Articles, Blog

Oral History: Dr. Griffin Rodgers, NIDDK Director

March 26, 2020

[music] RODGERS: I was born in New Orleans and was
raised in New Orleans in the ‘60s and early ‘70s before I left to go off to college. It is said that one can live in any city,
but New Orleans is the only city that lives in you and that has a lot to do with the influence
on me in terms of going into math and science, or the STEM disciplines as we understand it. My father was a high school science teacher,
my mother was a public health nurse, and they at an early age instilled in me a love of
science. And in particular medicine and serving others
were important principles. I also learned that through, it was called
then an elementary school, I guess it’s called middle school now, and then subsequently
in high school, that love of math and science persisted. And so I was pretty much sold on a career
in medicine at a very early age. INTERVIEWER: So medicine more than research? You wanted to be a doctor? RODGERS: Medicine more than research. There was great interest in the fields of
medicine and learning what I could, and I thought that would be a practical application
related to my love of both math and science. But something happened during high school
which tweaked that a bit and actually got me more interested in a subspecialty of medicine,
and more importantly doing research in medicine, and that was three good friends in high school
who—this was now in the late ‘60s, early ‘70s—who had sickle cell anemia. Back at that time there was very little that
you could do for individuals suffering with that condition. And when I say suffering, I really mean suffering. They would have these periodic bouts of just
excruciating pain, oftentimes requiring emergency room visits and hospitalizations and intravenous
fluids, and pain medications to get that under control. Oftentimes their anemia would be more profound,
requiring a blood transfusion, and of course they had infections they would be treated
with antibiotics at the time. But essentially, that’s all we had in terms
of treatment of them at the time. One of my friends passed away when I was still
in high school, I believe in 11th grade, and the other two passed away while I was in college. And somewhere during that time while I was
still focused on a career in medicine, in fact I had actually gotten accepted into medical
school straight out of high school in several programs- in combined programs- I decided
to consider what is necessary to subspecialize in blood diseases and then focussed on research,
particularly in this area, to see whether there was something I could bring to bear
on it. INTERVIEWER: What are the odds that you’d
have three friends that would have sickle cell disease? RODGERS: Well sickle cell disease as you probably
know is a genetic disease. It is oftentimes common among African Americans
or people of African ancestry. The prevalence seems to be a little bit higher
in the South because of the slave trade and the expansion of populations in that region. And you know, growing up in the late ‘60s
and early ‘70s, kind of in the still segregated South it was more likely that people I would
come in contact would be my race and my ethnic group. So on the surface you would probably say it’s
not that common, but actually the odds were stacked in favor of having friends and acquaintances
that have that disease. INTERVIEWER: So you went to Brown, I guess
with the intention of becoming a doctor pre-med. RODGERS: Yeah. So this program allowed people to be accepted,
this was called an accelerated medicine program. It allowed us the opportunity to get accepted
not only as an undergraduate, but at the time it was a six-year program allowing one to
get a Masters of Medical Science, and then they had a reciprocal relationship with several
of the other Ivy League schools. And so one could do the last two years at
Princeton – I mean not Princeton, but Harvard or Yale or the University of Pennsylvania
where you formally received your M.D. Fortunately after the first year I was there they had
attracted a sufficient number of clinical faculty at Brown, so they could offer a full
experience, and you could actually get your M.D. from Brown. The program moved from a six-year program
receiving a Bachelors and a Masters to a seven-year program receiving a Bachelors and an M.D.,
but I opted to also get a Master’s Degree, and so I was able to get three degrees in
seven years. INTERVIEWER: You’re starting to think about
becoming a scientist at this point? RODGERS: Yes. In fact, my focus of my Masters, I worked
with a fairly preeminent hematologist who had done outstanding work in the late ‘60s
and early ‘70s in New York, Dr. Herbert Lichtman. He worked in the area of sickle cell disease,
and so I was already trying to execute this plan. Unfortunately, there are not a lot of people
with sickle cell disease in Rhode Island, which is sort of the opposite of what I told
you what my experience was in New Orleans. However, there was no deficit of people who
were older age in Rhode Island, and so my thesis was to work on red blood cell function
among octogenarians. That was – but that got me acquainted with
the research method, and working with red blood cells, and the like. And I learned quite a bit from Dr. Lichtman
in terms of the process, the rigor and the importance of reproducibility and the conduct
of science during my graduate training. INTERVIEWER: You worked with a gentleman named
Dr. Galletti as well? RODGERS: Pierre Galletti was my advisor, my
scientific advisor. Dr. Galletti was from Switzerland and he was
a major figure in the medical device instrumentation industry. He developed an artificial kidney, an artificial
lung, and he actually merged them together. And so in my first year as an undergraduate
I worked in his lab on a system that he called an artificial Klung. This was in an animal lab and it simulated
the effects of the lung and the kidney, so it filtered blood and it also oxygenated the
blood. And my role in this research team was to collect
blood samples before they went into this device and then after it came out to see the effect
of his device, his novel device. It was very very large, though. I couldn’t see how it could be used, but
now with miniaturization it certainly is possible. And that sort of leads me to something that
hopefully we’ll conclude on and that is developing artificial organs to treat patients
that have the kinds of diseases that NIDDK is responsible for- INTERVIEWER: One of the benefits of having
worked all around blood, every way you could. RODGERS: That’s right, exactly. INTERVIEWER: At some point you got an M.D.
