This study of lifestyle change was published in the premier medical...
Dr. Dean Ornish is an American physician and researcher, the presid...
Coronary atherosclerosis affects arteries that carry blood to the h...
Quantitative coronary angiography is a a medical imaging technique ...
82% is a stunning result-> the percentage of patients whose arterie...
The lifestyle change that the patients underwent was only possible ...
This is a major diet change for these individuals, and they were la...
These support groups are essential to sustain behavior change (most...
This study is remarkable: only two other randomized control trials ...
336
Lancet
1990;
129
MEDICAL
SCIENCE
Can
lifestyle
changes
reverse
coronary
heart
disease?
The
Lifestyle
Heart
Trial
In
a
prospective,
randomised,
controlled
trial
to
determine
whether
comprehensive
lifestyle
changes
affect
coronary
atherosclerosis
after
1
year,
28
patients
were
assigned
to
an
experimental
group
(low-fat
vegetarian
diet,
stopping
smoking,
stress
management
training,
and
moderate
exercise)
and
20 to
a
usual-care
control
group. 195
coronary
artery
lesions
were
analysed
by
quantitative
coronary
angiography.
The
average
percentage
diameter
stenosis
regressed
from
40·0
(SD
16·9)%
to
37·8
(16·5)%
in
the
experimental
group
yet
progressed
from
42·7
(15·5)%
to
46·1
(18·5)%
in
the
control
group.
When
only
lesions
greater
than
50%
stenosed
were
analysed,
the
average
percentage
diameter
stenosis
regressed
from
61·1
(8·8)%
to
55·8
(11·0)%
in
the
experimental
group
and
progressed
from
61·7
(9·5)%
to
64·4
(16·3)%
in
the
control
group.
Overall,
82%
of
experimental-group
patients
had
an
average
change
towards
regression.
Comprehensive
lifestyle
changes
may
be
able
to
bring
about
regression
of
even
severe
coronary
atherosclerosis
after
only
1
year,
without
use
of
lipid-lowering
drugs.
Introduction
The
Lifestyle
Heart
Trial
is
the
first
randomised,
controlled
clinical
trial
to
determine
whether
patients
outside
hospital
can
be
motivated
to
make
and
sustain
comprehensive
lifestyle
changes
and,
if
so,
whether
regression
of
coronary
atherosclerosis
can
occur
as
a
result
of
lifestyle
changes
alone.
Over
twenty
clinical
trials
are
being
carried
out
to
determine
whether
the
progression
of
coronary
atherosclerosis
can
be
modified,
in
all
of
these,
cholesterol-
lowering
drugs,
plasmapheresis,
or
partial
ileal
bypass
surgery
are
the
primary
interventions.1
We
carried
out
trials
in
1977
and
1980
to
assess
the
short-term
effects
of
lifestyle
changes
on
coronary
heart
disease
with
non-invasive
endpoint
measures
(improvements
in
cardiac
risk
factors,
functional
status,
myocardial
perfusion,2
and
left
ventricular
function3).
However,
the
subjects
of
those
studies
were
not
living
in
the
community
during
the
trial,
and
we
did
not
use
angiography
to
assess
changes
in
coronary
atherosclerosis.
Patients
and
methods
Patients
with
angiographically
documented
coronary
artery
disease
were
randomly
assigned
to
an
experimental
group
or
to
a
usual-care
control
group.
Experimental-group
patients
were
prescribed
a
lifestyle
programme
that
included
a
low-fat
vegetarian
diet,
moderate
aerobic
exercise,
stress
management
training,
stopping
smoking,
and
group
support.
Control-group
patients
were
not
asked
to
make
lifestyle
changes,
although
they
were
free
to
do
so.
Progression
or
regression
of
coronary
artery
lesions
was
assessed
in
both
groups
by
quantitative
coronary
angiography
at
baseline
and
after
about
a
year.
ADDRESSES:
Pacific
Presbyterian
Medical
Center,
Preventive
Medicine
Research
Institute,
and
Departments
of
Medicine
and
Psychology,
University
of
California
San
Francisco
School
of
Medicine
(D.
Ornish,
MD,
S
E.
Brown,
MD,
J.
H.
Billings,
PhD);
UCSF
School
of
Dental
Public
Health
and
Hygiene
(L.
W.
Scherwitz,
PhD);
Cardiac
Catheterisation
Laboratories,
Pacific
Presbyterian
Medical
Center
(W.
T.
Armstrong,
MD);
Cardiovascular
Research
Institute,
UCSF
School
of
Medicine
(T.
A
Ports,
MD);
Integral
Health
Services,
Inc,
Richmond,
Virginia
(S.
M.
