Welcome to the Clinical Center Grand Rounds, a weekly series of educational lectures for physicians and health care professionals broadcast from the Clinical Center at the National Institutes of Health in Bethesda, MD. The NIH Clinical Center is the world's largest hospital totally dedicated to investigational research and leads the global effort in training today's investigators and discovering tomorrow's cures. Learn more by visiting us online at http://clinicalcenter.nih.gov TODAY WE'RE JOINED BY TWO COLLEAGUES FROM THE NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASE WHO WILL BE ADDRESSING DIABETES RISK, DIAGNOSIS AND PREVENTION. OUR FIRST SPEAKER IS DR. ANNE SUMNER WHO IS A SENIOR INVESTIGATOR AND CHIEF OF THE SECTION OF ETHNICITY AND HEALTH IN THE DIABETE ENDOCRINOLOGY AND OBESITY BRANCH AT NIDDK. DR. SUMMER HAS NOINT A-- SUMNER HAS A JOINT APPOINTMENT AS SENIOR INVESTIGATOR AT NATIONAL INSTITUTE OF MINORITY HEALTH AND HEALTH DISPARITIES AND IS FOUNDING DIRECTOR OF THE NIMHD NIDDK RA WANDAN HEALTH PROGRAM. DR. SUMNER EARNED HER MEDICAL DEGREE FROM UNIVERSITY OF PENNSYLVANIA SCHOOL OF MEDICINE, RESIDENCY IN INTERNAL MEDICINE AT THE REDDING HOSPITAL AND MEDICAL CENTER IN PENNSYLVANIA. AND FOLLOWED THAT BY A FELLOWSHIP IN NUTRITION AND METABOLISM AT THE HOSPITAL OF THE UNIVERSITY OF PENNSYLVANIA. SUBSEQUENTLY A FELLOWSHIP IN ENDOCRINOLOGY, DIABETES AND METABOLISM AT THE MEDICAL COLLEGE OF PENNSYLVANIA. SHE BEGAN HER ACADEMIC CAREER AS ASSISTANT PROFESSOR OF MEDICINE AND ENDOCRINOLOGY AT THE ALLEGHENY UNIVERSITY HEALTH SCIENCES AND THEN CAME TO THE NIH AS A CLINICAL INVESTIGATOR IN 1998. SHE'S BEEN A TENURED INVESTIGATOR AT NIDDK SINCE 2011. DR. SUMNER'S RESEARCH CENTERS ON THE PREVENTION OF CARDIOVASCULAR DISEASE AND DIABETES AND PEOPLE OF AFRICAN DESCENT, SHE FOCUSES ON DIFFERENCES IN CARDIOVASCULAR RISK FACTORS BY RACE AND ETHNICITY IN ORDER TO FIND WAYS TO MAXIMIZE THE EFFECTIVENESS OF SCREENING PROGRAMS FOR DETECTING EARLY STAGE DISEASE IN ALL POPULATIONS. AS THE DIRECTOR OF THE RA WAN DAN HEALTH PROGRAM SHE'S WORKING WITH THE MINISTER OF HEALTH TO ESTABLISH A NATIONAL DIABETES REGISTRY FOR THE COMPILATION OF HEALTH STATISTICS FOR USE IN RESOURCE ALLOCATION AND HEALTH LITERACY. DR. SUMNER'S FELLOW OF THE AMERICAN COLLEGE OF PHYSICIANS, HER MEMBERSHIPS INCLUDE THE ENDOCRINE SOCIETY, THE AMERICAN HEART ASSOCIATION AND FOR FOUR YEARS SHE SERVED ON THE BOARD OF GOVERNORS OF THE ASSOCIATION OF BLACK CARDIOLOGISTS. SHE'S THE RECIPIENT OF TWO NIDDK NANCY NOSALL OUTSTANDING MENTOR AWARDS AND NIH DIRECTORS HARVEY J. BULL LOCK JR. AWARD FOR OUTSTANDING MENTORING OF MINORITIES AND WOMEN. AND NATIONAL HEART LUNG AND BLOOD INSTITUTE DIRECTORS DIVERSITY AWARD. FOR EXPANDING THE DIVERSITY OF BOTH THE RESEARCH WORK FORCE AND THE POPULATIONS RECRUITED FOR PROTOCOLS. SHE IS THE ASSOCIATE EDITOR OF THE JOURNAL FRONTIERS IN ENDOCRINOLOGY AND HAS PUBLISHED MORE THAN 80 ORIGINAL MANUSCRIPTS IN THE BIOMEDICAL LITERATURE. THE TITLE OF HER PRESENTATION IS REVERSING THE TIDE DIAGNOSIS AND PREVENTION OF TYPE 2 DIABETES IN AFRICAN DESCENT POPULATIONS. OUR SECOND SPEAKER IS DR. STEPHANIE CHUNG WHO IS AN ASSISTANT CLINICAL INVESTIGATOR IN THE DIABETES OBESITY AND ENDOCRINOLOGY BRANCH AT NIDDK AND SHE'S ALSO ADJUNCT ASSISTANT PROFESSOR PEDIATRICS AT THE GEORGE WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND HEALTH SCIENCES. DR. CHUNG GRADUATED WITH HONORS FROM THE UNIVERSITY OF THE WEST ENDES MEDICAL SCHOOL IN JAMAICA AND COMPLETED COMBINED INTERNAL MEDICINE PEDIATRIC RESIDENCY TRAINING AT THE UNIVERSITY OF TEXAS MEDICAL CENTER. AND SHE ALSO COMPLETED TRAINING AT THE UNIVERSITY OF TEXAS MEDICAL BRANCH IN GALVESTON. SUBSEQUENTLY SHE COMPLETED A PEDIATRIC ENDOCRINOLOGY FELLOWSHIP AT BAILOR COLLEGE OF MEDICINE, HOUSTON. DR. CHUNG'S CLINICAL AND RESEARCH FOCUSES ON MINIMIZING THE BURDEN OF DIABETES HEALTH DISPARITIES ACROSS THE LIFE SPAN BY IMPROVING DIABETES PREVENTION AND MANAGEMENT. ESPECIALLY AMONG INDIVIDUALS OF AFRICAN DESCENT. SHE'S LEAD INVESTIGATOR OF THE FEDERAL WOMEN'S STUDY, DESIGNED TO EVALUATE UPSTREAM PATHWAYS AND LIPID AND GLUCOSE METABOLISM. AND THIS IS IMPORTANT BECAUSE THAT MAY EXPLAIN POPULATION SPECIFIC PHENOTYPES OF CARDIO METABOLIC RISK IN WOMEN OF AFRICAN DESCENT. SHE'S ALSO THE PRIMARY INVESTIGATOR FOR THE THERAPEUTIC TARGETS IN AFRICAN AMERICAN YOUTH WITH TYPE 2 DIABETES, A STUDY EVALUATING NEW PHARMACOLOGIC AND PHARMACOGENETIC TARGETS IN AFRICAN AMERICAN YOUTH WITH TYPE 2 DIABETES. THIS STUDY ALSO ADDRESSES REASONS FOR MEDICATION NON-RESPONSIVENESS. HER RESEARCH GROUP ALSO PARTNERS WITH VARIOUS NON-PROFIT ORGANIZATIONS AND THE CHILDREN'S NATIONAL MEDICAL CENTER TO ADVOCATE FOR PEDIATRIC HEALTH AND AWARENESS OF OBESITY AND DIABETES IN THE GREATER D.C. METRO AREA. DR. CHUNG IS BOARD CERTIFIEDED IN PEDIATRICS SPECIAL MEDICINE AND -- INTERNAL MEDICINE AND PEDIATRIC ENDOCRINOLOGY AND FELLOW OF THE AMERICAN ACADEMY OFPEDIATRICS. HERS INCLUDE THE PEDIATRIC ENDOCRINE SOCIETY WHERE SHE CHAIRS THE OBESITY COMMITTEE, SOCIETY FOR PEDIATRIC RERESEARCH, THE AMERICAN SOCIETY FOR CLINICAL INVESTIGATION, AND THE ASSOCIATION OF CLINICAL AND TRANSLATIONAL SCIENCE. HER WORKS INCLUDE THE NIDDK WILLIAM J. COLEMAN JR. AWARD FOR DIVERSITY AND INCLUSION AND NIH CLINICAL CENTER BENCH TO BEDSIDE PROGRAM AWARD. TODAY SHE WILL SPEAK ON RACE, ETHNIC VARIATIONS IN DIABETES RISK PREDICTION, INSIGHTS FROM METABOLIC STUDIES. SO LET'S BEGIN WITH DR. SUMNER. >> THANK YOU VERY MUCH. THANK YOU FOR INVITING ME TO SPEAK, THANK YOU FOR ATTENDING OUR LECTURES TODAY. I WILL TALK ABOUT DIABETES AND AFRICAN DESCENT POPULATIONS. I'M GOING TO FOCUS ON AFRICA BECAUSE BETWEEN 2017 AND 2045 AFRICA WILL EXPERIENCE 156% INCREASE IN THE PREVALENCE OF DIABETES. THIS IS THE HIGHEST ANTICIPATED INCREASE IN THE WORLD AND THAT'S WHY AFRICA APPEARS MOST BRIGHTLY ON THIS MAP. BY WAY OF COMPARISON, DURING THE SAME TIME PERIOD IN NORTH AMERICA THERE'S A 34% INCREASE IN DIABETES PREVALENCE. AFRICA HAS THE HIGHEST PROPORTION OF PEOPLE WHO DIE FROM DIABETES UNDER THE AGE OF 60 YEARS. NO COUNTRY IN AFRICA OR ANYWHERE IN THE WORLD CAN SUSTAIN A LOSS OF LARGE POPULATIONS BETWEEN THE AGES OF 40 AND 60. THIS IS ECONOMICALLY DEVASTATING AND IT'S DEVASTATING TO SOCIETIES. THE REASON PEOPLE ARE DYING IN