from Brown? RODGERS: Yes, 1979. I was in the fifth graduating class. INTERVIEWER: And where did you get your clinical
experience? RODGERS: So after I completed that, I was
accepted at Barnes Hospital in the Washington University School of Medicine in St. Louis. So I went there to do a residency in internal
medicine and was offered the opportunity to become the Chief Medical Resident at Wash
U as well. And that was from 1979 to 1982, and I had
a great time at Washington University. In fact, they wanted me to stay there to do
my resident- my fellowship training in hematology, but I opted to follow the advice of others
to leave St. Louis and to actually come to Bethesda. INTERVIEWER: So going to the hospital and
working in a clinical setting didn’t change your mind about doing research. RODGERS: Oh no. It actually inspired me even more. There were quite a large number of patients
in St. Louis with various blood diseases, and I developed an affinity for working in
those clinics in addition to my general internal medicine clinic. But at that time I was able to take on a large
number of patients that had sickle cell disease, and so I was still very much inspired to follow
that path that I had set out on high school. [music] RODGERS: During my second year of my training
there, one begins to think about what one is going to do after their last year. And so the options existed to do hematology
training at a number of places. But one of my mentors at Washington University
was a Dr. James Gavin who himself had worked in the intramural laboratory at NIDDK— or
one of its precursors— we’ve gone through the evolution of several different names. Dr. Gavin worked in the lab of Dr. Jesse Roth,
who was a former NIDDK scientific director. And working in his laboratory he discovered
the insulin receptor. And so this was really critical to the understanding
of the pathogenesis of diabetes, so this was very high on his list. Dr. Gavin was an assistant professor at Washington
University at the time and he says, “Griff, you should go and consider Bethesda, Maryland,
and doing some training at the NIH. I’m not sure whether they’re doing sickle
cell disease research, but it’s something that you should consider. It’s a great place, and I’m sure you’ll
have a great time there.” In fact, Dr. Gavin is really one of these
mentors that- there are a number of pieces of advice that he gave to me over the years
that I followed assiduously. One was when I was at Brown and looking at
residencies, I met with him among other people. But he took a half a day off and cancelled
his clinics so he could take me around and introduce me to various people. And you know while the places that I did interview
for were considered some of the better residencies, this was the first time that I had actually
had an experience where someone was looking at me and thinking about my career trajectory. So at the end of the day as I was off to the
airport he said, “You really should consider this place.” So when I came I said, “Look, I followed
your advice.” As I was leaving I turned to him, and he told
me to come here. And this is more or less what got to me- that
and a few other things I’ll mention. The third piece of advice that he gave me,
is he says, “You should learn to play golf.” He was a great golf player, and he wanted
someone to play with. And now that was something that my wife wasn’t
that excited about because it typically gets me away from her for four or five hours at
a time, but I followed that piece of advice as well. [music] RODGERS: So I came here my junior year. I followed his advice. Of course, we didn’t have the Internet back
then, so I had to go to the library at Wash U and read through and see who at the NIH
was doing research in sickle cell disease. And then I made a few phone calls actually
to the National Heart, Lung, and Blood Institute and I spoke with Dr. Clarice Reid who was
the head of their blood division. And she says, “Well if you’d like to come
to the NIH and work on this, the person that you should speak to is not at NI- NHLBI, he’s
actually at NIADDK, it’s Alan Schechter.” Because he had published a two-piece review
article in The New England Journal of Medicine, as it turns out, just a month before, and
he was already envisioning how one could attack this disease. Dr. Schechter came at this disease as someone
who had more of a biochemical perspective. He worked in the laboratory of chemical biology
under the lab chief who was one of the four intramural Nobel Laureates who worked here-
Dr. Chris Anfinsen. When I set up the interview, as was standard
back then, before you talk to the person that you are coming to work with you have to speak
with the lab chief first to get his or her approval that this person is appropriately
vetted, I’d like him to come, now you can talk to the person you want him to work with. And so in my interview with Dr. Anfinsen,
I had read that he was a Nobel Laureate. I tried to read up on how he received it and
why, so I could sound intelligent when I spoke to him about protein folding. And I guess after- we met in his office and
after about the first ten minutes I got a good feeling that things were going well. And he says, “Griff, this is great. I think you should come here. Don’t look at those other offers that you
have.” He says, “By the way, let’s go down to
the cafeteria and maybe we can talk more over coffee.” And while I was there, I said, “Wow, this
is great. This is the first Nobel Laureate I ever met.” As we were sitting there, coffee in hand,
he says, “Have you got two bucks I can borrow from you? I want to buy some cigarettes” [laughs]
My whole sort of opinion of Nobel Laureates, this guy asking me for money, how can I say
no. I said, “Sure, here it is.” And I have to say when I came back, he remembered,
and he offered to give me the money back. I said, “No, please keep it. I have a story to tell for the rest of my
life now on this.” I later met with Dr. Schechter and we clicked
immediately. He was working really more on sort of the
basic biology and trying to understand the molecular and cellular pathophysiology of
the disease. I told him I’d really like to work on that,
but I’d like to expand that somewhat to work in addition on some of the more clinical
aspects of the disease. And so when I came to join his lab in ‘82,
I continued as a collaboration of work that he was doing in some of the basics, but also
looked to expand the lab into projects involving clinical research as well. INTERVIEWER Had he, Dr. Schechter, made some
important findings about sickle cell disease at that point? RODGERS: He absolutely did. Most people thought that sickle cell disease,
as the name implied, was a problem when red blood cells lost their oxygen, as they’re
supposed to as they deliver oxygen to the tissue. The thought there, and this was something
that was initially argued by Linus Pauling and others, was that when the red blood cell
gives up its oxygen and picks up carbon dioxide from the peripheral tissues that unlike people
with normal hemoglobin, people with sickle hemoglobin, their red blood cells would begin
sickle, and it was that sickling process that caused obstruction to blood flow in the small
vessels. It was Dr. Schechter’s idea and actually
other people in our intramural program, Dr. Bill Eaton and Jim Hofrichter, that suggested
that it wasn’t the sickling per se, but it was actually the state of hemoglobin. This gets to be a little bit technical, but
the state of the hemoglobin, the mutation in sickle cell disease causes a substitution
for what’s called a hydrophobic amino acid valine at position 6. It substitutes for glutamic acid. And as a result of that substitution this
hydrophobic valine causes an interaction with an adjacent hemoglobin molecule upon deoxygenation,
and that causes these hemoglobin molecules to bind to one another almost like Velcro. And a process that gets set up where these
long strands of polymer form and it’s actually the polymer that’s inside the cell- you
can think about it as reinforced steel inside of a cell. As they elongate, they begin to change the
shape of the cell so that at very extremes you see the sickling of the cells, and that’s
what people were seeing under a microscope. But Dr. Schechter’s and Noguchi’s contribution,
and Dr. Hofrichter’s and Bill Eaton’s contribution, it was- it’s not actually
the sickling of the cell per se, but it’s the biophysical characteristic of the polymer,
whether it’s either a polymerized form or a non-polymerized form, that determines the
underlying pathogenesis of the disease. And so the goal now was, instead of developing
something that could unsickle the cell or desickle the cells, one is looking at potential
chemicals, and this is where his chemistry background came in, that could disrupt that
Velcro binding, that binding of neighboring deoxygenated hemoglobin molecules that would
lead to the depolymerization of deoxy sickle hemoglobin and thereby stabilize the disease. So that’s what I came to work with him on. He had a great model of explaining it, and
explaining it in those terms actually offered alternative targets in terms of getting at
the underlying pathogenesis of the disease. For example, they learned that the rate at
which this polymer occurs varies with the 32nd power of the intracellular hemoglobin
polymerization concentration, which means that if you could overhydrate the cell in
some way you can dilute out that concentration and thereby greatly perturb the rate at which
polymer forms under deoxygenated conditions. So now the challenge was to try to figure
out drugs that could cause red cells to swell. In fact, people showed that- people from Boston
and others showed that was actually a- I would say a viable approach. They proved the concept worked. It was somewhat untenable how people had to
go about doing it. They had to drink several gallons of water
a day along with something called DDAVP, a vasopressin analog, which caused their total
body water content to increase. These red cells act like small— as the concentration
of free water increased on the outside it would actually just move in- that would swell
the cells and would diminish it. Then you start to think about other things
that could cause that affect that as well. INTERVIEWER: So this- what year is this? RODGERS: We’re now talking about 1981, ‘82. Dr. Schechter’s idea came out in ‘79,
‘80, ‘81. And I arrived in the lab in ‘82, so we’re
now looking at proof of concepts of this theory that- that people here and other people around
the world were actually embracing now. INTERVIEWER: But you were working with Dr.