McLanahan,
MD);
Center
for
Cardiovascular
and
Imaging
Research,
University
of
Texas
Medical
School
(R.
L.
Kirkeeide,
PhD,
Prof
K. L.
Gould,
MD);
and
Department
of
Biomedical
and
Environmental
Heath
Science,
University
of
California
School
of
Public
Health,
Berkeley,
California,
USA
(Prof
R.
J.
Brand,
PhD).
Correspondence
to
Dr
D.
Ornish,
Preventive
Medicine
Research
Institute,
1001
Bridgeway
Box
305,
Sausalito,
California
94965,
USA.
130
Patients
were
recruited
from
Pacific
Presbyterian
Medical
Center
(PPMC)
and
from
Moffitt
Hospital
of
the
UCSF
School
of
Medicine
according
to
the
following
criteria:
age
35-75
years,
male
or
female;
residence
in
the
greater
San
Francisco
area;
no
other
life-threatening
illnesses;
no
myocardial
infarction
during
the
preceding
6
weeks,
and
no
history
of
receiving
streptokinase
or
alteplase;
not
currently
receiving
lipid-lowering
drugs;
one,
two,
or
three
vessel
coronary
artery
disease
(defined
as
any
measurable
coronary
atherosclerosis
in
a
non-dilated
or
non-bypassed
coronary
artery);
left
ventricular
ejection
fraction
greater
than
25%;
not
scheduled
to
have
coronary
artery
bypass
grafting;
and
permission
granted
by
patient’s
cardiologist
and
primary
care
physician.
We
screened
and
recruited
only
patients
who
were
having
angiograms
for
clinical
reasons
unrelated
to
this
study
so
that
only
one
additional
angiogram
was
needed
for
research
purposes.
A
total
of
193
patients
who
met
the
first
five
entry
criteria
underwent
quantitative
coronary
arteriography
at
UCSF
and
PPMC.
94
of
these
patients
(49%)
met
the
remaining
entry
criteria.
Of
the
94
eligible
patients,
53
were
randomly
assigned
to
the
experimental
group
and
43
to
the
control
group;
28
(53%)
and
20
(42%),
respectively,
agreed
to
take
part.
All
patients
who
were
eligible
and
volunteered
were
accepted
into
the
study.
These
patients
represented
a
cross-section
of
age,
gender,
race,
ethnic
group,
socioeconomic
status,
and
educational
level.
Each
gave
fully
informed
written
consent
and
the
study
was
approved
by
the
relevant
ethical
committees.
Follow-up
angiographic
data
were
not
available
for
7
patients:
1
control-group
patient
underwent
emergency,
non-quantitative
angiography
in
another
hospital;
and
of
the
6
experimental-group
patients,
1
died
while
greatly
exceeding
exercise
recommendations
in
an
unsupervised
gym,
1
could
not
be
tested
owing
to
a
large
unpaid
hospital
bill,
1
was
a
previously
undiagnosed
alcoholic
who
dropped
out,
1
patient’s
preintervention
angiogram
was
lost
in
transit
to
Houston
for
quantitative
analysis,
and
2
patients’
angiographic
views
before
and
after
intervention
did
not
match
adequately
owing
to
technical
difficulties.
Selective
coronary
angiography
was
done
by
the
percutaneous
femoral
technique.
The
two
laboratories
were
calibrated
at
baseline
and
every
6
months
thereafter.
Orthogonal
views
were
obtained,
and
the
angle,
skew,
rotation,
table
height,
and
type
of
catheter
were
recorded
during
the
baseline
angiogram
to
allow
these
measurements
to
be
reproduced
during
angiography
about
a
year
(15
[SD
3]
months)
later.
Baseline
and
follow-up
measures
were
identical
in
the
view
angles,
their
sequence,
type
of
contrast
dye,
the
angiographer,
and
the
cine
arteriographic
equipment.
Catheter
tips
were
saved
and
used
as
reference
measures
for
quantitative
analyses
of
films.
Cine
arteriograms
made
in
San
Francisco
were
sent
to
the
University
of
Texas
Medical
School
at
Houston
for
quantitative
analyses
by
a
protocol
described
elsewhere
in
detail.’
4
Blood
samples
for
measurement
of
serum
lipids
were
drawn
(after
a
14
h
fast)
at
baseline,
after
6
months,
and
after
a
year.
Total
cholesterol,
HDL-cholesterol,
and
triglyceride
concentrations
were
measured
by
’Astra’
enzymic
assays
(Beckman
Instruments,
Brea,
California).
LDL
was
calculated
as
total
cholesterol
minus
HDL-cholesterol
plus
0-16
x
triglycerides.
