Obesity: It’s More Complex than You Think | Fatima Cody Stanford || Radcliffe Institute

Obesity: It’s More Complex than You Think | Fatima Cody Stanford || Radcliffe Institute


– Good afternoon, and welcome
to the Radcliffe Institute for Advanced Study. My name is Janet Rich-Edwards. I am one of the advisors
to the academic Ventures Program, which
brings you programs like this here at Radcliffe. And I also happen to
be an epidemiologist. This has been a
banner year for me, because we have been able to
put on a series of lectures about epidemiology. This one, I’m glad you’re here,
is the penultimate lecture. We have one more on April 23
about Alzheimer’s disease. But I am absolutely
thrilled to welcome the team of Cody Stanford
to give a talk today about obesity, which is
arguably one of the greatest public health challenges
we face in our lifetime. She’s an instructor of
medicine and pediatrics at Harvard Medical School. A leading expert on
obesity, Dr. Stanford provides clinical care,
supervises trainees, administers a
clinic, and conducts research on obesity, health
policy, and health disparities to enhance knowledge
and quality of care. In addition to teaching in
clinical work at Harvard, and in the Massachusetts
MGH Weight Center, she conducts clinical
research to evaluate the efficacy of weight
loss medications as an adjunct to
weight loss surgery, delineate the metabolic changes
associated with adolescents who undergo weight loss surgery,
and evaluate obesity treatment coverage in the United States. She’s been featured in national
news, broadcasts, magazines, newspapers, web sites on
issues related to obesity. And I just learned that she
won the medical community’s equivalent of the Oscars. It’s called the Doxey Award. It’s a great golden statuette. Just, I think, like, last week. [APPLAUSE] In addition to all that, and
this long string of letters you see after her name, she’s
a recipient of the Harvard Medical School Diversity Award,
and the Massachusetts Medical Society’s Women’s Health Award. She received her master’s
in public health from Emory, her M.D. From the
medical college of Georgia School of
Medicine, and her master’s in public administration
from the Kennedy School. Please welcome Dr.
Fatima Cody Stanford. [APPLAUSE] – Good evening, everyone. Can you hear me? OK, good evening. I’m a walker and a
talker, so you’ll see me walk throughout the
course of this lecture. Today, you’re here to
learn about obesity. And I hope that by the
end of this lecture, you’ll leave with some new
insights about obesity, and its role in our
current structure as it relates to health,
and multiple of issues. I’m not going to spend
time talking about myself. Thank you, Dr. Rich-Edwards. So we will pass by that. So what are the questions
of interest today? What is obesity, and
what is its prevalence in the United States,
and throughout the world? We’ll learn about
the epidemiology. So we’ll talk about
that initially. Is obesity really complex? You think it may be not complex. Like, we are here to
understand why that is. And if it is really complex,
how do we understand it? How do we glean information? How prevalent is weight
bias, and how do we work to change it? And what are some
clinical interventions for the treatment of obesity? Now I’m going to step
on a soapbox moment at the very beginning
of this lecture to talk about our language
regarding obesity here in the United States. Often, we will refer to
patients as obese patient. We use words such as
morbid obesity, fat. I want us to change
that thinking because that thinking, our
language in and of itself, promotes weight bias and stigma. So this is a disease
process like any other. We talk about these as
patients with obesity, patients with severe obesity. We take out the term morbid,
because we don’t utilize it for any other disease process
i.e. cancer, heart disease, things that could
potentially kill patients. And so let’s remove that. You’ll hear me talk with
people first, language, throughout the course
of this lecture, and I challenge you to do
the same in your daily life. Now let’s look at obesity
and its prevalence compared to other
disease processes. We’ll start with commonly
discussed disease processes. HIV at the bottom of this list. We have 1.2 million people. We have colon cancer
here with 1.2 million. Breast cancer gets a lot
of attention, 2.8 million. All cancers combined,
13.8 million. Diabetes 37.2 million. NAFLD is nonalcoholic
fatty liver disease. You can see 80.3 million. And then obesity, 93.4 million. Let’s go look at how many people
own a TV here in the United States. 115.6 million. People that own a smartphone. We spend a lot more time
on our smartphones– 205.4 million. So what you can see here is
that 93 million adults struggle with obesity. Approximately 40% of the US
adult population has obesity. But why are we not
doing much about it? I think a lot of that has to do
with our lack of understanding, and a lot of are placing blame
on patients, which we can hope to change after this lecture. Now when we look at
obesity, often, we will look at it in terms of the
BMI, or the body mass index. It determines height and
weight, and then gives us a kind of a measure,
crude measure, to help determine
who has obesity. We’ll look at the guidelines
for children and adults that have obesity. There are different guidelines. So if you’re thinking about
your child or grandchild, I want you to realize that
there are different criteria. We’ll start looking at
the pediatric population. So how is obesity defined
in children and adolescents. It’s done based upon growth
measurements taken from the age of 2 up until the age of 20. So those that are
underweight have less than the fifth percentile. Those that are considered
to be a healthy weight between the fifth and less
than the 85th percentiles. Those that are
considered overweight, between the 85th and less
than the 95th percentile. And those that have
obesity greater than or equal to
the 95th percentile. Now there are criteria that
go beyond this, meaning as we get into severe obesity. I’m not going to specifically
focus on that here with regard to the children and
adolescent population. However, I won’t
do that for adults. Now when we look at
adults, because we’ve stopped growing
vertically, we actually have just a BMI criteria
that defines adults. And this is utilized, not only
here in the United States, but by the World
Health Organization throughout the world. So when we look at those that
are considered underweight, they have a BMI
of less than 18.5. And for those that
are considered of normal or healthy weight,
a BMI from 18.5 to 24.9, we start to get
into overweight when we get to BMIs from 25 to 29.9. And then we get into obesity. And what you can
see on the screen is we have class 1, class
2, and class 3 obesity– mild, moderate,
and severe obesity. Mild obesity being classified
as a BMI of 30 to 34.9. Class 2 obesity classified
as a BMI of 35 to 39.9. And then those that
have BMI and excess or equal to 40 being categorized
as having severe obesity. Now what I’m going to do is
just take you very briefly through some of
the epidemiology, starting very recently, 2011. Often, when I use the slides,
I’ll start back from 1980, and bring us up to now. But we all know that
obesity rates are climbing, that’s part of why you’re here. So I didn’t want to really
kind of belabor that point. But I do want to point
out some nuances here. So if you look at this graphic
here of the United States, this is looking at obesity
amongst US adults by state. I want to point out kind
of some key things in terms of the coloring
here on the graph. States that have less than
20% obesity rates, if you can find one, let me know
about it, but no one does. Colorado was the
last to hang onto it. 20% to 25% in green– so this is the percent
of the population. In yellow, 25% to less than 30%. In the orange, which
is just concentrated a lot here in the southeast
and in the Midwest, 30% to less than 35%. And then greater than or
equal to 35% obesity rates. Now I want to give you a
little bit more information– and this is for
the epidemiologists in the room– this is from
the Behavioral Risk Factor Surveillance System,
which is self-report data. And so that means that this
is probably not even accurate. I just want you to think back to
your driver’s license, and what weight you put on there, and
what weight you actually are, and you tell me
if those coincide. Now if they coincide, and
you’re actually accurate, that’s great. But most people, fudge
