But	funding	of
genetic	research	continues	to	spiral	upwards	in	the	belief	that	specific	genes
account	for	the	occurrence	of	specific	diseases,	in	the	hope	that	we	somehow
will	be	able	to	“turn	off”	these	nasty	genes. Drug	company	public	relations
programs	now	depict	a	future	where	each	of	us	will	have	a	personal	ID	card
cataloging	all	of	our	good	and	bad	genes. Using	this	card,	we	will	be	expected
to	go	to	our	doctor,	who	will	prescribe	a	single	pill	to	suppress	our	bad	genes. I	strongly	suspect	these	miracles	will	never	be	realized,	or	if	tried	they	will
have	serious,	unintended	consequences. These	futuristic	pipe	dreams	obscure
the	affordable,	efficacious	health	solutions	that	currently	exist:	solutions
based	in	nutrition. In	my	own	laboratory	we	have	shown	in	experimental	animals	that	cancer
growth	can	be	turned	on	and	off	by	nutrition,	despite	very	strong	genetic
predisposition. We	have	studied	these	effects	in	great	detail	and	have
published	our	findings	in	the	very	best	scientific	journals. As	you	will	see
later,	these	findings	are	nothing	short	of	spectacular,	and	the	same	effects
have	been	indicated	over	and	over	again	in	humans. Eating	the	right	way	not	only	prevents	disease	but	also	generates	health
and	a	sense	of	well-being,	both	physically	and	mentally. Some	world-class
athletes,	such	as	ironman	Dave	Scott,	track	stars	Carl	Lewis	and	EdwinMoses,	tennis	great	Martina	Navratilova,	world	champion	wrestler	Chris
Campbell	(no	relation)	and	sixty-eight-year-old	marathoner	Ruth	Heidrich
have	discovered	that	consuming	a	low-fat,	
plant-based	diet	gives	them	a
significant	edge	in	performance. In	the	laboratory,	we	fed	experimental	rats	a
diet	similar	to	the	usual	American	fare—rich	in	animal-based	protein—and
compared	them	with	other	rats	fed	a	diet	low	in	animal-based	protein. Guess
what	happened	when	both	sets	of	rats	had	an	opportunity	to	voluntarily	use
exercise	wheels? Those	fed	the	low-animal	protein	diet	exercised
substantially	more,	with	less	fatigue,	than	those	fed	the	type	of	diet	that	most
of	us	eat. This	was	the	same	effect	observed	by	these	world-class	athletes. This	shouldn’t	be	news	to	the	medical	establishment. A	century	ago,
Professor	Russell	Chittenden,	a	famous,	well	established	nutrition	researcher
at	Yale	University	Medical	School,	investigated	whether	eating	a	plant-based
diet	affected	students’	physical	capacities. 34,	35
	He	fed	some	students,	fellow
faculty	and	himself	a	plant-based	diet	and	measured	their	physical
performance	tests. He	got	the	same	results	as	our	rats	almost	a	century	later—
and	they	were	equally	spectacular. Then	there	is	the	question	of	our	excessive	dependence	on	drugs	and
surgery	to	control	our	health. In	its	simplest	form,	eating	the	right	way	would
largely	obviate	the	enormous	costs	of	using	drugs,	as	well	as	their	side	effects. Fewer	people	would	need	to	wage	lengthy,	expensive	battles	with	chronic
disease	in	hospitals	over	their	last	years	of	life. Health	care	costs	would	drop
and	medical	mistakes	would	wane	as	premature	death	plummeted. In	essence,
our	health	care	system	would	finally	protect	and	promote	our	health	as	it	is
meant	to	do.SIMPLE	BEGINNINGS
As	I	look	back,	I	often	think	about	life	on	the	farm	and	how	it	shaped	my
thinking	in	so	many	ways. My	family	was	immersed	in	nature	every	waking
moment. In	the	summer,	from	sunrise	to	sunset,	we	were	outdoors	planting
and	harvesting	the	crops	and	taking	care	of	the	animals. My	mother	had	the
best	garden	in	our	part	of	the	country	and	toiled	day	in	and	day	out	during	the
summer	to	keep	our	family	well	fed	with	fresh	food,	all	produced	on	our	own
farm. I’ve	had	an	amazing	journey,	to	be	sure. I	have	been	startled	time	and	time
again	by	what	I	have	learned. I	wish	that	my	family	and	others	around	us	had
had	the	same	information	back	in	the	mid-1900s	that	we	now	have	about	food
and	health. If	we	had,	my	father	could	have	prevented,	or	reversed,	his	heart
disease. He	could	have	met	my	youngest	son,	his	namesake,	who	is
collaborating	with	me	on	this	book. He	might	have	lived	for	several	more
years	with	a	higher	quality	of	health. My	journey	in	science	over	the	past
forty-five	years	has	convinced	me	that	it	is	now	more	urgent	than	ever	to
show	how	people	can	avoid	these	tragedies. The	science	is	there	and	it	must
be	made	known. We	cannot	let	the	status	quo	go	unchallenged	and	watch	our
loved	ones	suffer	unnecessarily. It	is	time	to	stand	up,	clear	the	air	and	take
control	of	our	health.2
A	House	of	Proteins
M
Y	ENTIRE	PROFESSIONAL	CAREER
	in	biomedical	research	has	centered	on
protein. Like	an	invisible	leash,	protein	tethered	me	wherever	I	went,	from	the
basic	research	laboratory	to	the	practical	programs	of	feeding	malnourished
children	in	the	Philippines	to	the	government	board-rooms	where	our	national
health	policy	was	being	formulated. Protein,	often	regarded	with	unsurpassed
awe,	is	the	common	thread	tying	together	past	and	present	knowledge	about
nutrition. The	story	of	protein	is	part	science,	part	culture	and	a	good	dose	of
mythology. I	am	reminded	of	the	words	of	Goethe,	first	brought	to	my
attention	by	my	friend	Howard	Lyman,	a	prominent	lecturer,	author	and
former	cattle	rancher:	“We	are	best	at	hiding	those	things	which	are	in	plain
sight.”	Nothing	has	been	so	well	hidden	as	the	untold	story	of	protein. The
dogma	surrounding	protein	censures,	reproaches	and	guides,	directly	or
indirectly,	almost	every	thought	we	have	in	biomedical	research. Ever	since	the	discovery	of	this	nitrogen-containing	chemical	in	1839	by
the	Dutch	chemist	Gerhard	Mulder,	protein	has	loomed	as	the	most	sacred	of
all	nutrients. The	word	protein	comes	from	the	Greek	word	
proteios,
	which
means	“of	prime	importance.”
In	the	nineteenth	century,	protein	was	synonymous	with	meat,	and	this
connection	has	stayed	with	us	for	well	over	a	hundred	years. Many	people
today	still	equate	protein	with	animal-based	food. If	you	were	to	name	the
first	food	that	comes	to	mind	when	I	say	protein,	you	might	say	beef. If	you
did,	you	aren’t	alone. Confusion	reigns	on	many	of	the	most	basic	questions	about	protein:
What	are	good	sources	of	protein?How	much	protein	should	one	consume? Is	plant	protein	as	good	as	animal	protein? Is	it	necessary	to	combine	certain	plant	foods	in	a	meal	to	get	complete
proteins? Is	it	advisable	to	take	protein	powders	or	amino	acid	supplements,
especially	for	someone	who	does	vigorous	exercise	or	plays	sport? Should	one	take	protein	supplements	to	build	muscle? Some	protein	is	considered	high	quality	some	low	quality;	what	does	this
mean? Where	do	vegetarians	get	protein? Can	vegetarian	children	grow	properly	without	animal	protein? Fundamental	to	many	of	these	common	questions	and	concerns	is	the
belief	that	meat	is	protein	and	protein	is	meat. This	belief	comes	from	the	fact
that	the	“soul”	of	animal-based	foods	is	protein. In	many	meat	and	dairy
products,	we	can	selectively	remove	the	fat	but	we	are	still	left	with
recognizable	meat	and	dairy	products. We	do	this	all	the	time,	with	lean	cuts
of	meat	and	skim	milk. But	if	we	selectively	remove	the	protein	from	animal-
based	foods,	we	are	left	with	nothing	like	the	original. A	non-protein	steak,
for	example,	would	be	a	puddle	of	water,	fat	and	a	small	amount	of	vitamins
and	minerals. Who	would	eat	that? In	brief,	for	a	food	to	be	recognized	as	an
animal-based	food,	it	must	have	protein. Protein	is	the	core	element	of
animal-based	foods. Early	scientists	like	Carl	Voit	(1831-1908),	a	prominent	German	scientist,
were	staunch	champions	of	protein. Voit	found	that	“man”	needed	only	48.5
grams	per	day,	but	nonetheless	he	recommended	a	whopping	118	grams	per
day	because	of	the	cultural	bias	of	the	time. Protein	equaled	meat,	and
everyone	aspired	to	have	meat	on	his	or	her	table,	just	as	we	aspire	to	have
bigger	houses	and	faster	cars. Voit	figured	you	can’t	get	too	much	of	a	good
thing. Voit	went	on	to	mentor	several	well-known	nutrition	researchers	of	the
early	1900s,	including	Max	Rubner	(1854-1932)	and	W.O. Atwater	(1844-
1907). Both	students	closely	followed	the	advice	of	their	teacher. Rubner
stated	that	protein	intake,	meaning	meat,	was	a	symbol	of	civilization	itself:
“a	large	protein	allowance	is	the	right	of	civilized	man.”	Atwater	went	on	to
organize	the	first	nutrition	laboratory	at	the	United	States	Department	of
Agriculture	(USDA). As	director	of	the	USDA,	he	
recommended	125	grams
per	day	(only	about	fifty-five	grams	per	day	is	now	recommended). Later,	we
will	see	how	important	this	early	precedent	was	to	this	government	agency. A	cultural	bias	had	become	firmly	entrenched. If	you	were	civilized,	youate	plenty	of	protein. If	you	were	rich,	you	ate	meat,	and	if	you	were	poor,
you	ate	staple	plant	foods,	like	potatoes	and	bread. The	lower	classes	were
considered	by	some	to	be	lazy	and	inept	as	a	result	of	not	eating	enough	meat,
or	protein. Elitism	and	arrogance	dominated	much	of	the	burgeoning	held	of
nutrition	in	the	nineteenth	century. The	entire	concept	that	bigger	is	better,
more	civilized	and	perhaps	even	more	spiritual	permeated	every	thought
about	protein. Major	McCay	a	prominent	English	physician	in	the	early	twentieth
century,	provided	one	of	the	more	entertaining,	but	most	unfortunate,
moments	in	this	history. Physician	McCay	was	stationed	in	the	English
colony	of	India	in	1912	in	order	to	identify	good	fighting	men	in	the	Indian
tribes. Among	other	things,	he	said	that	people	who	consumed	less	protein
were	of	a	“poor	physique,	and	a	cringing	effeminate	disposition	is	all	that	can
be	expected.”PRESSING	FOR	QUALITY
Protein,	fat,	carbohydrate	and	alcohol	provide	virtually	all	of	the	calories	that
we	consume. Fat,	carbohydrate	and	protein,	as	
macro
nutrients,	make	up
almost	all	the	weight	of	food,	aside	from	water,	with	the	remaining	small
amount	being	the	vitamin	and	mineral	
micro
nutrients. The	amounts	of	these
latter	
micro
nutrients	needed	for	optimum	health	are	tiny	(milligrams	to