Apolipoproteins
A-I
and
B
were
measured
by
disc
gel
electrophoresis
and
by
isoelectric
focusing.6
To
check
adherence
to
the
programme
patients
completed
a
3-day
diet
diary
at
baseline
and
after
a
year
to
assess
nutrient
intake
and
dietary
adherence.7
These
diaries
were
analysed
by
means
of
the
CBORD
diet
analyser
based
upon
the
USDA
database
(CBORD
Group
Inc,
Ithaca,
New
York,
USA).
Patients
were
asked
to
complete
a
questionnaire
describing
the
type,
frequency,
and
duration
of
exercise
and
of
each
stress
management
technique.
Patients
who
said
they
had
stopped
smoking
underwent
random
tests
of
plasma
cotinine.8
Information
from
the
adherence
questionnaires
was
quantified
by
a
formula
determined
before
the
study.
A
total
score
of
1
indicated
100%
adherence
to
the
recommended
lifestyle
change
programme,
and
0
indicated
no
adherence.
Patients
who
did
more
than
we
recommended
achieved
a
score
greater
than
1.
To
reduce
the
possibility
that
knowledge
of
group
assignment
might
bias
the
outcome
measurements,
the
investigators
carrying
TABLE
I-BASELINE
CHARACTERISTICS
OF
EXPERIMENTAL
AND
CONTROL GROUPS
out
all
medical
tests
remained
unaware
of
both
patient
group
assignment
and
the
order
of
the
tests.
Different
people provided
the
lifestyle
intervention,
carried
out
the
tests,
analysed
the
results,
and
carried
out
statistical
analyses.
Coronary
arteriograms
were
analysed
without
knowledge
of
sequence
or
of
group
assignment.
The
intervention
began
with
a
week-long
residential
retreat
at
a
hotel
to
teach
the
lifestyle
intervention
to
the
experimental-group
patients.
Patients
then
attended
regular
group
support
meetings
(4
h
twice
a
week).
Experimental-group
patients
were
asked
to
eat
a
low-fat
vegetarian
diet
for
at
least
a
year.
The
diet
included
fruits,
vegetables,
grains,
legumes,
and
soybean
products
without
caloric
restriction.
Some
take-home
meals
were
provided
for
those
who
wanted
them.
No
animal
products
were
allowed
except
egg
white
and
one
cup
per
day
of non-fat
milk
or
yoghurt.
The
diet
contained
approximately
10%
of
calories
as
fat
(polyunsaturated/saturated
ratio
greater
than
1),
15-20%
protein,
and
70-75%
predominantly
complex
carbohydrates.
Cholesterol
intake
was
limited
to
5
mg/day
or
less.
Salt
was
restricted
only
for
hypertensive
patients.
Caffeine
was
eliminated,
and
alcohol
was
limited
to
no
more
than
2
units
per
day
(alcohol
was
excluded
for
anyone
with
a
history
of
alcoholism,
and
no
one
was
encouraged
to
drink).
The
diet
was
nutritionally
adequate
and
met
the
recommended
daily
allowances
for
all
nutrients
except
vitamin
B12’
which
was
supplemented.
The
stress
management
techniques
included
stretching
exercises,
breathing
techniques,
meditation,
progressive
relaxation,
and
imagery.3,9-12
The
purpose
of
each
technique
was
to
increase
the
patient’s
sense
of
relaxation,
concentration,
and
awareness.
Patients
were
asked
to
practise
these
stress
management
techniques
for
at
least
1
h
per
day
and
were
given
a
1
h
audiocassette
tape
to
assist
them.
Only
1
patient
in
the
experimental
group
was
smoking
at
baseline,
and
she
agreed
to
stop
on
entry.
Patients
were
individually
prescribed
exercise
levels
(typically
walking)
according
to
their
baseline
treadmill
test
results.
Patients
were
asked
to
reach
a
target
training
heart
rate
of
50-80%
of
the
heart
rate
at
which
1
mm
ST
depression
occurred
during
baseline
treadmill
testing
or,
if
not
ischaemic,
to
50-80%
of
their
age-adjusted
maximum
heart
rate
based
on
level
of
conditioning.
Patients
were
also
trained
to
identify
exertional levels
by
means
of
the
Borg
rate
of
perceived
exertion
scale.13
Patients
were
asked
to
exercise
for
a
minimum
of 3 h
per
week
and
to
spend
a
minimum
of
30
min
per
session
exercising
within
their
target
heart
rates.
A
defibrillator
and
emergency
drugs
were
available
at
all
times.
The
twice-weekly
group
discussions
provided
social
support
to
help
patients
adhere
to
the
lifestyle
change
programme.’"
