WELL, GOOD AFTERNOON OR GOOD
MORNING.
I'M CATHERINE LAW AT THE
NATIONAL CENTER AT NCCIH
NATIONAL INSTITUTES OF HEALTH
AND ON BEHALF OF HELENE LANGEVIN
AND DR. DAVID SHURTLEFF I
WELCOME YOU TO THE 2023 STEPHEN
E. STRAUS DISTINGUISHED LECTURE
IN THE SCIENCE OF COMPLIMENTARY
THERAPIES.
OUR SPEAKER WILL BE DR. AHMED
TAWAKOL OF MASSACHUSETTS GENERAL
HOSPITAL AND HARVARD MEDICAL
SCHOOL IN MASSACHUSETTS AND THE
LINK IS BELOW THE STREAM FOR THE
FEEDBACK.
IF YOU CANNOT FIND THE LINK FOR
SOME REASON YOU CAN E-MAIL YOUR
QUESTIONS THE ADDRESS IS NCCIH
EVENTS AS ONE WORD AT MAIL DOT
NIH GOT GOV.
DURING THE Q&A WE'LL TRY TO GET
AS MANY QUESTIONS ANSWERED AS WE
CAN HOWEVER, WE MAY NOT BE ABLE
TO GET TO ALL QUESTIONS BUT
WE'LL SHARE THEM WITH
DR. TAWAKOL AFTER THE EVENT.
FINALLY THE PRESENTATION IS
BEING RECORDED AND WILL BE
ARCHIVED IN THE NIH VIDEOCAST
SITE FOR FUTURE VIEWING.
I'D LIKE TO TURN THINGS OVER TO
DR. HELENE LANGEVIN, DIRECTOR OF
NCCIH TO WELCOME OUR SPEAKER AND
SPEAK A LITTLE BIT ABOUT THE
STRAUS LECTURE.
PLEASE TAKE IT AWAY.
>> HELLO AND THANK YOU ALL FOR
TAKING TIME TO JOIN US TODAY WE
LOOK FORWARD TO THIS LECTURE
EACH YEAR AS A VERY SPECIAL TIME
TO HONOR THE MEMORY AND LEGACY
OF DR. STEPHEN E. STRAUS THE
CENTER'S FOUNDING DIRECTOR AND
LED NCCIH FROM 1989 TO 2006.
STEVE WAS AN IMMINENT PHYSICIAN
RESEARCHER AT NIH AND CHAMPIONED
EFFORTS TO ESTABLISH THE
EFFICACY AND SAFETY OF
COMPLIMENTARY AND INTEGRATIVE
HEALTH PRACTICES WHILE UPHOLD
NIH'S RIGOROUS STANDARDS AND
REMEMBERED THROUGHOUT NIH AND
VERY MUCH MISSED.
MRS. BARBARA STRAUSS IS
ATTENDING THE LIVE STREAM TODAY
AND WE WELCOME HERE AND ALWAYS A
GREAT SUPPORTER OF THIS EVENT.
AND I ALSO HAVE SOME ADDITIONAL
THANKS TO SHARE.
MR. BERNARD ORSHER AND
MRS. ORSHER MADE THIS POSSIBLE
AND WANT TO THANK MARY BITTERMAN
THE PRESIDENT OF THE BERNARD O
RSHER FOUNDATION WHO IS ALSO A
WONDERFUL SUPPORTER AND
APPRECIATE NIH'S LONG TERM
PARTNERSHIP WITH NCCIH ON THE
LECTURE SERIES.
THANK YOU ALL.
I'M NOW PLEASED TO WELCOME OUR
LECTURE YOU ARE, DR. AHMED
TAWAKOL WHO WILL SPEAK ON NOVEL
INSIGHTS INTO HEART-BRAIN
INTERACTIONS AND NEUROBIOLOGICAL
RESILIENCE.
WE'RE PLEASED DR. TAWAKOL WOULD
SAR HIS THOUGHTS WITH US TODAY
ON THIS VERY INTERESTING TOPIC.
DR. TAWAKOL IS A CARDIOLOGIST
WITH A CLINICAL AND RESEARCH
FOCUS ON CARDIOVASCULAR IMAGING.
HE IS THE DIRECTOR OF NUCLEAR
CARDIOLOGY AND RESEARCH CENTER
AT MASSACHUSETTS GENERAL
HOSPITAL AND ASSOCIATE PROFESSOR
OF MEDICINE AT HARVARD MEDICAL
SCHOOL.
HE RECEIVED HIS M.D. FROM
STANFORD AND DID A POST-DOCTORAL
TRAINING IN MEDICINE AND
CARDIOLOGY AT BRIGHAM AND
WOMEN'S AND NUCLEAR CARDIOLOGY
AT THE MASSACHUSETTS GENERAL
HOSPITAL.
THE NIH FUNDERS INCLUDE THE
NHLBI AND THE NATIONAL INSTITUTE
OF ARTHRITIS AND MUSCULOSKELETAL
AND SKIN DISEASES.
HIS PIONEERING WORK EXPLORES
CONNECTIONS ACROSS ORGANS AND
SYSTEMS OF THE BODY RELEVANT TO
NCCIH'S INTEREST OF THE WHOLE
PERSON AND FOCUSES ON THE EFFECT
OF STRESS, LIFESTYLE AND
RESILIENCE WHICH ARE OTHER AREAS
OF FOCUS AT NCCIH.
SO WE'RE ALL VERY MUCH LOOKING
FORWARD TO HEARING HIS LECTURE.
SO IT'S MY GREAT PLEASURE TO
WELCOME DR. AHMED TAWAKOL.
>> THANK YOU FOR THE KIND
INTRODUCTION.
IT TRULY IS AN HONOR TO GIVE THE
LECTURE IN THE MEMORY OF
DR. STRAUS.
INDEED HE'S DONE SO MUCH FOR THE
FIELD AND I'M HONORED TO BE HERE
IN THIS POSITION.
TODAY I'LL TALK ABOUT
PSYCHOSOCIAL STRESS AND HOW IT
LEADS TO DISEASE.
WE HAVE KNOWN THE ATTRIBUTE AND
STRESS IS ON PAR WITH SMOKING,
DYSLIPIDEMIA AND DIABETES AND
LITTLE HAD BEEN KNOWN OF THE
MECHANISMS THAT TRANSLATES
STRESS TO CARDIOVASCULAR EVENTS.
WE'VE KNOWN SINCE THE INNER
HEART STUDY, STRESS WHETHER
MEASURED THROUGH 24,000 PATIENTS
SHOWED 55% INCREASED RISK FOR
MYOCARDIAL INFARCTION AFTER
CONTROLLING FOR RISK FACTORS.
WE'VE KNOWN STRESS MAY AFFECT
HEART DISEASE RISK, FOR EXAMPLE,
INACTIVITY, OVER EATING,
HYPERTENSION AND AFTER
ACCOUNTING FOR ALL THESE WE FIND
THOSE FACTS DON'T EXPLAIN THE
OBSERVED EXCESS RISK.
WE STARTED TO LEARN QUITE ABOUT
THE MECHANISMS BY WHICH STRESS
LEADS TO HEART DISEASE THROUGH
ANNAL STUDIES.
IN PARTICULAR, STUDIES PUBLISHED
OVER A DECADE AGO SHOWED THAT
STRESSING MICE, YOU CAN DO SO BY
SHAKING CAGES, CHANGING LITTER
MATE OR PUTTING A CAT ON A MOUSE
CAGE CAN LEAD TO STIMULATION OF
THE BONE MARROW AND DOES SO BY
SYMPATHETIC NERVE GO FROM THE
BRAIN TO THE BONE MARROW AND
TRIGGER THE RELEASE OF
INFLAMMATORY CELLS AND IN THESE
STUDIES THEY FOUND THOSE
INFLAMMATORY CELLS CAN GO TO THE
SPLEEN WHERE THEY'RE READY FOR
THE NEXT INFLAMMATORY INSULT OR
DIRECTLY TO THE CORONARY
ARTERIES.
IN CASE THEY MEASURED THE
ARTERIES IN THE MICE AND FOUND
THE STRESSED MICE HAVE HIGHER
ARTERIAL INFLAMMATION.
WE ASKED IF THE SAME PATH OF
STRESS LEADING STIMULATION OF
THE BONE MARROW AND SPLEEN
RESERVOIRS TO ARTERIAL
INFLAMMATION LEADING TO EVENTS
WOULD BE SEEN ALSO IN HUMANS.
TO DO SO, WE WONDERED IF
INTEGRATIVE MULTI-SYSTEM IMAGING
CAN GIVE THOSE INSIGHT.
WHAT DO I MEAN BY THAT?
WE CAN USE PET CT TO IMAGE THE
BONE MARROW TO IMAGE THE SPLEEN
AND ALSO LOOK AT ARTERIAL
INFLAMMATION.
WE AND OTHERS HAVE SHOWN, FOR
EXAMPLE, THAT YOU CAN MEASURE
SPLENIC ACTIVITY AND BONE MARROW
ACTIVITY.
HERE YOU CAN SEE A BONE MARROW
WITH HIGH ACTIVITY AND HERE IS A
BONE MARROW WITH LOW METABOLIC
ACTIVITY WITH FTG PET.
THAT ACTIVITY ASSOCIATES WITH
THE BIOMARKERS OF INFLAMMATION
LIKE CRP AND IL1 BETA AND GENE
EXPRESSION IN THE CIRCULATING
CELLS.
MOREOVER, IF WE SIMPLY LOOK AT
HIGH VERSUS LOW ACTIVITY AND
FOLLOW PATIENTS OVER TIME WE
SHOW PATIENTS WITH RELATIVELY
LOW ACTIVITY, LESS THAN ME
MEDIAN HAVE FEWER MYOCARDIAL
INFARCTIONS WITH THOSE WITH
HIGHER ACTIVITY IN THE BONE
MARROW.
LIKEWISE WE CAN LOOK AT THE
ACTIVITY IN THE ARTERIES AND
HERE'S EXAMPLES OF AORTIC
ACTIVITY AND SEE ELEVATED
ACTIVITY IN THE WALLS OF THE
AORTA AND HERE IS ACTIVE IN THE
CAROTID ARTERIES AND HERE'S A
COMPLEX PLAQUE AND WITHIN THE
AREA OF THE PLAQUE YOU CAN SEE
INCREASED METABOLIC ACTIVITY AND
IF YOU LOOK AT IT AT A CROSS
SECTION HERE AGAIN IS A PLAQUE
AND THE AREA OF STENOSIS AND
WHERE THE BLOOD FLOW IS AND
HERE'S THE INTENSE METABOLIC
ACTIVITY.