micrograms). Protein,	the	most	sacred	of	all	nutrients,	is	a	vital	component	of	our	bodies
and	there	are	hundreds	of	thousands	of	different	kinds. They	function	as
enzymes,	hormones,	structural	tissue	and	transport	molecules,	all	of	which
make	life	possible. Proteins	are	constructed	as	long	chains	of	hundreds	or
thousands	of	amino	acids,	of	which	there	are	fifteen	to	twenty	different	kinds,
depending	on	how	they	are	counted. Proteins	wear	out	on	a	regular	basis	and
must	be	replaced. This	is	accomplished	by	consuming	foods	that	contain
protein. When	digested,	these	proteins	give	us	a	whole	new	supply	of	amino
acid	building	blocks	to	use	in	making	new	protein	replacements	for	those	that
wore	out. Various	food	proteins	are	said	to	be	of	different	quality,	depending
on	how	well	they	provide	the	needed	amino	acids	used	to	replace	our	body
proteins. This	process	of	disassembling	and	reassembling	the	amino	acids	of
proteins	is	like	someone	giving	us	a	multicolored	string	of	beads	to	replace	an
old	string	of	beads	that	we	lost. However,	the	colored	beads	on	the	string
given	to	us	are	not	in	the	same	order	as	the	string	we	lost. So,	we	break	the
string	and	collect	its	beads. Then,	we	reconstruct	our	new	string	so	that	the
colored	beads	are	in	the	same	order	as	our	lost	string. But	if	we	are	short	of
blue	beads,	for	example,	making	our	new	string	is	going	to	be	slowed	down
or	stopped	until	we	get	more	blue	beads. This	is	the	same	concept	as	in
making	new	tissue	proteins	to	match	our	old	worn	out	proteins. About	eight	amino	acids	(“colored	beads”)	that	are	needed	for	making	our
tissue	proteins	must	be	provided	by	the	food	we	eat. They	are	called
“essential”	because	our	bodies	cannot	make	them. If,	like	our	string	of	beads,
our	food	protein	lacks	enough	of	even	one	of	these	eight	“essential”	amino
acids,	then	the	synthesis	of	the	new	proteins	will	be	slowed	down	or	stopped. This	is	where	the	idea	of	protein	quality	comes	into	play. Food	proteins	of	the
highest	quality	are,	very	simply,	those	that	provide,	upon	digestion,	the	right
kinds	and	amounts	of	amino	acids	needed	to	efficiently	synthesize	our	new
tissue	proteins. This	is	what	that	word	“quality”	really	means:	it	is	the	ability
of	food	proteins	to	provide	the	right	kinds	and	amounts	of	amino	acids	to
make	our	new	proteins.Can	you	guess	what	food	we	might	eat	to	most	efficiently	provide	the
building	blocks	for	our	replacement	proteins? The	answer	is	human	flesh. Its
protein	has	just	the	right	amount	of	the	needed	amino	acids. But	while	our
fellow	men	and	women	are	not	for	dinner,	we	do	get	the	next	“best”	protein
by	eating	other	animals. The	proteins	of	other	animals	are	very	similar	to	our
proteins	because	they	mostly	have	the	right	amounts	of	each	of	the	needed
amino	acids. These	proteins	can	be	used	very	efficiently	and	therefore	are
called	“high	quality.”	Among	animal	foods,	the	proteins	of	milk	and	eggs
represent	the	best	amino	acid	matches	for	our	proteins,	and	thus	are
considered	the	highest	quality. While	the	“lower	quality”	plant	proteins	may
be	lacking	in	one	or	more	of	the	essential	amino	acids,	as	a	group	they	
do
contain	all	of	them. The	concept	of	quality	really	means	the	efficiency	with	which	food
proteins	are	used	to	promote	growth. This	would	be	well	and	good	if	the
greatest	efficiency	equaled	the	greatest	health,	but	it	doesn’t,	and	that’s	why
the	terms	efficiency	and	quality	are	misleading. In	fact,	to	give	you	a	taste	of
what’s	to	come,	there	is	a	mountain	of	compelling	research	
showing	that
“low-quality”	plant	protein,	which	allows	for	slow	but	steady	synthesis	of
new	proteins,	is	the	healthiest	type	of	protein. Slow	but	steady	wins	the	race. The	quality	of	protein	found	in	a	specific	food	is	determined	by	seeing	how
fast	animals	would	grow	while	consuming	it. Some	foods,	namely	those	from
animals,	emerge	with	a	very	high	protein	efficiency	ratio	and	value. 1
This	focus	on	efficiency	of	body	growth,	as	if	it	were	good	health,
encourages	the	consumption	of	protein	with	the	highest	“quality.”	As	any
marketer	will	tell	you,	a	product	that	is	defined	as	being	high	quality	instantly
earns	the	trust	of	consumers. For	well	over	100	years,	we	have	been	captive	to
this	misleading	language	and	have	oftentimes	made	the	unfortunate	leap	to
thinking	that	more	quality	equals	more	health. The	basis	for	this	concept	of	protein	quality	was	not	well	known	among
the	public,	but	its	impact	was—and	still	is—highly	significant. People,	for
example,	who	choose	to	consume	a	plant-based	diet	will	often	ask,	even
today,	“Where	do	I	get	my	protein?”	as	if	plants	don’t	have	protein. Even	if	it
is	known	that	plants	have	protein,	there	is	still	the	concern	about	its	perceived
poor	quality. This	has	led	people	to	believe	that	they	must	meticulously
combine	proteins	from	different	plant	sources	during	each	meal	so	that	they
can	mutually	compensate	for	each	other’s	amino	acid	deficits. However,	this
is	overstating	the	case. We	now	know	that	through	enormously	complex
metabolic	systems,	the	human	body	can	derive	all	the	essential	amino	acids
from	the	natural	variety	of	plant	proteins	that	we	encounter	every	day. It
doesn’t	require	eating	higher	quantities	of	plant	protein	or	meticulouslyplanning	every	meal. Unfortunately,	the	enduring	concept	of	protein	quality
has	greatly	obscured	this	information.THE	PROTEIN	GAP
The	most	important	issue	in	nutrition	and	agriculture	during	my	early	career
was	figuring	out	ways	to	increase	the	consumption	of	protein,	making	sure	it
was	of	the	highest	possible	quality. My	colleagues	and	I	all	believed	in	this
common	goal. From	my	early	years	on	the	farm	to	my	graduate	education,	I
accepted	this	virtual	reverence	for	protein. As	a	youngster,	I	remember	that
the	most	expensive	part	of	farm	animal	feed	was	the	protein	supplements	that
we	fed	to	our	cows	and	pigs. Then,	at	graduate	school,	I	spent	three	years
(1958-1961)	doing	my	Ph.D.	research	trying	to	improve	the	supply	of	high-
quality	protein	by	growing	cows	and	sheep	more	efficiently	so	we	could	eat
more	of	them. 2,	3
I	went	all	the	way	through	my	graduate	studies	with	a	profound	belief	that
promoting	high-quality	protein,	as	in	animal-based	foods,	was	a	very
important	task. My	graduate	research,	although	cited	a	few	times	over	the
next	decade	or	so,	was	only	a	small	part	of	much	larger	efforts	by	other
research	groups	to	address	a	protein	situation	worldwide. During	the	1960s
and	1970s,	I	was	to	hear	over	and	over	again	about	a	so-called	“protein	gap”
in	the	developing	world. 4
The	protein	gap	stipulated	that	world	hunger	and	malnutrition	among
children	in	the	third	world	was	a	result	of	not	having	enough	protein	to
consume,	especially	high-quality	(i.e. animal)	protein. 1,	4,	5
	According	to	this
view,	those	in	the	third	world	were	especially	deficient	in	“high-quality”
protein,	or	animal	protein. Projects	were	springing	up	all	over	the	place	to
address	this	“protein	gap”	problem. A	prominent	MIT	professor	and	his
younger	colleague	concluded	in	1976	that	“an	adequate	supply	of	protein	is	a
central	aspect	of	the	world	food	problem“
5
	and	further	that	“unless…
desirably	[supplemented]	by	modest	amounts	of	milk,	eggs,	meat	or	fish,	the
predominantly	cereal	diets	[of	poor	nations]	are…	deficient	in	protein	for
growing	children	….”	To	address	this	dire	problem:
MIT	was	developing	a	protein-rich	food	supplement	called	INCA-
PARINA. Purdue	University	was	breeding	corn	to	contain	more	lysine,	the
“deficient”	amino	acid	in	corn	protein. The	U.S.	government	was	subsidizing	the	production	of	dried	milk
powder	to	provide	high-quality	protein	for	the	world’s	poor. Cornell	University	was	providing	a	wealth	of	talent	to	the	Philippines	to
help	develop	both	a	high-protein	rice	variety	and	a	livestock	industry. Auburn	University	and	MIT	were	grinding	up	fish	to	produce	“fishprotein	concentrate”	to	feed	the	world’s	poor. The	United	Nations,	the	U.S.	Government	Food	for	Peace	Program,	major
universities	and	countless	other	organizations	and	universities	were	taking	up
the	battle	cry	to	eradicate	world	hunger	with	high-quality	protein. I	knew
most	of	the	projects	firsthand,	as	well	as	the	individuals	who	organized	and
directed	them. The	Food	and	Agriculture	Organization	(FAO)	of	the	United	Nations
exerts	considerable	influence	in	developing	countries	through	their	agriculture
development	programs. Two	of	its	staffers
6
	declared	in	1970	
that	“…by	and
large,	the	lack	of	protein	is	without	question	the	most	serious	qualitative
deficiency	in	the	nutrition	of	developing	countries. The	great	mass	of	the
population	of	these	countries	subsists	mainly	on	foods	derived	from	plants
frequently	deficient	in	protein,	which	results	in	poor	health	and	low
productivity	per	man.”	M.	Autret,	a	very	influential	man	from	the	FAO,	added
that	“owing	to	the	low-animal	protein	content	of	the	diet	and	lack	of	diversity
of	supplies	[in	developing	countries],	protein	quality	is	unsatisfactory.”
4
	He
reported	on	a	very	strong	association	between	consumption	of	animal-based
foods	and	annual	income. Autret	strongly	advocated	increasing	the	production
and	consumption	of	animal	protein	in	order	to	meet	the	growing	“protein	gap”
in	the	world. He	also	advocated	that	“all	resources	of	science	and	technology
must	be	mobilized	to	create	new	protein-rich	foods	or	to	derive	the	utmost
benefits	from	hitherto	insufficiently	utilized	resources	to	feed	mankind.”
4
Bruce	Stillings	at	the	University	of	Maryland	and	the	U.S.	Department	of
Commerce,	another	proponent	of	consuming	animal-based	diets,	admitted	in
1973	that	“although	there	is	no	requirement	for	animal	protein	in	the	diet	
per
se,
	the	quantity	of	dietary	protein	from	animal	sources	is	usually	accepted	as
being	indicative	of	the	overall	protein	quality	of	the	diet.”
1
	He	went	on	to	say
that	the	“…	supply	of	adequate	quantities	of	animal	products	is	generally
recognized	as	being	an	ideal	way	to	improve	world	protein	nutrition.”