The
TABLE
II-MEAN
LESION
CHARACTERISTICS
AT
BASELINE
____________________________________!____________
195
lesions:
105
experimental,
90 control.
131
TABLE
III-COMPLIANCE
WITH
EXERCISE,
STRESS
MANAGEMENT,
AND
DIETARY
CHANGES
*Percentage
of
minimum
recommended
level
of
combined
lifestyle
change;
Includes
all
the
above
plus
smoking
cessation
TABLE
IV-CHANGES
IN
RISK
FACTORS
sessions
were
led
by
a
clinical
psychologist
who
facilitated
discussions
of
strategies
for
maintaining
adherence
to
the
programme,
communication
skills,
and
expression
of feelings
about
relationships
at
work
and
at
home.
Differences
in
baseline
characteristics
of
the
two
groups
were
tested
for
statistical
significance
by
conventional
t
tests.
Comparisons
of
the
two
study
groups’
baseline
coronary
artery
lesion
characteristics
(measured
by
quantitative
coronary
angiography)
and
changes
in
lesion
characteristics
after
intervention
were
examined
by
a
mixed-model
analysis
of
variance.1S
These
analyses
used
lesion-specific
data
but
allowed
for
the
possibility
that
lesion
data
in
a
given
subject
could
be
statistically
dependent.
Mean
changes
in
other
endpoint
measures
were
analysed
for
statistical
significance
by
repeated-measures
analysis
of
variance.
Results
At
baseline,
there
were
no
significant
differences
between
the
experimental
and
control
groups
in
demographic
characteristics
(table
1),
diet
and
lifestyle
characteristics,
functional
status,
cardiac
history,
or
risk
factors
in
the
41
subjects
who
completed
angiography
before
and
after
the
intervention.
The
control
group
had
significantly
higher
levels
of HDL-cholesterol
(1-33
[SD
052]
vs
1-02
[031]
mmol/1;
p=0029)
and
apolipoprotein
A-1
(156
(36)
vs
133
(21)
mg/dl;
p
=
0-0155)
than
the
experimental
group,
but
the
ratios
of total/HDL
cholesterol
and
LDL/HDL
cholesterol
did
not
differ
significantly
between
the
groups
at
baseline.
The
experimental
and
control
groups
did
not
differ
significantly
in
disease
severity
at
baseline.
The
mean
values
in
table
n
do
not
fully
reflect
the
severity
of
coronary
atherosclerosis
in
these
patients
for
the
following
reasons:
quantitative
analyses
of
coronary
arteriograms
tend
to
assess
stenoses
as
being
less
severe
than
do
qualitative
assessments;
we
analysed
all
detectable
lesions,
including
minor
ones;
and
we
excluded
from
analysis
33
lesions
that
were
100%
occluded
at
baseline.
Adherence
to
the
diet,
exercise,
and
stress
management
components
of
the
lifestyle
programme
in
the
experimental
group
was
excellent
(table
ill).
Patients
in
the
control
group
made
more
moderate
changes
in
lifestyle
consistent
with
more
conventional
recommendations.
Table
IV
summarises
changes
in
risk
factors
during
the
intervention
period.
In
the
experimental
group,
total
cholesterol
fell
by
24-3%
and
LDL-cholesterol
by
37-4%.
These
falls
occurred
even
though
patients
had
already
reduced
fat
consumption
to
31 5%
of
calories
and
TABLE
V-CHANGES
IN
ANGINA
SYMPTOMS
*Scale
of
1
to
7,
1
least
severe.
132
Correlation
of
overall
adherence
score
and
changes
in
percentage
diameter
stenosis
in
experimental
group
only
(A)
and
in
whole
study
group
(B).
A=7
subjects
in
each
tertile;
B = 13, 14.
13.
cholesterol
intake
to
213
mg/day
on
average
before
baseline
testing.
HDL-cholesterol
did
not
change
significantly
in
either
group.
Apolipoprotein
B
fell
substantially
in
the
experimental
group
but
it
did
not
change
in
the
control
group.
Neither
group
had
significant
changes
in
apolipoprotein
A-1.
Patients
in
the
experimental
group
reported
a
91 %
reduction
in
the
frequency
of
angina,
a
42%
reduction
in
duration
of
angina,
and
a
28%
reduction
in
the
severity
of
angina.
In
contrast,
control-group
patients
reported
a
165 %
rise
in
frequency,
a
95%
rise
in
duration,
and
a
39%
rise
in
severity
of
angina
(table
v).
In
previous
studies,2,3
we
found
that
similar
improvements
in
functional
status
occurred
in
only
1
month,
which
suggests
that
improvements
in
angina
may
precede
regression
of
coronary
atherosclerosis,
perhaps
by
changing
platelet-endothelial
interactions,
vasomotor
tone,
or
other
dynamic
characteristics
of
stenoses.