WHEN THIS PERSON WENT FOR
SURGERY OF THE NARROWED VESSEL
WE HAVE THE SPECIMEN WHERE WE'RE
ABLE TO SLOW THE MEASURE
CORRELATED WITH THE DEGREE OF
ACTIVITY ACROSS THIS GROUP OF
PATIENTS SO ACROSS OUR PATIENTS
WE SEE THE MACROPHAGE DENSITY
AND HISTOLOGY WAS PREDICTIVE OF
HOW MUCH INFLAMMATION WAS SEEN.
AND IN FACT SEVERAL GROUPS HAVE
LONG SINCE SHOWN THAT THERE'S A
CORRELATION FROM WHAT'S SEEN
HIST
HISTOP
HISTOPATHOLOGICALLY AND IT
PREDICTS SUBSEQUENT
CARDIOVASCULAR DISEASE EVENTS.
INDIVIDUALS WITH HIGHER SIGNALS
TEND TO HAVE MORE EVENTS
COMPARED TO THOSE WITH LOWER
IMAGING SIGNALS.
HERE'S A STUDY DIVIDED ACROSS
THE MEDIAN AND HERE WITH THOSE
WITH THE HIGHEST IMAGING OF
ARTERIES ARE HIGHER EVENTS AND
THAT CAN TELL YOU SOMETHING
ABOUT SUBSEQUENT EVENTS.
IN FACT, NOW SEVERAL GROUPS AND
IN FACT THE GUIDELINE
RECOMMENDATIONS FOR EVALUATING
INFLAMMATION HAS TRIGGERED THE
ASSESSMENT OF INFLAMMATION FOR
AORTITIS AND DEVICE INFECTION
FOR CLINICAL INDICATIONS AMONG
OTHERS.
NOW WE HAVE AN OPPORTUNITY TO
LOOK AT MULTIPLE ORGANS BUT WHAT
ABOUT STRESS?
HOW SHOULD WE MEASURE STRESS?
WE COULD GIVE A PERCEIVED STRESS
TEST AND INVITE YOU TO TAKE THE
TEST AND WE CAN MEASURE THIS BY
IMAGING THE BRAIN.
FOR EXAMPLE, WE CAN MEASURE THE
PREFRONTAL CORTEX OR AMYGDALA,
TWO AREAS THAT IS HAVE IMPORTANT
ROLES IN THE ASSESSMENT OF
STRESS.
FOR EXAMPLE, THE PRE-FRONTAL
CORTEX WILL BE IMPORTANT DURING
ALERT NON-STRESS CONDITIONS
WHERE AS THE AMYGDALA TENDS TO
BE MORE ACTIVE DURING STRESS
CONDITIONS.
I'LL TELL YOU A LITTLE BIT MORE
ABOUT THAT.
OVER TIME WITH CHRONIC STRESS
THE AMYGDALA TENDS TO DEVELOP
MORE SPINAL DENDRITIC GROWTH.
THE NEURONS BECOME MORE
ARBORIZED WHEREAS IN STRESSFUL
CONDITIONS THE CORTEX STARTS TO
HAVE REVERSIBLE DENDRITIC
ATROPHY AND BECOMES LESS
RESPONSIVE OVER TIME.
WE CAN USE IMAGING TO ASSESS
SOME OF THESE.
FOR EXAMPLE, WE HAVE LONG KNOWN
THAT INDIVIDUALS WITH GREATER
AMYGDALA ACTIVITY MEASURED BY
FUNCTIONAL MRI HAVE GREATER
BLOOD PRESSURE REACTIVITY AND
PRODUCE MORE INFLAMMATORY
CYTOKINES AND MORE ATHEIR --
ATHEROSCLEROSIS AND WE CAN
MEASURE IN THE AMYGDALA AND IN
THE PRIMATE MODEL SHOWED THE
TEMPERAMENT OF THE PRIMATES
SHOWED WITH THE UPTAKE IN THE
AMYGD
AMYGDALA.
SO PUTTING THIS TOGETHER, WE CAN
MEASURE THE NEURON BIOLOGY OF
STRESS USING FGT PET TO LOOK AT
AMYGDALA ACTIVITY REGULAR TO
CORTICAL ACTIVITY.
IN THIS CASE THE RATIO OF THE
ACTIVITY IN THE AMYGDALA DIVIDED
BY THE ACTIVITY IN THE
PREFRONTAL CORTEX OR TEMPORAL
LOBE AND LOOK AT NEURAL ACTIVITY
AND ACTIVITY WHERE HEIGHTENED
ACTIVATION IS SEEN IN THE
AMYGDALA IN REPRESENTATION TO
STRESSFUL STIMULI OR SIMPLY
REDUCED ACTIVITY WITH REGULATORY
TISSUES AND MEASURE TISSUE
VOLUMES AND THE AMYGDALA SHRINKS
WHEN THERE'S CHRONIC STRESS
PROBABLY DUE TO LOSS OF COUNTER
REGULATORY CONNECTIONS AND LOOK
AT THE TENSER IMAGING OF THE
AXONS.
HERE'S AN OPPORTUNITY TO USE
INTEGRATIVE BIO IMAGING WITH PET
CT OR PET MR LOOKING AT RESTING
NEUROLOGICAL ACTIVITY AND LOOK
AT FUNCTIONAL MRI, STRUCTURE OF
THE ATHEROSCLEROSIS OR
ATHEROSCLEROTIC INFLAMMATION ALL
AT THE SAME TIME.
INDEED WE SAW HIGHER STRESSED
NEURAL ACTIVITY ASSOCIATES WITH
A HIGHER RISK OF CARDIOVASCULAR
DISEASE.
WE DID THIS USING THE IMAGING
WITH FTC PET GC AND PET MRI
QUANTIFYING THE ACTIVITY AND
LOOKED AT THE LEUKO POIETIC
ACTIVITY AND AFTER EXCLUSIONS WE
HAD A POPULATION OF 2 93
INDIVIDUALS WITH ADEQUATE
BASELINE DATA.
WHAT WE FOUND IS THE FOLLOWING.
FIRST, THAT AMYGDALA MEASURED
NICELY PREDICTED SUBSEQUENT
CARDIOVASCULAR DISEASE EVENTS
AND THAT'S AFTER ROBUST
ADJUSTMENT AND IT WAS STRING
STRINGESTRING
STRINGENTLY ASSOCIATED WITH
DEFINED EVENTS GOING FROM
CARDIOVASCULAR DISEASE EVENT TO
MAJOR ADVERSE CARDIAC EVENTS
FOUND HIGHER RISK ASSOCIATED
WITH THE IMAGING SIGNAL.
IF WE LOOKED AT THE TIMING WE
FOUND SOMETHING INTERESTING.
THOSE INDIVIDUALS WHO HAD NEAR
TERM EVENT WITHIN THE FIRST YEAR
HAD THE HIGHEST AMYGDALA SIGNALS
COMPARED TO THOSE WITH LATTER
EVENTS OR THOSE WHO NEVER
DEVELOPED AN EVENT.
INTERESTINGLY ALSO, WE FOUND
CORRELATIONS BETWEEN THE IMAGING
SIGNALS IN THE BRAIN WITH WHAT'S
HAPPENING IN THE ARTERIES AND
THE BONE MARROW.
INDIVIDUALS WITH SUBSEQUENT
EVENTS TENDED TO HAVE HIGHER
AMYGDALA SIGNALS AND HERE'S A
PERSON WITH THE SUBSEQUENT EVENT
AND THE AMYGDALA WITH A PERSON
WITH THE SUBSEQUENT EVENT.
THE PERSON WITH THE SUBSEQUENT
EVENT HAD HIGHER INFLAMMATION
AND LEUKOPOIETIC ACTIVITY IN THE
BONE MARROW AND FOUND
CORRELATIONS BETWEEN THE BRAIN
IMAGE AND ATHEROSCLEROTIC
ACTIVITY AND BONE MARROW
ACTIVITY AND NOT WITH SUB
CUTANEOUS FAT.
WE ALSO FOUND THAT THE AMYGDALA
ACTIVITY PREDICTED ARTERIAL
INFLAMMATION THROUGH THE BONE
MARROW ACTIVITY.
THIS WAS SEEN THROUGH SINGLE
MEDIATION ANALYSIS.
IN FACT 65% WAS EXPLAINED BY
CHANGES IN BONE MARROW AND THE
AMYGDALA AND EVENTS WAS
EXPLAINED BY CHANGES IN THE
ARTERIES.
IF WE LOOKED AT SERIAL MEDIATOR
PATHS THE AMYGDALA ASSOCIATED
WITH CARDIOVASCULAR DISEASE
THROUGH BONE AMARROW SUPPORT TH
PATHS PREDICTED IN MICE AND
SHOWN A MODEL STRESS THROUGH
ACTIVATION OF THE AMYGDALA
INCREASES BONE MARROW AND
STIMULATION AND LEADS TO
CARDIOVASCULAR EVENTS.
AND THERE'S BEEN SEVERAL
FEATURES.
THIS STUDY AND THERE'S AN
ASSOCIATION BETWEEN AMYGDALA
ACTIVITY AND THE MORE THERE WERE
HIGHER PLAQUES AND IN THE SAME
STUDY THE AMYGDALA ACTIVITY LEAD
TO FEATURES THROUGH THE BONE
MARROW.
THIS SHOWED AN ASSOCIATION
BETWEEN AMYGDALA AND ACUTE
MYOCARDIAL INFARCTIONS.
THEY HAD HIGHER AMYGDALA
ACTIVITY AND THERE WAS A NICE
ASSOCIATION BETWEEN PERCEIVED
STRESS AND AMYGDALA ACTIVITY.
MOREOVER, THEY ALSO FOUND
ASSOCIATIONS BETWEEN THE BRAIN
IMAGING AND ARTERIAL
INFLAMMATION AS WELL AS BONE
MARROW ACTIVITY.
RECENTLY HERE'S A STUDY THAT
SHOWED AMYGDALA ACTIVITY
PREDICTS RECURRING EVENTS IN
PATIENTS COMING IN WITH STROKES
AND IN FACT THEY FOUND THOSE
PRESENTING WITH LOWER AMYGDALA
ACTIVITY TENDED TO HAVE FEWER
RECURRENT STROKES COMPARED TO
THOSE WITH HIGHER AMYGDALA
ACTIVITY.
LIKEWISE THEY FOUND THE SAME
ASSOCIATIONS.
THOSE WITH HIGHER BONE MARROW
ACTIVITY WERE LIKELY TO COME
BACK WITH RECURRENT STROKES.
NOW, I'VE BEEN TALKING ABOUT THE
AMYGDALA AND I GIVE YOU THE
SHORTENED NAME OF THE A MMYGDAL
ACTIVITY BUT IT'S ABOUT THE
AMYGDALA CORTICAL INTERACTIONS.