Schechter and he was the one who came up with that insight. RODGERS: That’s right. INTERVIEWER: I suppose that helped a little
bit. Tell me how you, and I’m sure working with
Dr. Schechter, came up with your research plan and the decision of what to do next. RODGERS: Yeah so again, we were working on
that concept that he had and trying to look for circumstances that would either support
or reject that hypothesis. So anything that would swell the cells would
be favorable, anything that would dehydrate the cells would be unfavorable, and that would
be reflected by changes in their overall clinical and hematologic status. There were certain populations who had the
same disease, but their disease seemed to be more attenuated, they had milder forms
of the disease. And during that early time between ‘82 to
‘85, we began to show that people that had a second condition, alpha thalassemia, which
is a very prominent disease or condition among African-Americans and other groups that had
high prevalence of sickle mutation, that that seemed to attenuate the disease, and we figured
out how that worked. And it still worked through the same mechanism
of polymerization. Interestingly, we found that people that had
a second mutation causing a high level of another type of hemoglobin, fetal hemoglobin,
also had an attenuation in their disease manifestation. There weren’t many people in the U.S. with
this, but it was quite prevalent in Saudi Arabia and in India, and other places in the
Middle East that in addition to having sickle hemoglobin, they also inherited mutations
that led to high levels of fetal hemoglobin. And that’s what really was sort of the backdrop
was for the work that I did in sort of the late ‘80s, to see whether you could use
a drug that might stimulate the expression of fetal hemoglobin among people who had low
levels normally, it normally is between one to two percent in everyone, but if you could
get that up to 10 or 15 to 20 percent with a drug or some other pharmacologic approach,
that that might attenuate the disease in the same manner that we saw in those populations
that actually- their normal levels were in the range of 20 to 25 percent. INTERVIEWER: To get to the fetal hemoglobin
inside, was that a matter of looking through literature or talking to people? RODGERS: It was actually looking at these
various populations that had been described. So for example, the people that were in the
Middle East in particular, as people were going out doing surveys to actually determine
the origins of the sickle mutation, they were finding that it did exist at least in old
world Africa, in three predominant sites. Of course, countries didn’t exist thousands
of years ago. They were sort of artificial based upon where
there were mountains or rivers, or other geographical demarcation zones. But in general, it was found that with the
knowledge that we gained from so-called DNA haplotypes or restriction enzyme polymorphisms,
RFLP, which is really the basis for all of the legal aspects of genetics in which you
can use people’s DNA to rule them in or out as suspects or looking on
and these other groups that can tell what the linkage is with you and your family, they’re
all based upon the concept of haplotypes or RFLPs. That work was discovered by a prominent hematologist
at the University of California at San Francisco, Dr. Y.W. Kahn. He worked on thalassemia and sickle cell disease
disease, so he applied that knowledge initially to doing prenatal diagnosis. But he came up with this concept of haplotypes. So it’s a long story, but getting back to
Africa, they found that there were probably three areas in Africa where the sickle mutation
arose thousands of years ago. There was something that existed in Senegal,
the region around Senegal, the Central African Republic and also in Benin, which is sort
of in the middle. And as it turns out the people who were in
Benin, in spite of what the name sounds like, they actually had a more severe type. The people who were from the Central African
Republic haplotype had sort of a more intermediate type and the people from Senegal had a more
milder form of the disease. What distinguished those three groups, as
Dr. Kahn and others later found out, was that the people from Senegal had modest elevations
of their fetal hemoglobin level. So now with this in hand, people went to areas
of the Middle East around the ‘70s to begin to explore this. Actually one of the people who published a
lot of work on this was a fellow named James Bowman. James Bowman is the father of Valerie Jarrett,
the former advisor to President Obama. And she’ll tell you that she was actually
born in Iran and moved around in places because her father was a molecular geneticist. Well, people were moving into the Middle East,
particularly these large oil companies and they wanted to make sure that they had a healthy
population to do what’s needed in terms of drilling for oil and things like that. So there was a lot of money going into geneticists
and others who could screen the population for the presence of certain diseases that
might make them not great candidates to work with. He actually determined that in Saudi Arabia
and some of the other Middle Eastern countries there was a fairly high prevalence of the
sickle mutation, actually slightly higher than what was seen in Africa. But he also- he and his group also found that
what distinguished them was they also had fairly high levels of fetal hemoglobin. When you look very carefully, it turns out
when you go to India because of the trade between Indians and Saudi Arabia, it was that
same haplotype. So these people from Saudi Arabia, the Middle
East and India actually had a very mild form of sickle cell disease, in general, and what
distinguished them was this high level of fetal hemoglobin. This is the backdrop to the study as we get
into it. In India, the prevalence is actually so high
that there are actually more people in India with sickle cell disease than anywhere else
in the world. People think this is a disease exclusively
in Africans, but that’s not the case. It actually exists in good portions of the
Mediterranean, so in Southern Spain, Italy, Greece and other places, but large pockets
in India and also in the Middle East. High levels of fetal hemoglobin protects the
disease. And we know it protects it now because it
acts in the same way that swelling the cells and developing a chemical that could interfere
with the polymerization does. Nature really developed the best way of doing
that in the form of developing this other fetal hemoglobin- this other- not reinducing
but maintaining a fairly high level of this type of hemoglobin which normally gets turned
off at the time that we’re all born. But because of these other mutations they
have a persistent high level of expression. So that sets the stage for, can you develop
a drug or something that might be able to achieve that same objective pharmacologically
in people that have low levels, people who are from Beninian haplotype or the Central
African Republic haplotype, can you somehow reinduce that- INTERVIEW: Turn it on. RODGERS: Turn it back on, that’s right. And that was the goal. Again, as I got here there was a group in
the Heart, Lung, and Blood Institute who started working on this using a drug called 5-Azacytidine-
that’s one of the questions that you had. And 5-Azacytidine at the time was known to
potentially reactivate genes that had been turned off due to chemical changes that occurred
in a certain part of the gene that controls the gene expression. So more precisely, methylation of the promoter
element seems to turn off the genes. If you could demethylate it, and 5-Azacytidine
was a drug that causes demethylation, maybe you could reactivate the gene or turn it back
on in your words. And it turns out that was the case. But people- again scientists always argue
about mechanisms. And some people felt that well, that could
be one explanation, but another thing could be that, just like all chemotherapy, it first
causes some toxicity to the rapidly dividing cells, and then when you withdraw the drug
and you give the cells a chance to recover maybe that’s what’s turning on the genes. And that led us to actually consider this
drug Hydroxyurea because it’s a form of chemotherapy. It works on rapidly dividing cells. It doesn’t have the same toxicity profile
that drugs like 5-Azacytidine does. And so that was the basis of our work in the
late ‘80s and early ‘90s that using this drug in about 70 percent of hospitalized patients
we could turn on their fetal hemoglobin to modest levels and the longer you gave it to
them, the higher their values would go. And subsequently our work was replicated by