All
195
detectable
lesions
were
included
in
the
quantitative
analysis.
The
average
percentage
diameter
stenosis
decreased
from
40-0
(SD
16-9)%
to
37-8
(16-5)%
in
the
experimental
group
yet
progressed
from
42.7
(15 5)%
to
46.1
1 (18-5)%
in
the
control
group
(p = 0-001,
two-tailed).
When
only
lesions
greater
than
50%
stenosed
were
analysed,
the
average
percentage
diameter
stenosis
regressed
from
61-1
(8-8)%
to
55-8
(11 -0)%
in
the
experimental
group
but
progressed
from
61-7
(9-5)%
to
64-4
(163)%
in
the
control
group
(p
=
0-03,
two-tailed).
The
average
lesion
change
scores
(%
diameter
stenosis
after
intervention
minus
before
intervention)
in
the
experimental
group
were
in
the
direction
of
regression
of
coronary
atherosclerosis
in
18
of
the
22
patients
(82%)
including
the
1
woman,
in
the
direction
of
slight
progression
in
3
patients,
and
in
the
direction
of
substantial
progression
in
1
patient
with
poor
adherence.
In
contrast,
in
the
control
group
the
average
lesion
change
scores
were
in
the
direction
of
progression
of
coronary
atherosclerosis
in
10
of
19
(53%),
in
the
direction
of
regression
(including
all
4
women)
in
8,
and
1
showed
no
change.
In
the
experimental
group
and
in
the
whole
study
group,
overall
adherence
to
the
lifestyle
changes
was
strongly
related
to
changes
in
lesions
in
a
"dose-response"
manner,
suggesting
that
the
relation
was
causal.
The
differences
in
overall
adherence
are
sufficient
to
explain
the
observed
differences
in
percentage
diameter
stenosis.
To
assess
whether
programme
adherence
was
related
to
lesion
changes,
the
experimental
group
and
the
combined
study
group
were
divided
into
tertiles
based
on
overall
adherence
score.
Degree
of
adherence
was
directly
correlated
with
changes
in
percentage
diameter
stenosis
(see
accompanying
figure).
Discussion
This
clinical
trial
has
shown
that
a
heterogeneous
group
of
patients
with
coronary
heart
disease
can
be
motivated
to
make
comprehensive
changes
in
lifestyle
for
at
least
a
year
outside
hospital.
The
changes
in
serum
lipid
levels
are
similar
to
those
seen
with
cholesterol-lowering
drugs.
The
lifestyle
intervention
seems
safe
and
compatible
with
other
treatments
of
coronary
heart
disease.
After
a
year,
patients
in
the
experimental
group
showed
significant
overall
regression
of
coronary
atherosclerosis
as
measured
by
quantitative
coronary
arteriography.
Since
coronary
atherosclerosis
occurs
over
a
period
of
decades,
one
would
not
expect
to
find
larger
changes
in
only
a
year.
Perfusion
is
a
fourth-power
function
of
coronary
artery
diameter,
so
even
a
small
amount
of
regression
in
a
critically
stenosed
artery
has
a
large
effect
on
myocardial
perfusion
and
thus
on
functional
status.
In
contrast,
patients
in the
usual-care
control
group
who
were
making
less
comprehensive
changes
in
lifestyle
showed
significant
overall
progression
of
coronary
atherosclerosis.
This
finding
suggests
that
conventional
recommendations
for
patients
with
coronary
heart
disease
(such
as
a
30%
fat
diet)
are
not
sufficient
to
bring
about
regression
in
many
patients.
The
strong
relation
between
programme
adherence
and
lesion
changes
showed
that
most
patients
needed
to
follow
the
lifestyle
programme
as
prescribed
to
show
regression.
Those
who
made
the
greatest
changes
showed
the
biggest
improvement.
Since
degree
of
stenosis
change
was
correlated
with
extent
of
lifestyle
change
across
its
whole
range,
small
changes
in
lifestyle
may
slow
the
progression
of
atherosclerosis,
whereas
substantial
changes
in
lifestyle
may
be
required
to
halt
or
reverse
coronary
atherosclerosis.
The
5
women
in
our
study
(1
experimental
group,
4
control
group)
were
the
notable
exceptions.
All
5
made
only
moderate
lifestyle
changes,
yet
all
showed
overall
regression.
All
5
were
postmenopausal,
and
none was
taking
exogenous
oestrogens.
The
4
women
in
the
control
group
showed
more
133
regression
than
any
of
the
men
in
that
group,
even
though
some
men
made
greater
lifestyle
changes.