WE LOOKED AT PATIENTS WITH PTSD
VERSUS CONTROL EXPOSED TO TRAUMA
BUT DIDN'T DEVELOP PTSD AND
HEALTHY CONTROL AND WE DID BRAIN
IMAGING AND SHOW THE AVERAGE
BRAIN IMAGING FEATURES.
HEALTHY CONTROLS HAVE THE
HIGHEST PREFRONTAL CORTICAL
ACTIVITY IN RELATION TO THE
AMYGDALA AND LOOKING ACROSS THE
GROUP AMYGDALA TO CORTICAL
ACTIVITY WAS HIGHEST IN PTSD
FOLLOWED BY THE TRAUMA CONTROL
AND THE INDIVIDUALS WITH PTSD
HAD MODEST AMYGDALA ACTIVITY BUT
LOWER PREFRONTAL CORTICAL
ACTIVITY GIVING THEM THE RATIO
THAT WAS ELEVATED.
AND WE FOUND PEOPLE WITH PT. IS
SD HAD POORER AXONAL INTEGRITY
CONNECTING THE PREFRONTAL CORTEX
RELATIVE TO THE HEALTHY CONTROLS
AND WHEN WE SEE THE CORRELATION
WE ALSO FOUND THE AXONAL
INTEGRITY PREDICTED
ATHEROSCLEROSIS AND AMYGDALA
ACTIVITY PREDICTED THIS BURDEN.
IT'S IMPORTANT TO RECOGNIZE IT'S
NOT ALL ABOUT THE AMYGDALA BUT
THE AMYGDALA RELATIVE TO COUNTER
REGULATORY TISSUES.
DOCTORS LOOKED AT THE GENETICS
OF STRESS AND HAD A POLY GENIC
RISK STORE AND ASKED IF
INDIVIDUALS WITH HIGHER
STRESS-RELATED GENETICS HAD
GREATER AMYGDULAR ACTIVITY AND
IF YOU SEPARATE THE SIGNAL GOES
UP IN THE BRAIN.
AND IN CHRONIC STRESS SHRINKAGE
IN THE AMYGDALA AND YOU HAVE THE
SHRINKAGE OF THE AMYGDALA AS
WELL AND THEY FOUND AND THE
STRESS SENSITIVE GENES AS THE
SCORES WENT UP THE RISK FOR
CARDIOVASCULAR DISEASE EVENTS
ALSO WENT UP WHETHER YOU LOOKED
AT IS IN THE MASS BRIGHAM BIO
BANK OR U.K.
AND LESS TO CHANGES IN THE
BRAIN.
THIS IS AN IMPORTANT MECHANISM
BY WHY THE FINDINGS ARE LINKED.
ANOTHER ASPECT I WANT TO
INTRODUCE IS THE ARTERY-BRAIN
CIRCUIT.
ABC.
AND I'M GOING TO TELL YOU
SOMETHING ABOUT AN ARTERY
TERTIARY LYMPHOID ORGAN AND THIS
REPORTED IN NATURE '22 THAT MICE
HAD COLLECTIONS OF INFLAMMATION
AROUND THE ARTERIES AND THEY
WERE LINKED TO SYMPATHETIC
NERVES THAT WENT TO THE DORSAL
ROOT GANGLION AND TRACE IT BACK
TO THE CENTRAL AMYGDALA AND
FOUND THERE WAS A LINK.
AND THAT WAS AN INTERESTING
FINDING THEY WERE ABLE TO
SHRINK THE INFLAMMATION AND
ADDITIONAL FEATURE I WANT TO
SHARE WITH YOU IS THE ASPECT OF
MENTAL STRESS.
I'M A CARD CAN -- CARDIOLOGIST
AND CONVENTIONAL STRESS TESTING
IS SOMETHING I DO ON A DAILY
BASIS.
TO DO THAT WE LOOK FOR
BLOCKAGES.
EXERCISE INDUCED ISCHEMIA OCCURS
WHEN AS THE BLOCKAGE IN THE
CORONARIES AND THE HEART DOESN'T
GET ENOUGH BLOOD FLOW WITH
STRESS AND THERE'S A DEFICIT IN
BLOOD FLOW ON IMAGING.
WE CAN ALSO INDUCE ISCHEMIA WITH
MENSTRUAL STRESS AND THAT'S
USUALLY DUE TO THE SMALL VESSELS
AND LEADING TO LESS BLOOD FLOW
THAN WHAT IS REQUIRED.
IN THE STUDY WHERE THEY FOLLOWED
PATIENTS FOR SEVERAL YEARS AFTER
IMAGING, THEY FOUND THE
INDIVIDUALS WHO HAVE NO ISCHEMIA
HAD LOWEST EVENT RATE.
AND INDIVIDUALS WITH ISCHEMIA
DURING MENTAL STRESS HAD A
HIGHER EVENT RATE.
THAT WAS SURPRISING.
AND FOLKS WHO HAD THE WORSE
OUTCOMES WERE THE INDIVIDUALS
WHO HAD THE COMBINATION OF
MENTAL STRESS AND CONVENTIONAL
STRESS ISCHEMIA.
I DIDN'T MENTION THE MENTAL
STRESS ISCHEMIA COULD BE INDUCED
BY SIMPLY ASKING THE PARTICIPANT
TO GIVE A SPEECH OR TO DO MENTAL
MATH AND DURING THIS TEST, THE
PEOPLE PARTICIPATING IN THE
STUDY WOULD LOOK UNINTERESTED
AND IT WOULD INCREASE THE STRESS
PERCEIVED BY THE INDIVIDUAL AND
TO THE DEGREE TO WHICH THE
MENTAL STRESS LED TO PROFUSION
ABNORMALITIES ASSOCIATED WITH
THE OUTCOMES.
WE'VE BEEN TALKING ABOUT STRESS
AND ITS IMPACT ON THE PATHWAYS
AND IN MOST OF THESE CASES WE
TALK ABOUT THEM INDEPENDENTLY OF
RISK FACTORS.
THAT MEANS THE ASSOCIATION
BETWEEN MENTAL STRESS OR IN THE
OTHER STUDIES I WAS SHOWING THE
STRESS MEASURED IN THE BRAIN AND
CARDIOVASCULAR DISEASE EVENTS,
WE ADJUST FOR CARDIOVASCULAR
RISK FACTORS.
HOWEVER, STRESS ALSO ASSOCIATES
WITH AN INCREASE IN THE
DEVELOPMENT OF RISK FACTORS.
A GROUP LOOKED AT ANXIETY OR
DEPRESSION AND SHOWED AN
INCREASE RISK OF DEVELOPING
CARDIOVASCULAR DISEASE RISK
FACTORS AFTER THE DIAGNOSIS OF
ANXIETY OR DEPRESSION.
AND IS THIS IS EVEN AFTER YOU
ADJUST FOR AGE, SEX, SMOKING,
LIFESTYLE FACTORS AND COMBINING
EVERYTHING THERE'S STILL
SUBSTANTIAL INCREASED RISK NOT
ONLY THAT BUT THE TIME TO
DEVELOP ANY RISK FACTOR IN THE
FUTURE IS REDUCED.
HERE YOU CAN SEE INDIVIDUALS
WITHOUT ANXIETY AND DEPRESSION
DO HAVE A RISK OF DEVELOPING
STANDARD CARDIOVASCULAR RISK
FACTOR IT'S JUST THAT IT'S
ACCELERATED IN INDIVIDUALS WITH
DEPRESSION AND ANXIETY.
I ALSO WANT TO ADD IN ADDITION
TO THE INCREASE AND
ATHEROSCLEROTIC DISEASES THERE'S
AN INCREASE IN THROMBOTIC
DISEASES.
DOCTORS MEZUE AND RF -- ROSOVSKY
HAVE SHOWN THE INCREASE IN DVT
FOR THOSE WITH ANXIETY AND
DEPRESSION VERSUS THOSE WITHOUT.
LOOKING AT THE BRAIN WILL SHOW
THOSE WITH HIGHER AMYGDALAR
ACTIVITY HAVE INCREASED RISK.
ANXIETY -- DEPRESSION OR HIGH
STRESS ACTIVITY WILL EACH
PREDICT AN INCREASED RISK OF
THROMBOSIS.
PUTTING THEM TOGETHER I PROPOSE
THE RATIO OF AMYGDALAR ACTIVITY
TO PREFRONTAL CORTICAL ACTIVITY
AND IT'S OFF AND HIGHER
AMYGDALAR ACTIVITY LEADS TO MORE
HPA ACTIVATION AND MORE
SYMPATHETIC SYSTEM ACTIVATION.
THESE RESULT IN SEVERAL THINGS
INCLUDING CORTISOL AND
EPINEPHRINE AND LEADS TO CHRONIC
INFLAMMATION THROMBOSIS AND
ATHEROSCLEROTIC AND THE STRESSED
ISCHEMIA ALL OF WHICH COLLUDE TO
INCREASED CARDIOVASCULAR DISEASE
RISK.
SO I'VE BEEN TALKING ABOUT
CHRONIC STRESSORS AND I WANT TO
TALK NOW ABOUT THE DIFFERENCE
BETWEEN THE STRESS AND STRESSOR.
SO STRESSORS ARE WHAT CAUSE
STRESS AND WE HAVE SEVERAL
STRESSORS IN LOW SOCIO ECONOMIC
STATUS AND NOISE AND THEY'RE
WELL KNOWN TO ASSOCIATE WITH AN
INCREASED RISK OF CARDIOVASCULAR
DISEASE AND HYPOTHESIZED STRESS
ASSOCIATED PATHWAYS MEDIATE
BETWEEN NOISE AND SOCIO ECONOMIC
STATUS AND CARDIOVASCULAR
DISEASE.
HERE'S AN EXAMPLE OF PRIOR
STUDDOS THAT SHOW HOW INCOME
ASSOCIATES.
IF YOU LOOK AT INCOME WHETHER IN
THE 2000 OR 2015, THE EXPECTED
AGE OF DEATH FOR A 40-YEAR-OLD
WILL DIFFER DEPENDING ON INCOME
WHERE THOSE WITH THE LOWEST
INCOME ARE DIFFERENT THAN HIGHER
INCOME AND THE DIFFERENCES ARE
INCREASING OVER THE DECADES.
WHAT ABOUT CHANGE IN INCOME?
IN THIS PARTICULAR STUDY THEY
FOLLOWED PATIENTS FROM THE START
OF THE STUDY THROUGH 25 YEARS
AND FOUND INDIVIDUALS WHO HAD A
DROP IN INCOME HAD A HIGHER RATE
COMPARED TO THOSE WHO HAD NO
CHANGE IN INCOME OR INCOME RISE.