Of	course,	it’s	quite	correct	that	a	supply	of	protein	can	be	an	important
way	of	improving	nutrition	in	the	third	world,	particularly	if	populations	are
getting	all	of	their	calories	from	one	plant	source. But	it’s	not	the	only	way,
and,	as	we	shall	see,	it	isn’t	necessarily	the	way	most	consistent	with	long-
term	health.FEEDING	THE	CHILDREN
So	this	was	the	climate	at	that	time,	and	I	was	a	part	of	it	as	much	as	anyone
else. I	left	MIT	to	take	a	faculty	position	at	Virginia	Tech	in	1965. Professor
Charlie	Engel,	who	was	then	the	head	of	the	Department	of	Biochemistry	and
Nutrition	at	Virginia	Tech,	had	considerable	interest	in	developing	an
international	nutrition	program	for	malnourished	children. He	was	interested
in	implementing	a	“mothercraft”	self-help	project	in	the	Philippines. This
project	was	called	“mothercraft”	because	it	focused	on	educating	mothers	of
malnourished	children. The	idea	was	that	if	mothers	were	taught	that	the	right
kinds	of	locally	grown	foods	can	
make	their	children	well,	they	would	not
have	to	rely	on	scarce	medicines	and	the	mostly	nonexistent	doctors. Engel
started	the	program	in	1967	and	invited	me	to	be	his	Campus	Coordinator	and
to	come	for	extended	stays	in	the	Philippines	while	he	resided	full	time	in
Manila. Consistent	with	the	emphasis	on	protein	as	a	means	of	solving
malnutrition,	we	had	to	make	this	nutrient	the	centerpiece	of	our	educational
“mothercraft”	centers	and	thereby	help	to	increase	protein	consumption. Fish
as	a	source	of	protein	was	mostly	limited	to	the	seacoast	areas. Our	own
preference	was	to	develop	peanuts	as	a	source	of	protein	because	this	was	a
crop	that	could	be	grown	most	anywhere. The	peanut	is	a	legume,	like	alfalfa,
soybeans,	clover,	peas	and	other	beans. Like	these	other	nitrogen	“fixers,”
peanuts	are	rich	in	protein. There	was,	however,	a	nagging	problem	with	these	tasty	legumes. Considerable	evidence	had	been	emerging,	first	from	England
7–9
	and	later
from	MIT	(the	same	lab	that	I	had	worked	in)
10,	11
	to	show	that	peanuts	often
were	contaminated	with	a	fungus-produced	toxin	called	aflatoxin	(AF). It	was
an	alarming	problem	because	AF	was	being	shown	to	cause	liver	cancer	in
rats. It	was	said	to	be	the	most	potent	chemical	carcinogen	ever	discovered. So	we	had	to	tackle	two	closely	related	projects:	alleviate	childhood
malnutrition	and	resolve	the	AF	contamination	problem. Prior	to	going	to	the	Philippines,	I	had	traveled	to	Haiti	in	order	to	observe
a	few	experimental	mothercraft	centers	organized	by	my	colleagues	at
Virginia	Tech,	Professors	Ken	King	and	Ryland	Webb. It	was	my	first	trip	to
an	underdeveloped	country,	and	Haiti	certainly	fit	the	bill. Papa	Doc	Duvalier,
president	of	Haiti,	extracted	what	little	resources	the	country	had	for	his	own
rich	lifestyle. In	Haiti	at	that	time	54%	of	the	children	were	dead	before
reaching	their	fifth	birthday,	largely	because	of	malnutrition. I	subsequently	went	to	the	Philippines	and	encountered	more	of	the	same. We	decided	where	mothercraft	centers	were	to	be	located	based	on	how	muchmalnutrition	was	present	in	each	village. We	focused	our	efforts	on	the
villages	in	most	need. In	a	preliminary	survey	in	each	village	(barrio),
children	were	weighed	and	their	weight	for	age	was	compared	with	a	Western
reference	standard,	which	was	subdivided	into	first,	second	and	third	degree
malnutrition. Third	degree	malnutrition,	the	worst	kind,	represented	children
under	the	65
th
	percentile. Keep	in	mind	that	a	child	at	the	100
th
	percentile
represents	only	the	average	for	the	U.S. Being	less	than	the	65
th
	percentile
means	near	starvation. In	the	urban	areas	of	some	of	the	big	cities,	as	many	as	15-20%	of	the
children	aged	three	to	six	years	were	judged	to	be	third	degree. I	can	so	well
remember	some	of	my	initial	observations	of	these	children. A	mother,	hardly
more	than	a	wisp	herself,	holding	her	three-year-old	twins	with	bulging	eyes,
one	at	eleven	pounds,	the	other	at	fourteen	pounds,	trying	to	get	them	to	open
their	mouths	to	eat	some	porridge. Older	children	blind	from	malnutrition,
being	led	around	by	their	younger	siblings	to	seek	a	handout. Children
without	legs	or	arms	hoping	to	get	a	morsel	of	food.A	REVELATION	TO	DIE	FOR
Needless	to	say,	those	sights	gave	us	ample	motivation	to	press	ahead	with
our	project. As	I	mentioned	before,	we	first	had	to	resolve	the	problem	of	AF
contamination	in	peanuts,	our	preferred	protein	food. The	first	step	of	investigating	AF	was	to	gather	some	basic	information. Who	in	the	Philippines	was	consuming	AF,	and	who	was	subject	to	liver
cancer? To	answer	these	questions,	I	applied	for	and	received	a	National
Institutes	of	Health	(NIH)	research	grant. We	also	adopted	a	second	strategy
by	asking	another	question:	how	does	AF	actually	affect	liver	cancer? We
wanted	to	study	this	question	at	the	molecular	level	using	laboratory	rats. I
succeeded	in	getting	a	second	NIH	grant	for	this	in-depth	biochemical
research. These	two	grants	initiated	a	two-track	research	investigation,	one
basic	and	one	applied,	which	was	to	continue	for	the	rest	of	my	career. I	found
studying	questions	both	from	the	basic	and	applied	perspectives	rewarding
because	it	tells	us	not	only	the	impact	of	a	food	or	chemical	on	health,	but
also	why	it	has	that	impact. In	so	doing,	we	could	better	understand	not	only
the	biochemical	foundation	of	food	and	health,	but	also	how	it	might	relate	to
people	in	everyday	life. We	began	with	a	stepwise	series	of	surveys. First,	we	wanted	to	know
which	foods	contained	the	most	AF	We	learned	that	peanuts	and	corn	were
the	foods	most	contaminated. All	twenty-nine	jars	of	peanut	butter	we	had
purchased	in	the	local	groceries,	for	example,	were	contaminated,	with	levels
of	AF	as	much	as	300	times	the	amount	judged	to	be	acceptable	in	U.S.	food. Whole	peanuts	were	much	less	contaminated;	none	exceeded	the	AF	amounts
allowed	in	U.S.	commodities. This	disparity	between	peanut	butter	and	whole
peanuts	originated	at	the	peanut	factory. The	best	peanuts,	which	filled
“cocktail”	jars,	were	hand	selected	from	a	moving	conveyor	belt,	leaving	the
worst,	moldiest	nuts	to	be	delivered	to	the	end	of	the	belt	to	make	peanut
butter. Our	second	question	concerned	who	was	most	susceptible	to	this	AF
contamination	and	its	cancer-producing	effects. We	learned	that	it	was
children. They	were	the	ones	consuming	the	AF-laced	peanut	butter. We
estimated	AF	consumption	by	analyzing	the	excretion	of	AF	metabolic
products	in	the	urine	of	children	living	in	homes	with	a	partially	consumed
peanut	butter	jar. 12
	As	we	gathered	this	information	an	interesting	pattern
emerged:	the	two	areas	of	the	country	with	the	highest	rates	of	liver	cancer,
the	cities	of	Manila	and	Cebu,	also	were	the	same	areas	where	the	most	AF
was	being	consumed. Peanut	butter	was	almost	exclusively	consumed	in	the
Manila	area	while	corn	was	consumed	in	Cebu,	the	second	most	populatedcity	in	the	Philippines. But,	as	it	turned	out,	there	was	more	to	this	story. It	emerged	from	my
making	the	acquaintance	of	a	prominent	doctor,	Dr.	Jose	Caedo,	who	was	an
advisor	to	President	Marcos. He	told	me	that	the	liver	cancer	problem	in	the
Philippines	was	quite	serious. What	was	so	devastating	was	that	the	disease
was	claiming	the	lives	of	children	before	the	age	of	ten. Whereas	in	the	West,
this	disease	mostly	strikes	people	only	after	forty	years	of	age,	Caedo	told	me
that	he	had	personally	operated	on	children	younger	than	four	years	of	age	for
liver	cancer! That	alone	was	incredible,	but	what	he	then	told	me	was	even	more
striking. Namely,	the	children	who	got	liver	cancer	were	from	the	best-fed
families. The	families	with	the	most	money	ate	what	we	thought	were	the
healthiest	diets,	the	diets	most	like	our	own	meaty	American	diets. They
consumed	more	protein	than	anyone	else	in	the	country	(high	quality	animal
protein,	at	that),	and	yet	they	were	the	ones	getting	liver	cancer! How	could	this	be? Worldwide,	liver	cancer	rates	were	highest	in	countries
with	the	lowest	average	protein	intake. It	was	therefore	widely	believed	that
this	cancer	was	the	result	of	a	deficiency	in	protein. Further,	the	deficiency
problem	was	a	major	reason	we	were	working	in	the	Philippines:	to	increase
the	consumption	of	protein	by	as	many	malnourished	children	as	possible. But	now	Dr.	Caedo	and	his	colleagues	were	telling	me	that	the	most	protein-
rich	children	had	the	highest	rates	of	liver	cancer. This	seemed	strange	to	me,
at	first,	but	over	time	my	own	information	increasingly	confirmed	their
observations. At	that	time,	a	research	paper	from	India	surfaced	in	an	obscure	medical
journal. 13
	It	was	an	experiment	involving	liver	cancer	and	protein
consumption	in	two	groups	of	laboratory	rats. One	group	was	given	AF	and
then	fed	diets	containing	20%	protein. The	second	group	was	given	the	same
level	of	AF	and	then	fed	diets	containing	only	5%	protein. Every	single	rat
fed	20%	protein	got	liver	cancer	or	its	precursor	lesions,	but	not	a	single
animal	fed	a	5%	protein	diet	got	liver	cancer	or	its	precursor	lesions. It	was
not	a	trivial	difference;	it	was	100%	versus	0%. This	was	very	much
consistent	with	my	observations	for	the	Philippine	children. Those	who	were
most	vulnerable	to	liver	cancer	were	those	who	consumed	diets	higher	in
protein. No	one	seemed	to	accept	the	report	from	India. On	a	flight	from	Detroit
after	returning	from	a	presentation	at	a	conference,	I	traveled	with	a	former
but	much	senior	colleague	of	mine	from	MIT,	Professor	Paul	Newberne. At
the	time,	Newberne	was	one	of	the	only	people	who	had	given	much	thought
to	the	role	of	nutrition	in	the	development	of	cancer. I	told	him	about	myimpressions	in	the	Philippines	and	the	paper	from	India. He	summarily
dismissed	the	paper	by	saying,	“They	must	have	gotten	the	numbers	on	the
animal	cages	reversed. In	no	way	could	a	high-protein	diet	increase	the
development	of	cancer.”
I	realized	that	I	had	encountered	a	provocative	idea	that	stimulated
disbelief,	even	the	ire	of	fellow	colleagues. Should	I	take	seriously	the
observation	that	protein	increased	cancer	development	and	run	the	risk	of
being	thought	a	fool? Or	should	I	turn	my	back	on	this	story? In	some	ways	it	seemed	that	this	moment	in	my	career	had	been
foreshadowed	by	events	in	my	personal	life. When	I	was	five	years	old,	my
aunt	who	was	living	with	us	was	dying	of	cancer. On	several	occasions	my
uncle	took	my	brother	Jack	and	me	to	see	his	wife	in	the	hospital. Although	I
was	too	young	to	understand	everything	that	was	happening,	I	do	remember
being	struck	by	the	big	“C”	word:	cancer. I	would	think,	“When	I	get	big,	I
want	to	find	a	cure	for	cancer.”
