including	those	of	the	liver,
breast	and	pancreas,	and	some	of	the	most	impressive	data	from	China	were
related	to	cancer. For	this	lifetime	work,	the	American	Institute	for	Cancer
Research	kindly	presented	me	with	their	Research	Achievement	award	in
1998. An	exceptional	number	of	books	have	summarized	the	evidence	on	the
effects	of	nutrition	on	a	variety	of	cancers,	each	with	their	own	particularities. But	what	I’ve	found	is	that	the	nutritional	effects	on	the	cancers	I’ve	chosen
to	discuss	here	are	virtually	the	same	for	all	cancers,	regardless	of	whether
they	are	initiated	by	different	factors	or	are	located	in	different	parts	of	the
body. Using	this	principle,	I	can	limit	my	discussion	to	three	cancers,	which
will	allow	me	space	in	the	rest	of	the	book	to	address	diseases	other	than
cancer,	demonstrating	the	breadth	of	evidence	linking	food	to	many	health
concerns. I	have	chosen	to	comment	on	three	cancers	that	affect	hundreds	of
thousands	of	Americans	and	that	generally	represent	other	cancers	as	well:
two	reproductive	cancers	that	get	plenty	of	attention,	breast	and	
prostate,	and
one	digestive	cancer,	large	bowel—the	second	leading	cause	of	cancer	death,
behind	lung	cancer. BREAST	CANCER
It	was	spring	almost	ten	years	ago. I	was	in	my	office	at	Cornell	when	I	was
told	that	a	woman	with	a	question	regarding	breast	cancer	was	on	the	phone. “I	have	a	strong	history	of	breast	cancer	in	my	family,”	the	woman,	Betty,
said. “My	mother	and	grandmother	both	died	from	the	disease,	and	my	forty-
five-year-old	sister	was	recently	diagnosed	with	it. Given	this	family	problem,
I	can’t	help	but	be	afraid	for	my	nine-year-old	daughter. She’s	going	to	start
menstruating	soon	and	I	worry	about	her	risks	of	getting	breast	cancer. ”	Her
fear	was	evident	in	her	voice. “I’ve	seen	a	lot	of	research	showing	that	family
history	is	important,	and	I’m	afraid	that	it’s	inevitable	that	my	daughter	will
get	breast	cancer. One	of	the	options	I’ve	been	thinking	about	is	a	mastectomy
for	my	daughter,	to	remove	both	breasts. Do	you	have	any	advice. ”
This	woman	was	in	an	exceptionally	difficult	position. Does	she	let	her
daughter	grow	up	into	a	deathtrap,	or	grow	up	without	breasts. Although
extreme,	this	question	represents	a	variety	of	similar	questions	faced	every
day	by	thousands	of	women	around	the	world. These	questions	were	especially	encouraged	by	the	early	reports	on	the
discovery	of	the	breast	cancer	gene,	BRCA-1. Headline	articles	in	the	
New
York	Times
	and	other	newspapers	and	magazines	trumpeted	this	discovery	as
an	enormous	advance. The	hoopla	surrounding	BRCA-1,	which	now	also
includes	BRCA-2,	reinforced	the	idea	that	breast	cancer	was	due	to	genetic
misfortune. This	caused	great	fear	among	people	with	a	family	history	of
breast	cancer. It	also	generated	excitement	among	scientists	and
pharmaceutical	companies. The	possibility	was	high	that	new	technologies
would	be	able	to	assess	overall	breast	cancer	risk	in	women	by	doing	genetic
testing;	they	hoped	they	might	be	able	to	manipulate	this	new	gene	in	a	way
that	would	prevent	or	treat	breast	cancer. Journalists	busily	started	translating
selective	bits	of	this	information	for	the	public,	relying	heavily	on	the	genetic
fatalistic	attitude. No	doubt	this	contributed	to	the	concern	of	mothers	like
Betty. “Well,	let	me	first	tell	you	that	I	am	not	a	physician,”	I	said. “I	can’t	help
you	with	diagnosis	or	treatment	advice. That’s	for	your	physician	to	do. I	can
speak	about	the	current	research	in	a	more	general	way,	however,	if	that	is	of
any	help	to	you. ”
“Yes,”	she	said,	“that’s	what	I	wanted. ”
I	told	her	a	little	bit	about	the	China	Study	and	about	the	important	role	of
nutrition. I	told	her	that	just	because	a	person	has	the	gene	for	a	disease	does
not	mean	that	they	are	destined	to	get	the	cancer:	prominent	studies	reported
that	only	a	tiny	minority	of	cancers	can	be	solely	blamed	on	genes. I	was	surprised	at	how	little	she	knew	about	nutrition. She	thought