WHAT WAS INTERESTING IS THE
DIFFERENCES PERSIST AFTER
ADJUSTING FOR DISEASED RISK
FACTORS, HEALTH CARE AND INCOME
AT THE START OF THE STUDY.
THE NEW CONCEPT FROM THIS STUDY
WAS THAT CHANGE IN INCOME WAS
ALSO IMPORTANT AS A PREDICTOR
FOR CARDIOVASCULAR DISEASE.
WITH THAT AS A BACKGROUND, WE
CONDUCTED A STUDY WHERE WE ASKED
IF INCOME LED TO CARDIOVASCULAR
DISEASE THROUGH CHANGES IN THE
BRAIN.
WHAT WE FOUND FIRST IS THAT
INDIVIDUALS WITH THE LOWEST
INCOME HAD THE HIGHEST DISEASE
RISK COMPARED TO THOSE WITH
HIGHEST INCOME.
FINDINGS THAT WERE SHOWN IN
SEVERAL PRIOR STUDIES.
MOREOVER, WE OBSERVED THAT
AMYGDALAR ACTIVITY WAS HIGHEST
AMONG INDIVIDUALS WITH LOWEST
INCOME AND LOWEST AMONG
INDIVIDUALS WITH HIGHER INCOME
AND THE SAME TRENDS WERE SEEN
FOR ARTERIAL INFLAMMATION.
WE FURTHERMORE NOTED THE
ASSOCIATION BETWEEN SOCIO
ECONOMIC STATUS AND MAJOR
ADVERSE CARDIOVASCULAR EVENTS
WERE LINKED TO THE AMYGDALAR
ACTIVITY AND THE BONE MARROW AND
THE ARTERIES IN SERIES.
GOING TO THE OTHER STRESSOR, WE
HAVE NOISE AND CARDIOVASCULAR
DISEASE.
IT'S LONG BEEN SHOWN NOISE IS
UNHEALTHY, CHRONIC NOISE IN
PARTICULAR.
THERE'S EVEN AN UNHEALTHY
THRESHOLD FOR NOISE AS MENTIONED
BY SEVERAL AGENCIES INCLUDING
THE WORLD HEALTH ORGANIZATION
AND THERE'S BEEN SEVERAL
PATHWAYS THAT HAVE BEEN SHOWN TO
BE ASSOCIATED WITH INCREASED
NOISE INCLUDING DOWN STREAM
CHANGES IN THE CORONARY
ARTERIES.
THE QUESTION LONG OUT THERE IS
HOW IS DOES NOISE INITIATE THESE
PATHOBIOLOGICAL LINES IN THE
FIRST PLACE.
IT BEGINS WITH CHANGES IN THE
BRAIN.
WE FIRST LOOKED AT MAJOR ADVERSE
CARDIOVASCULAR EVENTS RELATIVE
TO NOISE EXPOSURE AND AS OTHER
GROUPS HAVE SHOWN, THOSE WHO ARE
CHRONICALLY EXPOSED TO HIGHER
NOISE HAD A HIGHER
CARDIOVASCULAR RISK.
INTERESTINGLY WE FOUND NOISE
ASSOCIATED WITH AMYGDALAR
ACTIVITY.
PEOPLE LIVING IN LESS NOISY
AREAS HAD THE LOWEST ACTIVITY
AND THOSE IN THE NOISEST AREA
HAD THE HIGHEST AMYGDALAR
ACTIVITY AND NOISE LED TO MAJOR
EVENTS AND LED TO INCREASE IN
ARTERIAL INFLAMMATION.
WE'VE BEEN TALKING ABOUT
STRESSORS BUT I WANT TO ASK, IS
IT THE STRESSOR OR STRESS
RESPONSE THAT CAUSES THE
DISEASE?
IS IT SIMPLY LIVING IN A NOISY
AREA OR WHAT'S HAPPENING IN YOUR
BRAIN?
WE LOOKED AT THE NUMBER OF
STRESSORS VERSUS AMYGDALAR
ACTIVITY AND HAD MEASURES OF
STRESSORS INCLUDING INCOME,
CRIME AND NOISE AND THE FIRST
THING I'LL SHOW IS THERE'S A
NICE INCREASE IN AMYGDALAR
ACTIVITY AS YOU INCREASE
EXPOSURE TO STRESSORS.
NOT SURPRISING.
WHAT WAS INTERESTING THOUGH IS
THAT NOT EVERYBODY WHO IS
EXPOSED TO MANY STRESSORS HAVE
THE SAME AMYGDALA RESPONSE.
LET ME TAKE YOU THREE THIS FOR A
SECOND.
INDIVIDUALS WHO ARE NOT EXPOSED
TO THOSE STRESSORS ON AVERAGE
HAVE LOWER AMYGDALA ACTIVITY.
LESS THAN ONE STANDARD DEVIATION
ACROSS THE MEDIAN AS LOWER
ACTIVITY AS IN YELLOW.
HERE ARE INDIVIDUALS EXPOSED TO
THE STRESSORS CHRONICALLY AND
MANY OF THEM HAD LOWER AMYGDALAR
ACTIVITY CALLING THEM
NEUROBIOLOGICAL ACTIVITY IS
LOWER DESPITE THE FACT THEY'RE
EXPOSED TO THE STRESSORS.
ON THE OTHER HAND THESE PEOPLE
HERE WHO DEVELOPED MORE AMYGDALA
ACTIVITY UPON EXPOSURE.
THEY'RE LESS NEUROBIO LOGICALLY
RESILIENT.
LET'S SEE IF IT MATTERS.
IN THIS CASE WE TOOK JUST THE
INDIVIDUALS EXPOSED TO STRESSOR
AND LOOKED AT THOSE WHO ARE LESS
VERSUS MORE NEUROBIOLOGICALLY
RESILIENT AND THEY HAD FEWER
EVENTS.
IF YOU WERE EXPOSED TO THESE
STRESSORS AND YET YOUR BRAIN
RESPONSE IS NOT HIGH, YOUR
NEUROBIOLOGICAL RESILIENCE IS
GOOD YOU'RE LESS LIKELY TO
DEVELOP EVENTS.
THERE'S A PAYOFF TO
NEUROBIOLOGICAL RESILIENCE, IN
OTHER WORDS.
ONE QUESTION WE WOULD HAVE,
COULD NEUROBIOLOGICAL RESILIENCE
INCREASE YOUR EVENTS TRIGGERED
BY ACUTE STRESS?
LET ME TAKE YOU THROUGH THE
ACUTE STRESSORS.
THERE ARE SEVERAL POTENTIAL
ACUTE STRESSORS.
THIS IS A PARTICULARLY FAMOUS
STRESSOR.
THE STUDY PUBLISHED IN THE '90s
SHOWED A SURGE IN HEART ATTACKS
AFTER EARTHQUAKES.
ON THIS PARTICULAR STUDY WHERE
THEY LOOKED AT THE DAILY RATES
OF CARDIOVASCULAR DISEASE THAT'S
IN THE LOS ANGELES AREA YOU CAN
SEE THERE'S A RATHER PREDICTABLE
NUMBER OF HEART ATTACKS THROUGH
1992 AND 1993 AND THE DAYS
PRECEDING THE EARTHQUAKE AND
THEN THERE'S A SURGE IN
EARTHQUAKES AROUND THE TIME OF
THE EARTHQUAKE.
IT DOESN'T HAVE TO BE AN
EARTHQUAKE.
IT COULD BE A CHAMPION GAME AND
HERE'S ACUTE STRESSORS WITH THE
WORLD CUP.
THIS COMPARED HEART ATTACK RATES
AROUND THE TIME OF THE WORLD CUP
CHAMPIONSHIP AND COMPARED IT TO
OTHER YEARS AS WELL.
THE RED LINES ARE FOR THE YEAR
OF THE QUARTERFINAL OF THE WORLD
CUP THE YELLOW AND BLUE LINES
ARE FROM PROCEEDING YEARS.
FOR YELLOW AND BLUE THERE'S
PREDICTABLE NUMBER OF
CARDIOVASCULAR DISEASE EVENTS
BUT DURING THE GAINS WHERE THE
HOME TEAM WAS PLAYING YOU CAN
SEE SURGES IN HEART ATTACKS.
THE HIGHEST SURGES OCCURRED
DURING THE QUARTERFINALS WIN
AFTER DRAMATIC PENALTY SHOOTOUT
AND DURING THE SEMIFINALS LOSS
AND LOOK AT THIS.
WHERE THE CONSOLATION PRIZE THE
EVENT WENT DOWN TO THE WEEDS AND
DURING THE FINALS WITHOUT THE
HOME TEAM THERE WAS A SLIGHT
INCREASE BUT NOT NEARLY AS
SPECTACULAR AS DURING THE MORE
EXCITING GAMES AND THE
BACKGROUND RATE IS LOWER AND SO
STRESSFUL PERIODS ARE WELL KNOWN
TO ASSOCIATE WITH CARDIOVASCULAR
DISEASE EVENTS.
WHY?
WELL, ONE WAY TO STUDY THIS IS A
CLASSIC TAKOTSUBO SYNDROME OFTEN
TRIGGERED BY AN ACUTE EMOTIONAL
OR PHYSICAL STRESSOR.
THE PATHOGENESIS HAS BEEN
DELINEATED BUT A LINK BETWEEN
THE BRAIN AND HEART HAS BEEN
PROPOSED AS A FACTOR.
AND THEY FOUND TAKOTSUBO
IMPAIRED CORTICO-LIMBIC ACTIVITY
INVOLVING THE AMYGDALA AND
PREFRONTAL CORTEX AND DIDN'T
KNOW IF IT WAS PRESENT PRIOR TO
THE ONSET OF THE DISEASE.
WE HAD 104 INDIVIDUALS WHO
UNDERWENT CT IMAGING.
41 DEVELOPED TAKOTSUBO AND THEN
IDENTIFIED 63 MATCH CONTROLS.
TACK AT SUBO AND THEY HAD LOWER
IMAGING AND THERE WAS A BIG
RANGE OF AMYGDALA ACTIVITY AMONG
THOSE WITH TAKOTSUBO AND THOSE
HAD A STANDARD DEVIATION OFFER
THE MEAN COMPARED TO THE REST
AND LOWER AMOUNT OF ACTIVITY.
WHAT WAS INTERESTING HERE IS
THERE WAS A RELATIONSHIP BETWEEN
AMYGDALA ACTIVITY AND TIMING OF
TAKOTSUBO.
THOSE WITH LOWER AMYGDALA AC
TENDED TO HAVE TAKOTSUBO YEARS
HEARD AND THOSE WITH LOWER
ACTIVITY DEVELOPED IT LESS THAN
A YEAR AFTER IMAGING.