AFRICA FROM DIABETES IS BECAUSE AFRICA HAS THE HIGHEST PROPORTION OF PEOPLE LIVING WITH DIABETES WHO ARE UNDIAGNOSED. UNDIAGNOSED DIABETES OCCURS BECAUSE OF THE LACK OF ACCESS TO CARE AND ALSO AS PUT FORWARD BY OUR SECTION ON ETHNICITY AND HEALTH BECAUSE THE SCREENING TESTS THAT WE HAVE FOR DIABETES THAT WERE DEVELOPED IN WHITE POPULATIONS AND EVEN IN AFRICAN AMERICANS ARE NOT APPLICABLE TO AFRICANS. WE NEED TO SOLVE THE PROBLEM OF UNDIAGNOSED DIABETES IN AFRICANS, WE NEED TO UNDERSTAND THE DIVERSITY WITHIN OUR AFRICAN DESCENT POPULATIONS AND APPRECIATE THE DIABETES IS MULTI-FACTORIAL. AND THOSE FACTORS INCLUDE CULTURE, DIET, EXERCISE, AND INCOME, WAR AND WEATHER, WAR AND WEATHER BECAUSE THEY LEAD TO BOTH FAMINE AND CROONIC MALL MYTRITION. EXPOSURE IN EARLY LIFE TO FAMINE OR CHRONIC MALNUTRITION LEADS TO BETA CELL DAMAGE AND DIABETES IN LATER LIFE. AND THEN THERE'S POLITICS AND PUBLIC POLICY WHICH LEADS ON THE ONE HAND TO FOOD DESERTS AND FAST FOOD ON THE OTHER WHICH CONTRIBUTE TO DEVELOPMENT OF OBESITY AND DIABETES AND THEN THERE'S GENETICS. AND GENETICS ARE DIFFERENT ACROSS AFRICAN DESCENT POPULATIONS. TO SOLVE THE PROBLEM OF DIABETES IN AFRICANS WE NEED TO APPRECIATE THAT THE PRESENTATION AND ETIOLOGY OF DIABETES DIFFERS IN AFRICAN DESCENT POPULATIONS. AND AFRICAN AMERICANS ARE THE MOST WELL STUDIED POPULATION OF AFRICAN DESCENT BUT STUDIES DONE IN AFRICAN AMERICANS ARE NOT DIRECTLY APPLICABLE TO AFRICAN CARIBBEANS OR AFRICANS. SO WE'RE GOING TO FOCUS ON AFRICANS AND DO THAT FIRST BY WORKING WITH AFRICAN IMMIGRANTS. WHY ARE WE WORKING WITH AFRICAN IMMIGRANTS? ONE REASON IS BECAUSE WE CAN. AFRICAN IMMIGRATION TO UNITED STATES HAS DOUBLED EVERY DECADE SINCE 1970. SO NOW 4% OF THE FOREIGN BORN ADULTS IN THE U.S. ARE AFRICAN IMMIGRANTS. LUCKY FOR US WHO WANTS TO STUDY AFRICAN IMMIGRANTS, THAT NORTHERN VIRGINIA, MARYLAND AND WASHINGTON D.C. ARE ONE OF THE FOUR AREAS OF THE COUNTRY WHICH 15% OF THE FOREIGN BORN ADULTS ARE AFRICANS, SO THAT HELPS WITH RECRUITMENT AND WHAT YOU SEE HERE ON THE LEFT IS OUR LOGO WHICH HAS BEEN DEVELOPED OVER THE YEARS AND REFINED BY OUR POST BACKS AND ON THE OTHER SIDE YOU SEE OUR FLYER, THIS FLYER APPEARS ALL ACROSS THE NIH CAMPUS YOU HAVE SEEN IT AND IN THE WASHINGTON POST EVERY TUESDAY. SO OUR MAIN THESIS, I HOPE YOU FIND THIS INNOVATIVE, IF I WERE WRITING A Ph.D. THIS WOULD BE IT. WORKING WITH DISPARATE COMMUNITIES PROVIDES THE OPPORTUNITY TO USE SOPHISTICATED TESTING AVAILABLE IN AMERICA TO CLARIFY OBSERVATIONS MADE IN AFRICA SO I SUGGEST A NEW PARADIGM THAT INSIGHT GAINED FROM WORKING WITH IMMIGRANTS COMMUNITIES, ANY IMMIGRANT COMMUNITY CAN LEAD TO IMPROVED HEALTH POLICY IN THE COUNTRY OF ORIGIN. THIS IS NOT AN ALTERNATIVE TO RESEARCH IN THE COUNTRY OF ORIGIN BUT AN ADDITIONAL DIRECTION. SO WORKING WITH AFRICAN IMMIGRANTS AND USING RESOURCES AVAILABLE IN AMERICA WE CAN IDENTIFY GENETIC FACTORS SPECIFIC TO AFRICAN HERITAGE WHICH INTERFERE WITH INTERPRETATION OF A 1C, MAYBE DIAGNOSTIC TEST FOR DIABETES. IN ADDITION WE CAN EVALUATE SCREENING TESTS FOR EFFICACY IN AFRICAN IMMIGRANTS BEFORE TESTING DE NOVO TESTING IN AFRICA. WE CAN PROVIDE THE METABOLIC BASIS FOR OBSERVATIONS MADE IN AFRICA AND HELP IN THE DEVELOPMENT OF GUIDELINES. SO STARTING FIRST WITH IDENTIFYING IDENTIFICATION OF GENETIC FACTORS THERE'S THREE FACTORS HEMOGLOBIN S HEMOGLOBIN C TRAIT AND G 16B DEFICIENCY ALL WHICH ARE ACCUSED OF INTERFERING WITH THE INTERPRETATION OF A 1C. THAT'S AN ACTIVE AREA OF RESEARCH. THESE ALLELES ALL OF WHICH DECREASE SEVERITY OF MALARIA, HAVE A HIGHER FREQUENCY IN AFRICA. SO IF THEY HAVE HIGHER FREQUENCY OR PREVALENCE IN AFRICA, THEN AFRICAN AMERICANS OR CARIBBEANS, WE CAN ENROLL FEWER INDIVIDUALS THAT GET THE ANSWER IF PROTOCOL ENROLLS AFRICANS AND IF WE WORK WITH AFRICAN IMMIGRANTS WE CAN USE TECHNOLOGY HERE IN THE U.S.. WE CAN VALUE WAIT SCREENING TESTS FOR EFFICACY AND AFRICAN IMMIGRANTS BEFORE INVESTING IN DE NOVO TESTING IN AFRICA. WE HAVE DEVOTED GREAT DEAL OF RESOURCES TO UNDERSTAND GLEE KATEED ALBUMIN AND FINDING IT HAVE BEEN SUCCESSFUL TEST FOR DIAGNOSIS OF DIABETES IN AFRICANS, IN FACT BETTER IN AN CANS THAN AFRICAN AMERICANS BUT THAT'S NOT GOING TO BE WHERE I'M GOING TO FOCUS TODAY. TODAY I WILL FOCUS ON METABOLIC BASIS FOR OBSERVATIONS MADE IN AFRICA. I WANT TO TALK ABOUT HOW WAIST CIRCUMFERENCE PREDICTS INSULIN RESISTANCE AND HOW OUR WORK CONTRIBUTES TO GUIDELINE DEVELOPMENT AS WE BUILD STUDIES INITIALLY DONE IN AFRICA. WHY AM I SO INTERESTED IN THE WAY CIRCUMFERENCE OF LISTK IN AFRICANS, WAIST CIRCUMFERENCE IS BETTER THAN BODY MASS INDEX IN PREDICTING DIABETES AND CARDIOVASCULAR DISEASE. IT'S LESS EXPENSIVE AND EASIER TO OBTAIN THAN BMI. YOU CAN GET IT IN A COMMUNITY EVENT, YOU CAN GET IT OUTSIDE, YOU CAN GET IT INSIDE. IT'S CULTURALLY ACCEPTABLE. AND WAIST CIRCUMFERENCE IS PART OF THE METABOLIC SYNDROME, THAT'S WHY IT'S PART OF THE MELBOTIC SYNDROME BECAUSE IT'S BETTER THAN BMI AND THE METABOLIC SYNDROME HAS FIVE CHARACTERISTICS, WAIST CIRCUMFERENCE BLOOD PRESSURE TRIGLYCERIDE HDL FASTING GLUCOSE ALL WHICH ARE INEXPENSIVE AND INDIVIDUALLY PREDICT MET -- INSULIN RESISTANCE SO THEY'RE PUT TOGETHER BECAUSE THEY'RE ASSOCIATED WITH INSULIN RESISTANCE AND IF YOU HAVE THE METABOLIC SYNDROME YOU HAVE THREE TO FIVE TIMES THE RATE OF DIABETES AND CARDIOVASCULAR DISEASE. BUT WASES CIRCUMFERENCE THRESHOLD ARE NOT ESTABLISHED OR VALIDATED IN AFRICANS. AFRICANS CANNOT BENEFIT FROM THIS COST FREE SCREENING TEST FOR THE PREDICTION OF CARDIOVASCULAR DISEASE AND DIABETES. UNTIL THE THRESHOLDS ARE RIGHT FOR AFRICANS. BY WAY OF BACKGROUND, OBESITY LEADS TO DIABETES AND THIS IS TRUE IN THE UNITED STATES, YOU HAVE SEEN THIS SLIDE, OVER 30 YEARS OBESITY WEPT FROM LESS THAN 20 -- WENT FROM LESS THAN 10% TO MORE THAN 30% AND THE DIABETES EPIDEMIC FOLLOWED FROM LESS THAN 5% TO MORE THAN 20%. -- 10. THIS SLIDE SHOWS YOU THAT OBESITY IS ALSO OCCURRING WORLDWIDE. AND ON THE Y AXIS IS THE REGION OF THE WORLD FROM HIGHEST PREVALENCE TO LOWEST PREVALENCE AND ON THE X AXIS IS CHANGE IN PREVALENCE OF OBESITY OVER A 30 YEAR PERIOD. YOU CAN SEE THAT SOUTH AFRICAN WEST, EAST AND CENTRAL AFRICAN MEN ARE ALSO AFFECTED BY THIS CHANGE IN BMI OVER TIME. SO ARE WOMEN. YOU CAN SEE SOUTH AFRICAN WOMEN ARE LEADING THE WAY IN THE PREVALENCE OF OBESITY AND THE RATE