genetics	was	the	only	factor	that	determined	risk. She	didn’t	realize	that	food
was	an	important	factor	in	breast	cancer	as	well. We	talked	for	twenty	or	thirty	minutes,	a	brief	time	for	such	an	important
matter. By	the	end	of	the	conversation	I	had	the	feeling	that	she	was	not
satisfied	with	what	I	told	her. Perhaps	it	was	my	conservative,	scientific	way
of	talking,	or	my	reluctance	to	give	her	a	recommendation. Maybe,	I	thought,
she	had	already	made	up	her	mind	to	do	the	procedure. She	thanked	me	for	my	time	and	I	wished	her	well. I	remember	thinking
about	how	often	I	receive	questions	from	people	about	specific	health
situations,	and	that	this	was	one	of	the	most	unusual. But	Betty	wasn’t	alone. One	other	woman	also	talked	to	me	regarding	the
possibility	of	her	young	daughter	undergoing	surgery	to	remove	both	breasts. Other	women	who	already	had	one	breast	removed	wondered	whether	to	have
the	second	breast	removed	as	a	preventative	measure. It’s	clear	that	breast	cancer	is	an	important	concern	in	our	society. One	out
of	eight	American	women	will	be	diagnosed	with	this	disease	during	their
lifetimes—one	of	the	highest	rates	in	the	world. Breast	cancer	grassroots
organizations	are	widespread,	strong,	relatively	well	funded	and	exceptionally
active	compared	to	other	health	activist	organizations. This	disease,	perhaps
more	than	any	other,	incites	panic	and	fear	in	many	women. When	I	think	back	to	that	conversation	I	had	with	Betty,	I	now	feel	that	I
could	have	made	a	stronger	statement	about	the	role	nutrition	plays	in	breast
cancer. I	still	would	not	have	been	able	to	give	her	clinical	advice,	but	the
information	I	now	know	might	have	been	of	more	use	to	her. So	what	would	I
tell	her	now. RISK	FACTORS
There	are	at	least	four	important	breast	cancer	risk	factors	that	are	affected	by
nutrition,	as	shown	in	
Chart	8. 1. Many	of	these	relationships	were	confirmed
in	the	China	Study	after	being	well	established	in	other	research. CHART	8. 1:	BREAST	CANCER	RISK	FACTORS	AND
NUTRITIONAL	INFLUENCE
Risk	of	breast	cancer	increases
when	a	woman	has…
A	diet	high	in	animal	foods	and
refined	carbohydrates…
…early	age	of	menarche	(first
menstruation)
…	lowers	the	age	of	menarche
…	late	age	of	menopause
…	raises	the	age	of	menopause
…	high	levels	of	female	hormones
in	the	blood
…	increases	female	hormone	levels
…	high	blood	cholesterol
…	increases	blood	cholesterol	levels
With	the	exception	of	blood	cholesterol,	these	risk	factors	are	variations	on
the	same	theme:	exposure	to	excess	amounts	of	female	hormones,	including
estrogen	and	progesterone,	leads	to	an	increased	risk	of	breast	cancer. Women
who	consume	a	diet	rich	in	animal-based	foods,	with	a	reduced	amount	of
whole,	plant-based	foods,	reach	puberty	earlier	and	menopause	later,	thus
extending	their	reproductive	lives. They	also	have	higher	levels	of	female
hormones	throughout	their	lifespan,	as	shown	in	
Chart	8. 2. According	to	our	China	Study	data,	lifetime	exposure	to	estrogen
1
	is	at
least	2. 5–3. 0	times	higher	among	Western	women	when	compared	with	rural
Chinese	women. This	is	a	huge	difference	for	such	a	critically	important
hormone. 2
	To	use	the	words	of	one	of	the	leading	breast	cancer	research
groups	in	the	world,
3
	“there	is	overwhelming	evidence	that	estrogen	levels	are
a	critical	determinant	of	breast	cancer	risk. ”
4,	5
	Estrogen	directly	participates
in	the	cancer	process. 6,	7
	It	also	tends	to	indicate	the	presence	of	other	female
hormones
8–12
	that	play	a	role	in	breast	cancer	risk. 6,	7
	Increased	levels	of
estrogen	and	related	hormones	are	a	result	of	the	consumption	of	typical
Western	diets,	high	in	fat	and	animal	protein	and	low	in	dietary	fiber. 3,	13–18CHART	8. 2:	DIETARY	INFLUENCE	ON	FEMALE	HORMONE
EXPOSURE	OVER	A	WOMAN’S	LIFETIME	(SCHEMATIC)
The	difference	in	estrogen	levels	between	rural	Chinese	women	and
Western	women