groups in Seattle and Harvard and Johns Hopkins, and that led the NIH to fund this fairly large
study of a cooperative randomized clinical trial, which tests whether the drug would
have a benefit. And just to cut to the chase, the study was
stopped a year early because one group, which was blinded at the time, was doing much much
better than the other group, and that group was the Hydroxyurea group. In 1990 our paper came out. In 1995, this NIH supported trial, this large
randomized trial, showed that Hydroxyurea was quite beneficial, and in 1998, the FDA
approved the drug as the first drug that was approved specifically to treat adult patients
with sickle cell disease. INTERVIEWER: Had you- you had done a clinical
trial on your own before the 1990 paper, is that right? RODGERS: We had. We were looking at a number of other agents
and smaller subsets of patients to determine whether they might have some role. For example, we thought that you know, since
the problem in sickle cell disease was fundamentally that these cells, because of the polymer content,
had a difficult a time negotiating the small arteries, arterials, and capillaries and venules,
maybe if we gave a drug that could dilate the vessels that that might improve the blood
flow, and so you could get the cells through the microcirculation and back on the oxygenated
side so that polymer would be removed. And in that circumstance that trial used the
eye as an example to directly measure that. And we showed that certain types of drugs,
specifically calcium channel blockers were actually quite efficacious in these patients. And this has been again replicated by other
groups. We did clinical trials going into this. INTERVIEWER: So you must have been very encouraged
when you read that there was going to be this very large trial. RODGERS: Absolutely, absolutely. Yeah, we collaborated with the people at Johns
Hopkins. In fact, since we- I won’t say the luxury,
but we had the benefit of being here in the intramural program that you could actually
bring people into the hospital without concerns about their insurance. They could be hospitalized for extended periods
of time. In fact, patients in our initial trial were
in the hospital for three or four months as they were getting the drug, we knew that they
were taking it, so drug compliance wasn’t an issue, and we could then modify the dose
and gradually escalate it and look for side effects. So what our trial was able to do was not only
show that it worked, but we could define what the starting dose should be, the average dose,
and what the maximum tolerated dose was. And that information was used to support the
large cooperative clinical trial that NHLBI supported. INTERVIEWER: So the success of part of this
trial- one of the groups- did that come to the FDA’s attention? Is that how this happens? RODGERS: It was after this large cooperative
trial, so-called the MSH, Multicenter Study of Hydroxyurea was ongoing. And as I said, it was stopped prematurely
because the Data Safety and Monitoring Board, who looked at the data, periodically noticed
that among the patients in one arm — of course it was blinded at the time — the group receiving
let’s say Treatment A they required fewer blood transfusions. They seemed to have less pain. They seemed to have less hospitalizations. Their blood values were actually increasing
compared to people who were receiving Treatment B, which turned out to be the placebo arm. So they start- their thought, which I think
was appropriate was, since you’re already seeing an effect and it seems to be non-random,
that it’s statistically significant, was we should stop this trial, it would be unethical
to keep this group of patients who don’t seem to be benefiting at all on whatever they’re
receiving because you can stop the trial, figure out, sort out who is getting what and
then offer what seems to have been given to Group A to Group B, and that’s sort of what
happened. That was published in 1995. Then the FDA, after thinking about this, finally
gave approval in 1998. Our result of about a 70 percent success rate
ultimately was replicated in this larger trial, so about 70 to 75 percent of adults given
the drug seemed to respond. The other 25 to 30 percent still for unclear
reasons, you know that they’re taking it, in our setting they knew they were taking
it, when you give patients drugs on an outpatient basis you don’t know what the adherence
rate is, but since it came out to be the same as ours we assumed that most of them were
in fact taking the medicine. But at least having unambiguous confirmation
here at the NIH set the stage for developing the right dose and the maximum dose, and parameters
that were to follow, and that was exciting. INTERVIEWER: This is a pretty big deal. RODGERS: It’s a pretty big deal. It turns out that when our study came out,
before he was a very famous author on the New York Times Best Seller List, Malcolm Gladwell
was a science writer for the Washington Post. And he actually published the results of our
results on the front page above the fold about this Hydroxyurea work. He and this other guy Warren Leary at the
New York Times, and another science writer at the Los Angeles Times actually covered
this on front-page stories, so it did make a bit of a splash. Of course at that time, we had a limited number
of patients, but we were excited that we had something of a 70 percent response rate, and
that is sort of what, after it was replicated vaulted this on to the NHLBI’s attention
that funded this multi-center trial. [music] RODGERS: I worked with Dr. Schechter and a
colleague Dr. Noguchi and we were able to show in the lab this effect that we had in
terms of increasing the fetal hemoglobin, what the bio- the molecular and cellular effects
are in terms of the inhibition of polymerization. I also worked with Dr. Arthur Nienhuis who
was at the National Heart, Lung, and Blood Institute. And while most of his work was actually in
basic molecular biology, he was quite accustomed to doing clinical trials and setting up appropriate
clinical trials. And so what I tell people is that I have a
foot in NHLBI and NIDDK. In fact, both of the institute directors at
that time claimed me as their own. Dr. Gorden – who I don’t know whether you’ve
interviewed yet, but I’m sure you will – was the Institute Director at NIDDK and he knew
that I was here doing this work. Dr. Claude Lenfant, who was the Institute
Director of the Heart, Lung, and Blood Institute at the time, was certain that I had worked
in the Heart, Lung, and Blood Institute. And so he was saying this was work that was
being done in their intramural program. That withstanding, Dr. Nienhuis taught me
a lot about the conduct of clinical trials, safety issues, how to recruit patients for
the trial and more. And so I started off more with the project
and that ultimately led to a program in terms of the clinical aspects of sickle cell disease. We shortly thereafter showed in another piece
in The New England Journal that if you add a drug, recombinant erythropoietin, you could
actually synergize the effects and actually get higher levels of fetal hemoglobin among
these patients. So yeah, doing those clinical trials was really
a great start to my career. [music] RODGERS: Our programs are reviewed every four
years, quadrennially. It turns out, in 1990, when that paper came
out, I was actually put in and received tenure that year, in 1990. In 1994 after my review, I did some additional
clinical and some basic work, and I was put in to become a Section Chief. I was still in the Laboratory of Chemical
Biology, and by this point, Dr. Schechter was now a lab chief. When I came to work with him, he himself was
a Section Chief, but about a year later, Dr. Anfinsen left and he then became the Lab Chief. So from 1984 to 1994, I got tenure in about
six years and then for the next four years I was a section chief. Then in 1998, I was granted my own lab, my
own branch in 1998. At that point I physically separated from
the laboratory that I was in, Dr. Schechter’s lab, and I began to recruit people to expand
the program of what I thought the next step should be in terms of sickle cell disease
clinical research. INTERVIEWER: Is this the clinical and molecular
hematology branch? RODGERS: Molecular and Clinical Hematology
Branch, that was 1998. Now, the person who Dr. Gavin worked with,
just going back a little bit in our interview, was Dr. Jesse Roth. He was a Branch Chief. But he subsequently became the Scientific
Director of the Institute. And in 1990 when I received tenure, I was
the very last candidate that he brought on under his wing as a tenured scientist. He subsequently left and Dr. Allen Spiegel