the things a little bit. So what you can see
here– this was 2011. Now in 2012, we
see a pretty shift. You’re like, wow, in
one year we shifted? 2013. 2014. 2015. OK? So we see a change,
and you guys you would agree with me that
there is a bit more orange. Some red has kind have
crept into the area. We start seeing some of
the southern states– Mississippi, Alabama, Louisiana,
and then West Virginia getting obesity rates
by self-report data in excess of 35%. We see Guam here
on the outlying, and we see some differences. So of course, everyone’s
looking up to Massachusetts. And we like to tout ourselves
on the back– we’re 20% to 25%. But really? Still 20% to 25% of the
population with obesity by self-report? I mean, do we really need to
pat ourselves on the back? I don’t know if we
should really get a pass. Now what I’m going to
do is I’m like to look at this by race and
ethnicity– by the three major racial ethnic groups
here in the United States. We’ll start looking
at white adults, we’ll go into looking
at Hispanic adults, and we’ll finish
looking at black adults here in the United States
by self-report data– remember that. So if we look here, you can see
that there is some distribution of obesity in West Virginia. And we have Puerto Rico here. For those that are white adults
here in the United States, Colorado does have
that less than 20%, specifically for white adults. DC, so the District of
Columbia, and Hawaii. I wanted to say Hawaii. So less than 20%. OK? Let’s look at what happens
when we look at Hispanic adults here in the United States. We do see an oranging,
a reddening of the map. Would you guys agree with that? So we start seeing a
lot more red distributed throughout the United States. I think that the graphic
that’s most concerning is this last one, which is
black adults here in the United States. This is a lot of what
brought me to this work. I mean, you guys probably
recognize that I’m an African-American woman. And so I was always
concerned at why was there such a huge disparity. You can see that most of
this map is red in nature. And while red is a lovely
color, in this situation, it’s not one that precludes
positive thoughts. And so part of my
work on disparities is really to address
and understand why there’s such a difference
in the prevalence of obesity by race and ethnicity
here in the United States. Now a lot of people
often say to me that this is just a US problem. When I go other places
around the world, I don’t really notice obesity. And I would challenge your
thinking on this notion. Greater than 10% of the
world’s population has obesity. So that means it is
pandemic in nature. And I want to focus on some of
the areas that might have been a little bit shocking to you. Obviously, we have
the United States. We have Alaska. We have Egypt. We have Libya, we have Saudi
Arabia, Iraq, and Turkey. Out here in New
Zealand, excess of 30% prevalence of obesity
in those countries. Those dark green colors
if we get to Australia. Lots of Europe. We would see a lot
of places still have pretty significant
obesity rates. I mean, here in Africa– so it’s interesting–
so we just talk about black adults
in the US have really severe obesity rates. But throughout much of Africa,
the prevalence of obesity is less than 10%. So there are some
things that might account for these nuances. So when we talk
about energy balance, we learned that energy
balance is very simple. Really, what are we
having this talk for? It’s really just about calories
in– the food and beverages that we eat– versus our bodily
functions, stool output, physical activity. And if we just get
this in balance, then we should all be lean, OK? But that’s not the
simplicity that makes this disease process
as prevalent as it is, not only here in the United
States, but around the world. We’ll learn why this
indeed, is incorrect, and why our focus
on this has led to this rise in obesity rate. So let’s get obesity. It’s a multi-factorial disorder
where genetics, environment, development, and behavior
all play a role in a person’s likelihood of having obesity. Now I’m going to get into
the complexity of this, and hopefully, you guys don’t
lose me, but don’t worry, I’ll bring it back to eighth
grade level in a few minutes. But we’re going to go to
PhD level for just a moment so that we can understand
the complexity of obesity. Now what do you regulate the
weight set point is the brain. So if we’re going to focus
on the part of the brain, we’re going to focus
here on the hypothalamus. The hypothalamus is getting
signals from leptin out here in the fat tissue. It’s getting signals from the
small intestine, the large, intestine the pancreas,
and the stomach. These are sending signals back
to the brain, and it tells you, it tells me, it tells my
patients not only how much to eat, but how much to store. So let’s look at the
substances that you saw that were hormones–
where they’re produced, and what their
effect on feeding is. We’ll look at ghrelin,
which is housed in part of the stomach,
the fundus of the stomach, and in the hypothalamus,
which I just pointed out. Its effect on feeding
is orexigenic. So orexigenic means it
promotes my appetite, it stimulates my appetite,
it’s what makes me hungry, OK? Anandamides, which are housed
in the small intestine– it is also an orexigenic or
appetite promoting hormone within the body. Now insulin, when we
talk about insulin, we’re talking about
endogenous insulin, meaning insulin inside
of the body, not insulin that we’re ministering
from external. And insulin is housed
in the pancreas. And it promotes satiety. It is anorexigenic. eugenics
So orexigenic, anorexigenic. Anorexigenic is the
opposite of orexigenic. So insulin inside of the
body promotes satiety, OK? Leptin, which is a hormone
you’ve likely heard of, in the Latin, it’s
leptos, which means thin. It is produced in the
short term in the stomach, and the long term in the
adipocytes or fat cells. And it is also anorexigenic
and promotes satiety, that feeling of fullness. CCK or cholecystokinin
is produced in the small intestine. It promotes early satiety. So you get full quicker. And also, it plays a role
in digestive enzymes, and release of acid
in the stomach. Finally, we have
peptide YY, which is produced in the last part of
the small intestine, the ileum, and the colon, which
is the large intestine. And it promotes satiety,
so it is also anorexigenic. Now this looks crazy,
but don’t worry, I’m going to take
you guys through it. I want you to guys think of this
as two lanes down the highway that we’ll travel. We’re going to focus on leptin,
which is a hormone here. And it’s going to
bind to this receptor. So this is going to be
lane one of the highway, and then you can
go down lane two. But we’ll focus on the
right part of this. So when leptin binds
to this receptor, it stimulates the
neuron in the brain called the POMC or the
proopiomelanocortin neuron in the brain. This is in the arcuate
nucleus of the hypothalamus. Now when we promote this, think
of this as a firing mechanism. It fires, and it
communicates information about what I’m supposed to do. So people that travele down this
lane of the brain or this lane down the highway, they
get an anorexigenic signal to their brain. They have high levels of what’s
called BDNF, which is brain derived neurotrophic factor. And for these people that travel
down this lane or this pathway in the brain, they
tend to be very lean. I often like to
bring up my husband. At this time of
lecture, he’s used to hearing me bring him up
because his brain signals perfectly down this pathway, OK? So he’s been with me it will
24 years next week, sorry and he can eat what
he would like to eat, he can work out as
much as he would like, and he is very, very lean. So at six feet tall,
and about 150 pounds, he stands, which is great. He’s also standing in
the back of the room. He doesn’t think
I know he came in. All right. He was late, though. [INAUDIBLE] [LAUGHTER] So leptin can bind to
this alternate receptor. It looks like it’s
the same receptor, but it stimulates a different
neuron in the brain. This is called Agouti-related
peptide neuron, and it’s specifically housed
here in the paraventricular nucleus of the hypothalamus. For these people, they
get low levels of BDNF. So low levels of brain
derived neurotrophic factor. And these patients will
often struggle with obesity. If you’re a person or
a person that gosh, they seem to be
eating very healthy, they seem to be
exercising all the time, but no matter what they do,
they seem to defend a higher set point, it’s a high likelihood