Many	years	later,	just	a	few	years	after	getting	married,	at	about	the	time
when	I	was	starting	my	work	in	the	Philippines,	my	wife’s	mother	was	dying
of	colon	cancer	at	the	young	age	of	fifty-one. At	that	time,	I	was	becoming
aware	of	a	possible	diet-cancer	connection	in	our	early	research. Her	case	was
particularly	difficult	because	she	did	not	receive	appropriate	medical	care	due
to	the	fact	that	she	did	not	have	health	insurance. My	wife	Karen	was	her	only
daughter	and	they	had	a	very	close	relationship. These	difficult	experiences
were	making	my	career	choice	easy:	I	would	go	wherever	our	research	led	me
to	help	get	a	better	understanding	of	this	horrific	disease. Looking	back	on	it,	this	was	the	beginning	of	my	career	focus	on	diet	and
cancer. The	moment	of	deciding	to	investigate	protein	and	cancer	was	the
turning	point. If	I	wanted	to	stay	with	this	story,	there	was	only	
one	solution:
start	doing	fundamental	laboratory	research	to	see	not	only	if,	but	also	how,
consuming	more	protein	leads	to	more	cancer. That’s	exactly	what	I	did. It
took	me	farther	than	I	had	ever	imagined. The	extraordinary	findings	my
colleagues,	students	and	I	generated	just	might	make	you	think	twice	about
your	current	diet. But	even	more	than	that,	the	findings	led	to	broader
questions,	questions	that	would	eventually	lead	to	cracks	in	the	very
foundations	of	nutrition	and	health.THE	NATURE	OF	SCIENCE—WHAT	YOU	NEED
TO	KNOW	TO	FOLLOW	THE	RESEARCH
Proof	in	science	is	elusive. Even	more	than	in	the	“core”	sciences	of	biology,
chemistry	and	physics,	establishing	
absolute
	proof	in	medicine	and	health	is
nearly	impossible. The	primary	objective	of	research	investigation	is	to
determine	only	what	is	
likely
	to	be	true. This	is	because	research	into	health	is
inherently	statistical. When	you	throw	a	ball	in	the	air,	will	it	come	down? Yes,	every	time. That’s	physics. If	you	smoke	four	packs	a	day,	will	you	get
lung	cancer? The	answer	is	maybe. We	know	that	your	odds	of	getting	lung
cancer	are	much	higher	than	if	you	didn’t	smoke,	and	we	can	tell	you	what
those	odds	(statistics)	are,	but	we	can’t	know	with	certainty	whether	you	as	an
individual	will	get	lung	cancer. In	nutrition	research,	untangling	the	relationship	between	diet	and	health	is
not	so	straightforward. Humans	live	all	sorts	of	different	ways,	have	different
genetic	backgrounds	and	eat	all	sorts	of	different	foods. Experimental
limitations	such	as	cost	restraints,	time	constraints	and	measurement	error	are
significant	obstacles. Perhaps	most	importantly,	food,	lifestyle	and	health
interact	through	such	complex,	multifaceted	systems	that	establishing	proof
for	any	one	factor	and	any	one	disease	is	nearly	impossible,	even	if	you	had
the	perfect	set	of	subjects,	unlimited	time	and	unlimited	financial	resources. Because	of	these	difficulties,	we	do	research	using	many	different
strategies. In	some	cases,	we	assess	whether	a	hypothetical	cause	produces	a
hypothetical	effect	by	
observing
	and	measuring	the	differences	that	already
exist	between	different	groups	of	people. We	might	
observe
	and	compare
societies	who	consume	different	amounts	of	fat,	then	
observe
	whether	these
differences	correspond	to	similar	differences	in	the	rates	of	breast	cancer	or
osteoporosis	or	some	other	disease	condition. We	might	
observe
	and	compare
the	dietary	characteristics	of	people	who	already	have	the	disease	with	a
comparable	group	of	people	who	don’t	have	the	disease. We	might	
observe
and	compare	disease	rates	in	1950	
with	disease	rates	in	1990,	then	
observe
whether	any	changes	in	disease	rates	correspond	to	dietary	changes. In	addition	to	
observing
	what	already	exists,	we	might	do	an	experiment
and	intentionally	
intervene
	with	a	hypothetical	treatment	to	see	what	happens. We	intervene,	for	example,	when	testing	lor	the	safety	and	efficacy	of	drugs. One	group	of	people	is	given	the	drug	and	a	second	group	a	placebo	(an
inactive	look-alike	substance	to	please	the	patient). Intervening
	with	diet,
however,	is	far	more	difficult,	especially	if	people	aren’t	confined	to	a	clinical
setting,	because	then	we	must	rely	on	everyone	to	faithfully	use	the	specifieddiets. As	we	do	
observational	and	interventional
	research,	we	begin	to	amass
the	findings	and	weigh	the	evidence	for	or	against	a	certain	hypothesis. When
the	weight	of	the	evidence	favors	an	idea	so	strongly	that	it	can	no	longer	be
plausibly	denied,	we	advance	the	idea	as	a	likely	truth. It	is	in	this	way	that	I
am	advancing	an	argument	for	a	whole	foods,	plant-based	diet. As	you
continue	reading,	realize	that	those	seeking	absolute	proof	of	optimal	nutrition
in	one	or	two	studies	will	be	disappointed	and	confused. However,	I	am
confident	that	those	seeking	the	truth	regarding	diet	and	health	by	surveying
the	weight	of	the	evidence	from	the	variety	of	available	studies	will	be
amazed	and	enlightened. There	are	several	ideas	to	keep	in	mind	when
determining	the	weight	of	the	evidence,	including	the	following	ideas.CORRELATION	VERSUS	CAUSATION
In	many	studies,	you	will	find	that	the	words	correlation	and	association	are
used	to	describe	a	relationship	between	two	factors,	perhaps	even	indicating	a
cause-and-effect	relationship. This	idea	is	featured	prominently	in	the	China
Study. We	observed	whether	there	were	patterns	of	associations	for	different
dietary,	lifestyle	and	disease	characteristics	within	the	survey	of	65	counties,
130	villages	and	6,500	adults	and	their	families. If	protein	consumption,	for
example,	is	higher	among	populations	that	have	a	
high
	incidence	of	liver
cancer,	we	can	say	that	protein	is	
positively
	correlated	or	associated	with	liver
cancer	incidence;	as	one	goes	up,	the	other	goes	up. If	protein	intake	is	higher
among	populations	that	have	a	
low
	incidence	of	liver	cancer,	we	can	say	that
protein	is	
inversely
	associated	with	liver	cancer	incidence. In	other	words,	the
two	factors	go	in	the	opposite	direction;	as	one	goes	up,	the	other	goes	down. In	our	hypothetical	example,	if	protein	is	correlated	with	liver	cancer
incidence,	this	does	not	prove	that	protein	causes	or	prevents	liver	
cancer. A
classic	illustration	of	this	difficulty	is	that	countries	with	more	telephone
poles	often	have	a	higher	incidence	of	heart	disease,	and	many	other	diseases. Therefore,	telephone	poles	and	heart	disease	are	positively	correlated. But	this
does	not	prove	that	telephone	poles	cause	heart	disease. In	effect,	correlation
does	not	equal	causation. This	does	not	mean	that	correlations	are	useless. When	they	are	properly
interpreted,	correlations	can	be	effectively	used	to	study	nutrition	and	health
relationships. The	China	Study,	for	example,	has	over	8,000	statistically
significant	correlations,	and	this	is	of	immense	value. When	so	many
correlations	like	this	are	available,	researchers	can	begin	to	identify	patterns
of	relationships	between	diet,	lifestyle	and	disease. These	patterns,	in	turn,	are
representative	of	how	diet	and	health	processes,	which	are	unusually
complex,	truly	operate. However,	if	someone	wants	proof	that	a	single	factor
causes	a	single	outcome,	a	correlation	is	not	good	enough.STATISTICAL	SIGNIFICANCE
You	might	think	that	deciding	whether	or	not	two	factors	are	correlated	is
obvious—either	they	are	or	they	aren’t. But	that	isn’t	the	case. When	you	are
looking	at	a	large	quantity	of	data,	you	have	to	undertake	a	statistical	analysis
to	determine	if	two	factors	are	correlated. The	answer	isn’t	yes	or	no. It’s	a
probability,	which	we	call	
statistical	significance. Statistical	significance	is	a
measure	of	whether	an	observed	experimental	effect	is	truly	reliable	or
whether	it	is	merely	due	to	the	play	of	chance. If	you	flip	a	coin	three	times
and	it	lands	on	heads	each	time,	it’s	probably	chance. If	you	flip	it	a	hundred
times	and	it	lands	on	heads	each	time,	you	can	be	pretty	sure	the	coin	has
heads	on	both	sides. That’s	the	concept	behind	
statistical	significance
—it’s
the	odds	that	the	correlation	(or	other	finding)	is	real,	that	it	isn’t	just	random
chance. A	finding	is	said	to	be	statistically	significant	when	there	is	less	than	5%
probability	that	it	is	due	to	chance. This	means,	for	example,	that	there	is	a
95%	chance	that	we	will	get	the	same	result	if	the	study	is	repeated. This	95%
cutoff	point	is	arbitrary,	but	it	is	the	standard,	nonetheless. Another	arbitrary
cutoff	point	is	99%. In	this	case,	when	the	result	meets	this	test,	it	is	said	to	be
highly	statistically	significant. In	the	discussions	of	diet	and	disease	research
in	this	book,	statistical	significance	pops	up	from	time	to	time,	and	it	can	be
used	to	help	judge	the	reliability,	or	“weight,”	of	the	evidence.MECHANISMS	OF	ACTION
Oftentimes	correlations	are	considered	more	reliable	if	other	research	shows
that	two	correlated	factors	are	biologically	related. For	example,	telephone
poles	and	heart	disease	are	positively	correlated,	but	there	is	no	research	that
shows	how	telephone	poles	are	biologically	related	to	heart	disease. However,
there	is	research	that	shows	the	processes	by	which	protein	intake	and	liver
cancer	might	be	biologically	and	causally	related	(as	you	will	see	in	chapter
three). Knowing	the	process	by	which	something	works	in	the	body	means
knowing	its	“mechanism	of	action.”	And	knowing	its	mechanism	of	action
strengthens	the	evidence. Another	way	of	saying	this	is	that	the	two	correlated
factors	are	related	in	a	“biologically	plausible”	way. If	a	relationship	is
biologically	plausible,	it	is	considered	much	more	reliable.METANALYSIS
Finally,	we	should	understand	the	concept	of	a	metanalysis. A	metanalysis
tabulates	the	combined	data	from	multiple	studies	and	analyzes	them	as	one
data	set. By	accumulating	and	analyzing	a	large	body	of	combined	data,	the
result	can	have	considerably	more	weight. Metanalysis	findings	are	therefore
more	substantial	than	the	findings	of	single	research	studies,	although,	as	with
everything	else,	there	may	be	exceptions. After	obtaining	the	results	from	a	variety	of	studies,	we	can	then	begin	to
use	these	tools	and	concepts	to	assess	the	weight	of	the	evidence. Through
this	effort,	we	can	begin	to	understand	what	is	most	likely	to	be	true,	and	we
can	behave	accordingly. Alternative	hypotheses	no	longer	seem	plausible,	and
we	can	be	very	confident	in	the	result. Absolute	proof,	in	the	technical	sense,
is	unattainable	and	unimportant. But	common	sense	proof	(99%	certainty)	is
attainable	and	critical. For	example,	it	was	through	this	process	of	interpreting
research	that	we	formed	our	beliefs	regarding	smoking	and	health. Smoking
has	never	been	“100%”	proven	to	cause	lung	cancer,	but	the	odds	that
smoking	is	unrelated	to	lung	cancer	are	so	astronomically	low	that	the	matter
has	long	been	considered	settled.3
Turning	Off	Cancer
A
MERICANS	DREAD	CANCER
	more	than	any	other	disease. Slowly	and	painfully
being	consumed	by	cancer	for	months,	even	years,	before	passing	away	is	a
terrifying	prospect. This	is	why	cancer	is	perhaps	the	most	feared	of	the	major
diseases. So	when	the	media	reports	a	newly	found	chemical	carcinogen,	the	public
takes	notice	and	reacts	quickly. Some	carcinogens	cause	outright	panic. Such
was	the	case	a	few	years	ago	with	Alar,	a	chemical	that	was	routinely	sprayed
on	apples	as	a	growth	regulator. Shortly	after	a	report	from	the	Natural
Resources	Defense	Council	(NRDC)	titled	“Intolerable	Risk:	Pesticides	in
Our	Children’s	Food,”
1
	the	television	program	
60	Minutes
	aired	a	segment	on
Alar. In	February	1989	a	representative	of	NRDC	said	on	CBS’s	
60	Minutes
that	the	apple	industry	chemical	was	“the	most	potent	carcinogen	in	the	food
supply.”