became the Intramural Scientific Director. And that’s important because in 1999, one
year after Dr. Spiegel had put me in to become a Branch Chief, he actually became the Director
of NIDDK. He succeeded Dr. Phil Gorden, who I think
you will be interviewing. That was in 1999. [music] RODGERS: Traditionally laboratories in NIDDK
studied basic and translational research whereas branches were focused mostly on clinical studies. That, somehow, 20 years ago, began to be a
little bit less clear cut. So even in this Laboratory of Chemical Biology
where I worked, I did a lot of clinical research, I did basic and translational work. But I thought that calling it a branch would
be true to the historical perspective of focusing more on clinical work but supporting that
with basic studies as well. And so I went about hiring people in my branch
as tenure track investigators to take up some of the clinical work that I had envisioned,
which would be the next step in this moving forward. INTERVIEWER: What were those hires? RODGERS: So the first person I hired was a
fellow named John Tisdale, who was actually one of my fellows when I was an attending
on the hematology branch. And I hired John with the idea to develop
a bone marrow transplant program to treat patients with sickle cell disease. Up until now that wasn’t available. And while most of the patients who had been
treated with bone marrow transplants who had sickle cell disease were pediatric patients
who had not yet suffered all the end-organ complications of sickle cell disease that
would occur after 20 or 25 or 30 years, since our focus was on adults, the goal was in my
mission statement to him was to develop a regimen that could be safely applied to adults
who had suitable bone marrow donors for them- be donors for them- to transplant them. And so, he took that on. First did work in animal models, rodents,
subsequently in primates before we then applied this to humans, and he developed what’s
called a non-myeloablative transplant regimen, which was actually quite unique. Instead of using high doses of chemotherapy
and radiation to completely wipe out the bone marrow and then transfuse the patient with
the bone marrow or hematopoietic stem cells from an HLH compatible donor, the goal was
to make a little space in the bone marrow, not completely ablate it. So mini-transplant, or non-myeloablative,
or there are a number of terms for it. But it was really based upon the observation
that in a number of these kids who had undergone full myeloablative bone marrow transplantation
with sickle cell disease, most of them continued years later after they were cured to show
a hundred percent of their cells in their peripheral blood were of donor origin. But a small number of them, as it turns out,
after a number of months to years, their own bone marrow started to come back. And so they had elements of both donor marrow
function as well as recipient, their own. And that state is called mixed chimerisms. You have a little bit of this and a little
bit of that. Unlike the patients who had a hundred percent
donor cells in them, the patients who were about 20 percent recipient and 80 percent
donor, or 60 percent, or 70 percent donor, and 30 percent recipient, they seemed to be
cured as well. So that raised the possibility well maybe
you don’t have to exactly wipe out the entire bone marrow. Maybe you can use less intense regimens to
open up some spaces where you can put these donor cells, because it seems like they can
live together quite well in this state of mixed chimerisms. He was able to test this hypothesis in a transplant
rejection-prone model in mice and then subsequently apply this to this non-human primate, and
actually showed that it worked, which ultimately led us to move forward with this clinically. Now the reason that you don’t want to use
high doses of radiation and chemotherapy, because after 20 years, 25, 30 years of sickle
cell disease and all the damage it does to the organs, the lungs, the liver and many
other organs, the heart, this high dose of radiation and chemotherapy, it could tip people
over the edge and cause partial compensation of these organs that were severely damaged
to then be fully damaged. So we estimated that the likelihood that adults
with sickle cell disease, particularly the severe patients that we often are referred,
could result in a 20, 30 percent mortality at a hundred days. Usually the hundred-day mark is when people
begin to count whether the transplant was successful or not. And in doing this non-myeloablative approach,
as it turns out, in the first 30 patients that we transplanted, all but one survived. The one who passed away, passed away from
a condition unrelated to the transplant itself. And then when we expanded that to 50 to an
excess of 60 patients, it turns out there’s a 95-percent disease-free survival and about
a 98 percent overall survival. So these are results that were similar to
what you see in kids. And really as it turns out and somewhat unexpectedly,
the beauty in this regimen is that most people who get an organ transplant, be it bone marrow
or kidney, or liver, you have to give them anti-rejection medicine. That’s one of the downsides. So yes, you have a new kidney and you don’t
have to be on dialysis anymore, but for the duration you’re going to have to take a
medicine to keep your immune system from rejecting what it still sees as a foreign tissue. With this regimen we’re able, after a year
or 18 months, to get them all off of anti-rejection medicine. So this really is kind of a gold standard
for organ transplantation to both successfully get in the organ as well as not requiring
immunosuppression, which has side effects on its own, as you can imagine. INTERVIEWER: So it sounds like this project
is still underway. You’re still refining it. RODGERS: It is, but we’re now about to move
onto the next phase. So as I told you from kind of a Hydroxyurea
story, it’s quite effective, 75 to 80 percent effective in adults. Just two years ago the FDA extended the approval
of the drug for infants and kids. In 2017 I believe. So it was funded for- in kids they respond
even better, but we realize that it’s not a cure. These transplants actually seem to cure the
disease, but unfortunately, only about one in four potential patients have a full sibling
match. So while it is a cure and it has a high cure
rate, it’s not going to be effective in everyone. The actual cure would be to actually take
their bone marrow cells and peripheral hematopoietic stem cells and modify them in a way that you
actually correct that initial genetic defect, so-called gene therapy of the disease. INTERVIEWER: Yet to come. RODGERS: Well it actually is happening. So the guy who works with me is working actually
with a company now. This company has developed a new beta globin
gene that has inside of it not only the normal beta globin, instead of sickle globin, but
it also has another mutation that if it ends up getting next to a sickle hemoglobin that’s
starting to polymerize it actually goes in and it causes a disruption in that to occur. So you melt away existing polymer, so that
you both increase normal hemoglobin that can deliver oxygen. But if there’s still some residual sickle
hemoglobin in there it sort of acts an anti-sickling agent in a sense. And based upon the results that John has gotten
with transplantation, they quickly contacted him to see whether he would be interested
in applying what he’s learned in the transplant world to this gene therapy. What I would say is, that work was actually
just reported on 60 Minutes about four months ago [in 2019]. And Dr. Collins was quoted that he’s optimistic
and he dared to say the word “cure.” But he said this is a cure. Now you know that’s good if you have access
to this company’s proprietary compound. But I thought a while ago, and Dr. Tisdale
and I are working on this- that if you can pick out the kids at high risk from the time
that they were born, so if you get a couple that are at high risk for having sickle cell
disease, and if you were able to collect their cord blood at the time of birth and then freeze
it away using the correct practices, that eventually you can actually take that cord
blood, manipulate it with gene editing technology and then ultimately give that cord blood that’s
now edited back to the child without doing any manipulation, because it’s their own
cord sample. And so about 15 years ago we began a cord
blood program here to collect. This was before CRISPR-Cas, the gene editing
technologies were available. We anticipated that eventually it would be
available. So now we have collections of cells, we’re
now working also with people in Northern Virginia to do this. And so we think when it’s ethically and