that they have a predilection to firing down this
pathway of the brain. And it’s unfair. We want to do with
my husband’s doing– I want that little bit
of that sometimes too– but it’s not what
the reality is. So then we have to figure out
how do we affect the pathway, the signaling to
change such that we can have an impact on
someone’s likelihood to go down this
preferential pathway as it relates to weight regulation. So let’s look at BDNF. We talked about brain derived
neurotropic factor regulation and obesity, talking
about the role it plays. And so what they
did was they looked at about 30,000 individuals,
and they tried to determine, what’s going on. What are we seeing, and
how does that differ, maybe by race and ethnicity? What they found were
that people with obesity had a CC pair of this
heterogeneous nucleotide, ribonuclear protein D0B– I’ll ask you guys
about that later– CC pair. And for those people
that have this pair, they have low levels of brain
derived neurotrophic factor, and higher levels of obesity. Those that had a TT
pair had high levels of brain derived
neurotrophic factor, and tended to have lean figures. And those that had a TC pair–
kind of fill in the middle– they had medium likelihood
of having obesity. Now when they looked at
this by race and ethnicity, Hispanic and
African-Americans were more likely to have either
a CC pair or a CT pair compared to white individuals. And so maybe this
is one factor that plays a role in the
difference in obesity rates here in the United States. Now I’m going to switch
gears a little bit and talk about the concept
of fetal programming, and what does fetal programming
mean as it relates to obesity. And why is it important? Why do I think it is probably
one of the untapped mechanisms of controlling obesity,
not only in the US, but around the world? So if a mom goes into pregnancy
with overweight or obesity, she has increased inflammation,
increased insulin resistance, breakdown of cholesterol, and
she has inflammatory markers that are elevated. That then exposes
the fetus to lipids. Lipids are kind of cholesterol. And it reprograms
their gene targets such that they not only have an
increased amount of lipids or cholesterol in
their liver, they’re also struggling with issues
in their skeletal muscle, their adipose, which is
fat tissue, their brain, and their pancreas. Then that leads to risk
of childhood disease. That NAFLD, that nonalcoholic
fatty liver disease that we talked about earlier. Insulin resistance,
obesity, hyperphasia, which means that I have an
insatiable desire to eat, and diabetes. So I just told you
that I think that there is an untapped strategy
of really targeting moms prior to conception,
and let’s look at why. We’re going to look at a
study that’s been conducted. This is a prospective
study, so going forward, about 20 years of
duration at this time, and it’s looking at
children that are born to the same mom and dad. One born before the mom
had weight loss surgery, The second born after the
mom had weight loss surgery. So same genetic makeup,
same mom and dad, but different levels of obesity. So BMS stands for
before maternal surgery. AMS stands for after
maternal surgery. And that surgery specifically
is weight loss surgery. So we’re going to compare
these two columns. So obviously here,
there’s similar numbers of males and females. You can see that the
birth weight of those born to the children that
were born before the mom had surgery, which means that
she had severe obesity, is different. Macrosomia means
children with a big body. So those that have
macrosomia, we can see much higher prevalence
in those born before surgery. There’s also going to be
an age difference, right? So we expect these to be
older because they were born before the mom had surgery. The mom had surgery. We recommend not getting
pregnant for at least the first year, sometimes
two years post-surgery. So they’re going to be younger. The body mass index
percentile lower here. Weight, lower. Body fat, lower. Insulin levels, lower. Glucose levels, lower. Same mom and dad, child
born after surgery. So when we look at children
born after maternal surgery versus those born
before surgery, there is a threefold
decrease in the prevalence of severe obesity
in the children that are born after maternal
surgery versus those before. There’s improved
insulin sensitivity. We talked about insulin in
the body being anorexigenic, promoting satiety. There’s improved lipid profile,
improved cholesterol profile. We have a decrease in
inflammatory markers like CRP. Decrease in leptin. increased ghrelin. And so what we see across the
board for these individuals is that the metabolic
profile has changed just by modifying the mother. And by modifying the mother,
we have modified her entry into her environment. And then the long
term consequences of obesity within
the population. So I told you I would bring it
back down from the PhD level. We’re talking about
the brain, right? The brain is playing a role in
weight and weight regulation, but it does get inputs
from things that we do. So diet quality is important. I ask patients about
what they’re eating, not the caloric value
of what they’re eating. The brain cares more about
the quality of the calories than it does about the
number of the calories. So if your diet looks like
this, the brain is happier. So if it looks more like this. Now physical activity is
one of my favorite things. Many of my lovely
gym members are here in this audience today. We spent a lot of
time at the gym. I think we like to come
and see each other, but we also like to work
out pretty aggressively. But I want us to
think about what role physical activity actually
plays in weight regulation. And what I want to
tell you guys is that on average, people
that are physically active maintain their weight. But at the beginning of the
year, every single year, people go and join the
gym to do what, you guys? Lose weight, right? And so after two months
of them going to the gym, and they don’t lose
weight, what happens? They stop going
to the gym, right? They stop going to
the gym because they didn’t lose weight. One of the questions that
I always ask my patients is, did you gain weight? And often, they say no, but
they went to lose weight. And so since that was not
what they accomplished, they stopped going to the gym. My thinking is that we
need to change what’s being stated about
physical activity, because we know in
big meta analyzes that the role that
physical activity plays is to help with
weight maintenance, not to drive significant loss. Sleep quality and duration
plays a large role. Now this is something I do
not model well for patients. For people that know me,
they don’t think I sleep. I do sleep– I just require a lot
less than most people. Not one of my stronger suits. I can model these other
things pretty well. Now medications that we as
physicians provide to patients can lead to significant
weight change– and I’ll spend a little
bit of time talking about that in a few minutes. Circadian rhythm disturbances. So when we go from being a shift
worker to a night shift worker, that affects the pathways
that we’ve already talked about that regulate weight. And just by making that
shift or transition, we see significant
shifts in weight, as studied by the
Nurses’ Health Study. And then finally, thermogenesis. Thermogenesis is how
much we’re burning at rest and with activity. And a lot of that’s
genetic in nature. So we can’t shift
that significantly. So all of these play a role in
how the body regulates weight. Now this is one of
my favorite slides. I only use it in almost
every single presentation. And these are all
of the contributors to obesity that we know
of as of right now. Now you guys remember
the kind of skills that I showed you, like
looking at calories in, calories out– the reason
why that was inaccurate is because it didn’t take
into account all the factors that you see on this slide. So what you see here are
that there are things that happen inside of an individual. There are things that happen
exterior to an individual. Things here at the top
increase how much you take in. These things here at
the bottom decrease how much you’re able to burn. And these things
here in the middle affect either what you take
in, or how much you burn, or what you might be able
to see here, it says, unknown, or we just
haven’t figured it out. Now these are all contributors
or influencers to obesity. And these colors
actually mean something. So these things