OF CHECK AND BUT WEST AFRICA EAST AND CENTRAL AFRICAN WOMEN ARE NOT EXEMPT. YOU WILL NOTICE WEST EAST AND CENTRAL AFRICANS OF BOTH MEN AND WOMEN ARE SIMILAR TO EACH OTHER IN PREVALENCE OF OBESITY AND THE RATE OF CHANGE. WHY ARE PEOPLE BECOMING OBESE? IN AFRICA THEY ARE EATING FAST FOOD, RESTAURANTS EVEN CALL MR. BIGS AND IT IS MODELED AFTER MCDONALDS, IT HAS 200 LOCATIONS IN NIGERIA, THE FIRST DRIVE THROUGH RESTAURANT SO YOU HAVE TO GET OUT OF YOUR CAR TO GET THIS DELICIOUS FOOD. WHAT IS THE DELICIOUS FOOD? THE FAVORITE LUNCH OF SCOTT EGGS FRIED CHICKEN SUGARED DONUTS AND SOFT DRINK. THAT'S ONE MEAL. WHAT ARE SCOTT EGGS? I DIDN'T KNOW. I HAD TO LOOK IT UP, IT'S HARD BOILED EGGS WRAPPED IN SAUSAGE MEAT COATED IN BRED CRUMBS AND DEEP FRIED. THEIR SLOGAN IS WHAT A DELICIOUS EXPERIENCE. IT'S NOT JUST NIGERIA, IT IS ACROSS AFRICA. I GET THE NEW YORK TIMES DELIVERED TO MY HOUSE EVERY MORNING AND THIS PICTURE WAS ON THE FRONT PAGE OF THE NEW YORK TIMES ON OCTOBER 2ND, 2017. AND THEY SAID OBESITY WAS RISING AS GHANA EMBRACED FAST FOOD. THEN CAME KFC. THEY DON'T SAY THAT KFC IS KENTUCKY FRIED CHICKEN BECAUSE KENTUCKY HAS NO MEANING THERE. BUT THEY DO SAY THEY HAVE A DRIVE THREW. -- THROUGH. SO OBESITY LEADS THE DIABETES BECAUSE OBESITY LEADS TO INSULIN RESISTANCE. AND INSULIN RESISTANCE MAKES IT DIFFICULT FOR GLUCOSE TO BE TRANSPORTED INTO THE CELLS. THEREFORE YOUR PANCREAS HAS TO PUT OUT MORE INSULINS AND YOU'LL BECOME HYPERINSULINEMI C. SO TWO INDIVIDUALS WITH THREE MEALS A DAY AND Y AXIS IS GLUCOSE CONCENTRATION ANT X AXIS IS TIME OF EACH MEAL AND YOU CAN SEE THE GLUCOSE RISE. THEN YOU CAN SEE IN THE INSULIN SENSITIVE PERSON THAT THEY NEED ONLY A LITTLE BIT OF INSULIN TO DRIVE THAT GLUCOSE INTO THE CELL. BUT THE INSULIN RESISTANT PERSON NEEDS A LOT OF INSULIN TO DRIVE THAT GLUCOSE INTO THE CELL SO THEY HAVE TO SELF-MEDICATE BY HAVING PANCREAS PUT OUT MORE SO THEY HAVE INSULIN RESISTANCE LEADING TO HYPERINSULINEMIA TO GET GLUCOSE IN THE CELLS. THE KEY IS GLUCOSE CONCENTRATIONS ALONE CANNOT REVEAL WHETHER INSULIN RESISTANCE IS PRESENT. YOU CANNOT DISTINGUISH INDIVIDUALS BY LOOKING AT GLUCOSE CONCENTRATION. YOU HAVE TO KNOW THE INSULIN CONCENTRATION. AND WHAT HAPPENS WITH THE INSULIN RESISTANT PERSON IS THAT THEIR PANCREAS GETS EXHAUSTED, THEY CAN'T CONTINUE TO MAINTAIN THAT LEVEL OF INSULIN SECRETION AND THEY GET RELATIVE BETA CELL FAILURE, INSULIN CONCENTRATION IS LOWER THAN IT WAS BEFORE AND THEY GET DEVELOP DIABETES. SO INSULIN RESISTANCE RELATIVE BETA CELL FAILURE LEADS TO DIABETES AND IS RELATIVE BETA CELL FAILURE GETS WORSE, SO DOES THE DIABETES WE ARE NOT ACTUALLY TALKING ABOUT OVERALL OBESITY. WE ARE TALKING ABOUT CENTRAL OBESITY. THAT CENTRAL OBESITY CAN BE MEASURED BY A TAPE MEASURE. ONE GREAT FEATURE. BUT YOU CAN ARGUE WHETHER IT -- WHERE IT SHOULD BE DONE IN THE EUROPEANS AND THE AMERICANS ARGUE WITH THE LEVEL THAT WAIST CIRCUMFERENCE COULD BE DETERMINED. I WILL TELL YOU WE HAVE DONE BOTH LEVELS AND RESULTS COME OUT THE SAME. SO WHEN YOU THINK OF CENTRAL OBESITY YOU THINK OF STATE VISCERAL FAT IT LEADS TO RESISTANCE BECAUSE OF ALTERED FREE FATTY METABOLISM, WE WON'T DISCUSS THE MECHANISM TODAY BUT CONSIDER WAIST CIRCUMFERENCE VISCERAL FAT AND INSULIN RESISTANCE TO BE VIRTUALLY INTERCHANGEABLE TERMS. WHEN YOU TALK ABOUT EXERCISE, INSULIN RESISTANCE AND VISCERAL TO GET AROUND NIGERIA LIKE INSED- THE TOP SLIDE AND TO SOME DEGREE THEY MAY STILL. BUT IN THE BOTTOM ONE, THAT STAND STILL BELT WAY IN NIGERIA. THAT'S STAND STILL TRAFFIC AND FOOD VENDORS ARE WALKING IN BETWEEN THOSE CARS SELLING FOOD. WHAT KIND OF FOOD SUGARED DONUTS, NO DOUBT. SO THIS IS A CROSS SECTIONAL DRAWING OF THE ABDOMEN AND THE ARROW POINTS TO THE VISCERAL FAT. THEY ARE EATING THAT ENERGY FOOD DISPENSED BY THE FOOD VENDORS AND THEY HAVE DECREASED PHYSICAL ACTIVITY SITTING IN THEIR CAR. STATE PRISON RAIL ADIPOSE TISSUE WILL INCREASE THEN THEY'LL HAVE EXPANDING WAISTLINES AND DIABETES. WHEN I WENT BACK AND LOOKED AT THIS PICTURE FROM NEW YORK TIMES AND READ THE SUBHEADLINE, THE GROWING POPULARITY OF FRIED CHICKEN AND PIZZA IN PARTS OF AFRICA UNDERSCORES HOW FAST FOOD IS CHANGING AND EXPANDING WAISTLINES. SO THE MEDICAL JURY ROOM OF THE NEW YORK TIMES UNDERSTANDS IT'S WAIST CIRCUMFERENCE. SO THERE ARE SEX RACE AND ETHNIC DIFFERENCES IN VISCERAL ADIPOSE TISSUE. AND WE'RE GOING TO TALK ABOUT SEX DIFFERENCES. THESE ARE CT SCANS FROM TWO INDIVIDUAL WHOSE PARTICIPATED IN OUR STUDY, A MAP FROM UGANDA AND A WOMAN FROM GHANA, YOU CAN SEE THEY HAVE THE SAME AGE, BODY MASS INDEX AND WAIST CIRCUMFERENCE. BUT THE MAN HAS MORE VISCERAL ADIPOSE TISSUE SHOE BY YELLOW ARROWS THAN THE WOMAN. BUT THE WOMAN HAS MORE SUBCUTANEOUS ADIPOSE TISSUE THAN THE MAN SO SAME WAIST CIRCUMFERENCE YOU HAVE A DIFFERENT INTERNAL ADIPOSE TISSUE SO THAT'S WHY WE NEED SEX SPECIFIC WAIST THRESHOLDS FOR THE PREDICTION OF INSULIN RESISTANCE. WHAT ARE THE SEX SPECIFIC WAIST CIRCUMFERENCE THRESHOLDS WE SHOULD USE FOR AFRICANS? THE WHO EXPERT CONSULTATION REPORT OF 2008 STATES, THERE IS INSUFFICIENT EVIDENCE FOR RECOMMENDING SPECIFIC WAIST CIRCUMFERENCE THRESHOLDS FOR SUBSAHARAN AFRICANS, THERE'S BEEN NO UPDATE OF THAT REPORT SINCE 2008. WHAT IS IBF AMERICAN HEART AND NHLBI SAY? FOR SUB-SAHARAN AFRICANS USE EUROPEAN AND AMERICAN DATA UNTIL MORE SPECIFIC DATA ARE AVAILABLE. BUT THEY DON'T AGREE AMONG THEMSELVES WHAT THOSE WAIST CIRCUMFERENCE SHOULD BE. SO IT SAY USES 94 SENT MER TEARS AND 80-CENTIMETERS IN WOMEN AND MEME RESPECTIVELY WHEREAS NHLBI USES 88-CENTIMETERS FOR WOMEN MEN AND WOMEN NOTICING THE WAIST CIRCUMFERENCE RISK IS HIGHER IN MEN THAN WOMEN. IN ALL THESE POPULATIONS YOU WILL SEE WAIST CIRCUMFERENCE IS HIGHER IN MEN AND WOMEN EXCEPT ONE GROUP. THAT IS THE JAPANESE. THE JAPANESE SAY THE WAIST CIRCUMFERENCE OF RISK IS HIGHER IN WOMEN THAN MEN. SO OUR QUESTION THOUGH IS ARE EITHER OF THESE SETS OF THRESHOLDS RIPE FOR AFRICANS? TURNS OUT IN THE LAST TEN YEARS SINCE THAT WHO ARTICLE WAS PUBLISHED, THERE'S BEEN EIGHT STUDIES CONDUCTED IN AFRICA, SOUTH AFRICA DEMOCRATIC PUB LINK -- REPUBLIC OF CONGO WHICH PREDICTS INSULIN RESISTANCE AND THEY SAY IN WOMEN IT'S BETWEEN 90 AND 99-CENTIMETERS AND IN MEN, THEY SAY BETWEEN 80 AND 94-CENTIMETERS IN OTHER WORDS LIKE JAPANESE HIGHER IN WOMEN THAN MEN. BUT HOW DID THEY MEASURE INSULIN