2,	3
The	public	reaction	was	swift. One	woman	called	state	police	to	chase
down	a	school	bus	to	confiscate	her	child’s	apple. 4
	School	systems	across	the
country,	in	New	York,	Los	Angeles,	Atlanta	and	Chicago,	among	others,
stopped	serving	apples	and	apple	products. According	to	John	Rice,	former
chairman	of	the	U.S.	Apple	Association,	the	apple	industry	took	an	economic
walloping,	losing	over	$250	million. 5
	Finally,	in	response	to	the	public	outcry,
the	production	and	use	of	Alar	came	to	a	halt	in	June	of	1989. 3
The	Alar	story	is	not	uncommon. Over	the	past	several	decades,	several
chemicals	have	been	identified	in	the	popular	press	as	cancer-causing	agents. You	may	have	heard	of	some:
Aminotriazole	(herbicide	used	on	cranberry	crops,	causing	the“cranberry	scare’”	of	1959)
DDT	(widely	known	after	Rachel	Carson’s	book,	
Silent	Spring)
Nitrites	(a	meat	preservative	and	color	and	flavor	enhancer	used	in	hot
dogs	and	bacon)
Red	Dye	Number	2
Artificial	sweeteners	(including	cyclamates	and	saccharin)
Dioxin	(a	contaminant	of	industrial	processes	and	of	Agent	Orange,	a
defoliant	used	during	the	Vietnam	War)
Aflatoxin	(a	fungal	toxin	found	on	moldy	peanuts	and	corn)
I	know	these	unsavory	chemicals	quite	well. I	was	a	member	of	the
National	Academy	of	Sciences	Expert	Panel	on	Saccharin	and	Food	Safety
Policy	(1978–79),	which	was	charged	with	evaluating	the	potential	danger	of
saccharin	at	a	time	when	the	public	was	up	in	arms	after	the	FDA	proposed
banning	the	artificial	sweetener. I	was	one	of	the	first	scientists	to	isolate
dioxin;	I	have	firsthand	knowledge	of	the	MIT	lab	that	did	the	key	work	on
nitrites,	and	I	spent	many	years	researching	and	publishing	on	aflatoxin,	one
of	the	most	carcinogenic	chemicals	ever	discovered—at	least	for	rats. But	while	these	chemicals	are	significantly	different	in	their	properties,
they	all	have	a	similar	story	with	regard	to	cancer. In	each	and	every	case,
research	has	demonstrated	that	these	chemicals	may	increase	cancer	rates	in
experimental	animals. The	case	of	nitrites	serves	as	an	excellent	example.THE	HOT	DOG	MISSILE
If	you	hazard	to	call	yourself	“middle-aged”	or	older,	when	I	say,	“Nitrites,
hot	dogs	and	cancer,”	you	might	rock	back	in	your	chair,	nod	your	head,	and
say,	“Oh	yeah,	I	remember	something	about	that.”	For	the	younger	folks—
well,	listen	up,	because	history	has	a	funny	way	of	repeating	itself. The	time:	the	early	1970s. The	scene:	the	Vietnam	War	was	beginning	to
wind	down,	Richard	Nixon	was	about	to	be	forever	linked	to	Watergate,	the
energy	crisis	was	about	to	create	lines	at	gas	stations	and	nitrite	was	becoming
a	headline	word. Sodium	Nitrite:
	A	meat	preservative	used	since	the	1920s. 6
	It	kills
bacteria	and	adds	a	happy	pink	color	and	desirable	taste	to	hot	dogs,
bacon	and	canned	meat. In	1970,	the	journal	
Nature
	reported	that	the	nitrite	we	consume	may	be
reacting	in	our	bodies	to	form	nitrosamines. 7
Nitrosamines:
	A	scary	family	of	chemicals. No	fewer	than	seventeen
nitrosamines	are	“reasonably	anticipated	to	be	human	carcinogens”	by
the	U.S.	National	Toxicology	Program. 8
Hold	on	a	second. Why	are	these	scary	nitrosamines	“anticipated	to	be
human	carcinogens”? The	short	answer:	animal	experiments	have	shown	that
as	chemical	exposure	increases,	incidence	of	cancer	also	increases. But	that’s
not	adequate. We	need	a	more	complete	answer. Let’s	look	at	one	nitrosamine,	NSAR	(N-nitrososarcosine). In	one	study,
twenty	rats	were	divided	into	two	groups,	each	exposed	to	a	different	level	of
NSAR. The	high-dose	rats	were	given	twice	the	amount	that	the	low-dose	rats
received. Of	rats	given	the	lower	level	of	NSAR,	just	over	35%	of	them	died
from	throat	cancer. Of	rats	given	the	higher	levels,	100%	died	of	cancer
during	the	second	year	of	the	experiment. 9–11
How	much	NSAR	did	the	rats	get? Both	groups	of	rats	were	given	an
incredible	amount. Let	me	translate	the	“low”	dose	by	giving	you	a	little
scenario. Let’s	say	you	go	over	to	your	friend’s	house	to	eat	every	meal. This
friend	is	sick	of	you	and	wants	to	give	you	throat	cancer	by	exposing	you	to
NSAR. So	he	gives	you	the	equivalent	of	the	“low”	level	given	to	the	rats. You	go	to	his	house,	and	your	friend	offers	you	a	bologna	sandwich	that	has	a
whole	pound	of	bologna	on	it! You	eat	it. He	offers	you	another,	and	another,
and	another	…. You’ll	have	to	eat	270,000	bologna	sandwiches	before	yourfriend	lets	you	leave. 9,	12
	You	better	like	bologna,	because	your	friend	is	going
to	have	to	feed	you	this	way	every	day	for	over	thirty	years! If	he	does	this,
you	will	have	had	about	as	much	exposure	to	NSAR	(per	body	weight)	as	the
rats	in	the	“low”-dose	group. Because	higher	cancer	rates	were	also	seen	in	mice	as	well	as	rats,	using	a
variety	of	methods	of	exposure,	NSAR	is	“reasonably	anticipated”	to	be	a
human	carcinogen. Although	no	human	studies	were	used	to	make	this
evaluation,	it	is	likely	that	a	chemical	such	as	this,	which	consistently	causes
cancer	in	both	mice	and	rats,	can	cause	cancer	in	humans	at	some	level. It	is
impossible	to	know,	however,	what	this	level	of	exposure	might	be,	especially
because	the	animal	dosages	are	so	astronomical. Nonetheless,	animal
experiments	alone	are	considered	enough	to	conclude	that	NSAR	is
“reasonably	anticipated”	to	be	a	human	carcinogen. 9
So,	in	1970,	when	an	article	in	the	prestigious	journal	
Nature
	concluded
that	nitrites	help	to	form	nitrosamines	in	the	body,	thereby	implying	that	they
help	to	cause	cancer,	people	became	alarmed. Here	was	the	official	line:
“Reduction	of	human	exposure	to	nitrites	and	certain	secondary	amines,
particularly	in	foods,	may	result	in	a	decrease	in	the	incidence	of	human
cancer.”
7
	Suddenly	nitrites	became	a	potential	killer. Because	we	humans	get
exposed	to	nitrites	through	consumption	of	processed	meat	such	as	hot	dogs
and	bacon,	some	products	came	under	fire. Hot	dogs	were	an	easy	target. Besides	containing	additives	like	nitrites,	hot	dogs	can	be	made	out	of
ground-up	lips,	snouts,	spleens,	tongues,	throats	and	other	“variety	meats.”
13
So	as	the	nitrite/nitrosamine	issue	heated	up,	hot	dogs	weren’t	looking	so	hot. Ralph	Nader	had	called	hot	dogs	“among	America’s	deadliest	missiles.”
14
Some	consumer	advocacy	groups	were	calling	for	a	nitrite	additive	ban,	and
government	officials	began	a	serious	review	of	nitrite’s	potential	health
problems. 3
The	issue	jolted	forward	again	in	1978,	when	a	study	at	the	Massachusetts
Institute	of	Technology	(MIT)	found	that	nitrite	increased	lymphatic	cancer	in
rats. The	study,	as	reported	in	a	1979	issue	of	
Science
,
15
	found	that,	on
average,	rats	led	nitrite	got	lymphatic	cancer	10.2%	of	the	time,	while	animals
not	led	nitrite	got	cancer	only	5.4%	of	the	time. This	finding	was	enough	to
create	a	public	uproar. Fierce	debate	ensued	in	the	government,	industry	and
research	communities. When	the	dust	settled,	expert	panels	made
recommendations,	industry	cut	back	on	nitrite	usage	and	the	issue	fell	out	of
the	spotlight. To	summarize	the	story:	marginal	scientific	results	can	make	very	big
waves	in	the	public	when	it	comes	to	cancer-causing	chemicals. A	rise	incancer	incidence	from	5%	to	10%	in	rats	fed	large	quantities	of	nitrite	caused
an	explosive	controversy. Undoubtedly	millions	of	dollars	were	spent
following	the	MIT	study	to	investigate	and	discuss	the	findings. And	NSAR,
a	nitrosamine	possibly	formed	from	nitrite,	was	“reasonably	anticipated	to	be
a	human	carcinogen”	after	several	animal	experiments	where	exceptionally
high	levels	of	chemical	were	fed	to	animals	for	almost	half	their	lifespan.BACK	TO	PROTEIN
The	point	isn’t	that	nitrite	is	safe. It	is	the	mere	possibility,	however	unlikely
it	may	be,	that	it	could	cause	cancer	that	alarms	the	public. But	what	if
researchers	produced	considerably	more	impressive	scientific	
results	that
were	far	more	substantial? What	if	there	was	a	chemical	that	experimentally
turned	on	cancer	in	100%	of	the	test	animals	and	its	relative	absence	limited
cancer	to	0%	of	the	animals? Furthermore,	what	if	this	chemical	were	capable
of	acting	in	this	way	at	routine	levels	of	intake	and	not	the	extraordinary
levels	used	in	the	NSAR	experiments? Finding	such	a	chemical	would	be	the
holy	grail	of	cancer	research. The	implications	for	human	health	would	be
enormous. One	would	assume	that	this	chemical	would	be	of	considerably
more	concern	than	nitrite	and	Alar,	and	even	more	significant	than	aflatoxin,	a
highly	ranked	carcinogen. This	is	exactly	what	I	saw	in	the	Indian	research	paper
16
	when	I	was	in	the
Philippines. The	chemical	was	protein,	fed	to	rats	at	levels	that	are	well	within
the	range	of	normal	consumption. Protein! These	results	were	more	than
startling. In	the	Indian	study,	when	all	the	rats	had	been	predisposed	to	get
liver	cancer	after	being	given	aflatoxin,	only	the	animals	fed	20%	protein	got
the	cancer	while	those	fed	5%	got	none. Scientists,	myself	included,	tend	to	be	a	skeptical	bunch,	especially	when
confronted	with	eye-popping	results. In	fact,	it	is	our	responsibility	as
researchers	to	question	and	explore	such	provocative	findings. We	might
suspect	that	this	finding	was	unique	to	rats	exposed	to	aflatoxin	and	for	no
other	species,	including	humans. Maybe	there	were	other	unknown	nutrients
that	were	affecting	the	data. Maybe	my	friend,	the	distinguished	MIT
professor,	was	right;	maybe	the	animal	identities	in	the	Indian	study	got
mixed	up. The	questions	begged	for	answers. To	further	study	this	question,	I	sought
and	received	the	two	National	Institutes	of	Health	(NIH)	research	grants	that	I
mentioned	earlier. One	was	for	a	human	study,	the	other	for	an	experimental
animal	study. I	did	not	“cry	wolf”	in	either	application	by	suggesting	that
protein	might	promote	cancer. I	had	everything	to	lose	and	nothing	to	gain	by
acting	like	a	heretic. Besides,	I	wasn’t	convinced	that	protein	actually	might
be	harmful. In	the	experimental	animal	study,	I	proposed	to	investigate	the
“effect	of	
various	factors
	[my	italics]	on	aflatoxin	metabolism.”	The	human
study,	mostly	focused	on	aflatoxin’s	effects	on	liver	cancer	in	the	Philippines,
was	briefly	reviewed	in	the	last	chapter	and	was	concluded	after	three	years. It	was	later	renewed	in	a	much	more	sophisticated	study	in	China	(chapter
four).A	study	of	this	protein	effect	on	tumor	development	had	to	be	done
extremely	well. Anything	less	would	not	have	convinced	anyone,	especially
my	peers	who	would	review	my	future	request	for	renewed	funding! In
hindsight,	we	must	have	succeeded. The	NIH	funding	for	this	study	continued
for	the	next	nineteen	years	and	led	to	additional	funding	from	other	research
agencies	(American	Cancer	Society	the	American	Institute	for	Cancer
Research	and	the	Cancer	Research	Foundation	of	America). On	these
experimental	animal	findings	alone,	this	project	gave	rise	to	more	than	100
scientific	papers	published	in	some	of	the	best	journals,	many	public
presentations	and	several	invitations	to	participate	on	expert	panels. ANIMAL	RIGHTS
The	rest	of	this	chapter	concerns	experimental	animal	research,	all	of
which	included	rodents	(rats	and	mice). I	know	well	that	many	oppose	the
use	of	experimental	animals	in	research. I	respect	this	concern. I
respectfully	suggest,	however,	that	you	consider	this:	very	likely,	I	would
not	be	advocating	a	plant-based	diet	today	if	it	were	not	for	these	animal
experiments. The	findings	and	the	principles	derived	from	these	animal
studies	greatly	contributed	to	my	interpretations	of	my	later	work,
including	the	China	Study,	as	you	will	come	to	see. One	obvious	question	regarding	this	issue	is	whether	there	was	an
alternative	way	to	get	the	same	information	without	using	experimental