here in the purple, these are environmental
pressures on physical activity. These things here
in the lavender that you see kind of
scattered throughout more inside of the individual are
biological or medical reasons why someone may have obesity. Here in the yellow, maternal
or developmental reasons why someone may
struggle with obesity. The only things we
ever hear about, not only in the lay population,
but also in medicine, are these things that are
here in the pink and orange– economic reasons why someone
may struggle with weight. In orange, food and beverage
behaviors, and environments. Here in this kind
of green color, these are psychological
reasons that might be associated with weight. And then here in the blue,
we have social reasons. OK? So these are the contributors
and influencers to obesity. I’m not going to go
through each one of those. I’ll give you guys
the reference for that later if you so desire. But these are contributors to
obesity inside of the person. You can see things that might
affect increasing intake. Might be hyper reactivity
to environmental food cues. Delayed satiety, so it takes
a longer time to feel full. Or disordered eating. So if we are restricting
binging, purging, things of that sort. Decreased expenditure
may be associated with a gut microbiota. You’re like, what does
the gut microbiota have to do with this? When we look at the
gut microbiota, which is the bacteria in the gut
of individuals that are lean versus those that
have obesity, we see different bacteria
housed in the gut. We see a shift in the bacteria
after weight loss surgery. And we also often see a
shift if someone gets what’s called a fecal transplant. So if they’re getting feces
from an individual for treatment of something like C. Diff,
which is Clostridium difficile. We can see people lose
weight without making any significant
changes if they’re getting the bacteria of the
gut of a lean individual. The alternate is also
true– if they’re getting the bacteria of
someone that has obesity, they may gain weight. So thermogenesis, how
the body’s burned. Physical disabilities
might affect expenditure. Increase intake and
decreased expenditure may be secondary to genetic
and epigenetic factors. Age related changes. Menopause– huge
in causing changes and how weight is distributed. I do whole hour long
lectures on that, so we won’t talk about that. Mood disturbances can also
affect intake and expenditure. Those things outside
of the person. Environmental or
chemical toxins. Pervasive food advertising. Large portion sizes. The built environment,
sedentary time, and labor saving devices
might decrease expenditure. And things that might increase
intake and decrease expenditure may be things like
stress, or weight cycling. What people don’t
realize is that when they restrict their eating,
the body recognize what it’s baseline or set point is. As we diet to lose weight, the
body gets very angry with us, and it rebounds, usually
at a higher set point. So weight cycling leads to a
consistent increase in weight over time. And then maternal
and paternal obesity can affect this as well. So I’m going to take you
back to my childhood, because I want to shift into
talking about weight bias. And I think this
is very important because weight bias, I think,
does preclude our ability to focus on this disease and
the treatment of this disease. This is me back when I was
like, I don’t know, six. This is my little sister. My little sister is also
37, but I talk about her like she’s a child. The reason why I
bring this up is because at a recent
obesity convention, I was approached by a
childhood friend of mine from about this time
frame, who came up to me, and she said, well, Fatima,
I’m trying to talk to you. And I’m like, OK. Different people kept trying
to pull me aside to talk about other different issues. She kept trying to get me alone. Couldn’t figure
out why this was. And she was like,
well, Fatima, I just want you to know that there
is a reason why I’ve always been relatively standoffish
as it relates to your. I just had not noticed. I just thought that’s
how she was since I’ve known her since I was six. I didn’t know. So she was like, do
you know why that is? And I was like, no I’m not. She’s like, well, you came
up to me in dance class when we were about six,
and you called me fat. Right. I don’t like to be
vulnerable on stage, either. So I was like, well, I’m sure
she remembers that correctly. I’m devastated that
as the person that’s supposed to be undoing weight
bias, that this has impacted her life so much
that she has gone into a career in obesity
medicine and academics. But she told me– this is what
was the most striking portion of what she said– she said, well I feel as though
if you’re capable of change, anyone is capable of change. [LAUGHTER] So I think a choked back
a tear when that happened. But I think that it
was a point well taken. And it led me to recognize that
something that I did or said– I was very apologetic
that I said this when I was six years old– had a huge impact on her life. For her, it ended up
being a positive thing. But in any way, you can tell
that this has a huge impact. So that’s my story. Now let’s look at bias
in Western societies. And bias that we talk
about, we don’t usually hear much about weight bias. I mean although, I
think it’s becoming more of a prominent issue. We hear more about race bias. So if you did a Google
search back in 2012– this was actually not reported
on in the Washington Post until 2016– if you Googled young
black male, these were the images that came up. They supposedly
changed the algorithm– I didn’t try this
before this talk. When you Googled young teens
without race qualifiers, you got kind of happy
looking pictures like this, which is
very, very different from what you see at the top. Glamour, back in 2012,
wanted to give adjectives to describe how we
think of young women that either are lean versus
those that have obesity. And so you can see these
adjectives that are often used to describe a lean woman– seated, ambitious,
confident, mean. For someone that has
obesity, the presumption is she’s undisciplined,
insecure, giving, lazy, passive, nice. And so we do have these. I would say that what’s become
the most common form of bias that’s accepted is weight bias. Really, you know these are kind
of terms that we think about. So how early does
weight bias begin? And it’s going to be
shocking to recognize that we start seeing weight bias
as early as 32 months of age. In this particular study, they
looked at 70 mother and child pairs, where they showed
the infants pictures. And those that were
11 months of age had a preference for looking
at figures with obesity. So this is is kind of the
pictures they were shown. By the time they got
to 32 months however, they changed to
going to the more average or lean individuals. And that was specifically
based on the maternal’s anti-fat attitudes. So if the mom had significant
anti-fat attitudes, we saw a significant
shift with average age of 32 months of these
children beginning to demonstrate weight bias
against those that had obesity. Now this study was
a study that was done looking at three-year-old
children and their parents, 279. And they conducted
interviews of the children. And what they saw was that
over the time of the study, there were more
negative attitudes towards large
bodied individuals, and there was awareness
of weight loss strategies that were really coming more
from the father, actually, in this situation. So this is a little bit
of a deviation from what you saw in the previous
study, but the previous only looked at mom and
children, whereas these looked at both mom,
dad, and their children. So here, we’re transmitting
through social cues, weight bias. This is a great study. So this looked at weight
teething and adolescence, and what that meant with regards
to weight related outcomes in adult adulthood. What they did was
they identified whether weight based
teasing, and adolescent predicted adverse eating,
and weight related outcomes 15 years later. They determined whether
the teasing source, the source was either
the peers or the family, affected these outcomes. And they collected this
data for 1,830 individuals from 1999 to 2015 in diverse
group of adolescents. So they looked at
race and ethnicity also along these lines. What they found was that weight
based teasing in adolescence did predict higher
body mass index and obesity 15 years later. So what they found was
that BMI increased. That led to binge eating,
more dieting, unhealthy weight control, which then