RESISTANCE? THEY TOOK A PRACTICAL APPROACH, THEY USED INEXPENSIVE READILY AVAILABLE DATA, DATA FROM METABOLIC SYNDROME. THEY SAID THE METABOLIC SYNDROME HAS FIVE VARIABLES EACH SUPPOSED TO BE ASSOCIATED WITH INSULIN RESISTANCE. SO WE CAN USE THESE FOUR VARIABLES TO PREDICT THE WAIST CIRCUMFERENCE, THAT'S NOT HOW THE METABOLIC SYNDROME WAS DESIGNED, IT WASN'T DESIGNED FOR ANY ONE VARIABLE TO PREDICT OTHERS. AND THEY DIDN'T MEASURE INSULIN CONCENTRATION SO THEY DIDN'T DIRECTLY MEASURE INSULIN RESISTANCE. THEY DIDN'T MEASURE VISCERAL ADIPOSE TISSUE, SO THOSE STUDIES IN AFRICA MAYBE IMPORTANT BUT CAN'T BE USED FOR GUIDELINE DEVELOPMENT AT THIS TIME. HOWEVER, WORKING WITH THE AFRICANS IN AMERICA COHORT WE CAN WORK WITH AFRICAN BORN MEN AND WOMEN AND DETERMINE WAIST CIRCUMFERENCE WHICH PREDICTS INSULIN RESISTANCE AND THEN DETERMINE HOW SEX DIFFERENCES IN DISTRIBUTION OF VAT AND SAT CONTRIBUTE TO SEX DIFFERENCES IN WAIST CIRCUMFERENCE OF RISK. WE HAD 385 AFRICAN IMMIGRANTS WHO PARTICIPATED, AND YOU CAN SEE THEIR CHARACTERISTICS. THEY HAVE GLUCOSE TOLERANCE STATUS, WAIST CIRCUMFERENCE MEASURE, INSULIN RESISTANCE AND MOST IMPORTANTLY, THEY HAD SRISCAL AND SUBCUTANEOUS ABDOMINAL ADIPOSITY MEASURED BY CT SCAN. AS WE GET TO THE RESULTS, THE FIRST QUESTION YOU MIGHT ASK IS CAN AFRICANS WEST CENTRAL AND EAST AFRICA BE COMBINED INTO A SINGLE GROUP? WHEN WE LOOK AT ANTHROPOE METRIC METABOLIC AND SOCIAL FACTOR THERE'S NO DIFFERENCE IN MEN AND WOMEN IN THOSE CHARACTERISTICS SO WE PROVIDE THEM INTO SEX SPECIFIC GROUPS. WHAT IS THEIR GLUCOSE TOLERANCE STATUS? EVERYONE SELF-IDENTIFIED AS HEALTHY BUT WE FOUND OUT 40% OF MEN AND 25% OF WOMEN HAD PRE-DIABETES AND 3% OF BOTH HAD DIABETES. SO WE COMBINE THEM AND CALL THIS ABNORMAL GLUCOSE TOLERANCE. SO WHAT ARE THE GLUCOSE TOLERANCE CATEGORIES THAT PEOPLE WERE DIVIDED INTO? NORMAL GLUCOSE TOLERANCE, NORMAL GLUCOSE TOLERANCE AND INSULIN RESISTANCE. ABNORMAL GLUCOSE TOLERANCE AND INSULIN RESISTANT, GLUCOSE TOLERANT AND NO INSULIN RESISTANCE. SO THESE HAVE -- THIS IS THE DISTRIBUTION BY GLUCOSE TOLERANCE CATEGORY OF OUR PARTICIPANTS, AND THESE ARE THE PEOPLE THAT WILL BE ABLE TO IDENTIFY THE PEOPLE THAT HAVE INSULIN RESISTANCE. SO WHEN WE LOOK AT THE VISCERAL ADIPOSE TISSUE IN MEN, THE FIRST COLUMN REPRESENT THE NORMAL GLUCOSE TOLERANCE GROUP, OUR REFERENCE GROUP, NEXT IS NORMAL GLUCOSE TOLL RAN AND INSULIN RESISTANT, ABOUT NORMAL GLUCOSE TOLERANT INSULIN RESISTANT AND ABNORMAL GLUCOSE TOLERANT AND NOT INSIN RESISTANT. THE TWO STARS REPRESENT THE GROUPS THAT WE CAN IDENTIFY AND THE STARS REPRESENT A P VALUE OF LESS THAN .001 IN COMPARISON TO THE REFERENCE GROUP. FROM THIS IS TRUE MORE INSULIN RESISTANCE HIGHER VAT IN MEN, ALSO TRUE IN IN WOMEN AND HIGHER IN MEN THAN WOMEN. FOR SUBCUTANEOUS ADIPOSE TISSUE GROUPS WITH INSULIN RESISTANCE HAD MORE SUBCUTANEOUS ADIPOSE TISSUE THAN NORMAL GLUCOSE TOLL RAPT WOMEN, NORMAL GLUCOSE TOLERANT IN WOMEN HAD NOR SUBCUTANEOUS ADIPOSE TISSUE THAN MEN, SO HOW DOES IT TRAN LATE TO WAIST CIRCUMFERENCE OF RISK? USING THE ARROWS FOR THE PREDICTION OF INSULINS RESISTANCE BY WAIST, THE ERROR WAS 0.8 SO WAIST CIRCUMFERENCE IS DOING AN EXCELLENT JOB PREDICTING INSULIN RESISTANCE. AND THE WAIST CIRCUMFERENCE PREDICT INSULIN RESISTANCE IN MEN WAS 91 SENTENCE METERS AND IN WOMEN, 96 CENTIMETERS. IN OTHER WORDS, THE OPTIMAL WAIST CIRCUMFERENCE LIKE THE JAPANESE TO PREDICT INSULIN RESISTANCE WAS HIGHER IN WOMEN THAN MEN. THE JAPANESE ALSO FOUND WHEN THEY DID CT SCANS LIKE WE HAVE DONE YOU HAVE WAIST CIRCUMFERENCE ON THE Y AXIS AND VAT ON THE X AXIS AND THE WOMEN IN RED AND THE MEN IN BLUE. YOU CAN SEE EVERY LEVEL OF VAT WAIST CIRCUMFERENCE IS HIGHER IN THE WOMEN THAN MEN. THAT'S BECAUSE AT EVERY LEVEL OF VAT SUBCUTANEOUS ADIPOSE TISSUE IS HIGHER IN WOMEN THAN MEN. ARE EITHER OF THESE SETS OF THRESHOLDS RIGHT FOR AFRICANS? FOR AFRICAN WOMEN 80 CENTIMETERSES AND 88 SENT ME REFERS ARE TOO LOW CENTIMETERS ARE TOO LOW. YOU'VE OVERSCREEN AND NOT DIRECT THEM WISELY. FOR AFRICAN MEN, THE 94 SEPTEMBER-METERS FOR PRE-- CENTIMETERS IS REASONABLE BUT IF YOU USE THE AMERICAN THRESHOLD OF 102 YOU WOULD HAVE MANY UNDIAGNOSED PEOPLE AND AGAIN, NOT GOING IN THE RIGHT DIRECTION. HOW ARE OUR RESULTS RELATE TO THE STUDIES THAT HAVE BEEN DONE EARLIER IN AFRICA? THEY SAID THE OPTIMAL WAIST CIRCUMFERENCE PREDICT INSULIN RESISTANCE USING TECHNOLOGY THEY HAD WAS BETWEEN 90 AND 99-CENTIMETERS, SIMILAR TO 96-CENTIMETERS. THEY SAID HIGHER IN WOMEN THAN MEN. JUST LIKE WE HAVE DONE. SO WITH AFRICANS LIVING IN AMERICA, WE WERE ABLE TO VALIDATE THIS METABOLIC STUDIES IN CT SCANS OBSERVATIONS MADE IN AFRICA. AND THE KEY IS, THE KEY RESOURCE THAT WE HAVE FOR THIS STUDY WERE THOSE CT SCANS. SO REMEMBERING THAT MY MAIN THESIS IS WORKING WITH DISPARATE COMMUNITIES PROVIDES US THE OPPORTUNITY TO SOPHISTICATED TESTING AVAILABLE IN AMERICA TO CLARIFY OBSERVATIONS MADE IN AFRICA. SO THE OBSERVATIONS IN AFRICA FOR THE PREDICTION OF WAIST CIRCUMFERENCE WERE RIGHT AND SO AFTER PUBLICATION OF OUR PAPER WE'RE GOING TO TAKE IT TO WHO AND REQUEST A NEW CONSENSUS CONFERENCE BECAUSE THE RIGHT WAIST CIRCUMFERENCE WILL MAKE A DIFFERENCE. WHAT I'M TRYING TO DO IS BUILD A CLINICAL BRIDGE, A CLINICAL DATA BRIDGE BETWEEN AFRICAN IMMIGRANTS AND AFRICANS, THAT'S THE LOGO I'M CONSIDERING. YOU CAN LET ME KNOW. I PRESENTED THIS DATA AT EAST AFRICAN DIABETES CONGRESS IN RWANDA IN MARCH, SO DID DR. PHYSICIAN WORKING WITH ME, THERE HE IS, HAVE THIS POSTER AND YOU CAN SEE THE INTEREST THAT WE GENERATED AT THAT CONFERENCE. THIS IS OUR GROUP. A GREAT WONDERFUL GROUP OF PEOPLE. STEPHANIE WILL BE THE NEXT SPEAKER. THANK YOU VERY MUCH. [APPLAUSE] >> GOOD AFTERNOON, EVERYONE, THANK YOU FOR BEING HERE, IT'S AN HONOR TO BE PRESENTING ALONGSIDE DR. SUMNER AND TO PRESENT TO YOU TODAY A LITTLE BIT OF OUR WORK SPECIFICALLY IN RACE AND ETHNIC DISPARITIES AND THE METABOLIC WORK WE DO AT THE NIH CLINICAL CENTER. I HAVE NO DISCLOSURES. OVER THE NEXT FEW MINUTES, I'M GOING TO SUMMARIZE THE TYPE 2 DIABETES SCREENING TEST. AND THEN FOCUS QUITE A BIT ON ONE OF THOSE TESTS, THE FASTING GLUCOSE TEST, AND ITS ABILITY TO PREDICT DIABETES AND DETECT DIABETES, ESPECIALLY IN AFRICAN ANCESTRY POPULATIONS AND THEN I'LL FINISH WITH A LITTLE BIT OF THE WORK WE'RE DOING TO LOOK AT ALTERNATIVE MARKERS