animals. To	date,	I	have	found	none,	even	after	seeking	advice	from	my
“animal	rights”	colleagues. These	experimental	animal	studies	elaborated
some	very	important	principles	of	cancer	causation	not	obtainable	in
human-based	studies. These	principles	now	have	enormous	potential	to
benefit	all	of	our	fellow	creatures,	our	environment	and	ourselves.THREE	STAGES	OF	CANCER
Cancer	proceeds	through	three	stages:	initiation,	promotion	and	progression. To	use	a	rough	analogy,	the	cancer	process	is	similar	to	planting	a	lawn. Initiation	is	when	you	put	the	seeds	in	the	soil,	promotion	is	when	the	grass
starts	to	grow	and	progression	is	when	the	grass	gets	completely	out	of
control,	invading	the	driveway,	the	shrubbery	and	the	sidewalk. So	what	is	the	process	that	successfully	“implants”	the	grass	seed	in	the
soil	in	the	first	place,	i.e.,	initiates	cancer-prone	cells? Chemicals	that	do	this
are	called	carcinogens. These	chemicals	are	most	often	
the	byproducts	of
industrial	processes,	although	small	amounts	may	be	formed	in	nature,	as	is
the	case	with	aflatoxin. These	carcinogens	genetically	transform,	or	mutate,
normal	cells	into	cancer-prone	cells. A	mutation	involves	permanent	alteration
of	the	genes	of	the	cell,	with	damage	to	its	DNA. CHART	3.1:	TUMOR	INITIATION	BY	AFLATOXIN	INSIDE	A	LIVER
CELL
The	entire	initiation	stage	(
Chart	3.1
)	can	take	place	in	a	very	short	period
of	time,	even	minutes. It	is	the	time	required	for	the	chemical	carcinogen	tobe	consumed,	absorbed	into	the	blood,	transported	into	cells,	changed	into	its
active	product,	bonded	to	DNA	and	passed	on	to	the	daughter	cells. When	the
new	daughter	cells	are	formed,	the	process	is	complete. These	daughter	cells
and	all	their	progeny	will	forever	be	genetically	damaged,	giving	rise	to	the
potential	for	cancer. Except	in	rare	instances,	completion	of	the	initiation
phase	is	considered	irreversible. At	this	point	in	our	lawn	analogy,	the	grass	seeds	have	been	put	in	the	soil
and	are	ready	to	germinate. Initiation	is	complete. The	second	growth	stage	is
called	promotion. Like	seeds	ready	to	sprout	blades	of	grass	and	turn	into	a
green	lawn,	our	newly	formed	cancer-prone	cells	are	ready	to	grow	and
multiply	until	they	become	a	visibly	detectable	cancer. This	stage	occurs	over
a	far	longer	period	of	time	than	initiation,	often	many	years	for	humans. It	is
when	the	newly	initiated	cluster	multiplies	and	grows	into	larger	and	larger
masses	and	a	clinically	visible	tumor	is	formed. But	just	like	seeds	in	the	soil,	the	initial	cancer	cells	will	not	grow	and
multiply	unless	the	right	conditions	are	met. The	seeds	in	the	soil,	for
example,	need	a	healthy	amount	of	water,	sunlight	and	other	nutrients	before
they	make	a	full	lawn. If	any	of	these	factors	are	denied	or	are	missing,	the
seeds	will	not	grow. If	any	of	these	factors	are	missing	after	growth	starts,	the
new	seedlings	will	become	dormant,	while	awaiting	further	supply	of	the
missing	factors. This	is	one	of	the	most	profound	features	of	promotion. Promotion	is	reversible,	depending	on	whether	the	early	cancer	growth	is
given	the	right	conditions	in	which	to	grow. This	is	where	certain	dietary
factors	become	so	important. These	dietary	factors,	called	promoters,	feed
cancer	growth. Other	dietary	factors,	called	anti-promoters,	slow	cancer
growth. Cancer	growth	flourishes	when	there	are	more	promoters	than	anti-
promoters;	when	anti-promoters	prevail	cancer	growth	slows	or	stops. It	is	a
push-pull	process. The	profound	importance	of	this	reversibility	cannot	be
overemphasized. The	third	phase,	progression,	begins	when	a	bunch	of	advanced	cancer
cells	progress	in	their	growth	until	they	have	done	their	final	damage. It	is	like
the	fully-grown	lawn	invading	everything	around	it:	the	garden,	driveway	and
sidewalk. Similarly,	a	developing	cancer	tumor	may	wander	away	from	its
initial	site	in	the	body	and	invade	neighboring	or	distant	tissues. When	the
cancer	takes	on	these	deadly	properties,	it	is	considered	malignant. When	it
actually	breaks	away	from	its	initial	home	and	wanders,	it	is	metastasizing. This	final	stage	of	cancer	results	in	death. At	the	start	of	our	research,	the	stages	of	cancer	formation	were	known
only	in	vague	outline. But	we	knew	enough	about	these	stages	of	cancer	to	be
able	to	structure	our	research	more	intelligently. We	had	no	shortage	ofquestions. Could	we	confirm	the	findings	from	India	that	a	low-protein	diet
represses	tumor	formation? More	importantly,	why	does	protein	affect	the
cancer	process? What	are	the	mechanisms;	that	is,	how	does	protein	work? With	plenty	of	questions	to	be	answered,	we	
went	about	our	experimental
studies	meticulously	and	in	depth	in	order	to	obtain	results	that	would
withstand	the	harshest	of	scrutiny.PROTEIN	AND	INITIATION
How	does	protein	intake	affect	cancer	initiation? Our	first	test	was	to	see
whether	protein	intake	affected	the	enzyme	principally	responsible	for
aflatoxin	metabolism,	the	mixed	function	oxidase	(MFO). This	enzyme	is
very	complex	because	it	also	metabolizes	pharmaceuticals	and	other
chemicals,	friend	or	foe	to	the	body	Paradoxically,	this	enzyme	both
detoxifies	and	activates	aflatoxin. It	is	an	extraordinary	transformation
substance. THE	ENZYME	“FACTORY”
In	a	simplistic	way,	the	MFO	enzyme	system	can	be	thought	of	as	a	factory
within	the	industrious	workings	of	the	cell. Various	chemical	“raw
materials”	are	fed	into	the	factory,	where	all	the	complex	reactions	are
performed. The	raw	materials	may	be	disassembled	or	assembled. After	a
transforming	process,	the	“raw	material”	chemicals	are	ready	to	be	shipped
out	of	the	factory	as	mostly	normal,	safe	products. But	there	also	may	be
byproducts	of	these	complex	processes	that	are	exceptionally	dangerous. Think	of	the	smokestack	at	a	real-life	factory. If	someone	told	you	to	stick
your	face	down	a	smokestack	and	breathe	deeply	for	a	couple	hours,	you’d
refuse. Within	the	cell,	the	dangerous	byproducts,	if	not	held	in	check,	are
the	highly	reactive	aflatoxin	metabolites	that	go	on	to	attack	the	cell’s	DNA
and	damage	its	genetic	blueprint. At	the	time	we	started	our	research,	we	hypothesized	that	the	protein	we
consume	alters	tumor	growth	by	changing	how	aflatoxin	is	detoxified	by	the
enzymes	present	in	the	liver. We	initially	determined	whether	the	amount	of	protein	that	we	eat	could
change	this	enzyme	activity. After	a	series	of	experiments	(
Chart	3.2
18
),	the
answer	was	clear. Enzyme	activity	could	be	easily	modified	simply	bychanging	the	level	of	protein	intake. 18–21
Decreasing	protein	intake	like	that	done	in	the	original	research	in	India
(20%	to	5%)	not	only	greatly	decreased	enzyme	activity	but	did	so	very
quickly. 22
	What	does	this	mean? Decreasing	enzyme	activity	via	low-protein
diets	implied	that	less	aflatoxin	was	being	transformed	into	the	dangerous
aflatoxin	metabolite	that	had	the	potential	to	bind	and	to	mutate	the	DNA. We	decided	to	test	this	implication:	did	a	low-protein	diet	actually
decrease	the	binding	of	aflatoxin	product	to	DNA,	resulting	in	fewer	adducts? An	undergraduate	student	in	my	lab,	Rachel	Preston,	did	the	experiment
(
Chart	3.3
)	and	showed	that	the	lower	the	protein	intake,	the	lower	the	amount
of	aflatoxin-DNA	adducts. 23
CHART	3.2:	EFFECT	OF	DIETARY	PROTEIN	ON	ENZYME
ACTIVITY
	
CHART	3.3:	DECREASE	IN	CARCINOGEN	BINDING	TO	NUCLEUS
COMPONENTS	CAUSED	BY	LOW-PROTEIN	FEEDING
We	now	had	impressive	evidence	that	low	protein	intake	could	markedly
decrease	enzyme	activity	and	prevent	dangerous	carcinogen	binding	to	DNA. These	were	very	impressive	findings,	to	be	sure. It	might	even	be	enough
information	to	“explain”	how	consuming	less	protein	leads	to	less	cancer. But
we	wanted	to	know	more	and	be	doubly	assured	of	this	effect,	so	we
continued	to	look	for	other	explanations. As	time	passed,	we	were	to	learn
something	really	quite	remarkable. Almost	
every	time	we	searched	for	a	way,
or	mechanism,	by	which	protein	works	to	produce	its	effects,	we	found	one! For	example,	we	came	to	discover	that	low-protein	diets,	or	their	equivalents,
reduce	tumors	by	the	following	mechanisms:
less	aflatoxin	entered	the	cell
24–26
cells	multiplied	more	slowly
18
multiple	changes	occurred	within	the	enzyme	complex	to	reduce	its
activity
27
the	quantity	of	critical	components	of	the	relevant	enzymes	was
reduced
28,	29
less	aflatoxin-DNA	adducts	were	formed
23,	30
The	fact	that	we	found	more	than	one	way	(mechanism)	that	low-protein
diets	work	was	eye-opening. It	added	a	great	deal	of	weight	to	the	results	of
the	Indian	researchers. It	also	suggested	that	biological	effects,	although	often
described	as	operating	through	single	reactions,	more	likely	operate	through	a
large	number	of	varied	simultaneous	reactions,	very	likely	acting	in	a	highly
integrated	and	concerted	manner. Could	this	mean	that	the	body	had	lots	of
backup	systems	in	case	one	was	bypassed	in	some	way? As	research	unfolded
in	the	subsequent	years,	the	truth	of	this	thesis	became	increasingly	evident. From	our	extensive	research,	one	idea	seemed	to	be	clear:	lower	protein
intake	dramatically	decreased	tumor	initiation. This	finding,	even	though	well
substantiated,	would	be	enormously	provocative	for	many	people.PROTEIN	AND	PROMOTION
To	go	back	to	the	lawn	analogy,	sowing	the	grass	seeds	in	the	soil	was	the
initiation	process. We	found,	conclusively,	through	a	number	of	experiments,
that	a	low-protein	diet	could	decrease,	at	the	time	of	planting,	the	number	of
seeds	in	our	“cancerous”	lawn. That	was	an	incredible	finding,	but	we	needed
to	do	more. We	wondered:	what	happens	during	the	promotion	stage	of
cancer,	the	all-important	reversible	stage? Would	the	benefits	of	low	protein
intake	achieved	during	initiation	continue	through	promotion? Practically	speaking,	it	was	difficult	to	study	this	stage	of	cancer	because
of	time	and	money. It	is	an	expensive	study	that	allows	rats	to	live	until	they
develop	full	tumors. Each	such	experiment	would	take	more	than	two	years
(the	normal	lifetime	of	rats)	and	would	have	cost	well	over	$100,000	(even
more	money	today). To	answer	the	many	questions	that	we	had,	we	could	not
proceed	by	studying	full	tumor	development;	I	would	still	be	in	the	lab,	thirty-
five	years	later! This	is	when	we	learned	of	some	exciting	work	just	published	by	others
31
that	showed	how	to	measure	tiny	clusters	of	cancer-like	cells	that	appear	right
after	initiation	is	complete. These	little	microscopic	cell	clusters	were	called
foci. Foci	are	precursor	clusters	of	cells	that	grow	into	tumors. Although	most
foci	do	not	become	full-blown	tumor	cells,	they	are	predictive	of	tumor
development. By	watching	foci	develop	and	measuring	how	many	there	are	and	how	big
they	become,
32
	we	could	learn	indirectly	how	tumors	also	develop	and	what
effect	protein	might	have. By	studying	the	effects	of	protein	on	the	promotion
of	foci	instead	of	tumors	we	could	avoid	spending	a	lifetime	and	a	few
million	dollars	working	in	the	lab. What	we	found	was	truly	remarkable. Foci	development	was	almost
entirely	dependent	on	how	much	protein	was	consumed,	regardless	of	how
much	aflatoxin	was	consumed! This	was	documented	in	many	interesting	ways,	first	done	by	my	graduate
students	Scott	Appleton
33
	and	George	Dunaif
34
	(a	typical	comparison	is
shown	in	
Chart	3.4
). After	initiation	with	aflatoxin,	foci	grew	(were
promoted)	far	more	with	the	20%	protein	diet	than	with	the	5%	protein	diet. 33,
34
Up	to	this	point,	all	of	the	animals	were	exposed	to	the	same	amount	of
aflatoxin. But	what	if	the	initial	aflatoxin	exposure	is	varied? Would	protein
still	have	an	effect? We	investigated	this	question	by	giving	two	groups	of	ratseither	a	high-aflatoxin	dose	or	a	low-aflatoxin	dose,	along	with	a	standard
baseline	diet.