affected the body image. Now for females, both peers
and family based teasing had implications for leading
to increased disorders, eating, and having a higher BMI. Whereas for males,
only peer based teasing seemed to affect them. They weren’t quite as moved by
what their family was doing. But regardless of who
the teasing is from, you can see that what a patient
experiences in adolescence does have huge implications for what
they experience in adulthood. So let’s look at weight
bias internalization and metabolic syndrome. When we look at blood pressure,
waist circumference, fasting, blood sugar, triglycerides,
which is a type of cholesterol, and then HDL, which
is a good cholesterol, measured in 178 adults with
obesity in a weight loss trial. Of these adults, they
completed a weight by internalization scale, and
a patient health questionnaire. 32% met criteria for
metabolic syndrome, which means they have a
predilection for developing type 2 diabetes. And this high weight
based internalization predicted the greater odds
of having metabolic syndrome and high triglycerides, which
is one of our bad cholesterols. So even though it just
seems like it’s not very hurtful to
individuals, this study demonstrated that it could
be very hurtful and harmful. And also, when we look at mental
health of persons with obesity who experience bias,
physiologic stress leads to weight gain, which
then leads to disordered eating, and then, maladaptive behaviors. So it affects the mental
health of these individuals. Now in terms of
overcoming weight stigma and the treatment
of obesity, there are many different areas
that we need to work on. First, when stress
is involved, we start seeing issues
that affect food eating and physical
activity behaviors. We start seeing binge eating,
increased caloric consumption, or maladaptive weight
control, meaning using methods that aren’t going
to lead to long term weight regulation. Disordered eating, lower
motivation for exercise, less physical activity. There are actual physiologic
response to weight stigma. We have increased
levels of cortisol, CRP, these are stress
hormones within the body. A1C, which is
average blood sugar. And also, elevated
blood pressure. With regards to
health care services, they have poorer
treatment adherence. They don’t trust their
health providers. They avoid follow up care. They delay in preventive
health screenings. And there’s poor communication. Psychological
health distress, we see depression, anxiety, low
self-esteem, poor body image, substance abuse,
and suicidality. And then physiologic
health or distress, we see poor glycemic control,
less effect of chronic disease self management, more
advanced and poorly controlled chronic disease, and lower
health related quality of life. So you can see that this weight
stigma has huge implications for the individual. Now we’re going to go
quickly into looking at obesity treatments. What do we do for those
that have obesity. We talked about
93.4 million adults having obesity here
in the United States. What do I do in the clinic
setting to treat them, and what guidelines
is it based on. So here, we’re looking
at BMI category, and we’re looking at those that
fall into having overweight, which would be 25 to 29.9. And then class 1, mild,
class 2, moderate, or class 3, severe obesity. Now you can see diet,
physical activity, and behavioral therapy, we
can use across the spectrum of weight class. With regards to pharmacotherapy,
meaning medications we use for weight loss, we
don’t begin to entertain those until we have a BMI of 27 with
co-morbidities, meaning heart disease, type 2 diabetes,
obstructive sleep apnea. And then weight loss
surgery, we start to really get into when we get
into class 1, 2, and 3 obesity. The current criteria,
technically, is class 2 with
co-morbidities or for those that have a BMI an
excess or equal to 40 without co-morbidities. So let’s first explore common
weight promoting drugs. These are medications that
are prescribed by doctors, which lead to weight gain. I like to do a laundry list
here with all of my patients, and I ask them if they’ve taken
lithium, Depakote, Tegretol, Alexis, Cymbalta, Effexor,
Paxil, Prozac, Ambien, Trazodone, Lunesta, Gabapentin,
Glyburide, Glipizide, Glimepiride,
Atenolol, Metoprolol, Propanolol, long term insulin,
or long term Prednisone. And if they are taking any of
those for a month or longer, there’s a high
likelihood that there was a weight contributing factor. I’ve put them up
here on the screen. You might have seen, I
use the generic names. But if you’ve been on
any of these medications, and noticed a shift
in weight, you might want to discuss
with your doctor, because I can tell you that in
medical school, in residency– and my fellowship, we
did learn about this because I did an obesity
medicine fellowship– we don’t learn
about the likelihood that a lot of these drugs
lead to weight gain, and that we might need
to use alternatives to control the weight
gain that is occurring from these medications. So what I do is when
a patient comes in, I investigate whether
medications are a likely source of weight gain. If I can discontinue the drug,
that would be my first step. But if I’m unable to discontinue
it because I’m treating, let’s say, a psychiatric
illness like bipolar disorder, I then need to utilize
weight-loss medications to control the weight
gain that they have. So you guys are like, weight
loss medications, really, they use those? Yes, we do. And there are three classes
of medications– those that act centrally,
meaning in the brain to impair dietary intake. Those that act more
peripherally, so out here in the periphery, to
impair absorption. And those that increase
energy expenditure. These are the FDA approved
anti-obesity pharmacotherapy agents as of today. You’ll notice
things with a star. These are approved for long
term weight regulation. And many of the star agents
were approved from 2012 to now. Phentermine is a long term drug
that you might have heard of, and people get really scared
when they hear Phentermine because fen-phen, which was
withdrawn from the market, and it did include Phentermine. But the fen that was
removed from the market was fenfluramine– that’s
the F-E-N– fenfluramine. It caused heart valve issues. Phentermine has
remained continuously on the market since 1959. Phentermine
Topiramate in combos, so the most effective
drug that we have in the general population
for weight regulation. Bupropion,
Wellbutrin– people are used to hearing that name–
and Naltrexone is very commonly used. Naltrexone is what we call
an opioid antagonists. So I always warn my patients
when they go on this medicine that if they need opioid
medications for let’s say, a surgery, then we would
need to remove that drug. And also, I would warn them
that the stigma surrounding the opioid epidemic here
in the United States is such that when
people see Naltrexone, they will immediately
assume that they had an opioid issue, as opposed
to recognizing that it’s used for weight regulation. These are other
anti-obesity agents that I might utilize that
aren’t necessarily FDA approved. You may have seen them
in combination approved, not approved as
individual agents. But we will utilize
these readily. Now with weight loss
surgery, we talked about using weight
loss surgery for those that have been trying
to lose weight, still struggle with moderate
to severe obesity. For those that have class
2 or moderate obesity, they do need to have a
serious co-morbidity of type 2 diabetes, heart disease,
or obstructive sleep apnea. Prior unsuccessful
weight loss attempts, acceptable operative
risk, and the ability to participate long term
treatment and follow up. And an understanding of the
operation and the lifestyle changes needed to
sustain weight loss. These are the two most
commonly performed procedures here in the United States. The sleeve gastrectomy here
is the most common procedure. People think that the
bypass is the most common, but that has not been the
most common procedure here in the United States at least
for the last seven years. So this is the most common. So you might wonder, oh, it’s
because the stomach is smaller. No, it’s because we
remove the stomach, and ghrelin, which you guys
remember, which is orexigenic, or promoted appetite,
is housed here in the fundus of the stomach. Same with the Roux-en-Y
gastric bypass. We are circumventing all of
this portion of the stomach and the beginning portion
of the small intestine. When someone eats something,