IF YOU PUT THIS TOGETHER, WE CAN
THINK OF A CONCEPT BY WHICH
INDIVIDUALS WHO ARE LESS
NEUROBIOLOGICALLY RESILIENT AND
AFFECTED BY STRESSFUL EVENTS AND
LEAD TO GREATER TRIGGERING OF
EXAGGERATED RESPONSE TO STRESS
LEADING TO ARRHYTHMIA AND SUDDEN
DEATH AND TAKOTSUBO AND THOSE
MORE RESILIENT WILL HAVE LOWER
SUSCEPTIBILITY TO ACTIVATION TO
STRESS WITH FEWER RESPONSES AND
BENIGN COURSE.
THAT BEING SAID, CAN YOU DO
ANYTHING ABOUT OUR RESILIENCE?
THERE'S LONG BEEN AN OBSERVATION
THAT CHANGES IN PERCEIVED STRESS
CAN BE SHOWN TO ASSOCIATE WITH
CHANGES IN WHAT HAPPENS IN THE
AMYGDALA.
THAT'S PROMISING.
HERE'S A STUDY.
IT SHOWED THAT STRESS REDUCTION
ON TOP OF EXERCISE CAN IMPART
GREATER CARDIOVASCULAR DISEASE
BENEFITS.
WHAT DO I MEAN BY THAT?
IN THIS PARTICULAR STUDY THEY
LOOKED AT INDIVIDUALS WITH A
RECENT ACUTE CORONARY SYSTEM OR
REVASCULARIZATION AND RANDOMIZED
A PORTION OF SUBJECTS TO
STANDARD CARDIOVASCULAR REHAB
WHICH FOCUSES ON EXERCISE VERSUS
CARDIOVASCULAR REHAB WITH STRESS
REDUCTION.
LET'S CALL THIS ENHANCED
CARDIOVASCULAR REHAB AND
COMPARED THESE GROUPS TO
INDIVIDUALS WHO HAVE NO
CARDIOVASCULAR REHAB AND THEN
FOLLOWED FOR FIVE YEARS FOR
CARDIOVASCULAR DISEASE EVENTS.
FIRST, THE INDIVIDUALS WITH NO
INTERVENTIONS WERE MOST LIKELY
TO DEVELOP CARDIOVASCULAR
DISEASE EVENTS.
HERE, FREE FROM CLINICAL EVENTS.
THOSE WITH NO INTERVENTION WERE
FAR MORE LIKELY TO HAVE EVENTS.
NO SURPRISE, THERE WAS A
SUBSTANTIAL IMPROVEMENT IN
OUTCOMES AMONG INDIVIDUALS WHO
HAD EXERCISE.
BUT WHAT WAS A SURPRISE WAS THAT
THE ADDITION OF STRESS REDUCTION
ON TOP OF EXERCISE BOUGHT AN
ADDITIONAL 50% RELATIVE RISK
REDUCTION IN TERMS OF HEART
EVENTS.
I WOULD ADD THAT OTHER FORMS OF
STRESS REDUCTION ALSO IMPROVE
BUT HAPPENS IN THE BRAIN.
FOR EXAMPLE, TAI CHI HAS BEEN
KNOWN TO IMPROVE CORTICAL
ACTIVITY AND TAI CHI HAS BEEN
SHOWN TO LEAD TO THICKER
CORTICAL REGIONS.
TWO ATTRACTIVE SIGNS.
SIMPLE IMPROVEMENT IN
RESPIRATIONS, RESPIRATORY
EXERCISES CAN LEAD TO CHANGES IN
ACTIVITY WITHIN THE AMYGDALA.
SO THERE ARE GROWING DATA TO
SUPPORT THAT STRESS REDUCTION
TECHNIQUES AND APPROACHES SUCH
AS TAI CHI HAVE IMPORTANT
IMPACTS ON THE BRAIN.
WHAT ABOUT LIFESTYLE FACTORS?
THERE'S SEVERAL WE'VE LOOKED AT
CAREFULLY IN THE CONTEXT OF THE
MASS GENERAL BRIGHAM BIO BANK.
IN THE BIO BANK WE HAVE OVER
50,000 INDIVIDUALS WHO HAVE
REPORTED THEIR LIFESTYLE DATA
INCLUDING SLEEP, PHYSICAL
ACTIVITY AND ALCOHOL AND A
SUBSET WHO HAVE BRAIN IMAGING
DATA FOR OUR ANALYSIS.
THIS IS WHAT WE FOUND.
IN ONE STUDY WE FOUND IF ALCOHOL
LIGHT TO MODERATE ALCOHOL WILL
IMPACT THE BRAIN REGIONS I JUST
DESCRIBED.
WE OBSERVED LIGHT TO MODERATE
ALCOHOL REDUCES CARDIOVASCULAR
DISEASE EVENTS.
SO HERE ARE 10-YEAR MACE EVENT
RATE IS REDUCED AND WHEN WE
ADJUST FOR HEALTH BEHAVIORS AND
SOCIO ECONOMIC AND PSYCHOLOGICAL
AND OTHER COMORBIDITIES WE
CONTINUED TO SEE A NICE
REDUCTION IN CARDIOVASCULAR
DISEASE EVENTS.
MOREOVER, IF YOU LOOK AT ALL
MAJOR ADVERSE CARDIOVASCULAR
EVENTS OR THE COMPONENTS SUCH AS
HEART FAILURE, PERIPHERAL
VASCULAR DISEASE OR STROKE IT
ALL GOES DOWN NICELY.
BUT BEFORE PEOPLE GET EXCITED
LOOK AT WHAT HAPPENS WITH
CANCERS.
LIGHT TO MODERATE ALCOHOL INTAKE
ALSO ASSOCIATES WITH AN
INCREASED RATE OF CANCER SO IT'S
NOT ALL GOOD.
FOCUSSING BACK ON ALCOHOL AND
THE BRAIN, THIS IS WHAT WE FOUND
WHEN WE LOOK AT AMYGDALAR
ACTIVITY GOES DOWN NICELY WITH
LIGHT TO MODERATE ALCOHOL INTAKE
AND WITH HIGH ALCOHOL IT GOES
BACK UP.
I ALSO WANT TO MENTION HOW
AMYGDALAR ACTIVITY GOES DOWN.
NOTICE I KEEP REFERRING TO
AMYGDALAR ACTIVITY AND PUT A C
THERE.
THIS IS FOR THE CORTICAL
ACTIVITY BECAUSE THE AMYGDALA
ACTIVITY IS RATIO AMYGDALA TO
THE CORTEX.
IS AMYGDALA ACTIVITY BECAUSE OF
REDUCTIONS IN THE AMYGDALA OR
INCREASES IN THE PRE FRONTAL
CORTEX, THE AMYGDALA HAS LOWER
METABOLIC ACTIVITY IN
INDIVIDUALS WHO DRINK LIGHT TO
MODERATE ALCOHOL.
ON THE OTHER HAND WE DID NOT SEE
A SIGNIFICANT INCREASE IN
PREFRONTAL CORTICAL ACTIVITY AND
NO SURPRISE ALCOHOL IS NOT
MAKING YOU SMARTER.
WHAT WE DID FIND AS A CAUTIONARY
NOTE IS WITH HIGHER AMOUNTS OF
ALCOHOL THERE WAS A TREND
TOWARDS REDUCTION IN OVER ALL
BRAIN METABOLIC ACTIVITY.
SO THIS IS NOT A SURPRISE BUT
AGAIN A NOTE OF CAUTION AS
DRINKS GO OVER 14 THERE WAS A
CONCERNING SIGNAL AS WELL.
WE ASKED IF MODERATE ALCOHOL
ASSOCIATES WITH IMPROVEMENTS IN
MACE RISK THROUGH THE BRAIN AND
FOUND MODERATE ALCOHOL REDUCES
MACE RISK IN PART THROUGH
REDUCTIONS IN THE STRESS
ASSOCIATED NEURAL NETWORK
ACTIVITY.
WITH THAT IF INDEED ALCOHOL IN
PART REDUCING HEART ATTACKS
THROUGH IMPACTS ON THE BRAIN, WE
WOULD EXPECT IT TO BE MORE
EFFECTIVE AT REDUCING HEART
ATTACKS AMONG INDIVIDUALS
ANXIOUS TO BEGIN WITH.
IN FACT WE TESTED THAT SO WE
LOOKED AT 10-YEAR RISK OF HEART
ATTACKS AMONG INDIVIDUALS WITH
OR WITHOUT PRE EXISTING ANXIETY
AND FOUND THAT THOSE WITH
PRE-EXISTING ANXIETY HAD A
GREATER REDUCTION IN THE HEART
ATTACK RISK COMPARED TO THOSE
WITHOUT ANXIETY.
ALCOHOL IS REDUCING HEART ATTACK
RATES DUE IN PART TO THE IMPACT
ON THE BRAIN AFFECT WAS ROUGHLY
DOUBLE AMONG INDIVIDUALS WITH
PRE-EXISTING ANXIETY.
AND ATTENUATED STRESS-RELATED
PATHWAYS HOWEVER, THERE'S NO
SAFE LEVEL OF ALCOHOL AND NEED
ADDITIONAL INTERVENTIONS THAT
REDUCE NEURAL MECHANISMS WITHOUT
THE SIDE EFFECTS OF ALCOHOL
WHICH TAKES ME TO EXERCISE.
WE ADDED EVERY INDIVIDUAL WAS
THEN PUT INTO QUINTILES
DEPENDING ON THEIR OVER ALL
ACTIVITY AND THOSE WITH THE
GREATEST ACTIVITY HAVE THE
LOWEST AMYGDALA ACTIVITY AND
NICE DOSE RESPONSE BETWEEN
PHYSICAL AND AMYGDALA ACTIVITY
AND THIS REMAINED SIGNIFICANT
AFTER ADJUSTING FOR MULTIPLE
CONFOUNDERS.
NOW IS PHYSICAL ACTIVITY ACTING
MORE ON THE AMYGDALA OR MORE ON
THE PREFRONTAL CORTEX AND WE
FOUND A NICE INCREASE IN PRE
FRONTAL CORTICAL CONTROL AND
ENHANCES THE CONTROL AND
PHYSICAL ACTIVITY REDUCES MAJOR
ADVERSE CARDIAC EVENTS IN PART
THROUGH CHANGES IN THE BRAIN.
THE NEXT QUESTION WE ASKED IF
EXERCISE REDUCES HEART ATTACKS
IN PART BY ATTENUATING
STRESS-ASSOCIATED MECHANISMS
THEN EXERCISE SHOULD HAVE A
LARGER IMPACT ON MACE RISK AMONG
INDIVIDUALS WITH CHRONIC HIGHER
AMYGDALA ACTIVITY SUCH AS
INDIVIDUALS WITH DEPRESSION OR
ANXIETY.
IN INDIVIDUALS WITHOUT
DEPRESSION, EXERCISE WAS
EFFECTIVE.