scientifically justifiable we’ll be moving forward. We’re doing preliminary studies to test
it right now, but this might be really the cure that could be more widely applied. INTERVIEWER: Well, we’ve taken the science
right up to the present day. And right up to the possibility of a cure,
which is great. But there’s this whole other track that we
have to do, which is the administrative side. When did you get a sense that you might be
tapped as Deputy Director? RODGERS: I didn’t until the time I was asked. My Scientific Director at the time who had
thought enough of me to move from Section Chief and have me start my own branch, in
1998, the very next year, he became the Institute Director. And because he was now freeing up his position
as the Scientific Director in early 2000, and the person who was his Deputy Director
at the time was someone who wasn’t a scientist, he was a businessperson, but he was about
to retire. And so Allen turned to me and said, “I would
like you to consider moving in this administrative track. You could either considering doing the position
that I had, the Scientific Director, or because this person will be retiring in a year you
could wait and become a candidate for the Deputy Director slot.” And so I said, “You know what, let me wait
a year because my research is going well.” So in January 2001, I became the Deputy Director
of the Institute. INTERVIEWER: And you got an M.B.A. as well? RODGERS: So as I said the person that he had
that was his deputy was a businessperson and he was managing a lot of the budget and the
financial aspects of the work. And I think Dr. Spiegel confided in me and
wanted me to take over that aspect. I said, “I’d love to do that, but I don’t
have any business experience per se, finance, accounting, and the like.” It turns out that they had just started a
program at Johns Hopkins, and it was a Master’s of Business Administration but it was focused
principally on the business of medicine and science. And it wasn’t one of these executive programs
where you get a degree in 18 months or two years. It was actually a full program but every part
of it was focusing on either medicine or science, and so in accounting, in finance, negotiations
of legal aspects, in economics. It all centered around case studies that dealt
with the business of medicine. And so after three years I was able to get
that M.B.A., and that’s what I started doing as a deputy, managing aspects of the budget
and other things within the Institute. I’m someone who believes in continuous learning. And in fact, in 2017, I went back and I got
a degree in law as well. INTERVIEWER: Well let’s talk a little bit
about becoming Director. I don’t want to miss how you and Dr. Spiegel
split things up. It sounds like he really- his intention was
for you to run things that are sort of the nuts and bolts. RODGERS: That’s right. Yeah. And I sort of searched as his- to actually
split up some of the scientific aspects of it. This is a very large institute dealing with
diabetes and endocrine disorders and inborn errors of metabolism, a lot of congenital
defects. We also have digestive disease and nutrition,
obesity and liver disease, and then we have kidney and urologic and hematologic diseases. And each of those organizations expect you
to attend their national meetings and meet with them regularly. At last count we had about 68 different advocacy
groups, there are three Celiac disease advocacy groups, Inflammatory Bowel Crohn’s and Colitis
Foundation. There’s not only the American Diabetes Association,
but also Juvenile Diabetes Group [JDRF, formerly the Juvenile Diabetes Research Foundation],
and it goes on and on. There were about 68 at last count. So he wanted to divvy up the scientific aspects
of this as well, so we really developed a nice way of managing that. And then I had my own areas that I focused
on like the budget, and we have an intramural program not only here, but we have one out
in Phoenix. And so I would, several times a year I would
go out and manage certain aspects of what was going on out there as well. [music] RODGERS: And so in 2005, Dr. Spiegel- so I
was Deputy from 2001— now about four years later he told me that, “Griff, I’m going
to be looking at-” I think you’ve interviewed Dr. Spiegel and so he may have said this more
eloquently than I can because he’s tends to speak in paragraphs, he’s so brilliant,
“I’m looking at another opportunity that I will consider to be my final push.” He told me that he was looking at positions,
considering positions. Ultimately in 2006, he had accepted a position
to be the Dean at Albert Einstein College of Medicine. And upon him accepting that position I was
asked by the Director, then Dr. Elias Zerhouni, to step into the company of the Acting Director,
and I continued to be the Deputy Director as well and I did that for a year. And after a national search, which was co-chaired
as it turns out by Dr. Francis Collins, who was then an Institute Director, and Dr. Tony
Fauci, I was offered the permanent job on April 1, 2007. So I told Dr. Zerhouni, and I still joke with
him, “I know you picked that date because you could always say that ‘I was just joking.’” You could always- it was April 1st, right. So I’ve been the formal Director since 2007,
so now a little bit beyond 12 years. [music] RODGERS: Well this was an organization that
historically did extremely well. And I learned in business that there are generally
four types of businesses in a situation where a new director or CEO comes in. There are start-ups. This obviously wasn’t a start-up. It had a rich history. There are organizations that were turnarounds
that started off going well, but you had to completely put it in a different direction. There were areas that you just had to realign
some of the minor aspects of it to keep it on its ongoing successful mission. Then there are very successful organizations,
which I think this is. And there you want to put your own stamp on
it and really continue to do more of what you had been doing historically. That’s how I view this. And so I set in motion, after talking with
a number of people, five objectives that I tried to accomplish. The most important thing was we wanted to
maintain a vigorous connection to our investigator-initiated portfolio. In terms of our budget, we have 85 percent
of that budget that goes extramurally out to individuals at universities, medical schools
throughout the country, and a small amount of money internationally. But we wanted to make sure that people with
great ideas could succeed in applying to our Institute and considering this a place to
have a viable research career for their entire career. And then of course we wanted to make sure
that there were exceptional training and mentoring opportunities. We wanted to make sure that we get cutting-edge
clinical research that would have a beneficial and demonstrable effect on people’s lives. It was important that we consider in both
the clinical trials and in both our early scientists and our established scientists
that we make sure that we were an institute that was diverse and inclusive, particularly
given the kinds of diseases that we were responsible for, as they disproportionately affect women
and certain under-represented groups. We wanted to make sure that not only did the
patient population that we recruited for our clinical trials reflected that diversity,
but also the individuals who would actually be performing those studies. Our principal investigators and their supported
staff also felt that NIDDK was a welcome home for them as well. And of course since we’re a publicly funded
institution, we wanted to make sure that the results of our trials, be they positive or
negative, were immediately spread in a way with public education, awareness, and outreach. Not only to the public, but also to practitioners
and the policymakers who ultimately decide what our budget is going to be, we wanted
to make sure that our outward- face in terms of both the Internet, and increasingly, social
media, reflected the things that we were doing and achieving with this public support. INTERVIEWER: Speaking of public support, you’ve
had to testify before Congress and things like that? RODGERS: Yes. Multiple times. INTERVIEWER: Tell me about the first time
you did that and what you learned. RODGERS: So I came into this job on April
1, 2007 and I think the first committee [hearing] that I attended was only about two weeks later. It was the Senate Appropriations Committee. And it’s funny that you mention that because
I can send you a video that was just done. On that committee [hearing] we were all asked
questions. We testified along with Dr. Zerhouni, who