they go and bypass that portion, and it comes
right into the small intestine. So it’s not really the sides– it’s the change in the brain
and gut communication that leads to the weight loss change. And I’ll take you through a
few cases, and then we’ll end, and I’ll entertain
some questions. So I should be finished
relatively soon. But I want to give you
guys a few patients. I thought about whether
or not to do this, but I think it’s
important for you to understand what it
looks like in real life. So this is a
54-year-old one that came into me with hypertension–
untreated hypertension– migraine headaches. She had reflux,
irritable bowel syndrome, and metabolic syndrome. She retained 20 pounds with
each of her two pregnancies, and she’s tried many
commercial programs, which lead to 20 pounds of
unsustainable weight loss with each attempt. Her most significant weight loss
was with the use of fen-phen in the 1990’s. She lost over 50 pounds over
the course of six months. She comes in to me specifically
interest of weight loss medications, plus
behavioral therapy. These graphs– you’ll see
a couple more after this. We have weight in pounds here. We have BMI or body
mass index here. And we have time here. So you can see for
this individual is that every time she would
lose that 20 pounds, she would gain it back. She’s lose the 20 pounds,
she gained it back. So of course, she comes to
see me here at a BMI of 40. And she has a significant
drop to a BMI of 31. I’m going to have you guys
yell out from the audience. What do you guys
think I did for her? Weight loss surgery. Absolutely. That’s a good guess. Anyone else want to
guess differently? This was all behavioral. Now this shocked me just
as much as it shocks you, because she’d try, right? She tried and lost,
tried and lost. And for some reason,
when she came in and did our Healthy
Habits for Life program, she was able to
achieve a BMI 31. Now you can see that she’s
stabilized here at a BMI of 30, and she’s had some
subsequent drops. And that was when I added
medication and to keep her at this different set point. You can see that she comes down. But a typical graph here–
behavior, medication, surgery– is they’ll come down,
and they rebound. I caught her when she rebounded,
I added another medicine. And so she is now here
with two different drugs, on board for the
utilization for weight loss. Let’s take you to case 2. This is a 57-year-old woman. You might be like, why am I
using all 50-year-old women. The typical patient that
presents for weight management is a Caucasian
post-menopausal woman. That’s who we will
typically see in the office. Those are the people that
are like, what is going on, I’m doing all the right
things, why am I struggling. OK, so this woman had a
history of dyslipidemia, which means high cholesterol,
breast cancer, high blood pressure, depression. You can see her diet–
pretty good, right? Brown rice, cashews,
goat cheese. She eats fish. She eats some nuts, and
spinach, salad for dinner. She exercises quite a bit. She does cardio interval
circuit three times per week. Two videos for a half hour. She does yoga at night. She sleeps for eight hours. So you’re kind of like, what
do I do differently, right? She’s doing a lot. So remember, the
same graph, right? Now it’s graph. Weight in pounds on this axis. BMI, body mass index here. She starts off at a BMI of 56. Pretty severe obesity, right? BMIs in excess of 40
are considered severe. And she has this lovely
drop to a BMI of 33. This is back– you can see– many years ago, 2003. And what do you think
drove about this change? Everybody’s whispering. Surgery. That’s a reasonable thought. This was medication. Now you might be like, wow,
that’s pretty impressive. That’s why she makes my graphs. But she has a rebound. So she comes back up
to this BMI of 40. Her BMI 40 is not
that BMI of 56, but something happens, and
it drives her back down to this BMI of 33. So that was back in
2005, end of 2005. What drove her back? I mean, she goes from 40
to 33– not a huge shift, but you know– what do you guys think? No, she dropped. She [INAUDIBLE] the drop. Menopause and drop– I can tell you, my
patients will love that. What do you guys think? You said something,
what did you say? Romantic? A romantic involvement–
that’s the first. I like that answer. That’s when she had her
Roux-en-Y gastric bypass. So her surgery didn’t
really do very much, would you guys agree with that? Very, very low
amount of efficacy. She comes in, of
course, to see me here, because that’s when patients
like to come in to me. I would have loved to have
seen her anywhere in here, but that’s just not what I get. So she comes into
the BMI of 44.5, she gets driven down
to a BMI of 28.5. And what do you guys think
I did for her at this point? Behavior? You guys are coming
on to something. I will not do anything until
the behavior is controlled. What else? I put her back on
the drug she was on. So her doctor stopped these
medications because he said, oh, well, you can’t be on
the medications long term. Remember, I told you these are
approved for long term use. When we’re using
medications to treat a chronic disease, this
chronic disease being obesity, when I withdraw those
agents, the brain gets back to where it was, and
you will regain the weight. So I do have to keep
her on these long term. So that’s important for me
to discuss with my patients. I have a 49-year-old
Hispanic woman coming in with the issue
of anxiety and depression. She has a ventricular
tachycardia, which means that
her heart beats, and she had an ablation,
which controlled that. She has mixed connection of
tissue disease, hypertension, reflux. This is her diet, this
is her exercise regimen. She noticed that her weight
gain became prominent after childbirth. She gained 10 pounds with
each of her six pregnancies. She also noticed
that she gain weight when she stopped
smoking, and when she went on Metoprolol, which
is a commonly used beta blocker, which she went on initially
for her ventricular tachycardia up here. So you can see this
is what she’s doing. She comes in to see me
here at a BMI of 52. Remember, that is
severe obesity– BMIs of greater than 40. She does have a drop
here to BMI of 26.5. So what do we think happened
for this individual? Also, notice how her brain
was defending that set point kind of in this range of
severe obesity with some ups and downs, but never down here,
or never significantly up here. So initially, I did behavioral. So I figure I’ll always
start with behavioral. She had a significant drop. And then subsequently,
I did surgery for her. And so you can see
that we’ve been able to drive her into a
completely different set point for her weight. Finally, we have a
36-year-old woman coming in with hypothyroidism,
dysthymia, meaning low mood, allergic rhinitis, chronic
back pain, migraine headaches. Has a pretty virtuous diet here. Cardio at the gym
five days per week. She’s on the
elliptical for an hour. She walks at lunchtime
for 45 minutes. She strength trains three
times per week for one hour. Her trainer sends in
the information to me on a weekly basis during the
time I was taking care for. Sleeps six to seven hours
a night of restful sleep. Comes in at a BMI of 36. You guys will remember that
class 2 or moderate obesity. She does drop here
to this BMI of 29.5. So she comes out of obesity
right into what is considered overweight category. That was with the use of drugs. But notice she comes back
within a four month period. She comes back with BMI of 36. So what happened to
this lovely individual? Why does she come back? She stopped taking
the medication. Why, as a 36-year-old
woman, did she stop taking these medications. She wanted to get pregnant. Absolutely. So for all of my women
of childbearing age that went to go to
these meds, I tell them, I have to stop these because
they’re contraindicated during use of pregnancy. And it took us two years
for her to lose the weight. Four months for her to
gain the weight back. So it shows you that if
I stop these medications, that is quite an issue. I promise in two
minutes, we’ll be done. The costs of obesity around
the world– pretty steep. And this is taken
from 2014 data, so the numbers are
probably even steeper. There’s is no good study that
supports the new numbers. You can see the United States
down here to $147 billion. Some estimates are
upwards of $350 billion here in the United States. When we look at it from its
impact on the global GDP, $2.1 trillion for smoking,
$2.1 for armed violence, war on terrorism. $2 trillion for obesity.