Although
the
numbers
are
small,
these
findings
suggest
the
possibility
that
gender
may
affect
progression
and
regression
of
atherosclerosis.
Futher
studies
may
determine
whether
women
can
reverse
coronary
atherosclerosis
with
more
moderate
lifestyle
changes
than
men.
5
men
in
the
control
group
showed
very
slight
regression
of
atherosclerosis.
These
patients
exercised
more
often,
for
longer
periods,
and
consumed
fewer
calories
and
less
cholesterol
than
the
control-group
patients
who
showed
progression
of
atherosclerosis.
We
found
that
the
severely
stenosed
lesions
showed
the
greatest
improvement.
Although
the
opposite
of
what
we
expected,
the
finding
is
important
since
more
severely
stenosed
lesions
are
the
most
important
clinically.
More
work
is
needed
to
determine
the
extent
to
which
the
relation
between
change
and
initial
site
of
lesions
is
affected
by
the
phenomenon
of
regression
to
the
mean.
Increasing
evidence
supports
the
roles
of
diet,
exercise,
emotional
stress,
and
smoking
in
the
pathogenesis
of
coronary
heart
disease,16-18
but
until
lately
evidence
for
regression
of
coronary
atherosclerosis
was
limited
or
anecdotal.
There
are
case-reports
of
regression
involving
femoral’9
and
renal
arteries,z°
and
one
case-report
of
spontaneous
regression
in
a
coronary
artery.21
However,
several
studies
have
found
that
regression
of
coronary
atherosclerosis
can
occur
spontaneously
in
the
absence
of
lifestyle
changes
or
treatment
with
drugs,22-24
thereby
making
it
necessary
for
intervention
trials
to
be
controlled.
Only
two
other
randomised,
controlled
trials
showing
regression
of
coronary
atherosclerosis
have
been
reported ’222325
and
both
used
cholesterol-lowering
drugs
as
the
primary
interventions.
Some
important
questions
remain
unanswered.
Can
these
comprehensive
lifestyle
changes
be
sustained
in
larger
populations
of
patients
with
coronary
heart
disease?
The
point
of
our
study
was
to
determine
what
is
true,
not
what
is
practicable.
The
adherence
measures
and
the
angiographic
findings
suggest
that
adherence
to
this
lifestyle
programme
needs
to
be
very
good
for
overall
regresion
to
occur,
although
more
moderate
changes
have
some
beneficial
effects.
Further
research
will
be
necessary
to
determine
the
relative
contribution
of
each
component
of
the
lifestyle
programme
and
the
mechanisms
of
changes
in
coronary
atherosclerosis.
It
would
be
interesting
to
examine
the
effects
of
lifestyle
changes
in
a
larger
sample
of
postmenopausal
women
with
coronary
atherosclerosis.
Also,
direct
comparison
of
intensive
lifestyle
changes
with
pharmacological
or
surgical
interventions
would
be
interesting.
Our
trial
suggests
that
comprehensive
lifestyle
changes
may
begin
to
reverse
coronary
atherosclerosis
in
only
a
year.
This
study
was
supported
by
grants
from
the
National
Heart,
Lung,
and
Blood
Institute
of
the
National
Institutes
of
Health
(ROl
HL42554),
the
Department
of
Health
Services
of
the
State
of
California
(no
1256SC-01),
Gerald
D.
Hines
Interests,
Houston
Endowment
Inc,
the
Henry
J.
Kaiser
Family
Foundation.
the
John
E.
Fetzer
Institute,
Continental
Airlines,
the
Enron
Foundation,
the
Nathan
Cummings
Foundation,
the
Pritzker
Foundation,
the
First
Boston
Corporation,
Quaker
Oats
Co.,
Texas
Commerce
Bank,
Corrine
and
David
Gould,
Pacific
Presbyterian
Medical
Center
Foundation,
General
Growth
Companies,
Arthur
Andersen
and
Co.,
and
others.