was the [NIH] Director at the time. But Senator Daniel Inouye from Hawaii was
on that Appropriations Committee and I remember this very distinctly. We had set up a program in Hawaii to train
the next generation of biomedical researchers at a college level. And then that spilled over to looking at feeder
high schools in the Hawaiian Islands that could potentially bring these talented kids
ultimately to the University of Hawaii as college students. And then from there they might expand to get
graduate degrees or medical degrees, or other affiliated STEM degrees. Senator Inouye turned to me and said, [paraphrasing]
“I’m very much aware of this program that you’re doing, but I would like you to consider
expanding that somewhat to the American territories that exist in the Pacific Islands because
these are a lot of places where people just don’t have these opportunities.” So, hearing his remarks, we set up a program
very quickly in Guam and then in American Samoa, and in Saipan, and Palau, and the Marshall
Islands and others. And in fact, just earlier this month at the
University of Hawaii, because I happened to be in Honolulu for attending another meeting,
I recognized the person who was very helpful, now it’s ten years in action, who set up
that program and expanded it so greatly. Of course Senator Inouye is no longer alive,
but representatives from Senator Schatz’s [and Congressman Ed Case’s] office, as well
as a local representative, sent representatives with proclamations because they were so impressed
with how the program was going. I’ve testified at different times to the
House as well as to the Senate. Every two years there is a special committee
that I testify to, it’s actually the Aging Committee, which is co-chaired by Senator
Susan Collins and more recently, on the Democratic side, Senator Casey from Pennsylvania. There it’s set up specifically [to talk
about] for a pool of funds called a Special Diabetes Program to focus on Type 1 diabetes. The second time I testified— it’s every
other year— the other people- people who testified with me, it was an interesting group. On my right-hand side was Mary Tyler Moore,
then I was here, and next to me was Sugar Ray Leonard, and the person at the very end
was Nick Jonas. There must have been maybe 500 people all
in this room. Of course, they were all there to see Nick
Jonas, especially these kids. But all of these senators showed up and they
all wanted his autograph. And of course, they said they wanted this
for their grandkids. It was the first time- someone from Rolling
Stone magazine took a picture. Actually, I have it here on the wall. So I appeared in Rolling Stone magazine. I said, “Life can’t get any better than
this.” We were very successful during that time. Senator Collins asked me, “When are you
going to be able to develop an artificial pancreas so that these kids won’t have to
prick their finger and go through the kinds of very tedious and arduous painstaking way
of managing their diabetes?” And I said, “We’re going to work on this.” This was maybe around 2011. In 2016, the FDA approved the very first [hybrid]
artificial pancreas. And now there are five additional ones on
the market. So we’ve been able to stimulate the biotech
industry to really move very quickly in this space, and we’re developing other things
that make life living with Type 1 diabetes much more manageable. So those are very exciting. INTERVIEWER: The artificial pancreas? Did NIDDK help fund the research? RODGERS: It’s funded through the Special
Diabetes [Program] allotment that we get. In fact, most of the major- the early work
on the various components of an artificial pancreas – which consist of a pump to continuously
deliver insulin and then bolus certain levels during the time of a meal. It consists of something to continuously measure
glucose as your pancreas does, and then some device, a Bluetooth device that detects those
changes and then signals the insulin pump to give- to either increase or decrease or
bolus the appropriate level. All of that fundamental work was funded in
the early stages by NIDDK, and then it was in many instances later taken over by private
industry. Two things that you might hear on the television,
there is a system of continuous glucose monitoring called the Freestyle Libre that Abbott puts
out that doesn’t require a finger stick at all. You don’t have to calibrate it. This is something you just take your smartphone,
put it next to it and it tells you what your blood glucose level is. The early funding of that was done through
NIDDK. There is an implantable device called the
Eversense that can stay in place for several months at a time and you can get the same
information. That was also our work we funded a different
type of hormone. Not only does your pancreas make insulin,
it makes something called glucagon, which if your blood sugar gets too low the body
kicks in this glucagon to raise your value. We worked with chemists to develop a more
chemically stable agent that has a longer half-life, a shelf life, so you can actually
put it in the pump as well, so have a bi-hormonal pump. And again that was some of our work. I can go on and tell you about many of those. But this work with industry, at least in my
mind, was greatly assisted, I think, not only because of my general interest in this, but
by some of the business training that I was able to obtain. [music] RODGERS: A major one, sticking with the diabetes
phase, is the Diabetes Prevention Program [Outcomes Study]. While at the moment there are about 30 million
Americans with diabetes, most of whom know that they have it, but some don’t or are
unaware. There are another 84 million Americans that
have what’s known as prediabetes. Their blood sugar levels are not normal, but
they’re not quite yet high enough to categorize them as having frank diabetes. But they’re on the cusp and sometime within
the next five to ten years they’re at a high risk of developing type 2 diabetes. So this Diabetes Prevention Program was set
up to answer a very simple question: If, for example, you were to treat these individuals
with a lifestyle intervention to get them to lose about five to seven percent of their
weight through diet and exercise, would that be sufficiently be enough to greatly reduce,
compared to the standard instructions, the rate at which people go on to develop diabetes? And we had a third arm to this trial, [a drug]
called metformin, which is a standard pill that one uses to treat patients once they
have a diagnosis. Well after three years it became clear that
the metformin reduced the conversion to diabetes by about 31 percent with this lifestyle intervention
resulting in about 58 percent reduction in the conversion. We went on to extend that study, to do a Outcomes
Study, with a later follow-up. Even at ten years, the benefits were durable. There were demonstrable, statistically significant
results with [more in the] lifestyle group [and metformin] of patients who still either
had pre-diabetes or the blood levels went back to normal [compared to the placebo group]. And the metformin arm remained statistically
stable. I guess we were wise enough to know that of
the things that are at high risk of putting one in this category of pre-diabetes [converting
to diabetes] includes women who have had a history of gestational diabetes, it includes
the same ratio in ethnic groups that are at a high risk for diabetes, but it also includes
people over 60. And so, working with our colleagues in the
Aging Institute, we tried to over-sample for people who were 60 or older at the time of
randomization. And the reason, as it turns out in hindsight,
that was a good thing, was that while overall population, about 58 percent of the people
responded to the lifestyle. If you look only at the people who were 60
or older at the time that they were randomized, they had a 71 percent reduction in the rate
of transformation to diabetes. And it was funny because people said you’re
never going to get people over 60 to exercise, and even if you do, they’re not going to
sustain it. Well, both of those things have proven to
be not correct. The thing is, with this one-on-one counseling,
it required six sessions and then a boost every month after they had gone through the
formal sessions. But it was a very expensive enterprise with
one-on-one. There’s no way that you can make a dent
in this 84 million people at risk. So we figured we’d try to scale this up
in a way that, instead of doing this one-on-one, we’d do it in a group setting and we chose
the YMCA as a venue to do this. So you might ask, why the Y? Well it turns out there are 2,600 YMCAs in