DR. SUMNER ALLUDED TO BEFORE. SO SHE GAVE A WONDERFUL PRESENTATION HIGHLIGHTING THE GLOBAL EPIDEMIC OF TYPE 2 DIABETES AND THE FACT THAT IT AFFECTS PEOPLE OF ALL AGES, RACES AND SOCIO COMMISSION BACKGROUNDS. WE'RE ALL AWARE THAT CERTAIN GROUPS EXPERIENCE A DISPROPORTIONATE BURDEN OF DISEASE. IN NORTH AMERICA CARIBBEAN FOR EXAMPLE PREVALENCE OF TYPE 2 DIABETES IS TWICE AS HIGH IN AFRICAN ANCESTRY POPULATIONS COMPARED TO WHITE ADD MIXTURE POPULATIONS BUT THE BURDEN IS FURTHER MAGNIFIED. AS MENTIONED BEFORE ONE-THIRD OF THESE INDIVIDUALS DON'T YET KNOW THAT THEY HAVE DISEASE. IN AFRICA THE TRUE BURDEN IS JUST COMING INTO FOCUS. WE HAVE RELIABLE DATA ON 12 OF THE 37 COUNTRIES. AND IN THIS -- IN THESE COUNTRIES WE KNOW UP TO TWO-THIRDS OF THE 14 MILLION AFRICANS WITH DIABETES ARE UNDIAGNOSED. HIGH UNDIAGNOSED RATES REPRESENT AN IMPORTANT DIAGNOSTIC CHALLENGE. THERE'S THE MISSED OPPORTUNITY FOR EARLY INTERVENTION AND PREVENTION OF DIABETES RELATED COMPLICATIONS OR EVEN REVERSAL OF DISEASE. MULTIPLE FACTORS CONTRIBUTE TO HIGH UNDIAGNOSED RATES. SOCIAL, ENVIRONMENTAL, LACK OF ACCESS TO HEALTHCARE, BUT THE UNDERAPPRECIATED STRUCTURE WE ARE TRYING TO PUT FORWARD IS THE FACT THAT SOME OF THESE SCREENING TESTS THEY JUST DON'T WORK AS WELL. SO OUR APPROACH TO DIABETES PREVENTION AS SHE MENTIONED IS THAT WE'RE LOOKING AT RESEARCH TO IMPROVE EARLY DETECTION. BY EVALUATING THE SCREENING TEST IN THAT POPULATION SPECIFIC BANNER TO APPRECIATE THE DIVERSITIES IN DIET AND LIFESTYLE, NOT JUST BY RACE BUT ETHNICITY. MY FOCUS IS ALSO TO TAKE A DEEPER LOOK, MORE MECHANISTIC VIEW OF RISK MARKERS SO WE CAN OPTIMIZE TESTS AND DEVELOP HOPEFULLY NEW AND BETTER ONES. BEFORE I GO INTO THAT, I HAVE A COUPLE OF SLIDES REVIEWING THE BACKGROUND OF NATURAL HISTORY OF TYPE 2 DIABETES, WITH THE PURPOSE OF SHOWING WHY THESE SCREENING TESTS WERE CHOSEN IN THE FIRST PLACE. THE LAST FEW DECADES HAVE BEEN EXCITING FOR DIABETES RESEARCHERS. WE HAVE REALLY EXPANDED OUR KNOWLEDGE IN TERMS OF THE MULTIPLE ORGAN SYSTEMS THAT ARE INVOLVED IN THE DEVELOPMENT OF TYPE 2 DIABETES. BUT AT ITS CORE WE HAVE TWO MAIN PATHOPHYSIOLOGICAL DEFECTS THAT ARE NOT GOING ANYWHERE. INCREASING INSULIN RESISTANCE, AND DECLINING BETA CELL FUNCTION. THOSE TWO FEATURES WORSEN WITH TIME. SUCH THAT TYPE 2 DIABETES IS THAT SPECTRUM OF DISEASE. WHICH YOU PROGRESS FROM NORMAL GLUCOSE TOLERANCE AND INSULIN RESISTANCE TO PRE-DIABETES AND TYPE 2 DIABETES. AND WHAT CHARACTERIZES THAT IS THE INCREASE IN GLUCOSE THAT OCCURS GARAGE JULIE BUT THAT COMPENSATES INITIAL INSULIN RESPONSE EVIDENCE HERE AS RED LINE AND THEN THE DECLINING BETA CELL SECRETION THAT OCCURS GRADUALLY, AS THE BETA CELL LAX ABILITY TO COMPENSATE WE SEE THE DEVELOPMENT OF SEVERE HYPERGLYCEMIA. IF YOU'RE GOING TO DEVELOP A SCREENING TEST, YOU WANT THEM TO TRY TO CATCH PEOPLE IN THIS INTERMEDIATE STAGE, THE PRE-DIABETES STAGE WHERE YOU CAN IDENTIFY INDIVIDUALS HOPEFULLY KEEP THEM IN THAT STAGE OR REVERSE THE DISEASE AND -- OR IF THEY HAVE EARLY TYPE 2 DIABETES, TO BRING >> GLUCOSE DOWN BEFORE THEY START FEELING SYMPTOMS. THERE IS WORLDWIDE CONSENSUS, THE ADA EDF, SUGGESTING THAT BOTH FASTING GLUCOSE AND HEMOGLOBIN A 1C ARE THE OPTIMAL TEST FOR SCREENING AND THERE'S A CONSENSUS ON THE ACTUAL LEVELS THAT WE SHOULD HAVE, FASTING GLUCOSE REPRESENTS THAT HEPATIC INSULIN RESISTANCE AS I ALLUDED TO, AS I MENTIONED BEFORE, INSULIN RESISTANCE IS AN IMPORTANT PART AND IT COMES IN TWO FLAVORS HEMATOIC INSULIN RESISTANCE WHICH THERE'S INCREASE OUTPUT FROM THE LIVER, GIVING RISE TO FASTING GLUCOSE AND PERIPHERAL INSULIN RESISTANCE WHICH THERE IS MORE DECREASE IN GLUCOSE DISPOSAL AS WELL AS ADIPOSE INCREASE ADIPOSE TISSUE HIGH POLICIES AND INSULIN RESISTANCE. FASTING GLUCOSE IS TAKEN AFTER AN OVERNIGHT FAST SO 8 TO 10 HOUR FAST USUALLY. HEMOGLOBIN A 1C IS COMPOSITE AND GIVES AN AVERAGE OF GLUCOSE OVER THE PREVIOUS THREE MONTHS ZOBOS TESTS WERE CHOSEN NOT ONLY BECAUSE THERE ARE ESTABLISHED THRESHOLDS FOR DIABETES, BUT ALSO BECAUSE THEY PREDICT DEVELOPMENT OF MICROVASCULAR COMPLICATIONS, THEY'RE EASY, THEY'RE OBTAINED IN A SINGLE BLOOD DRAW, AND THEY'RE RELATIVELY COST EFFECTIVE. WHEN YOU PUT TOGETHER WITH RISK MARKERS OBTAINED ON A REGULAR HISTORY AND PHYSICAL EXAM AND MAYBE A QUICK LAB TEST FOR TRIGLYCERIDES, THERE ARE DIABETES PREDICTION MODELS THAT HAVE BEEN DEVELOPED AND CAN BE USED ON A POPULATION SPECIFIC BASIS THAT CAN PREDICT DIABETES RISK DEVELOPMENT BY 90% ACCURACY IN THE GENERAL POPULATION. THIS TABLE SIMPLY ILLUSTRATES THREE MAIN COHORTS, THAT WERE USED TO DEVELOP THESE PREDICTION MODELS, ATHEROSCLEROSIS RISK IN COMMUNITY STUDY, THE FRAMINGHAM STUDY OUT OF MASSACHUSETTS AND SAN ANTONIO HEART STUDY OUT OF TEXAS. WHAT IS EVIDENT IS THAT THESE COHORTS WERE PREDOMINANTLY WHITE, EXCEPT FOR SAN ANTONIO HEART STUDY WHICH HAD -- INCLUDED MEXICAN AMERICANS SO IT WAS GENERALLY ASSUMED FOR SEVERAL YEARS THAT IT DIDN'T REALLY MATTER WHAT RACE ETHNICITY YOU WERE, THE MODELS WOULD BE GOOD ANYWAY. THAT SEEMS TO CHANGE TWO YEARS AGO WHEN LACI AND COLLEAGUE PUBLISHED DATA FROM THE CARDIO STUDY IN WHICH THEY LOOKED AT THE EQUATIONS IN A BIRACIAL POPULATION. WHAT THEY FOUND WAS THAT IF YOU ARE AFRICAN MESH, RISK PREDICTION WAS OKAY, QUITE GOOD BUT IT WAS 20% LOWER COMPARED TO USING THE SAME MODEL IN WHITE INDIVIDUALS. THEY DANCED AROUND ISSUE IN THE DISCUSSION BUT THEY DIDN'T PROPOSE A MECHANISM OF WHY THERE IS THIS LOWER RISK PREDICTION. WHEN YOU TAKE A CLOSER LOOK INTO THE OVERALL LITERATURE AND THE LARGE AMOUNT OF EPIDEMIOLOGIC DATA THAT IS AVAILABLE, IF YOU LOOK SOMETIMES IN THE SUPPLEMENTAL MATERIALS YOU'LL FIND EVIDENCE THAT FASTING GLUCOSE WAS NOT A GOOD TEST FOR THE DIAGNOSIS OF PRE-DIABETES AND DIABETES IN AFRICAN DESCENT INDIVIDUALS SO WE POSTULATED THAT THIS LOWER MODEL DISCRIMINATION IS RELATED TO LOWER PREVALENCE OF FASTING HYPERGLYCEMIA, BECAUSE A MODEL IS ONLY AS GOOD AS INPUT. AND SOURCE OF ITS EQUATIONS. WHAT AM I TALKING ABOUT? WHAT IS THIS EVIDENCE? SLIDE LOOKING AT EVIDENCE OF PRE-DIABETES IN THE UNITED STATES, IT'S TAKEN FROM N HAYNES NATIONAL SURVEY DATA, BETWEEN 1999 AND 2010 AND THESE PREVALENCE RATES WERE ADJUSTED FOR AGE, SEX, BMI AND POVERTY AND INCOME RATIO. AND PRE-DIABETES ILLUSTRATES IN THE RED BARS WAS DIAGNOSED BY EITHER HAVING ELEVATED FASTING GLUCOSE, IMPAIRED