$1.4 trillion for alcoholism. So this is a big policy issue. So it’s the big
policy issue, and we should have some targets. Let’s look at what we’re doing
here in the United States. We have some obesity
targets, but do we have any national
obesity policy? No. State long policy, it depends. Guidance– so surgery
and drugs– yes. So why is it that we haven’t
looked at all of these things? I can tell you that
right now before Congress is the Treat and Reduce
Obesity Act, which has gone now before
Congress for the third time. I’ve been on Capitol Hill
way too often lately. And it’s really to support
the treatment of obesity for those individuals
that have obesity. It does have bipartisan
support, but it just has not risen to the
level of importance such that it ever gets passed. So what’s the summary? Obesity is a
multi-factorial disorder, and conventional weight
loss should consist of diet and exercise first,
but we may need to utilize additional
tools to treat individuals that struggle with obesity. Pharmacotherapy and/or
bariatric surgery should be considered
as an option for appropriate patients. And that weight bias is
seen as early as infancy. Maternal and paternal
anti-fat bias does significantly influence
children’s behavior, and that can have huge
implications for individuals. We know that weight stigma
has a negative impact on the health and psychological
health of patients who struggle with obesity. Obesity is a chronic
disease, which requires lifelong
treatment and management. I’d like to thank you
so much for your time. And I don’t know if I have
time to entertain questions, but I’m available to
entertain questions. So thank you so much. [APPLAUSE] I think they’re going
to bring up mics. I can hear very
well, so I’m going to repeat back the question. You have a question. – What do you know about the
[INAUDIBLE] to talking about [INAUDIBLE] – 80-20. Tell me talk about the 80-20. – Like the 20% of
factors [INAUDIBLE].. – OK. So the question was, what
do we know, basically, about the contributing factors,
and the relative importance, or how they play a role. I’m going to say that the only
thing we definitively know is that genetics
contributes to 60% to 70% of obesity in this country. And that’s been well
studied and well regulated. No one has done a really
great study looking at promoting medications. We do know sleep, quality of
diet, and all of those things play a role. But it’s hard to say. And I think that one
of the things we do is we try to generalize it. And it’s important for
me, as an individual, when I’m working with
patients, to personalize it. Because one
individual may walk in and you can see that they
respond very differently. And so I have to listen to
the nuances of what they’re telling me when I’m treating. Now in terms of that
prevention side of things, I think there’s some
universal themes with regard to prevention. You know, we can’t change
our mom and dad, right? So if your mom and
dad have obesity, the likelihood you have
obesity is relatively high. You can’t pick the parents. But we can modify
maybe the mom going in before she has a child to
modify her as much as we can. Recognizing that we
can’t fix the genetics or the epigenetic
piece of things. And so I think about that– those broad statements are more
applicable to the prevention side of things as
opposed to what I do for the individual patient
that’s sitting in front of me in that chair in the office. Hopefully, that explains
kind of some of the things. Yes? – Hi, thanks. – Hi, how are you? – Good, thank you. Two questions. – We’ll start with
one, and then I’ll do the second one, because
my brain may not remember. – OK. Behavioral methods– what
do they usually involve? Just dietary change? – OK, so she asked
about behavioral methods for weight regulation. It depends. I think of behavior
as encompassing not only the diet
quality, but also, looking at the quality
and consistency of physical activity, right? So we need at least 150
minutes of moderate intensity physical activity per week
based upon the 2008 guidelines from the US department of
Health and Human Services. I can tell you that by
the end of this year, there are new guidelines
that will likely come out, which will be much
more aggressive. Because what we’ve
seen– and I don’t know if you guys have seen
the study that came out last week– that activity
levels have actually increased dramatically over
the last 10 years amongst the US population. But the obesity
rates also increase. So it goes to show you
that physical activity is one thing that can
potentially help quell the obesity epidemic, but
it is not the end all, be all. When we’re looking at
behavior, many of our patients do struggle with
psychological contributors to weight and weight regulation. So they may need intensive
work with psychologists or psychiatrists to
delve into issues that are leading to maladaptive
behaviors like we talked about. So that may be part of that. So it depends on the individual. So that kind of
encompasses a lot of the behavioral motivational
intervening surrounding some of those issues. Now you had a second question. – The second question is
about medications that reduce the absorption of nutrients. And I’m thinking of
something different. Recently, I started taking
proton pump inhibitors. – Does that affect obesity? – No, it was just [INAUDIBLE]. But I am wondering if it would
make somebody hungrier not to have the use of
all the nutrients. – Not necessarily. She’s talking about Omeprazole. I think that’s probably
what you’re on. You’re using Omeprazole. Those are proton
pump inhibitors. We have not seen anything
that consistently demonstrates that they affect either
hunger or satiety by changing the amount of acid being
produced in the stomach. Usually, it’s decreasing it
to a level that’s more normal. So we haven’t seen that as
something that’s implicated. – Thank you for sharing
so much of the things that you’ve studied
for all these years. I’m just so impressed with
the quality of the information that you shared. I’m so lucky to be here. So my question has to
do with medication. When I studied nutrition in
college a million years ago, nobody gave me drugs, never. And then in the years
up until very recently, it was like a no no– like, why would you
take amphetamines. It’s really an artificial thing. Now from what I was
watching you say, it seems that drugs
are more adapting to some physical
problem the person has with absorption, or energy
expenditure, or whatever. So that’s a whole new thing. When people go on these, do
they have to take them for life? And how much weight you lose,
and then do they plateau out? How does that really work
over a long period of time? – Yeah, so you saw me shaking
my head, so I kind of answered. But you can stay
up, if you want, since I want to make
sure I’m answering you. Because not, you can
come back, and be like, that’s not the answer. So yes, these medications do
need to be used chronically. Much like just treating any
other chronic disease process, if I am using a blood pressure
for high blood pressure, I withdraw that
agent, what happens? The blood pressure returns. And so we have to change our
thinking surrounding obesity to recognize it’s a
chronic disease very much like high blood pressure
or type 2 diabetes. And when we withdraw
whatever that agent is, you see that graph, which
is why I specifically used that last graph to
demonstrate what happens. I see these medications as
complementary to someone that has improved
already either diet quality and physical activity. These are the
patients that come in, and they’re doing
everything right. I love what they’re
doing, and I’m like, there’s not anything
else I can do. But we do need to modify how
your brain sees its weight set point. So most of them are
actually centrally. The ones that are most
effective tend to act centrally, but they also are
associated with higher level of side effects, right? Because if they’re
acting on the brain, they may cause
cognitive slowing, they may cause word
finding difficulties, things of that sort,
which we don’t want. So when I’m using
these medications, I’m very gingerly in
how I increase them, and I only increase
them when necessary. Your second question was like,
OK, so what do we expect. A good response to
medication will be 5% to 10% of total body weight loss
over the course of treatment. Now they will have–
and I said this with every single
patient– they have a drop. They’ll come down
to what’s considered the [INAUDIBLE] weight, and
they will rebound and stabilize at a level that’s slightly
above where they got to their [INAUDIBLE]. At that time, I