this country [at the time] and the average person lives about three miles from a YMCA. So we thought this would work and we could
scale it up and you would have a great way of starting to achieve that. And it turns out that again I’ll cut to the
chase: the benefits that you saw in a Y setting, giving group counseling, could achieve similar
weight reduction and the same values of diabetes prevention as we saw with one-on-one counseling. Now you’re making it cost-effective and
the fact that we’re able to get a lot of people at the age of 60 and over, Medicaid
and Medicare services, or CMS looked at this and said maybe we should offer this as a benefit
for people 65 or older. And just last year it became an approved benefit. So anyone who’s 65 or older [with Medicare]
can go in and be tested. If they have pre-diabetes then they would
cover this counseling service. It’s very unusual to actually have a clinical
trial result, in relatively short order, about 15 years, to actually make this a policy. That’s one of the things I guess I’m most
proud of. [music] RODGERS: About 12, 13 years ago, locally there
was a radio station that decided that they would host an event at a local hospital that’s
now closed, called Providence Hospital, and it was called “Take Your Loved One to the
Doctor.” A lot of people, particularly in urban settings,
particularly men, don’t like to see a doctor. So they used as an occasion every year to
encourage people, they would do different types of screening there, and they asked me
and several other people would you come and host a radio show where people can call in
and ask questions. They knew that at the time I was the Director
of the Institute with diabetes, obesity, and kidney disease, so there would be a lot of
interest in calling up and saying, “Doctor, I have heartburn, what should I take for it
or what does it mean?” So I did that and that went pretty well. They asked me the next year, but rather than
having a local radio personality they actually had someone who had a national slot, a fellow
named Tom Joyner, who has a fairly large reach. And that went well, and he actually said,
maybe you could consider doing this not just locally, but on a national scale. So about 10, 11 years ago we actually set
up a program with him and we went to the radio stations initially here in Washington but
then we expanded to Baltimore and Philadelphia and Richmond. The goal initially was just to do those areas
because I could use this venue to try to recruit patients to come to the NIH to get involved
in clinical studies. But then we expanded that even more to Atlanta
and places in the Midwest. And then over time, we actually expanded it
to another personality who’s actually in 41 markets around the country. So what started off just here in Baltimore
and Washington with maybe 10 or 20,000 listeners, is actually a program that’s now in 41 markets
with 60 million listeners on a weekly basis. And I expanded it to go beyond what we do
just in this Institute. I have other co-hosts from other institutes
like Dr. Fauci, for example, who will talk about HIV or people from the Office of Research
on Women’s Health talking about that aspect, complementary and alternative medicine, bioengineers
coming in and talking about new sensors, smart watches and Fitbits, and things like that. But I’ve also opened it up for people, celebrities
[to discuss their health concerns]. Remember I told you the Rolling Stone thing-
I was able to get Sugar Ray Leonard for example to talk about diabetes. I was able to get Sean Elliott a former basketball
player who was on the San Antonio Spurs, he’s had a kidney transplant, he talked about kidney
transplants. More recently I’ve collaborated with Barbra
Streisand. And that’s gotten a lot of likes and hits
because she’s very interested in the fact that heart disease affects women differently
than it affects men. She actually set up a foundation to do educational
awareness around this. She came to visit NIH and I mentioned to her
that some of the reason that women had it differently is a lot of those women had diabetes. And women with diabetes- women generally benefit-
pre-menopausal women benefit from the estrogen effect, and so their disease is not— usually
it is several years to a decade before traditionally they started having effects. But with diabetes, you erase all the beneficial
effects that you have due to estrogen. I made her aware of that and so she agreed
to partner with me. We did a month-long series on heart disease
in women, particularly those with diabetes. As I said that’s grown and it gets a lot
of listeners. Of course, with social media, we just don’t
have it on the radio now, it’s on the web, it’s on Twitter, and other places where
you can see it. INTERVIEWER: You’ve talked about reaching
out. I want to wrap up by looking back in again
though. One of the things that people tell me- the
old timers- it’s sort of like at NIDDK, you can do anything. There’s people doing everything here. And there’s not necessarily a discipline
or a science that holds it all together. I want to get a sense from you, having been
here and having held it all together, what do you think the glue is that is keeping this
institute as a coherent whole? RODGERS: I don’t want to argue with the
great scientists that you talked about. I would just differ a little bit. There are areas we focused on that are absolutely
clear to our mission. And so we have an intramural program that
focuses on liver disease, and one on diabetes, and obesity, kidney disease and others. We have basic scientists who actually support
some of the research moving into that, but maybe what they’re expressing is we have
people who do very basic basic work in structural biology, for example, without an obvious connection
to the clinical arena. So they seem to be outside of what our disease
mission is, but their work is so fundamental and so impactful that it has really has changed
how we think about it. It turns out that it has that application
that was unanticipated before. I would say the glue that keeps things together
is that, and again this is something I inherited so I think I can’t take credit for this,
is that this is a place where people like to work. Year after year in terms of ranking, in terms
of global satisfaction, and employee engagement and other things we tend to rank one among
all the large to medium size institutes at the NIH. There is something called the FEVS, the Federal
Employee Viewpoint Survey that ranks things in various domains and we tend to do quite
well. As you leave you’ll see our picture from
2018. We’re waiting on the 2019 result. We’re about somewhere between five to 10
percentage points above everyone else. And in fact, people think that the best institution
as they look across is actually NASA where it always tends to be the number one ranked
institute. But if you look at our numbers as an institute
compared with theirs as an agency, we actually outperform even NASA. People like to work here, and I think that-
again it’s not just satisfaction, it’s engagement, people feel like they’re family. Even our outfacing elements— we try to make
sure that people realize the importance of their work and what effect this has on the
American population. And so we’re ranked it turns out in the
top three of mobile devices for our website, for example. So except for Social Security and the IRS
at the time of taxes, we actually get more hits on our website, particularly now with
our mobile sites, than any other services that the federal government ranks. With that regard in terms of personal engagement,
it’s actually reflected by the fact that we have a fairly long turnaround. People stay here 30, 40 years. There’s one employee that works here who
turned a hundred last year [in 2018] and he’s actually worked with the federal government
with our institute now for 65 years. Next year we will celebrate our 70th anniversary
and 65 of those years he’s been with us. He has been a federal employee for I think
70 years because he was with the Coast Guard for five years before he came to us. INTERVIEWER: Herb Tabor. RODGERS: You know him! Herb Tabor, exactly. And so he- I think reflects the same sentiment
of people who have been here for 60 years, you know like Marty Gellert and Gary Felsenfeld,
and others. This is a place that people enjoy working
and I think their mission focus, even people doing basic science, they interact a lot with
the more clinical people to understand how they connect. The basic scientists work hand in glove with
some of the clinical people to expand their work into the clinical arena. So I think that’s the special sauce or the
glue that keeps it together. [music]

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