Investigators
who
took
part
in
the
trial
include:
administrator,
Myma
Melling;
counsellors,
Pamela
Lea
Byrne,
Carol
Naber;
stress
management
instructor,
Mary
Dale
Scheller;
exercise
instructors,
Terri
Merrit,
Lawrence
Spann,
Sarah
Spann;
chefs,
Celeste
Burwell,
Mary
Carroll,
Carol
Connell,
Jean-Marc
Fullsack,
Mark
Hall,
Jules
Stenzel;
quantitative
angiography
analysers,
Dale
Jones,
Yvonne
Stuart;
head
angiography
nurses,
LaVeta
Luce,
Geogie
Hesse;
angiographers,
Craig
Brandman,
Bruce
Brent,
Ralph
Clark,
Keith
Cohn,
James
Cullen,
Richard
Francoz,
Gabriel
Gregoratos,
Lester
Jacobsen,
Roy
Meyer,
Gene
Shafton,
Brian
Strunk,
Anne
Thorson;
radiologists
Robert
Bernstein,
Myron
Marx,
Gerald
Needleman,
John
Wack;
lipid
laboratory
directors,
Washington
Bums,
John
Kane,
Steve
Kunitake;
medical
liaison,
Patricia
McKenna;
research
assistants,
Patricia
Chung,
Stephen
Sparier;
secretaries,
Claire
Finn,
Kathy
Rainbird.
REFERENCES
1.
Arntzenius
AC.
Regression
of
atherosclerosis.
Presented
at
the
Second
International
Conference
on
Preventive
Cardiology,
Washington,
DC,
June,
1989.
2.
Ornish
DM,
Gotto
AM,
Miller
RR,
et
al.
Effects
of
a
vegetarian
diet
and
selected
yoga
techniques
in
the
treatment
of coronary
heart
disease.
Clin
Res
1979;
27: :
720A.
3. Ornish
DM,
Scherwitz
LW,
Doody
RS,
et
al.
Effects
of
stress
management
training
and
dietary
changes
in
treating
ischemic
heart
disease.
JAMA
1983;
249: 54-59.
4.
Gould
KL.
Identifying
and
measuring
severity
of
coronary
artery
stenosis.
Quantitative
coronary
arteriography
and
positron
emission
tomography.
Circulation
1988;
78: 237-45.
5.
Current
status
of blood
cholesterol
measurement
in
clinical
laboratories
in
the
US:
a
report
from
the
Laboratory
Standardization
Panel
of
the
National
Cholesterol
Education
Program.
Clin
Chem
1988;
34: 193.
6.
Kane
JP,
Sata
T,
Hamilton
RK,
Havel
RJ.
Apoprotein
composition
of
very
low
density
lipoproteins
of
human
serum.
J
Clin
Invest
1975;
56:
1622-34.
7.
Stuff
JE,
Garza
C,
Smith
EO,
et
al. A
comparison
of
dietary
methods
in
nutritional
studies.
Am J
Clin
Nutr
1983;
37:
300-06.
8.
Benowitz
NL.
Pharmacologic
aspects
of
cigarette
smoking
and
nicotine
addiction.
N
Engl J
Med
1988;
319:
1318-30.
9.
Ornish
DM.
Reversing
heart
disease.
New
York:
Random
House,
1990.
10.
Patel
C,
North
WR.
Randomised
controlled
trial
of
yoga
and
bio-
feedback
in
management
of
hypertension.
Lancet
1975;
ii:
93-95.
11.
Patel
C,
Marmot
MG,
Terry
DJ,
Carruthers
M,
Hunt
B,
Patel
M.
Trial
of
relaxation
in
reducing
coronary
risk:
four
year
follow
up.
Br
Med J
1985;
290: 1103-06.
12.
Benson
H,
Rosner
BA,
Marzetta
BR,
Klemchuk
HM.
Decreased
blood
pressure
in
pharmacologically
treated
hypertensive
patients
who
regularly
elicited
the
relaxation
response.
Lancet
1974;
i:
289-91.
13.
American
College
of
Sports
Medicine.
Guidelines
for
exercise testing
and
prescription.
Philadelphia:
Lea
&
Febiger,
1986.
14.
Orth-Gomer
K,
Unden
AL,
Edwards
ME.
Social
isolation
and
mortality
in
ischemic
heart
disease.
Acta
Med
Scand
1988;
224:
205-15.
15.
Dixon
WS,
ed,
et
al.
BMDP3V
statistical
software,
1983
printing
with
additions.
Berkeley:
University
of
California
Press,
1983.
16.
Kornitzer
M,
DeBacker
G,
Dramaix
M,
et
al.
Belgian
heart
disease
prevention
project:
incidence
and
mortality
results.
Lancet
1983;
i:
1066-70.
17.
Kaplan
JR,
Manuck
SB,
Clarkson
TB,
et
al.
Social
stress
and
atherosclerosis
in
normocholesterolemic
monkeys.
Science
1983;
220:
733-35.
18.
US
Department
of
Health
and
Human
Services.
Reducing
the
health
consequences
of
smoking:
25
years
of progress.
A
report
of the
Surgeon
General.
Washington
DC:
DHHS
Publication
#
(CDC)
89-8411,
1989.
19.
Barndt
R,
Blankenhorn
DH,
Crawford
DW,
et
al.