19
	is	all	the	more	remarkable	because	a	previous	report
20
found	that	a	mere	17%	decrease	in	estrogen	levels	could	account	for	a	huge
difference	in	breast	cancer	rates	when	comparing	different	countries. Imagine,
then,	what	26-63%	lower	blood	estrogen	levels	and	eight	to	nine	fewer
reproductive	years	of	blood	estrogen	exposure	could	mean,	as	we	found	in	the
China	Study. This	idea	that	breast	cancer	is	centered	on	estrogen	exposure
3,	21,	22
	is
profound	because	diet	plays	a	major	role	in	establishing	estrogen	exposure. This	suggests	that	the	risk	of	breast	cancer	is	preventable	if	we	eat	foods	that
will	keep	estrogen	levels	under	control. The	sad	truth	is	that	most	women
simply	are	not	aware	of	this	evidence. If	this	information	were	properly
reported	by	responsible	and	credible	public	health	agencies,	I	suspect	that
many	more	young	women	might	be	taking	very	real,	very	effective	steps	to
avoid	this	awful	disease. THE	COMMON	ISSUES
Genes
Understandably,	women	who	are	most	afraid	of	this	disease	have	a	family
history	of	breast	cancer. Family	history	implies	that	genes	do	play	a	role	in	the
development	of	breast	cancer. But	I	hear	too	many	people	say,	in	effect,	that
“it’s	all	in	the	family”	and	deny	that	they	can	do	anything	to	help	themselves. This	fatalistic	attitude	removes	a	sense	of	personal	responsibility	for	one’s
own	health	and	profoundly	limits	available	options. It	is	true	that	if	you	have	a	family	history	of	breast	cancer,	you	are	at	an
increased	risk	of	getting	the	disease. 23,	24
	However,	one	research	group	found
that	less	than	3%	of	all	breast	cancer	cases	can	be	attributed	to	family
history. 24
	Even	though	other	groups	have	estimated	that	a	higher	percentage
of	cases	are	due	to	family	history
25
	the	vast	majority	of	breast	
cancer	in
American	women	is	not	due	to	family	history	or	genes. But	genetic	fatalism
continues	to	define	the	nation’s	mindset. Among	the	genes	that	influence	breast	cancer	risk,	BRCA-1	and	BRCA-2
have	received	the	most	attention	since	their	discovery	in	1994. 26–29
	These
genes,	when	mutated,	confer	a	higher	risk	both	for	breast	and	ovarian
cancers. 30,	31
	These	mutated	genes	may	be	passed	on	from	generation	to
generation;	that	is,	they	are	inherited	genes. In	the	excitement	over	these	discoveries,	however,	other	information	has
been	ignored. First,	only	0. 2%	of	individuals	in	the	general	population	(1	in
500)	carry	the	mutated	forms	of	these	genes. 25
	Because	of	the	rarity	of	these
genetic	aberrations,	only	a	few	percent	of	the	breast	cancer	cases	in	the
general	population	can	be	attributed	to	mutated	BRCA-1	or	BRCA-2	genes. 32,
33
	Second,	these	genes	are	not	the	only	genes	that	participate	in	the
development	of	this	disease
32
;	many	more	will	surely	be	discovered. Third,
the	mere	presence	of	BRCA-1,	BRCA-2	or	any	other	breast	cancer	gene	does
not	guarantee	disease	occurrence. Environmental	and	dietary	factors	play	a
central	role	in	determining	whether	these	genes	are	expressed. A	recent	paper
31
	reviewed	twenty-two	studies	that	assessed	the	risk	of
breast	(and	ovarian)	cancer	among	women	who	carried	mutated	BRCA-1	and
BRCA-2	genes. Overall,	disease	risk	was	65%	for	breast	cancer	and	39%	for
ovarian	cancer	by	age	seventy	for	BRCA-1	women,	and	45%	and	11%,
respectively,	for	BRCA-2	women. Women	with	these	genes	certainly	face
high	risks	for	breast	cancer. But	even	among	these	high-risk	women,	there	is
still	good	reason	to	believe	that	more	attention	to	diet	is	likely	to	payhandsome	rewards. About	half	of	the	women	who	carry	these	rare,	potent
genes	do	not	get	breast	cancer. In	short,	although	the	discovery	of	BRCA-1	and	BRCA-2	added	an
important	dimension	to	the	breast	cancer	story,	the	excessive	emphasis	given
to	these	particular	genes	and	genetic	causation	in	general	is	not	warranted. I	do	not	mean	to	diminish	the	importance	of	knowing	all	there	is	to	know
about	these	genes	for	the	small	minority	of	women	who	carry	them. But	we