FASTK GLUCOSE OR IFG OR HEMOGLOBIN A 1C WAS ALSO ELEVATED, IT WAS A 30 TO 33% PREVALENCES WITH NO DIFFERENCE BY RACE OR ETHNICITY. IF YOU THEN LOOK AT PREVALENCE OF IMPAIRED FASTING GLUCOS, THEN YOU STRATIFY THAT BY RACE, THIS GRAPH ILLUSTRATES 30% LOWER PREVALENCE OF FASTING HYPERGLYCEMIA IN THE BLACK INDIVIDUALS SHOWN IN BLUE BARS COMPARED TO THE WHITE INDIVIDUALS SHOWN IN GREEN BARS. THE LOWER DIAGNOSTIC ABILITY OF FASTING GLUCOSE FOR DIABETES HAS ALSO BEEN DOCUMENTED IN JAMAICA, SO POPULATION AFRO CARIBBEAN POPULATION AND IN SMALLER STUDIES IN SOUTH AFRICA AS WELL AS TANZANIA AND CAMEROON. LOCALLY, DR. SUMNER AND I HAVE ALSO LOOKED AT THE SENSITIVITY OF THIS SINGLE FASTING GLUCOSE TESTING IN AFRICANS. WE COMPARED TO GOLD STANDARD OR OGGT SHE MENTIONED BEFORE THE TWO HOUR VALUE, WHAT WE FOUND WAS DISAPPOINTING BUT NOT SURPRISING SURPRISING, THE FASTING GLUCOSE ALONE HAD SENSE TVTY OF 30%. IF YOU USE A 1C WE IMPROVED IT BUT ONLY DETECTED HALF OF THE PEOPLE. SO IT WASN'T UNTIL WE PUT THE TWO TESTS TOGETHER THAT WE IMPROVED SENSITIVITY TO MORE THAN 60%. SO IF YOU TAKE ALL OF THIS DATA TOGETHER WHAT IT IS SUGGESTING IS THERE MIGHT BE DIFFERENCES IN THE PATHWAY TOWARDS DIABETES OR THE DEVELOPMENT OF SPECIFICALLY IMPAIRED FASTING GLUCOSE. WHAT AM I TALKING ABOUT? TRADITIONALLY THE OBESITY AND INSULIN RESISTANCE IS A COMPOSITE AND CLUSTERING OF CARDIO METABOLIC RISK FACTORS. SOME AS SHE SAID CALLS THIS METABOLIC SYNDROME. BUT IN UNCANNINESSESTRY POPULATIONS, NOT JUST AFRICAN AMERICANS, WE DON'T SEE THAT CLUSTERING OF THESE HEPATIC RISK MARKERS. THERE IS OBESITY, THERE IS INSULIN RESISTANCE IN THE ENTIRE BODY, BUT NOT THAT MARKED INCREASE IN HEPATIC OR VISCERAL FAT, LOWER GLOW DOSE AND LESS FASTING HYPERTRIGLYCERIDEEMIA OR DISLIPIDEMIA OF LIPID RESISTANCE. SO THE HYPOTHESIS IS THAT THERE IS A DIFFERENCE IN HEPATIC VERSUS PERIPHERAL INSULIN RESISTANCE SUCH THAT IF YOU ARE OF AFRICAN ANCESTRY, THE LOWER PREVALENCE OF FASTING HYPERGLYCEMIA IS RELATED TO THOSE DIFFERENCES IN BODY COMPOSITION. SPECIFICALLY LOWER TENDENCY TO ACCUMULATE THE HEPATIC FAT AND LOWER GLUCOSE PRODUCTION. SO WHAT DO WE DO? WE WANTS TO TEST THE HYPOTHESIS. SO WE RECRUITED WOMEN IN THE FEDERAL WOMEN'S STUDY, WHICH IS A COHORT OF AFRICAN IMMIGRANT, AFRICAN AMERICAN AN WHITE WOMEN, THEY ARE ALL SELF-IDENTIFIED AS HEALTHY AND THEY'RE ALL FEDERAL EMPLOYEES. SO THAT EVERYONE WOULD HAVE ACCESS TO HEALTHCARE AND ACCESS TO HEALTH INSURANCE. THESE WOMEN CAME IN FOR SERIES OF FOUR VISITS, HERE THE NIH CLINICAL CENTER, AFTER YOUR TYPICAL SCREENING WE ASSESS THE HABITUAL DIETARY INTAKE AND ACTIVITY LEVELS. AT HOME OVER 5 TO 7 DAY PERIOD, THEY HAD GLUCOSE TOLERANCE STATUS MEASURED WITHIN OGTT. THEN THEY CAME FOR A LITTLE BIT MORE OF DEEP PHENOTYPING. SO WE LOOKED AT THEIR INSULIN LYNN SENSITIVITY WHOLE BODY AS WELL AS INSULIN RESPONSE AND A SUBSET OF WOMEN IN THE NESTED TRACER STUDY WE ALSO LOOKED AT THEIR TISSUE SPECIFIC INSULIN SENSITIVITY, PAYING CLOSER ATTENTION TO GLUCOSE AND LIPID METABOLISM. ALL WOMEN FINISHED UP WITH A MEAL TEST WHICH I THOUGHT WAS THE MOST INTERESTING TEST IN TERMS OF UNDERSTANDING THE PHYSIOLOGIC RESPONSE OF INSULIN AND GLUCOSE AFTER BREAKFAST MEAL. THEY HAD PROTON MAGNETIC RESONANCE SPECTROSCOPY TO LOOK AT LIVER AND VISCERAL FAT. SO WE HAD 147 WOMEN, 135 UNDERWENT OGTT AND FIVE HAD DIABETES SO THE DATA WILL BE PRESENTING IS ON THE 130 PARTICIPANTS WHO COMPLETED THE FOUR VISITS AS WELL AS 46 OF THOSE 130 THAT DID THE NESTED TRACER STUDY. ALL WOMEN WERE MATCHED, THEY WEREN'T MATCHED ON PURPOSE, THEY WERE SIMILAR IN AGE, BMI AND PERCENT BODY FAT, BECAUSE WE& WERE RECRUITING ONLY WOMEN WHO SELF-IDENTIFIED AS HEALTHY AND WITHIN CERTAIN AGE AND BMI CUT OFFS. SO LET'S GET RIGHT INTO IT. SO THE DIET AND ACTIVITY LEVELS WERE THE SAME THEY WERE NOT DIFFERENT BY RACE OR ETHNICITY, THESE PIE CHARTS SHOWING THE SAME SO WE UNDERSTAND AND LOOK AT THE PREVALENCE OF THESE RISK MARKERS WITHOUT CO-VARIANTS OF DIET AND EXERCISE. OF THIS DATA IS UNADJUSTED AT THIS POINT. PREVALENCE OF PRE-DIABETES WAS 33%, RIGHT AT THAT NATIONAL AVERAGE THAT I MENTIONED BEFORE WITH NO DIFFERENCE BY RACE OR ETHNICITY. BUT WHEN YOU STRATIFY INTO THOSE WHO HAD FASTING HYPERGLYCEMIA AND THOSE WHO HAD JUST AN ELEVATION IN TO OUR GLUCOSE, WE SEE A TREND FOR LOWER FAKING HYPERGLYCEMIA IN AFRICAN AMERICANS, HIGHLIGHTED IN BLUE, COMPARED TO WHITES, HIGHLIGHTED IN GREEN. THESE ONLY IN 130 WOMEN BUT CERTAINLY WAS IN KEEPING WITH OUR HYPOTHESIS. JUST TO REMIND YOU WHAT WAS THE PURPOSE OF DOING THIS STUDY, PURPOSE IN TRIGLYCERIDES, FATS, INSULIN RESISTANCE AND GLUCOSE. SO THIS FIRST SLIDE ILLUSTRATES THE FASTING TRIGLYCERIDE RICH LIPOPROTEINS IN BOTH GROUPS OF AFRICAN DESCENT WOMEN COMPARED TO WHITES. AFRICAN DESCENT WOMEN HAD COMPARABLE TRIGLYCERIDES SIGNIFICANTLY LOWER THAN WHITE COUNTER PARTS. THIS IS ASSOCIATED WITH LOWER HEPATIC FAT IN AFRICAN IMMIGRANT AND AFRICAN AMERICAN WOMEN AND SINCE THE AFRICAN IMMIGRANT AND AFRICAN AMERICAN WOMEN HAD THAT SIMILAR HEPATIC PHENOTYPE WE TALKED ABOUT BEFORE, THEIR DATA IS AGGRAVATED FOR THE REST OF THE TALK. WHOLE BODY INSULIN SENSITIVETIVE WAS NOT DIFFERENT IN THESE THREE GROUPS OF WOMEN SO THIS LOOKS AT THE RELATIONSHIP OF HEPATIC FAT WITH THEIR WHOLE BODY INSULIN SENSITIVITY. IT IS AS WE EXPECT, AS YOU ACCUMULATE MORE HEPATIC FAT YOU HAVE LOWER WHOLE BODY INSULIN SENSITIVITY. BUT THERE IS INTERACTION BETWEEN RACE AND HEPATIC FAT SUCH THAT THE SLOPE OF THE REGRESSION LINE IS MUCH STEEPER IF YOU ARE OF WHITE DESCENT. SO TRYING TO UNDERSTAND THE MECHANISM BEHIND THIS, WHY HEPATIC FAT IS LOWER? IS IT RELATED TO DIET, RELATED TO NEW LIVER FAT MADE? IN ORDER TO LOOK AT THIS WE LOOKED AT A MARKER OF DE NOVO LIPO GENESIS OR NEW FAT MADE IN THE LIVER AND THAT MARKER IS SCD 1 ACTIVITY, STERILE IS ONE ACTIVITY, DERIVEDED FROM THE MOLAR RATIO OF PAL METHYLATE ACID THE FATETY ACID PROFILE AND IS COLLABORATION WITH DR. ALLEN LICHENSTEIN, TUFTS YOUTH. YOU CAN SEE THAT BLACK WOMEN HAD LOWER SCD 1 ACTIVITY, SO THIS SUGGESTS THERE COULD BE LOWER HEPATIC FAT BECAUSE THE LIVER IS JUST NOT MAKING AS MUCH IF YOU ARE AFRICAN DESCENT. SO IF THERE'S THIS SOMEWHAT DIFFERENT RELATIONSHIP BETWEEN FAT TRIGLYCERIDES AND INSULIN RESISTANCE, WHAT ABOUT INSULIN SECRETION, THE INSULIN RESPONSE? IS THERE A