Regression
and
progression
of
early
femoral
atherosclerosis
in
treated
hyperlipoproteinemic
patients.
Ann
Intern
Med
1977;
86: 139-46.
20.
Basta
LL,
Williams
C,
Kioschos
JM.
Regression
of
atherosclerotic
stenosing
lesions
of
the
renal
arteries
and
spontaneous
cure
of
systemic
hypertension
through
control
of hyperlipidemia.
Am
J
Med
1976;
61:
420-23.
21.
Roth
D,
Kostuk
WJ.
Noninvasive
and
invasive
demonstration
of
spontaneous
regression
of coronary
artery
disease.
Circulation
1980;
62:
888-96.
22.
Blankenhom
DH,
Nessim
SA,
Johnson
RL,
et
al.
Beneficial
effects
of
combined
colestipol-niacin
therapy
on
coronary
atherosclerosis
and
coronary
venous
bypass
grafts.
JAMA
1987;
257:
3233-40.
23.
Brown
BG,
Lin
JT,
Schaefer
SM,
et
al.
Niacin
or
lovastatin,
combined
with
colestipol,
regress
coronary
atherosclerosis
and
prevent
clinical
events
in
men
with
elevated
apolipoprotein
B.
Circulation
1989;
80:
II-266.
24.
Brown
BG,
Bolson
EL,
Dodge
HT
Arteriographic
assessment
of
coronary
atherosclerosis.
Review
of
current
methods,
their
limitations,
and
clinical
applications.
Arteriosclerosis
1982;
2: 2-15.
25.
Blankenhom
DH,
Johnson
RL,
El
Zein
HA,
et
al.
Dietary
fat
influences
human
coronary
lesion
formation.
Circulation
1988;
78
(suppl
II):
11.

Discussion

This is a major diet change for these individuals, and they were largely able to stick to it for an entire year, with most people preparing their own meals. Ornish tracked the patients for 5 years after the study and found that the patients had changed their lifestyle for good, with 99 percent stopping or reversing the progress of heart disease. These support groups are essential to sustain behavior change (most famous example is Alcoholics Anonymous). This study is remarkable: only two other randomized control trials had shown regression of coronary atherosclerosis up that point, and they both were drug interventions. This study of lifestyle change was published in the premier medical journal: The Lancet. It generated significant press and discussion because the general medical audience did not have "lifestyle changes" in their belief systems or "frames" (to use a behavior science term). The lifestyle change that the patients underwent was only possible because the patients wanted to change. The three R's of behavioral change are Relate, Repeat, and Reframe. Support groups and empathy exercises help the patients Relate at the beginning of the lifestyle change period, so that they are motivated to repeat the good behavior and make it into a habit. Coronary atherosclerosis affects arteries that carry blood to the heart muscle and is called coronary artery disease. Coronary artery disease is the No. 1 cause of death of Americans. Most of these deaths come from heart attacks caused by blood clots. ![Imgur](https://i.imgur.com/3gsmHY5.png) Quantitative coronary angiography is a a medical imaging technique that visualizes the inside of blood vessels and organs of the body, with particular interest in the arteries, veins and the heart chambers. This is usually done by injecting a radio-opaque contrast agent into the blood vessel and imaging using X-ray based techniques like fluoroscopy. Angiography was first developed in 1927 by the Portuguese physician and neurologist Egas Moniz at the University of Lisbon. ![Imgur](https://i.imgur.com/l2jyDQL.png) 82% is a stunning result-> the percentage of patients whose arteries were not as clogged after only 1 year of lifestyle change. Amazingly, despite the results of this study, as well as numerous other lifestyle studies performed by Dr. Ornish and others that changed the lives of the patients involved, the medical establishment has not changed. Critics says that plant-based diets can work in places like SF, but not in the American mainland. Amazingly, Ornish's next major study, published in 1993 and funded by an insurance company called Mutual of Omaha, had remarkable results all around the country: in Omaha, Des Moines, and Columbia, and South Carolina. Dr. Dean Ornish is an American physician and researcher, the president and founder of the nonprofit Preventive Medicine Research Institute, and a Clinical Professor of Medicine at UCSF. Dr. Ornish is a strong advocate for using diet and lifestyle changes (like plant-based diets, exercise, stress management, psychosocial support) to treat and prevent heart disease as well as other chronic diseases. In 1993, Dr. Ornish was the first person to gain approval for insurance reimbursement for a non-surgical, non-pharmaceutical therapy for heart disease. The therapy combined diet, meditation, exercise and support groups interventions for people with heart disease and had remarkable success. Besides chiropractic care, it was the first alternative medical technique to gain approval by any major insurance carrier.