NO SURPRISE AND WE FOUND ABOUT A
12% REDUCTION IN HEART ATTACK
RATE.
BUT, AMONG INDIVIDUALS WITH
DEPRESSION, EXERCISING TO THE
GUIDELINES ACTUALLY
SUBSTANTIALLY IMPROVES YOUR RISK
OF HEART ATTACKS EVEN FURTHER.
LET ME WALK YOU THROUGH THIS.
FIRST, THIS IS THE ADJUSTED
HAZARD RATIO FOR INDIVIDUALS
WITHOUT PRIOR DEPRESSION ACROSS
QUINTILES OF EXERCISE.
AND THE EXERCISE
RECOMMENDATIONS.
WE TELL PATIENTS TO ACHIEVE 150
TO 300 MINUTES OF MODERATE
INTENSITY EXERCISE PER WEEK.
WE CAN SEE HERE THAT THERE IS A
STEEP REDUCTION IN EVENTS
FOLLOWED BY A PLATEAU.
MULTIPLE PRIOR STUDIES HAVE
SHOWN SIMILAR CURVES FOR
EXERCISE VERSUS HEART ATTACK
RATES AND HENCE WE TALK ABOUT
THIS 150 TO 300 MINUTES OF
MODERATE EXERCISE BECAUSE OF THE
PLATEAU WE SEE AFTERWARDS.
THERE'S MINIMAL RETURNS ABOVE A
CERTAIN THRESHOLD OF EXERCISE
AND AMONG THOSE WITH DEPRESSION
WE SAW CONTINUED IMPROVEMENTS
AND NO PLATEAU WHICH WE
HYPOTHESIZED WAS DUE TO THE FACT
MAYBE INDIVIDUALS WITH
DEPRESSION STAND TO GAIN MORE
FROM EXERCISE BECAUSE OF THOSE
INCREASED IMPACTS ON THE BRAIN.
AND IN THE RELATIVE SMALL
PERSPECTIVE STUDY EVALUATING
EXERCISE, THEY FOUND THAT
INDIVIDUALS WHO WENT TO EXERCISE
HAD A NICE REDUCTION IN AMYGDALA
ACTIVITY FOLLOWING EXERCISE.
>> WE HAVE FIVE MINUTES JUST A
HEADS UP.
>> I ALSO WANT TO TALK ABOUT
SLEEP.
SO HERE IS AND SLEEP CAN ALSO
INCREASE CARDIOVASCULAR DISEASE
RISK.
HERE'S TIME TO HEART ATTACKS AND
THIS IS HEART SURVIVAL IN
INDIVIDUALS WITHOUT SLEEP
DEPRIVATION THERE'S A LOWER RATE
COMPARED TO INDIVIDUALS WITH
SLEEP DEF RIFFATION AND FOUND
THE INTERACTION BETWEEN GENETICS
AND SLEEP AND LET ME TAKE YOU
THROUGH THIS.
INDIVIDUALS WITH HIGHER STRESS
SENSITIVITY -- A HIGHER
POLYGENIC RISK SCORE FOR MORE
LIKELY TO DEVELOP HEART ATTACKS
IN RELATION TO SLEEP DEPRIVATION
AND THOSE WITH LOWER STRESS HAD
LESS EVENTS BUT THOSE WITH A
HIGHER STRESS SENSITIVITY HAD A
GREATER RISK.
SO YOUR GENETICS OF STRESS WILL
SOMEHOW MODIFY YOUR RISK OF
HEART ATTACKS WHEN YOU'RE SLEEP
DEPRIVED.
AS YOU FOLLOW THE CARTOON HERE,
THOSE WHO ARE UNHEALTHY SLEEP
BUT LOWER STRESS SENSITIVE GENES
HAVE A MODERATELY INCREASED RISK
OF MAJOR ADVERSE EVENTS WHEREAS
THOSE WITH A HIGHER STRESS
SENSITIVITY GENETICS HAVE DOUBLE
THE MACE RISK.
I ALSO WANT TO TALK ABOUT STRESS
AND CANCER.
SO HERE IN THE PARTICULAR STUDY
WE LOOKED AT INDIVIDUALS WHO
WERE COMING TO OUR HOSPITAL WITH
A SUSPICION OF HEAD AND NECK
CANCER AND GETTING THEIR STAGES
PET CTs.
THAT GAVE US AN OPPORTUNITY TO
MEASURE THE ACTIVITY IN THEIR
BRAIN.
FIRST, WHAT WE FOUND IS THAT THE
BRAIN ACTIVITY PREDICTED THE
BONE MARROW ACTIVITY IN THE
PATIENTS AND THE BRAIN ACTIVITY
ALSO RELATED TO INFLAMMATORY
BIOMARKERS.
BUT MORE IMPORTANTLY, WE FOUND
THAT INDIVIDUALS WITH HEIGHTENED
BRAIN ACTIVITY HERE IN BLUE HAD
A HIGHER RISK OF DYING FROM
THEIR HEAD AND NECK CANCER AND
THAT'S OVER ALL SURVIVAL FOR ALL
THE PATIENTS AND EVEN IF THEY
CAME IN WITH AN ADVANCED STAGE
OF CANCER WE STILL FOUND AN
ASSOCIATION BETWEEN THE BRAIN
IMAGING AND LIKELIHOOD OF
SURVIVING THEIR CANCER.
HERE IF YOU LOOK AT THE BRAIN
IMAGING, THOSE WHO SURVIVED WITH
NO PROGRESSION OF DISEASE CAME
IN WITH LOWER SIGNALS OF STRESS
COMPARED TO THOSE WHO SURVIVED
WITH SOME PROGRESSION VERSUS
THOSE WHO DIED IN THE COURSE OF
THERAPY.
THERE'S AN ASSOCIATION BETWEEN
THE BRAIN IMAGING OF STRESS AND
THE OUTCOMES.
SO WITH THIS ALL BEING TOGETHER,
STRESS AND STRESS-RELATED
DISORDERS ARE IMPORTANT RISK
FACTORS FOR CARDIOVASCULAR
DISEASE.
IT'S ATTRIBUTABLE RISK ON PAR
WITH HIGHER TENSION, SMOKING AND
DIABETES AND RELATED TO POIETIC
ACTIVITY AND NON-CALCIFIED
PLAQUE AND CARDIOVASCULAR
DISEASE IMPACTS MAY BE
MODIFIABLE BUT LARGE TRIALS ARE
NEEDED TO PROVE CAUSATION AND
DETERMINE EFFICACY OF
INTERVENTIONS.
UNTIL THEN, WE WOULD RECOMMEND
THAT FOR INDIVIDUALS WITH HIGHER
ATHEROSCLEROTIC EVENTS AND
STRESS TO UNDER GO STRESS
REDUCTION APPROACHES, LOOK FOR
PHYSICAL ACTIVITY AND HEALTHY
SLEEP.
THANK YOU VERY MUCH FOR YOUR
ATTENTION.
>> THANK YOU, FOR THE WONDERFUL
TALK AND FASCINATING INFORMATION
WITH THAT WE'LL MOVE INTO OUR
Q&A SESSION.
I BELIEVE DR. TAWAKOL YOU WANT
TO KEEP YOUR SLIDES UP FOR THE
Q&A AND REMINDER FOR OUR
AUDIENCE, USE THE FEEDBACK FORM
LINK IF YOU HAVE QUESTIONS YOU
WANT TO SUBMIT AND LET'S KICK
THIS OFF AND LEN AND DAVID, DO
YOU HAVE A FIRST QUESTION YOU'D
LIKE TO POSE TO DR. TAWAKOL TO
START OUR Q&A SESSION?
>> YOU COVERED A GREAT DEAL.
I WANTED TO BACK TO THE
BEGINNING OF THE PRESENTATION TO
TALK ABOUT SO MANY QUESTIONS I'D
LIKE TO ASK BUT THIS QUESTION
I'M CURIOUS, YOU TALKED ABOUT
USING PET IMAGING TO LOOK AT
VARIOUS DIFFERENT PARTS OF THE
BODY.
SAME METHOD AS TOMOGRAPHY
LOOKING AT THE BRAIN AND
ARTERIES AND BONE MARROW,
THERE'S A TENDENCY IN PET
IMAGING FOR THE WHOLE BODY AND
WHAT ABOUT THE LIVER OR OTHER
MUSCLE -- IS THAT SOMETHING YOU
THINK IS POSSIBLE IN THE NEAR
FUTURE TOO LOOK AT THE EFFECTS
OF STRESS ON ALL THE OTHER
PARTS?
>> IF YOU'RE INTERESTED IN A
DISEASE PROCESS THAT INVOLVES
MULTIPLE ORGANS YOU NEED TO
BROADEN THE WAY TO OBTAIN YOUR
DATA.
AND PET IMAGING GIVES YOU BE AN
OPPORTUNITY TO LOOK AT THE
ENTIRE BODY AT THE SAME TIME AND
GO BACK AND LOOK AT SEVERAL
ASPECTS AND ASK QUESTIONS ONE
DAY ABOUT ONE GROUP OF ORGANS
AND ON ANOTHER DAY RECESS OTHER
ORGANS.
AND WE LOOM AT LYMPHNODES AND
MEASURE MUSCLE AND LOTS OF END
POINTS?
IT CAN GROW FROM THERE.
WITH SOME OF THE LATEST PET
TECHNIQUES THE OPPORTUNITIES ARE
IMPROVING BECAUSE THE RESOLUTION
IS IMPROVING AND THE ABILITY TO
GET MORE AND MORE SENSITIVE
MEASURES OF METABOLIC ACTIVITY
AREN'T PROVEN.
NOT ONLY THAT WE DON'T ONLY HAVE
TO LOOK AT METABOLIC ACTIVITY.
WITH PET WE CAN USE DIFFERENT
TRACERS THAT WILL TARGET OTHER
METABOLIC PROCESSES OR OTHER
BIOLOGICAL PROCESSES.
SO IT'S QUITE AN EXCITING TOOL.
>> SOUND LIKE A WHOLE WORLD
OPENING UP.
>> THERE IS.
>> DAVID.
>> A GREAT PRESENTATION AND
MAKING THE CONNECTION BETWEEN
MIND AND BODY AND HEALTH AND
DISEASE AND SPEAKS TO NCCIH'S
MISSION TO UNDERSTAND WHOLE
PERSON HEALTH.
WHAT I WANTED TO ASK YOU ABOUT
IS YOU BROUGHT UP AN IMPORTANT
OTHER ASPECT OF YOUR WORK IS THE
GENE ENVIRONMENT INTERACTIONS
HAPPENING.