need	to	remind	ourselves	that	these	genes	need	to	be	“expressed”	in	order	for
them	to	participate	in	disease	formation,	and	nutrition	can	affect	this. We’ve
already	seen	in	chapter	three	how	a	diet	high	in	animal-based	protein	has	the
potential	to	control	genetic	expression. Screening	and	Non-Nutritional	Prevention
With	all	of	this	new	information	regarding	genetic	risk	and	family	history,
women	are	often	encouraged	to	get	screened	for	breast	cancer. Screening	is	a
reasonable	step,	especially	for	women	who	may	have	tested	positive	for	the
BRCA	genes. But	it’s	important	to	remember	that	doing	a	mammography	or
getting	a	genetic	test	to	see	if	you	harbor	BRCA	genes	does	not	constitute
prevention	of	breast	cancer. Screening	is	merely	an	observation	to	see	whether	the	disease	has
progressed	to	an	observable	state. Some	studies
34–36
	have	found	that	groups
of	women	who	undergo	frequent	mammography	have	slightly	lower	mortality
rates	than	groups	of	women	who	do	not	undergo	frequent	mammography. This	implies	that	our	cancer	treatments	are	more	likely	to	be	successful	if	the
cancer	is	found	at	an	earlier	stage. This	is	likely	to	be	true,	but	there	is	some
concern	over	the	way	statistics	are	used	in	this	debate. One	of	the	statistics	used	to	support	early	detection	and	the	ensuing
treatments	is	that	once	diagnosed	with	breast	cancer,	the	likelihood	of
surviving	for	at	least	five	years	is	higher	than	ever	before. 37
	What	this	really
means	is	that	with	the	aggressive	campaign	for	regular	screening,	many
women	are	discovering	their	breast	cancer	at	an	earlier	stage	of	disease. When
disease	is	discovered	at	an	earlier	stage	it	is	less	likely	to	lead	to	death	within
five	years,	
regardless	of	treatment. As	a	consequence,	we	may	have	an
improved	five-year	survival	rate	simply	because	women	find	out	that	they
have	breast	cancer	earlier	in	the	disease	progression,	not	because	our
treatments	have	improved	over	time. 38
Beyond	the	current	screening	methods,	there	are	other	non-nutritional
options	for	prevention	that	have	been	promoted. They	are	especially	of
interest	to	women	who	have	a	high	risk	of	breast	cancer	due	to	family	history
and/or	to	the	presence	of	the	BRCA	genes. These	options	include	taking	a
drug	such	as	tamoxifen	and/or	mastectomy. Tamoxifen	is	one	of	the	most	popular	drugs	taken	to	prevent	breast
cancer,
39,	40
	but	the	long-term	benefits	of	this	option	are	not	clear. One	major
U. S. study	showed	that	tamoxifen	administered	over	a	period	of	four	years	to
women	at	increased	risk	of	breast	cancer	reduced	the	number	of	cases	by	an
impressive	49%. 41
	This	benefit,	however,	may	be	limited	to	women	whose
estrogen	levels	are	very	high. It	was	this	result	that	led	the	U.
Dr. Anderson's research focuses on the relationship between diet and disease, particularly in the context of diabetes and cancer.
What is the primary focus of Dr. Anderson's research?
The main concern is that this perspective oversimplifies the complexity of the issue and ignores the potential impact of environmental and dietary factors.
What is the main concern with the idea that breast cancer is caused by genetic factors?
The study found that the patients were able to discontinue their insulin medication, with some patients being able to stop taking insulin after just three weeks.
What is the key finding of the study on the effects of a high-fiber, low-fat diet on diabetic patients?
The study found that a plant-based diet can lead to a significant decrease in the risk of breast cancer, and that the consumption of animal-based foods increases the risk.
What is the significance of the China Study?
The main concern is that the relationship between fiber and colon cancer is more complex and influenced by a combination of factors, including diet and lifestyle.
What is the main concern with the idea that fiber is the magic bullet for preventing colon cancer?