_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:

        But	funding	of
genetic	research	continues	to	spiral	upwards	in	the	belief	that	specific	genes
account	for	the	occurrence	of	specific	diseases,	in	the	hope	that	we	somehow
will	be	able	to	“turn	off”	these	nasty	genes. Drug	company	public	relations
programs	now	depict	a	future	where	each	of	us	will	have	a	personal	ID	card
cataloging	all	of	our	good	and	bad	genes. Using	this	card,	we	will	be	expected
to	go	to	our	doctor,	who	will	prescribe	a	single	pill	to	suppress	our	bad	genes. I	strongly	suspect	these	miracles	will	never	be	realized,	or	if	tried	they	will
have	serious,	unintended	consequences. These	futuristic	pipe	dreams	obscure
the	affordable,	efficacious	health	solutions	that	currently	exist:	solutions
based	in	nutrition. In	my	own	laboratory	we	have	shown	in	experimental	animals	that	cancer
growth	can	be	turned	on	and	off	by	nutrition,	despite	very	strong	genetic
predisposition. We	have	studied	these	effects	in	great	detail	and	have
published	our	findings	in	the	very	best	scientific	journals. As	you	will	see
later,	these	findings	are	nothing	short	of	spectacular,	and	the	same	effects
have	been	indicated	over	and	over	again	in	humans. Eating	the	right	way	not	only	prevents	disease	but	also	generates	health
and	a	sense	of	well-being,	both	physically	and	mentally. Some	world-class
athletes,	such	as	ironman	Dave	Scott,	track	stars	Carl	Lewis	and	EdwinMoses,	tennis	great	Martina	Navratilova,	world	champion	wrestler	Chris
Campbell	(no	relation)	and	sixty-eight-year-old	marathoner	Ruth	Heidrich
have	discovered	that	consuming	a	low-fat,	
plant-based	diet	gives	them	a
significant	edge	in	performance. In	the	laboratory,	we	fed	experimental	rats	a
diet	similar	to	the	usual	American	fare—rich	in	animal-based	protein—and
compared	them	with	other	rats	fed	a	diet	low	in	animal-based	protein. Guess
what	happened	when	both	sets	of	rats	had	an	opportunity	to	voluntarily	use
exercise	wheels. Those	fed	the	low-animal	protein	diet	exercised
substantially	more,	with	less	fatigue,	than	those	fed	the	type	of	diet	that	most
of	us	eat. This	was	the	same	effect	observed	by	these	world-class	athletes. This	shouldn’t	be	news	to	the	medical	establishment. A	century	ago,
Professor	Russell	Chittenden,	a	famous,	well	established	nutrition	researcher
at	Yale	University	Medical	School,	investigated	whether	eating	a	plant-based
diet	affected	students’	physical	capacities. 34,	35
	He	fed	some	students,	fellow
faculty	and	himself	a	plant-based	diet	and	measured	their	physical
performance	tests. He	got	the	same	results	as	our	rats	almost	a	century	later—
and	they	were	equally	spectacular. Then	there	is	the	question	of	our	excessive	dependence	on	drugs	and
surgery	to	control	our	health. In	its	simplest	form,	eating	the	right	way	would
largely	obviate	the	enormous	costs	of	using	drugs,	as	well	as	their	side	effects. Fewer	people	would	need	to	wage	lengthy,	expensive	battles	with	chronic
disease	in	hospitals	over	their	last	years	of	life. Health	care	costs	would	drop
and	medical	mistakes	would	wane	as	premature	death	plummeted. In	essence,
our	health	care	system	would	finally	protect	and	promote	our	health	as	it	is
meant	to	do. SIMPLE	BEGINNINGS
As	I	look	back,	I	often	think	about	life	on	the	farm	and	how	it	shaped	my
thinking	in	so	many	ways. My	family	was	immersed	in	nature	every	waking
moment. In	the	summer,	from	sunrise	to	sunset,	we	were	outdoors	planting
and	harvesting	the	crops	and	taking	care	of	the	animals. My	mother	had	the
best	garden	in	our	part	of	the	country	and	toiled	day	in	and	day	out	during	the
summer	to	keep	our	family	well	fed	with	fresh	food,	all	produced	on	our	own
farm. I’ve	had	an	amazing	journey,	to	be	sure. I	have	been	startled	time	and	time
again	by	what	I	have	learned. I	wish	that	my	family	and	others	around	us	had
had	the	same	information	back	in	the	mid-1900s	that	we	now	have	about	food
and	health. If	we	had,	my	father	could	have	prevented,	or	reversed,	his	heart
disease. He	could	have	met	my	youngest	son,	his	namesake,	who	is
collaborating	with	me	on	this	book. He	might	have	lived	for	several	more
years	with	a	higher	quality	of	health. My	journey	in	science	over	the	past
forty-five	years	has	convinced	me	that	it	is	now	more	urgent	than	ever	to
show	how	people	can	avoid	these	tragedies. The	science	is	there	and	it	must
be	made	known. We	cannot	let	the	status	quo	go	unchallenged	and	watch	our
loved	ones	suffer	unnecessarily. It	is	time	to	stand	up,	clear	the	air	and	take
control	of	our	health. 2
A	House	of	Proteins
M
Y	ENTIRE	PROFESSIONAL	CAREER
	in	biomedical	research	has	centered	on
protein. Like	an	invisible	leash,	protein	tethered	me	wherever	I	went,	from	the
basic	research	laboratory	to	the	practical	programs	of	feeding	malnourished
children	in	the	Philippines	to	the	government	board-rooms	where	our	national
health	policy	was	being	formulated. Protein,	often	regarded	with	unsurpassed
awe,	is	the	common	thread	tying	together	past	and	present	knowledge	about
nutrition. The	story	of	protein	is	part	science,	part	culture	and	a	good	dose	of
mythology. I	am	reminded	of	the	words	of	Goethe,	first	brought	to	my
attention	by	my	friend	Howard	Lyman,	a	prominent	lecturer,	author	and
former	cattle	rancher:	“We	are	best	at	hiding	those	things	which	are	in	plain
sight. ”	Nothing	has	been	so	well	hidden	as	the	untold	story	of	protein. The
dogma	surrounding	protein	censures,	reproaches	and	guides,	directly	or
indirectly,	almost	every	thought	we	have	in	biomedical	research. Ever	since	the	discovery	of	this	nitrogen-containing	chemical	in	1839	by
the	Dutch	chemist	Gerhard	Mulder,	protein	has	loomed	as	the	most	sacred	of
all	nutrients. The	word	protein	comes	from	the	Greek	word	
proteios,
	which
means	“of	prime	importance. ”
In	the	nineteenth	century,	protein	was	synonymous	with	meat,	and	this
connection	has	stayed	with	us	for	well	over	a	hundred	years. Many	people
today	still	equate	protein	with	animal-based	food. If	you	were	to	name	the
first	food	that	comes	to	mind	when	I	say	protein,	you	might	say	beef. If	you
did,	you	aren’t	alone. Confusion	reigns	on	many	of	the	most	basic	questions	about	protein:
What	are	good	sources	of	protein. How	much	protein	should	one	consume. Is	plant	protein	as	good	as	animal	protein. Is	it	necessary	to	combine	certain	plant	foods	in	a	meal	to	get	complete
proteins. Is	it	advisable	to	take	protein	powders	or	amino	acid	supplements,
especially	for	someone	who	does	vigorous	exercise	or	plays	sport. Should	one	take	protein	supplements	to	build	muscle. Some	protein	is	considered	high	quality	some	low	quality;	what	does	this
mean. Where	do	vegetarians	get	protein. Can	vegetarian	children	grow	properly	without	animal	protein. Fundamental	to	many	of	these	common	questions	and	concerns	is	the
belief	that	meat	is	protein	and	protein	is	meat. This	belief	comes	from	the	fact
that	the	“soul”	of	animal-based	foods	is	protein. In	many	meat	and	dairy
products,	we	can	selectively	remove	the	fat	but	we	are	still	left	with
recognizable	meat	and	dairy	products. We	do	this	all	the	time,	with	lean	cuts
of	meat	and	skim	milk. But	if	we	selectively	remove	the	protein	from	animal-
based	foods,	we	are	left	with	nothing	like	the	original. A	non-protein	steak,
for	example,	would	be	a	puddle	of	water,	fat	and	a	small	amount	of	vitamins
and	minerals. Who	would	eat	that. In	brief,	for	a	food	to	be	recognized	as	an
animal-based	food,	it	must	have	protein. Protein	is	the	core	element	of
animal-based	foods. Early	scientists	like	Carl	Voit	(1831-1908),	a	prominent	German	scientist,
were	staunch	champions	of	protein. Voit	found	that	“man”	needed	only	48. 5
grams	per	day,	but	nonetheless	he	recommended	a	whopping	118	grams	per
day	because	of	the	cultural	bias	of	the	time. Protein	equaled	meat,	and
everyone	aspired	to	have	meat	on	his	or	her	table,	just	as	we	aspire	to	have
bigger	houses	and	faster	cars. Voit	figured	you	can’t	get	too	much	of	a	good
thing. Voit	went	on	to	mentor	several	well-known	nutrition	researchers	of	the
early	1900s,	including	Max	Rubner	(1854-1932)	and	W. O. Atwater	(1844-
1907). Both	students	closely	followed	the	advice	of	their	teacher. Rubner
stated	that	protein	intake,	meaning	meat,	was	a	symbol	of	civilization	itself:
“a	large	protein	allowance	is	the	right	of	civilized	man. ”	Atwater	went	on	to
organize	the	first	nutrition	laboratory	at	the	United	States	Department	of
Agriculture	(USDA). As	director	of	the	USDA,	he	
recommended	125	grams
per	day	(only	about	fifty-five	grams	per	day	is	now	recommended). Later,	we
will	see	how	important	this	early	precedent	was	to	this	government	agency. A	cultural	bias	had	become	firmly	entrenched. If	you	were	civilized,	youate	plenty	of	protein. If	you	were	rich,	you	ate	meat,	and	if	you	were	poor,
you	ate	staple	plant	foods,	like	potatoes	and	bread. The	lower	classes	were
considered	by	some	to	be	lazy	and	inept	as	a	result	of	not	eating	enough	meat,
or	protein. Elitism	and	arrogance	dominated	much	of	the	burgeoning	held	of
nutrition	in	the	nineteenth	century. The	entire	concept	that	bigger	is	better,
more	civilized	and	perhaps	even	more	spiritual	permeated	every	thought
about	protein. Major	McCay	a	prominent	English	physician	in	the	early	twentieth
century,	provided	one	of	the	more	entertaining,	but	most	unfortunate,
moments	in	this	history. Physician	McCay	was	stationed	in	the	English
colony	of	India	in	1912	in	order	to	identify	good	fighting	men	in	the	Indian
tribes. Among	other	things,	he	said	that	people	who	consumed	less	protein
were	of	a	“poor	physique,	and	a	cringing	effeminate	disposition	is	all	that	can