AND WHEN YOU LOOK AT HOW SELF
CARE MIGHT OUT AND AROUND THE
DEVELOPMENT OF PRECISION
MEDICINE AND HOW THAT CAN BE
USED TO MAYBE TAKE YOUR FINDINGS
A STEP INTO THE CLINIC AND CARE
FOR PATIENTS GENERALLY.
>> THAT'S A VERY NICE QUESTION.
I APPRECIATE IT.
IT'S INTERESTING HOW DIFFERENT
BIOMARKERS YOU CAN GET WITH
GENETIC TOOLS AND POLY GENIC
RISK SCORES CAN GIVE YOU INSIGHT
TO DISEASE.
WE'VE BEEN LOOKING AT THE POLY
GENIC RISK SCORE FOR LOOKING AT
CARDIOVASCULAR DISEASE RISK.
IN THIS CASE WE'VE BEEN LOOKING
ALSO AT STRESS SENSITIVITY
GENES.
THERE'S SEVERAL WAYS YOU CAN DO
THAT.
WE'VE BEEN USING THE POLY GENIC
RISK SCORE THAT CRUNCHES ALL THE
NUMBERS AND GIVES A RELATIVE
RISK FOR THE LIKELIHOOD YOU'LL
DEVELOP A STRESS-RELATED
SYNDROME SOME TIME IN YOUR LIFE.
I GAVE YOU ONE EXAMPLE.
THERE ARE SEVERAL OTHERS IN THE
BACKGROUND.
ONE EXAMPLE I GAVE YOU IS A
SIMPLE ONE WHICH IS IF YOU HAVE
A GREATER THAN AVERAGE ONE
RECOMMENDATION I HAD IF SOMEHOW
EVERYONE WAS GETTING THEIR
POLYGENIC RISK SCORE THE
RECOMMENDATION I HAVE WITH
INDIVIDUALS FOR GREATER THAN
MEDIAN RISK STORE BE CAREFUL
ABOUT SLEEP SCORE AND THAT'S ONE
OPPORTUNITY FOR GIVING PRECISE
RECOMMENDATIONS FOR INDIVIDUALS
AND I HYPOTHESIZE MULTIPLE DOWN
STREAM OPPORTUNITIES.
SOME I CAN TALK ABOUT.
FOR EXAMPLE, ONE COLLEAGUE
RECENTLY PUBLISHED IF YOU LOOK
AT INCOME DISPARITIES, THERE'S
ANY INTERACTION BETWEEN INCOME
AND SOME OF THESE POLY GENIC
RISK SCORES AND PEOPLE WITH
LOWER STRESS SENSITIVE GENES
DON'T HAVE AS MUCH AS OF A
DISEASE CONSEQUENCE OF LOWER
INCOME WHERE PEOPLE WITH MORE
STRESSFUL GENE HAVE A GREATER
CONSEQUENCE.
WE LOOK FOR MORE LIFESTYLE
INTERVENTIONS DEPENDING ON THE
STRESS-RELATED GENES.
>> FASCINATING.
THANK YOU SO MUCH.
>> YOU DISCUSS MENTAL STRESS CAN
LEAD TO ISCHEMIA.
WOULD THE INCREASED MENTAL
STRESS BE INDUCED BY A CHRONIC
SYMPATHETIC OVERDRIVE WHERE THE
CORONARIES LEAD TO THE
VASOCONSTRICTION AND ISCHEMIA.
THIS COMES IN FROM AN AUDIENCE
MEMBER.
>> THEY LEAD TO OTHER RISK
FACTORS THAT TEND TO IMPAIR
CORONARY FLOW INCLUDING CHRONIC
INFLAMMATION ADIS POPAUC POPADI
INFLAMMATION AND INCREASE THE
FLOW RESPONSE WHEN NEEDED.
IT'S A COMBINATION OF ALL THESE
THINGS.
AND THERE'S ADIPOSITY THAT
COMES.
>> AND THERE'S ANOTHER QUESTION
FROM THE MEMBER OF THE AUDIENCE
WATCHING.
WITH EXERCISE SO EFFECTIVE IN
REDUCING STRESS AND THUS
CARDIOVASCULAR EVENTS, WHY ISN'T
EXERCISE IN STANDARD
CARDIOVASCULAR REHABILITATION
SUFFICIENT WHY DOES FURTHER
STRESS REDUCTION NEED TO BE
INCLUDED?
>> I'M SHOWING THE DATA I
REFERRED TO BEFORE.
THE ADDITION OF STRESS REDUCTION
GIVES FURTHER BENEFITS BECAUSE
WE BELIEVE STRESS REDUCTION IS
AUGMENTING WHAT HAPPENS WITH
EXERCISE.
SO EXERCISE GETS YOU SO FAR WITH
THE IMPROVED BIOLOGY AND STRESS
REDUCTION ADDS TO THOSE
IMPRESSIVE CHANGES.
I HYPOTHESIZE EXERCISE MAY BE
WORKING MORE ON THE PREFRONTAL
CORTEX AND STRESS REDUCTION MAY
BE WORKING MORE ON THE AMYGDALA.
THE COMBINATION OF THE TWO MAY
GIVE YOU GREATER IMPROVEMENTS IN
STRESS NEURAL ACTIVITY.
ALSO, EXERCISE HAS A BUNCH OF
BENEFITS THAT LEAD TO
IMPROVEMENTS IN HEART HEALTH
THAT HAVE LITTLE TO DO WITH THE
BRAIN.
IT GIVES YOU OTHER COURSES OF
BENEFITS.
SO THE COMBINATION OF THE
VARIOUS COURSES GETS YOU TO AN
IMPROVEMENT IN OUTCOMES.
>> ANOTHER QUESTION FROM THE
VIDEOCAST AUDIENCE.
I'M CURIOUS TO KNOW WHETHER YOU
HAVE DATA OR IS THERE IS DATA IN
THE LITERATURE SHOWING AN
ASSOCIATION BETWEEN ARIDGE
CARDIAC DISEASES SUCH AS ATRAIL
DEFIBRILLATION AND STRESS AND
NEUROPSYCHIATRIC DISORDERS?
ANY COMMENTS THERE OR THOUGHTS?
>> YES, THERE'S BEEN STUDIES
THAT SHOW ASSOCIATIONS WITH
ATRIAL FIBRILLATION AND MORE
RESEARCH IS NEEDED IN THAT AREA.
ON ONE HAND STRESS ASSOCIATES
WITH THE RISK FACTORS THAT
INCREASE THIS AND ADIPOSITY AND
INFLAMMATION.
ALL WILL INCREASE THE LIKELIHOOD
OF THE DEVELOPMENT OF ATRIAL
DEFIBRILLATION.
HOW ROBUST IS THE ASSOCIATION
BETWEEN STRESS AND ATRIAL
DEFIBRILLATION AFTER ADJUSTING
FOR THE RISK FACTORS.
THOSE STUDIES ARE STILL NEEDED.
>> RIGHT.
OKAY.
>> WE HAVE ANOTHER QUESTION
COMING IN, I'M CURIOUS ABOUT
MINDFULNESS.
DID YOU RESEARCH THE AFFECT OF
THIS AND THE AMYGDALA AND
RESULTING CARDIOVASCULAR
DISEASE?
>> ABSOLUTELY.
MINDFULNESS IS REALLY EFFECTIVE
IN REDUCING THE DOWN STREAM
SIGNALS I'VE BEEN DESCRIBING.
IT IMPROVES THE INFLAMMATORY
SIGNALS AND NICELY IMPROVES
BLOOD PRESSURE RESPONSE AND WE
ARE DOING STUDIES NOW TO ASK IF
A MINDFULNESS INTERVENTION WILL
IMPROVE THE BRAIN SIGNALS
WHETHER THAT IMPROVEMENT IN THE
BRAIN SIGNALS WILL LEAD TO
IMPROVEMENTS IN THE BONE MARROW
AND RESULT IN IMPROVEMENTS IN
THE ARTERIES AS WELL.
WE CURRENTLY HAVE TWO STUDIES
ONGOING WHERE WE'RE TESTING THIS
INTERVENTION AND PEOPLE ARE
RANDOMIZED TO EITHER AN
EIGHT-WEEK COURSE OF THIS
MINDFULNESS BASED STRESS
REDUCTION VERSUS NO INTERVENTION
TO SEE CHANGES IN OUTCOME.
>> OKAY.
WE HAD ANOTHER SIMILAR QUESTION
THAT CAME IN SOMEBODY ASKING
ABOUT MINDFULNESS BASED
INTERVENTIONS AND AMYGDALA
ACTIVITY OR STUDIES ON THAT AND
I THINK YOU'VE JUST ANSWERED
THAT QUESTION.
I WANT TO REMIND OUR VIDEOCAST
AUDIENCE IF YOU HAVE ADDITIONAL
QUESTIONS TO -- I'M SEEING MORE
AND HERE'S A FEW MORE POPPING
UP.
THE PERSON IS ASKING AND I'M
GOING TO DROP THIS IN TO OUR
CHAT FOR YOU SO YOU CAN SEE IT.
AND THE PERSON ASKED THIS
QUESTION.
CURRENTLY, ASSESSMENT OF CBD
RISK AND STATINS RELIES ON BLOOD
WITH THE PANELS A MEASURE OF
ARTERIAL INFLAMMATION.
HOW DO YOU SEE THE FINDINGS,
CHANGES, INFLUENCING THE
DIAGNOSIS AND CHANGES IN CBD.
WHAT ROLE OR HEALTH STYLE
MEDICINE AND COACHING DO YOU
SEE?
>> SO, THERE'S EMERGING
LITERATURE THAT SHOWS CHRONIC
STRESS MAY IMPEDE THE ACTIONS OF
SOME EFFECTIVE DRUGS SUCH AS
STATINS.
SO STATINS NICELY LOWER ARTERIAL
INFLAMMATION.
IT TURNS OUT THE LIPIDS THAT
STATINS LOWER ARE SOME OF THE
MOST POTENT INDUCERS OF
INFLAMMATION IN THE ARTERIAL
WALL.
WHAT WE ALSO FIND IS INDIVIDUALS
WHO ARE CHRONICALLY STRESSED
TEND TO HAVE ONGOING BONE MARROW
PRODUCTION OF INFLAMMATORY CELLS
SO IF YOU ONLY LOWER THE LIPIDS
BUT DON'T IMPROVE THE STRESS YOU
DON'T SEE THE AMOUNT YOU
ANTICIPATED TO SEE.
IT'S A COMPLEX SCENARIO.
THERE'S ONGOING STUDIES BUT
FASCINATING ANIMAL STUDIES THAT
SHOW THAT STRESSED MICE RESOLVE
THEIR ATHEROSCLEROTIC
INFLAMMATION HALF AS WELL AS
NON-STRESSED MICE.
>> INTERESTING.