DIFFERENCE IN THAT RELATIONSHIP AS WELL BY RACE ETHNICITY? THE ANSWER IS YES. THERE IS A GREATER INSULIN RESPONSE IN BLACK WOMEN BUT IT IS NOT RELATED TO GREATER INSULIN SECRETION. THIS GRAPH ILLUSTRATES POSTPRANDIALLY SO AFTER THE MEAL AND SHOWS C PEPTIDE D CONVOLUTION AND MODELING THAT THERE IS NO DIFFERENCE IN SECRETION RATE EARLY OR LATE. WHAT WAS DIFFERENT WAS THE CLEARANCE IN INSULIN. AT THE SAME WHOLE BODY INSULIN RESISTANCE, BLACK WOMEN HAD LOWER INSULIN CLEARANCE, SO MORE INSULIN WAS STICKING AROUND. EXACTLY HOW THAT CAUSES OR RELATES TO LOWER LIVER FAT IS -- CANNOT BE ANSWERED BY THIS PARTICULAR STUDY BUT WE DO KNOW THAT THE LOWER LIVER FAT IS RELATED TO LOWER SCD 1 ACTIVITY, LOWER TRIGLYCERIDES, AND WE HYPOTHESIS THAT IT IS ALSO RELATED TO THE LOWER PREVALENCE OF FASTING HYPERGLYCEMIA. NOW WE TOOK THIS SMALLER GROUP OF WOMEN, 46, 24 BLACK AND 22 WHITE, WE INVITED THEM TO STAY OVERNIGHT IN THE METABOLIC UNIT ON 5 SOUTHWEST NORTH AND THEY RECEIVED STABLE ISOTOPE TRACERS OVER NIGHT. DINNER MEAL STANDARD, ACTIVITY WAS KEPT THE SAME, WE LOOKED A AT THEIR METABOLIC RATES AND WHAT THE RATES WAS DOING IS ALLOWING US TO PARTITION GLUCOSE PRODUCTION INTO ITS TWO COMPONENT PARTS. GLUCO GENESIS OR NEW GLUCOSE MADE BY LIVER AND GLYCO GENERALLOLOGISTS THE BREAK DOWN OF GLYCO GENERAL, IN THE MORNING THEY GOT ISOTOPE RACERS GLUCOSE GLYCEROL, TO LOOK AT GLUCOSE TURN OVER AND RESPECTIVELY AND THE GLYCEROL IS TO LOOK AT THE WHOLE BODY LIE POLICIES AND MEASURE THE WHOLE BODY INSULIN SENSITIVITY AGAIN WITH FREQUENT SAMPLED ID GLUCOSE TEST. BUT IN ADDITION TO WHOLE BODY INSULIN SENSITIVITY, WE PARTITIONED OUT INSULIN SINCETIVETY TO HEPATIC COMPONENT AS WELL AS ADIPOSE TISSUE SENSITIVITY INDEX. CUT TO CHASE FOR SAKE OF TIME. IN THESE WOMEN MATCHED FOR AGE AND BMI AND ALL PRE-MENOPAUSAL THEY HAD A 10% LOWER GLUCOSE PRODUCTION AND THIS IS IN THE PRESENCE OF SIMILAR STEADY STATE GLUCOSE AND SIMILAR STEADY STATE INSULIN CONCENTRATION. SO JUST TAKING A FASTING GLUCOSE YOU WOULD NOT HAVE BEEN ABLE TO PICK THIS UP. THIS LOWER GLUCOSE PRODUCTION WAS DIRECTLY CAUSED BY LOWER GLUCO GENESIS WITH NO DIFFERENCE IN GLYCO GENERAL ROLLSIS. BUT THE LOWER GLUCO GENESIS IS NOT RELATED TO HIGHER TURN OVER OF FAT SO THERE WAS NO DIFFERENCE IN GLYCEROL OR WHOLE BODY LIE POLICIES AND NO DIFFERENCE IN ADIPOSE TISSUE INSULIN SENSITIVITY. IT WAS HOWEVER RELATED TO LOWER FREE FATTY ACID CONCENTRATIONS, SO FINALLY IN THIS COMPARISON OF HEPATIC WHOLE BODY INSULIN SENSITIVITY, I SHOW YOU MY LAST SCATTER PLOT WHICH ILLUSTRATES THIS EXPECTED POSITIVE RELATIONSHIP BETWEEN THE TWO RACES BUT THE REGRESSION LINE FOR THE AFRICAN AMERICANS AND AFRICAN IMMIGRANTS IS SHIFTED UPWARDS INTO THE LEFT. IT SAYS AT THE SAME WHOLE BODY INSULIN SENSITIVITY, AFRICAN DESCENT WOMEN HAD HIGHER HEPATIC INSULIN SENSITIVITY. IN KEEPING WITH OUR HYPOTHESIS, THIS PHENOTYPE IN THE AFRICAN ANCESTRY WOMEN IS ASSOCIATED WITH LOWER GLUCOSE PRODUCTION CAUSED BY LOWER GLUCO GENESIS. THAT'S ASSOCIATED WITH BOTH HIGHER HEPATIC INSULIN SENSITIVITY AND LOWER FREE FATTY ACIDS WHICH THOUGH NOT DIRECT SUBSTRATE FOR GLUCO GENESIS, PROVIDES THE ENERGY STORES TO FUEL THE GLUCO NEOGENIC PATHWAY. SO WE JUST SPENT ALL THAT TIME AND TOLD YOU GLUCOSE IS NOT A GOOD TEST SO WHAT ARE WE GOING TO USE WE LOOKED AT A COUPLE OF ALTERNATIVES, ONE PREVIOUSLY MENTIONED, GLEE KATEED ALBUMIN, THIS SHOWS A 1C AND GLYCATED ALBUMIN HAS GOOD SENSE TVTY OF 80% AND THESE TESTS ARE COMPLIMENTARY. WE CAN ALSO LOOK AT HISTORY, WE CAN LEARN FROM THE PAST. THE TIME TO GLUCOSE PEAK WAS A MORPHOLOGICAL FEATURE OF GLUCOSE CURVE NOT NECESSARILY NEW, IT HAS BEEN DESCRIBED IN THE LITERATURE EVER SINCE WE STARTED DOING MULTIPLE SAMPLING OGTTs BUT NOBODY REALLY PAID ATTENTION TO IT. THEY WERE ONLY LOOKING AT ABSOLUTE GLUCOSE THRESHOLDS. AND LAST YEAR, WE PUBLISHED THAT YOU CAN LOOK AT THE TIMING OF THE PEAK. SO IN THESE TWO INDIVIDUALS ONE PERSON HAS A PEAK AT 30 MINUTE, IN THE OTHER ONE THE PEAK IS AFTER 30 MINUTES OR AT 60 MINUTES. IF YOU LOOK AT THIS SIMPLE DICHOTOMOUS VARIABLE THAT CAN BE OBTAINED EITHER DURING ONE HOUR OR TWO HOUR OGTT, THE TIME TO GLUCOSE PEAK OF GREATER THAN 30 MINUTES IS ASSOCIATED WITH A FOUR FOLD INCREASE ODD OF PRE-DIABETES AS WELL AS PREDICTOR OF BETA CELL FUNCTION. SO I HOPE I HAVE BEEN ABLE TO PROVIDE A LITTLE BIT MECHANISTIC INSIGHT INTO WHY FASTING GLUCOSE IS A POOR EARLY MARKER FOR DIABETES. THE FACT IT HAS TO IN AFRICAN POPULATIONS AN DIFFERENCE IN BODY COMPOSITION AND GLUCO NEOGENESIS REMAINS LOW IN THE PRESENCE OF WHOLE BODY INSULIN RESISTANCE. WE NEED TO DO MORE RESEARCH, WE NEED TO EXPAND STUDIES SO WE CAN TEST SOME OF THESE ALTERNATIVE MARKERS AND HELP AUGMENT TYPE 2 DIABETES PREVENTION IN THESE POPULATIONS. THANK YOU AGAIN, ESPECIALLY FOR ALL YOUR ATTENTION TO THE PATIENTS, TO THE FAMILIES, I WANT TO THANK MARIA AND ANTHONY IN PARTICULAR, THEY HAVE BEEN THE MOST WONDERFUL POST BACKS AND OUR RESEARCH NURSE, BUT TO ALL, EVERYBODY IN IN OUR TEAM, ALL ARE INTRAMURAL AND EXTRAMURAL COLLABORATORS, WE COULD NOT HAVE DONE THIS WITHOUT YOU. THANK YOU. [APPLAUSE] >> SO WE HAVE TIME FOR QUESTIONS. FROM IF YOU COULD USE THE MICROPHONES HERE ON THE AISLE. WE'LL GET STARTED. SO I WILL ASK MY QUESTION. SO IF I UNDERSTOOD THEN WHAT YOUR FINDINGS WILL GO AWAY FROM DETECTION AND START THINKING ABOUT INTERVENTION AND TREATMENT. TOWARD THIS COHORT, WOULD IT BE NECESSARY TO TRY TO INCREASE GLUCOSE UTILIZATION TO DECREASE THE RESIDUAL BLOOD SUGAR IN THESE PATIENTS? HOW ARE YOU GOING TO DO THAT? EXERCISE ALONE THAT COULD RESULT IN THAT OR ARE YOU GOING TO GO THE PHARMACOLOGIC ROUTE, DO IT THAT WAY? >> THAT'S A RAY WILL I GOOD QUESTION, THAT'S THE ENTIRE POINT. HOW ARE WE GOING TO PREVENT IT, WHAT CAN WE DO TO INTERVENE AND MOST DEFINITELY WE NEED TO APPROACH DICTION IN A MOR TARGET -- DIABETES IN A MORE TARGETED FASHION SO INDIVIDUALIZED MEDICINE, UNDERSTANDING IF YOU ARE FROM CERTAIN POPULATIONS, OR EVEN JUST A CERTAIN PHENOTYPE REGARDLESS OF WHICH POPULATION YOU ARE FROM, YOU NEED TO HAVE THERAPEUTICS, WHETHER PHARMACOLOGICAL OR NON-PHARMACOLOGICAL, THAT WILL BE THAT TARGETS THE PATHWAY THAT'S DERANGED SO BY PHARMACOLOGY, YOU CAN SAY HELP IMPROVE PERIPHERAL INSENSITIVITY BUT THE FIRST LINE FOR DIABETES MANAGEMENT IS TO TRY TO GET AT THE DIET AND LIFESTYLE