be	expected. ”PRESSING	FOR	QUALITY
Protein,	fat,	carbohydrate	and	alcohol	provide	virtually	all	of	the	calories	that
we	consume. Fat,	carbohydrate	and	protein,	as	
macro
nutrients,	make	up
almost	all	the	weight	of	food,	aside	from	water,	with	the	remaining	small
amount	being	the	vitamin	and	mineral	
micro
nutrients. The	amounts	of	these
latter	
micro
nutrients	needed	for	optimum	health	are	tiny	(milligrams	to
micrograms). Protein,	the	most	sacred	of	all	nutrients,	is	a	vital	component	of	our	bodies
and	there	are	hundreds	of	thousands	of	different	kinds. They	function	as
enzymes,	hormones,	structural	tissue	and	transport	molecules,	all	of	which
make	life	possible. Proteins	are	constructed	as	long	chains	of	hundreds	or
thousands	of	amino	acids,	of	which	there	are	fifteen	to	twenty	different	kinds,
depending	on	how	they	are	counted. Proteins	wear	out	on	a	regular	basis	and
must	be	replaced. This	is	accomplished	by	consuming	foods	that	contain
protein. When	digested,	these	proteins	give	us	a	whole	new	supply	of	amino
acid	building	blocks	to	use	in	making	new	protein	replacements	for	those	that
wore	out. Various	food	proteins	are	said	to	be	of	different	quality,	depending
on	how	well	they	provide	the	needed	amino	acids	used	to	replace	our	body
proteins. This	process	of	disassembling	and	reassembling	the	amino	acids	of
proteins	is	like	someone	giving	us	a	multicolored	string	of	beads	to	replace	an
old	string	of	beads	that	we	lost. However,	the	colored	beads	on	the	string
given	to	us	are	not	in	the	same	order	as	the	string	we	lost. So,	we	break	the
string	and	collect	its	beads. Then,	we	reconstruct	our	new	string	so	that	the
colored	beads	are	in	the	same	order	as	our	lost	string. But	if	we	are	short	of
blue	beads,	for	example,	making	our	new	string	is	going	to	be	slowed	down
or	stopped	until	we	get	more	blue	beads. This	is	the	same	concept	as	in
making	new	tissue	proteins	to	match	our	old	worn	out	proteins. About	eight	amino	acids	(“colored	beads”)	that	are	needed	for	making	our
tissue	proteins	must	be	provided	by	the	food	we	eat. They	are	called
“essential”	because	our	bodies	cannot	make	them. If,	like	our	string	of	beads,
our	food	protein	lacks	enough	of	even	one	of	these	eight	“essential”	amino
acids,	then	the	synthesis	of	the	new	proteins	will	be	slowed	down	or	stopped. This	is	where	the	idea	of	protein	quality	comes	into	play. Food	proteins	of	the
highest	quality	are,	very	simply,	those	that	provide,	upon	digestion,	the	right
kinds	and	amounts	of	amino	acids	needed	to	efficiently	synthesize	our	new
tissue	proteins. This	is	what	that	word	“quality”	really	means:	it	is	the	ability
of	food	proteins	to	provide	the	right	kinds	and	amounts	of	amino	acids	to
make	our	new	proteins. Can	you	guess	what	food	we	might	eat	to	most	efficiently	provide	the
building	blocks	for	our	replacement	proteins. The	answer	is	human	flesh. Its
protein	has	just	the	right	amount	of	the	needed	amino	acids. But	while	our
fellow	men	and	women	are	not	for	dinner,	we	do	get	the	next	“best”	protein
by	eating	other	animals. The	proteins	of	other	animals	are	very	similar	to	our
proteins	because	they	mostly	have	the	right	amounts	of	each	of	the	needed
amino	acids. These	proteins	can	be	used	very	efficiently	and	therefore	are
called	“high	quality. ”	Among	animal	foods,	the	proteins	of	milk	and	eggs
represent	the	best	amino	acid	matches	for	our	proteins,	and	thus	are
considered	the	highest	quality. While	the	“lower	quality”	plant	proteins	may
be	lacking	in	one	or	more	of	the	essential	amino	acids,	as	a	group	they	
do
contain	all	of	them. The	concept	of	quality	really	means	the	efficiency	with	which	food
proteins	are	used	to	promote	growth. This	would	be	well	and	good	if	the
greatest	efficiency	equaled	the	greatest	health,	but	it	doesn’t,	and	that’s	why
the	terms	efficiency	and	quality	are	misleading. In	fact,	to	give	you	a	taste	of
what’s	to	come,	there	is	a	mountain	of	compelling	research	
showing	that
“low-quality”	plant	protein,	which	allows	for	slow	but	steady	synthesis	of
new	proteins,	is	the	healthiest	type	of	protein. Slow	but	steady	wins	the	race. The	quality	of	protein	found	in	a	specific	food	is	determined	by	seeing	how
fast	animals	would	grow	while	consuming	it. Some	foods,	namely	those	from
animals,	emerge	with	a	very	high	protein	efficiency	ratio	and	value. 1
This	focus	on	efficiency	of	body	growth,	as	if	it	were	good	health,
encourages	the	consumption	of	protein	with	the	highest	“quality. ”	As	any
marketer	will	tell	you,	a	product	that	is	defined	as	being	high	quality	instantly
earns	the	trust	of	consumers. For	well	over	100	years,	we	have	been	captive	to
this	misleading	language	and	have	oftentimes	made	the	unfortunate	leap	to
thinking	that	more	quality	equals	more	health. The	basis	for	this	concept	of	protein	quality	was	not	well	known	among
the	public,	but	its	impact	was—and	still	is—highly	significant. People,	for
example,	who	choose	to	consume	a	plant-based	diet	will	often	ask,	even
today,	“Where	do	I	get	my	protein. ”	as	if	plants	don’t	have	protein. Even	if	it
is	known	that	plants	have	protein,	there	is	still	the	concern	about	its	perceived
poor	quality. This	has	led	people	to	believe	that	they	must	meticulously
combine	proteins	from	different	plant	sources	during	each	meal	so	that	they
can	mutually	compensate	for	each	other’s	amino	acid	deficits. However,	this
is	overstating	the	case. We	now	know	that	through	enormously	complex
metabolic	systems,	the	human	body	can	derive	all	the	essential	amino	acids
from	the	natural	variety	of	plant	proteins	that	we	encounter	every	day. It
doesn’t	require	eating	higher	quantities	of	plant	protein	or	meticulouslyplanning	every	meal. Unfortunately,	the	enduring	concept	of	protein	quality
has	greatly	obscured	this	information. THE	PROTEIN	GAP
The	most	important	issue	in	nutrition	and	agriculture	during	my	early	career
was	figuring	out	ways	to	increase	the	consumption	of	protein,	making	sure	it
was	of	the	highest	possible	quality. My	colleagues	and	I	all	believed	in	this
common	goal. From	my	early	years	on	the	farm	to	my	graduate	education,	I
accepted	this	virtual	reverence	for	protein. As	a	youngster,	I	remember	that
the	most	expensive	part	of	farm	animal	feed	was	the	protein	supplements	that
we	fed	to	our	cows	and	pigs. Then,	at	graduate	school,	I	spent	three	years
(1958-1961)	doing	my	Ph. D. research	trying	to	improve	the	supply	of	high-
quality	protein	by	growing	cows	and	sheep	more	efficiently	so	we	could	eat
more	of	them. 2,	3
I	went	all	the	way	through	my	graduate	studies	with	a	profound	belief	that
promoting	high-quality	protein,	as	in	animal-based	foods,	was	a	very
important	task. My	graduate	research,	although	cited	a	few	times	over	the
next	decade	or	so,	was	only	a	small	part	of	much	larger	efforts	by	other
research	groups	to	address	a	protein	situation	worldwide. During	the	1960s
and	1970s,	I	was	to	hear	over	and	over	again	about	a	so-called	“protein	gap”
in	the	developing	world. 4
The	protein	gap	stipulated	that	world	hunger	and	malnutrition	among
children	in	the	third	world	was	a	result	of	not	having	enough	protein	to
consume,	especially	high-quality	(i. e. animal)	protein. 1,	4,	5
	According	to	this
view,	those	in	the	third	world	were	especially	deficient	in	“high-quality”
protein,	or	animal	protein. Projects	were	springing	up	all	over	the	place	to
address	this	“protein	gap”	problem. A	prominent	MIT	professor	and	his
younger	colleague	concluded	in	1976	that	“an	adequate	supply	of	protein	is	a
central	aspect	of	the	world	food	problem“
5
	and	further	that	“unless…
desirably	[supplemented]	by	modest	amounts	of	milk,	eggs,	meat	or	fish,	the
predominantly	cereal	diets	[of	poor	nations]	are…	deficient	in	protein	for
growing	children	…. ”	To	address	this	dire	problem:
MIT	was	developing	a	protein-rich	food	supplement	called	INCA-
PARINA. Purdue	University	was	breeding	corn	to	contain	more	lysine,	the
“deficient”	amino	acid	in	corn	protein. The	U. S. government	was	subsidizing	the	production	of	dried	milk
powder	to	provide	high-quality	protein	for	the	world’s	poor. Cornell	University	was	providing	a	wealth	of	talent	to	the	Philippines	to
help	develop	both	a	high-protein	rice	variety	and	a	livestock	industry. Auburn	University	and	MIT	were	grinding	up	fish	to	produce	“fishprotein	concentrate”	to	feed	the	world’s	poor. The	United	Nations,	the	U.
The author strongly suspects that this idea will never be realized, or if tried, will have serious, unintended consequences.
What is the author's stance on the idea that specific genes account for the occurrence of specific diseases?
The author believes that nutrition, particularly a plant-based diet, can be a more effective and sustainable solution.
What is the author's alternative approach to improving health and preventing disease?
The author's initial focus was on increasing the consumption of high-quality protein, particularly in the context of malnutrition in the Philippines.
What was the author's initial focus in their research career?
The author emphasizes the importance of understanding the complexity of the relationship between diet and health, and highlights the limitations of correlation analysis in determining causality.
What is the author's opinion on the concept of correlation and causation in scientific research?
The author's approach involves conducting in-depth experiments and analyzing the effects of different factors on cancer growth, including the role of protein in the process.
What is the author's approach to studying the relationship between diet and cancer?