IN TERMS OF THE LIFESTYLE
COACHING DO YOU SEE ANYTHING
THERE?
WHAT DO YOU THINK IS --
>> I THINK WE NEED TO SPEND MORE
TIME DEVELOPING A LITERATURE
THAT SHOWS THE EFFICACY OF SOME
OF THESE INTERVENTIONS.
FOR INDIVIDUAL WHO'S HAVE
ATHEROSCLEROTIC DISEASE,
LIFESTYLE IS AN INCREDIBLY
EFFECTIVE WAY TO REDUCE YOUR
RISK.
I WOULD SAY A DECADE AGO HUMBLY,
I WOULD NOT HAVE ANTICIPATED THE
STRENGTH OF THE DATA THAT WE'RE
SEEING EMERGE FROM THE
LITERATURE SHOWING HOW EFFECTIVE
LIFESTYLE INTERVENTIONS ARE.
WE SHOW, FOR EXAMPLE, GREAT AN
IMPACT EXERCISE HAS ON THE BRAIN
AS WELL.
WE'VE BEEN TALKING ABOUT STRESS
AND I'VE BEEN TALKING ABOUT
PREFRONTAL CORTEX AND DIDN'T
MENTION COGNITION AND PROFOUND
ASPECTS YOU EXPECT TO SEE WITH
CHANGES IN THE PREFRONTAL
CORTEX.
WHEN I RECOMMEND EXERCISE TO MY
PATIENTS IN CLINICS I TALK ABOUT
CARDIOVASCULAR EVENTS AS A CARD
CARRYING MEMBER OF CARDIOLOGY
BUT HAS GREAT IMPACTS ON
COGNITION AS WELL AND OF COURSE
STRESS.
SO HALF YOUR PATIENTS RECOGNIZE
THE MULTIPLE PATHS SOME OF THE
LIFESTYLE INTERVENTIONS HAVE
TOWARDS IMPROVING HEALTH AND
CAUSES MANY OF THEM AND THEY'LL
BE MORE ENGAGED IN THE LIFESTYLE
INTERVENTIONS BECAUSE THEY HAVE
A BETTER UNDERSTANDING AS TO HOW
IT MIGHT WORK AND HOW IT MIGHT
BENEFIT THEM.
AT THE END OF THE DAY WHEN
YOU'RE CHOOSING TO EXERCISE YOUR
OFTEN HAVING TO CHOOSE IT OVER
SOMETHING ELSE.
KNOWING THE DEGREE TO WHICH IT'S
HELPING YOU PERSONALLY ALLOWS
YOU TO BETTER UNDERSTAND WHEN TO
PRIORITIZE THESE LIFESTYLE
INTERVENTIONS.
>> THANK YOU.
I THINK THAT'S A WONDERFUL
ANSWER.
WE ACTUALLY HAVE A DIFFERENT
QUESTION SO I'LL MOVE IT ON THE
NEXT ONE.
HOW DO YOU DETERMINE YOUR POLY
GENIC SENSITIVITY AND WHAT GENES
ARE INVOLVED?
>> POLY GENIC RISK SCORES ARE
THROUGH ANALYSES AND AN
INDIVIDUAL GETS THEIR GENES
ASSESSED.
WE DO IT IN THE CONTEXT OF OUR
BIO BANK STUDIES.
THE MASS GENERAL BRIGHAM BIO
BANK BUT THERE ARE LARGER
STUDIES INCLUDING THE U.K. BIO
BANK THAT ALSO DO THAT.
ANOTHER WAY TO DO THAT IS YOU
CAN GO TO ONE OF THE GROUPS THAT
WILL TAKE YOUR BLOOD SAMPLES AND
MEASURE YOUR GENETICS, 23 AND ME
FOR EXAMPLE NOT PUT IN A PLUG
FOR ANY PARTICULAR COMPANY BUT
THAT WOULD BE ONE PLACE YOU CAN
GO.
THEN YOU WOULD HAVE TO HAVE A
GROUP MEASURE THAT POLY GENIC
RISK SCORE.
THAT'S NOT SO STRAIGHTFORWARD
AND TRADITIONALLY DONE.
SOME GROUP NEEDS TO HAVE ACCESS
TO POINT THE 2.2 MILLION SNIPS,
INDIVIDUAL GENES AND CALCULATE
THAT WEIGHTED SCORE FOR YOU.
I WISH I HAD A DIRECTOR ANSWER
HOW THAT COULD BE ACHIEVED
EASILY BUT I DON'T AT THIS
POINT.
>> THANK YOU.
I THINK IT'S A GOOD INSIGHT INTO
THE FACT THAT THERE'S STILL MORE
TO BE DONE THERE EVEN IN THE
INDICATOR.
WE HAVE A QUESTION THAT CAME IN
FROM A COLLEGIATE NIAID.
AND THEY WERE ASKING IN THE WORK
SHOWING PREFRONTAL CORTEX
AMYGDALA DIFFERENCES BETWEEN
STUDIED POPULATIONS AND
CONTROLS.
ARE CONDITIONS LIKE ADHD
CONTROLLED FOR SINCE IT INT
INHERENTLY HAS LESS PHD UPTAKE.
>> NOT REGULARLY.
WE HAVE PSYCHO METRIC ANALYSES
AND WE WILL ASSESS FOR SEVERAL
STRESS-RELATED DISORDERS.
>> AND WE HAVE A COUPLE
QUESTIONS FROM MEMBERS OF THE
AUDIENCE ASKING WHAT TYPES OF
STRESS REDUCTION ACTIVITIES ARE
RECOMMENDED?
>> WELL, THE FIRST
RECOMMENDATION I WOULD HAVE IS
TO MAKE SURE YOU HAVE HEALTHY
SLEEP BECAUSE UNHEALTHY SLEEP IS
GOING TO REALLY HURT YOUR STRESS
CONTROL AND REDUCE YOUR
RESILIENCE AS A RESULT.
YOU'RE MORE LIKELY TO HAVE
INFLAMMATORY REACTIONS IS WHEN
YOU'RE STUDYING FOR YOUR EXAMS
AND SLEEP DEPRIVED.
BUT FROM THERE WE SEE ALL SORTS
OF RISKS OVER A LIFE TIME THAT
ASSOCIATES WITH SLEEP
DEPRIVATION.
NEXT IS EXERCISE.
IT'S A WONDERFUL WAY TO REDUCE
YOUR STRESS.
I USED TO THINK IT WAS ALL ABOUT
THE FLASH IN THE PAN YOUR
INCREASED PROTEINS THAT WILL
REDUCE YOUR SENSE OF STRESS BUT
SINCE THEN WE'VE LEARNED IT'S
BECAUSE THE WIRING OF YOUR BRAIN
CHANGES.
IN ANIMAL MODELS WE SEE EXERCISE
LEADS TO ARBORIZATION OF THE
NEURONS ESPECIALLY IN THE PRE
FRONTAL CORTEX.
HOW ELSE WILL YOU INCREASE THE
ARBORIZATION OF YOUR NERVES?
THAT'S A BEAUTIFUL WAY TO DO
THAT.
STRESS REDUCTION CAN BE ACHIEVED
THROUGH ADDITIONAL APPROACH AND
I GAVE SLIDES IN REGARDS TO TAI
CHI, YOGA, BREATHING EXERCISE
CAN BE EFFECTIVE AND
MINDFULNESS-BASED, STRESS
REDUCTION TECHNIQUES HAVE A NICE
LITERATURE SHOWING THAT IT
REDUCES SEVERAL OF THE
INFLAMMATORY END POINTS.
A LOT OF THE SYNTHETIC NERVOUS
ACTIVITIES THINGS WE ASSOCIATE
WITH THE HIGHER DISEASE RISK AND
TRY TO COMBINE THE TECHNIQUES
YOU CAN COMBINE THAT DO AS MANY
OF THE TECHNIQUES THAT YOU THINK
WORK WELL WITHIN YOUR LIFE AND
PRIORITIZE THE ONES THAT YOU
THINK WILL BENEFIT YOU THE MOST.
AS LONG AS YOU AT LEAST PUT IT
ON YOUR RADAR SCREEN THAT STRESS
AND STRESS RELATED DISORDERS ARE
REALLY GOING TO WREAK HAVOC IN
TERMS OF CARDIOVASCULAR HEALTH
AND CANCER RISK AND ADVERSE
OUTCOMES, THEN YOU'LL PRIORITIZE
REDUCING IT AND BY THE WAY, BY
REDUCING THE STRESS YOU'LL FEEL
BETTER.
IT HAS IMMEDIATE BENEFITS AND
LONG TERM BENEFITS AND KEY IS TO
PRIORITIZE IT AND GET LONG TERM
BENEFITS FROM THEM.
>> THANK YOU, DR. TAWAKOL.
I THINK WE'RE BRINGING THINGS TO
A CLOSE FOR OUR Q&A SESSION
WHICH WAS VERY ROBUST AND WE
HAVE A FEW QUESTIONS WE DIDN'T
GET TO BUT DO NOT FEAR, FOLKS,
WE'RE GOING TO GATHER THE
QUESTIONS AND SHARE THEM WITH
DR. TAWAKOL.
AT THIS POINT I WANT TO REMIND
OUR VIEWERS AND THANK YOU FOR
JOINING US AND REMIND YOU THIS
HAS BEEN RECORDED AND WILL BE
ARCHIVED IN THE NIH VIDEOCAST
WEBSITE FOR FUTURE VIEWING.
WITH THAT I'D LIKE TO TURN
HELENE FOR ANY CLOSING THOUGHTS
FOR THE LECTURE.
>> I THINK YOU'VE GIVEN US A
BEAUTIFUL DEMONSTRATION OF
INTEGRATIVE RESEARCH.
THIS IS A POINT WE MAKE
NECESSARY ALL THE TIME THAT IN
RESEARCH WE CAN DO IT ANALYSIS
AND BREAK THINGS DOWN AND REALLY
LOOK AND DRILL INTO SPECIFIC
GENES AND MOLECULES.
BUT EVENTUALLY YOU HAVE TO PUT
THINGS BACK TOGETHER TO
UNDERSTAND WHAT'S GOING ON AND
YOU ARE DOING THAT IN SPADES.
I WANT TO CONGRATULATE FOR ALL
THE WORK AND THIS WAS A LOVELY
LECTURE YOU JUST GAVE US.
THANK YOU.
>> THANK YOU SO MUCH.
>> THANK YOU AS MUCH AND AGAIN
THANK YOU TO OUR AUDIENCE FOR
JOINING US AND WE LOOK FORWARD
TO SEEING YOU AS FUTURE ACTIVES
AT NCCIH AND WITH THAT I'LL NOW
CONCLUDE THIS VIDEOCAST.
THANK YOU AND HAVE A LOVELY DAY EVERYONE.