AND EXERCISE FIRST. SO EXERCISE WILL MOST DEFINITELY IMPROVE PERIPHERAL GLUCOSE UTILIZATION, WITH ADDED BENEFIT OF IMPROVING HEPATIC INSULIN SENSITIVITY AS WELL. >> FOR DR. SUMNER, HOW DO YOU GET COUNTRIES TO GET PEOPLE MOVING TO DO EXERCISE, ACTUALLY AFFECT THAT? LOOKS LIKE IT'S GOING IN THE OPPOSITE DIRECTION. >> RAW WANDA IS LEADING THE WAY AND IT HAS CAR FREE DAYS SO AFRICAN COUNTRIES ARE BECOMING AWARE. YOU NEED TO SORT OF CHANGE PEOPLE'S CULTURAL IDEAS BECAUSE PEOPLE ARE NOT -- LIKE HERE IN AMERICA THEY DON'T UNDERSTAND WHY ARE YOU SPENDING MONEY TO EXERCISE? SO PEOPLE NEED TO THINK NOT GOING TO GO TO GYMS BUT WE ARE GOING TO WALK INSTEAD OF TAKE THE BUS IN THE METRO, AND WE'LL STAY OUT OF OUR CARS. >> PARTICIPATE IN NIH TAKE A HIKE DAY TOO. ON THURSDAY, YES. >> YOU SHOWED THE AFRICAN DATA WHERE THEY DID THE PRACTICAL THING OF LOOKING AT MET BOLL UK SYNDROME COMPONENTS WHICH DOESN'T HAVE ANY VALIDITY BUT THEN YOU SHOWED YOUR RIGOROUS DATA LOOKING BACK IT LOOKS LIKE IT SORT OF WORKED. IN A WAY YOU MAY HAVE UNIQUE OPPORTUNITY TO ASK WAS THAT NAIVE THING ACTUALLY REASONABLE? AND IN YOUR COHORT, WAS IT? >> WHAT I TELL MY PEOPLE IS YOU CAN DO THE RIGHT STATISTICAL TEST OR THE WRONG STATISTICAL TESTS BUT THE RESULT IS VERY STATISTICALLY SIGNIFICANT, IT WN'T MATTER WHICH TEST YOU USE BUT WHEN YOU PUBLISH YOU HAVE TO USE THE RIGHT STATISTICAL TEST. AND IN TERMS OF WHAT THEY DID IN AFRICA, IT DID WORK BECAUSE ALL OF THOSE VARIABLES ARE RELATED INSULIN RESISTANCE. BUT THERE HAS TO BE A FOUNDATION WHICH TO BUILD BECAUSE IT WASN'T SUFFICIENT FOR GUIDELINES AND IT WASN'T SUFFICIENT TO MEASURE INSULIN CONCENTRATION. BUT TO HAVE THAT VAT AND SAT MEASUREMENT TO SEE WHY IT WAS HIGHER IN WOMEN THAN MEN BECAUSE YOU WERE USING A NON-STANDARD TEST AND FINDING A NON-STANDARD RESULT, YOU HAD TO HAVE METABOLIC VALIDATION. THAT'S WHAT MADE IT POSSIBLE WORKING WITH AFRICAN IMMIGRANTS HERE IN THIS COUNTRY. >> DO YOU KNOW WHAT EXPLAINS THE DIFFERENCE BETWEEN THE POSITION IN MALES AND FEMALES HOW THERE'S A DIFFERENCE IN VISCERAL VERSUS SUBCUTANEOUS LIKE THE SAME BMIs? >> WHY? >> YES. >> OKAY. WELL TESTOSTERONE, I'LL LEAVE IT AT THAT. I HAVE NO IDEA. >> >> THANK YOU FOR YOUR TALKS. VERY GOOD. WONDERING WHETHER THIS INFORMATION LEAVES SOMEONE WHO IS AFRICAN AMERICAN WHETHER WE MIGHT BE MORE LIKELY TO BE LIKE THE AMERICAN RESEARCH SUGGESTS IN TERMS OF WAIST CIRCUMFERENCE OR FASTING BLOOD SUGAR OR MORE LIKE AFRICAN AMERICAN SO WHETHER A PERSON SHOULD FEEL COMFORTABLE IF THEY SEEM NORMAL BLOOD SUGAR FASTING BLOOD SUGAR NOW AND MAYBE THEY'RE OKAY OR SHOULD BE CONSIDERING WHAT WE MIGHT BE SEEING IN OUR AFRICAN COUNTERPARTS AND THINK THAT PERHAPS IT MAYBE GOOD TO LOOK AT A DIFFERENT TEST LIKE A GLUCOSE TOLERANCE TEST. SHOULD AFRICAN AMERICANS THINK ABOUT ASKING THAT ARE DOCTORS FOR A DIFFERENT KIND OF TEST? >> I'LL TACKLE THE FASTING GLUCOSE QUESTION, THE REASON WE LOOK AT IT IN MULTI-ETHNIC POPULATION, AFRICAN AMERICANS AND AFRICAN IMMIGRANTS IS BECAUSE PHENOTYPE OF LOWER PREVALENCE OF FASTING HYPERGLEE SEEMIA IS CONSISTENT NO MATTER WHICH AFRICAN ANCESTRY YOU'RE FROM. SO DEFINITELY WE HOPE TO USE THIS INFORMATION TO HELP GUIDE THE TRUE LEADERS IN T FIELD WHO WILL SHAPE THE GUIDELINES AND PROMOTE NOT JUST USING A FASTING GLUCOSE TEST BUT COMBINING THAT WITH SOMETHING ELSE. SO MAYBE USING AND DOING THE FULL OGTT AS YOU MENTION BEFORE OR DOING FASTING GLUCOSE WITH A 1C WHICH CAPTURES THE ENTIRE GLYCEMIC PROFILE. >> THAT WAS VERY GOOD. IN TERMS OF WAIST CIRCUMFERENCE OF RISK WE COMPARED ASP CAN IMMIGRANTS, SOUTH AFRICAN WOMEN TO WEST AFRICAN WOMEN CT SCANS IN COLLABORATION WITH INVESTIGATORS IN SOUTH AFRICA AND WITH CHARLES (INAUDIBLE) AND WE FOUND THAT AFRICAN AMERICANS AFRICAN IMMIGRANTS AND AFRICAN AMERICANS HAD SIMILAR WAIST CIRCUMFERENCE AND IT WAS HIGH THAN CURRENT RECOMMENDATIONS OF 88-CENTIMETERS THAT'S CURRENTLY USED. WHETHERREN WE COMPARED AFRICAN IMMIGRANT MEN TO AFRICAN AMERICANS WE FOUND A DIFFERNCE WITHIN SEX -- BETWEEN -- ETHNIC DIFFERENCE WITHIN MEN SO THAT AFRICAN IMMIGRANT MEN HAD MORE ADIPOSE TISSUE AND LOWER BODY MASS INDEX AND LOWER WAIST CIRCUMFERENCE SUCH THAT AFRICAN IMGRAND MEN SHOULD BE SCREENED AT LOWER THRESHOLD THAN AFRICAN AMERICAN MEN, IF NOT THAT LEADS TO LATE DIAGNOSIS AND LOST OPPORTUNITY. >> THANK YOU. >> FINAL QUESTION. >> THANK YOU VERY MUCH, TOUCHING ON THOSE GOOD PRESENTATIONS. I HAVE TWO QUESTIONS FOR YOU. WHAT DO YOU THINK OF NON-REGULATORY DIAGNOSTIC TOOLS FOR DIABETES? (INDISCERNIBLE) FIND RISK IN THE ACTIVITY DR. SUMNER MENTIONED FOR INSTANCE, 500 PEOPLE TO DO BLOOD SUGAR IN EVERYONE YET WE ALSO KNOW FASTING IS NOT A GOOD DIAGNOSTIC TEST WOULD YOU FOR INSTANCE ADVISE DEVELOPING SUCH TOOLS SKS SCREENING BEFORE YOU PROGRESS TO CONFIRMATORY TESTS? SECOND, WHAT DO YOU THINK OF FASTING BLOOD SUGAR IS NOT GOOD BECAUSE OF -- GLUCO GENESIS IN AFRICAN, WHAT ABOUT RANDOM BLOOD SUGAR AND THE USEFULNESS. >> SECOND FIRST, NO I DON'T THINK RANDOM GLUCOSE IS A VERY GOOD MARKER. IT'S JUST NOT SENSITIVE ENOUGH. IT'S GOING TO BE AFFECTED BY RECENT MEALS AND IF YOU'RE ME YOU EAT EVERY TWO HOURS IT'S ALWAYS HIGHER. I WILL NOT RECOMMEND TOWARDS USING RANDOM BLOOD GLUCOSE, I WOULD DEFINITELY AGREE OR GO ALONG WITH THE WHO GUIDELINES WHICH IS THAT EVERY SCREENING TEST, WE'RE TALKING DIABETES BUT IT ENCOMPASSES THE LARGER PUBLIC HEALTH RECOMMENDATION THAT WE NEED TO DEVELOP THESE SCREENING TESTS AND RISK TOOLS BUT THEY THEN NEED TO BE TESTED IN A POPULATION SPECIFIC MANNER. SO I THINK MOST DEFINITELY, FOR AFRICAN COUNTRIES BUT AROUND THE WORLD, ESPECIALLY IN RESOURCE POOR ALLOCATION -- COUNTRIES, WE NEED NON-LABORATORY COST EFFECTIVE PREDICTION TOOLS. AND I THINK THEY WOULD WORK RELATIVELY WELL IF WE HAVE THE RIGHT WAIST CIRCUMFERENCE THRESHOLDS BUT THEY HAVE TO BE TESTED IN THAT POPULATION BEFORE THEIR ROLLED OUT AND USED ON A PUBLISH HEALTH LARGE PUBLIC HEALTH ARENA. >> I THINK WE'RE AT THE END OF OUR PRESENTATION. WE WANT TO THANK BOTH SPEAKERS, EXCELLENT PRESENTATIONS. [APPLAUSE] I WILL REMIND YOU THAT NEXT WEEK IS THE ANNUAL JOHN DECKER LECTURE, THE DECKER LECTURE HONORS THE RECIPIENT OF THE DISTINGUISHED CLINICAL TEACHER AWARD. WE HOPE THAT WE WILL SEE ALL OF YOU IN THE AUDIENCE TO HONOR DR. JIM KATZ WHO WILL BE DELIVERING THE DECKER LECTURE. THANKS. [APPLAUSE]