can potentially try to introduce additional
agents to shift them down even further. But recognize that even
once they shift them down, there’s likely going
to be a rebound. If the body’s physiologic
response to either behavior, to medications, or to surgery. So they will come down, and
they’ll rebound to a level. Not back to where
they were, but they’ll rebound to a level that is not
the number that they remember when they bought
those new Prada pants. Because they got it at the
lowest weight set point. Because I have a
patient that wants to get into these Prada pants,
so of course that comes up. So yes, you had
another question. – So once they get down
to that weight loss, it’s not like they’ll
stay on that medication, like taking an ultra
vitamin dose or something. Like oh, we we’ve
stopped the anemia now, so you just stay at this
the rest of your life. You’re always tugging. – You’re always looking,
I’m always tweaking, I may be adding. I know, I know, I’m sorry. It’s the reality. And that’s what I tell patients
before we commit to it. Because if the medicine
works, then I’m going to keep you on it. If it doesn’t work,
then obviously, we’re not going
to keep you on it. We’re going to keep trying. Now what I did not
talk about, and where I think the new horizon– and no one is really doing
this, and maybe somebody will fund me to start
thinking about this– is that you obviously saw
that different people respond to different therapies. Something about
the genetic makeup of that woman that allowed
her to lose more weight than I would have anticipated from
any surgery from just two medicines– unbelievable. I told you an average 5% to
10% total body weight loss. She lost 35% of her total body
weight loss on two medicines. I wouldn’t have predicted that,
but that’s how she responded. Now I can tell you I’m
treating her sister now, and her sister is
responding quite similarly. So something about them allows
them to respond in that way, so much so that I would
recommend that therapy to that family, first
line, even though we’re dealing with severe obesity. Does that make sense? – Yeah. I don’t want to take up– – Yeah, absolutely. – What a great talk. Thank you so much great. I really appreciate the
multifactorial look, all encompassing
look at this problem. In the spirit of
I have a hammer, everything is a nail,
one of the things I look at and research is
the impact of early childhood trauma on diabetes,
and then on obesity. And then we try to unpack that. It looks like a lot of it
travels through food addiction, which you also had up there,
and particularly, early sexual abuse. – Absolutely. – Which is really prevalent. So I’m wondering about how
you see that in the clinic. Do you screen for it? Do you treat it? What works, what doesn’t? Do the medicines work? What does that do
to at this point? – Very good question. Actually, so what you didn’t say
when you did my introduction– because my CV is 59
pages– is that I worked for a rape crisis
center for two years before medical school. And I could never
figure out what that work was going to
mean for what I do, but now in the work that I do, I
do see that about a third of the women that
I treat have been a victim of sexual violence– or survivor, I
don’t like victim. Victims sounds bad. But survivor of sexual violence. Although if you look
in the literature, there’s a paucity of literature
surrounding sexual violence and obesity, just in general. What I find is my
psychologists do a bit more of that work in terms
of working with them, using motivational interviewing,
but they will also key me in into which agents or
medications might not be effective medications. Ones that have a higher
likelihood of promoting anxiety, they’ll say, I would
warn against the use of, which would likely
include Phentramine, might include
Bupropion, it depends. And they are very in tune
to what I’m thinking. So they’re probably
thinking, oh, Dr. Stanford wants to use medicines,
but let me tell her, I’m really concerned
about these things. For many of our patients
that have struggled with early childhood
trauma or sexual violence, they are in lifelong therapy,
either with our psychologists at the weight center or
their own therapists. They may have another
psychiatric team, and maybe most of
their care is really within the psychological realm. You know, it looks
different for every patient. And things that I would be
sometimes reticent to consider that we may consider
after finding that certain agents,
let’s say for medications, are ineffective,
and I’m like, let me try a low dose of Phentramine
might work without causing any negative
consequences, but I have to be watching that
patient on a weekly basis to make sure things are going
OK for those individuals. I think there’s so much
to be learned, Gina, in this realm of looking
at trauma, early childhood trauma, sexual violence, and
the implication it plays. Because it definitely has
huge implications for weight regulation in later life. – Thank you. I think I may also
be the last question, so I can take the opportunity
to thank you yet again. Oh wait, there’s
another question. Can I pass you the mic? – Yes. – You were excited. Why not? Why not? I’m here. Might as well. – Hi. It was a really terrific job. Thank you so much. So you had a side way back
where you were talking about changes in birth weight. – Where we were talking mothers
before and after surgery. – Pre and post
weight loss surgery. And the difference in
the baby’s birth weight. And I was wondering
whether there was any work done to look
at whether there was a link to inflammation, or whether
if it’s just attributed to the double C chromosome. – No, we know it’s inflammation. Remember, the second slide, we
looked at inflammatory markers within those individuals
that were after surgery, and then we saw
the lower levels. So inflammation
played a large role. Aisle 1, aisle 6, CRP-1. All of those things play a role. Those are inflammatory
markers, and we saw a significant decrease
in the inflammatory markers for both the mom, and the
child born after surgery. So I do think that
plays a large role. Yes? – So I had a question. You hinted at issues with
post-menopausal women. And I was wondering if hormone
replacement is ever a component of the overall package. – No. So hormone replacement
has never been shown to drive weight loss down. But I can explain– I didn’t talk about
post-menopausal women specifically, but I
guess people might want to know what is it that
causes the shift in weight. What happens is at
menopause, we see a change in distribution
of adipose tissue from being a gynoid
distribution, which means it’s in the hip,
buttock, and thigh region, to a more android distribution,
which is the central region. Which means that we
begin to assimilate more of the male body phenotype. When that shift occurs, we
start to deposit weight in areas that we are not typically
used to depositing them, but we also see this
gradual incline in weight, because estrogen helped
control or regulate some of these factors prior
to the onset of menopause. So hormone replacement therapy– I work closely with Joanne
Manson at the Brigham, who has done a lot of the
work with the Women’s Health Initiative, and all
of her work has never demonstrated that HRT,
which was a lot of her work back in the ’80s, early ’90s,
really led to any weight drops. What I do find that
works pretty effectively for these individuals
are weight loss pharmacotherapy for
those individuals that have mild or moderate obesity. And then for those that have
severe weight loss surgery, I would entertain if
they’re in those ranges. Often, they come in with
these very virtuous diets. The dietitian is like,
I can’t change anything. Psychologist is like, everything
looks good on their part. And so then we have to
start to begin to think of other treatment strategies. And I think about
using the right tool for the size of the problem. So people are like, really,
weight loss surgery? Isn’t that a method
of last resort? That’s kind of a pet
peeve when I hear that. Because we think about– I kind of use an analogy
of snow in Boston. We get 14 inches in eight hours. Do I go to use a
teaspoon or a tablespoon to scoop up the snow? Maybe it would work, but it’s
going to take me a long time. I’m going to use
the appropriate tool for the size of the problem. So I’m going to probably
use a big bulldozer to bulldoze the
snow out of the way so that the traffic
can continue. And I use the appropriate tool
for the size of the problem. Some people need bigger tools. Some people need smaller tools. Some people, hey,
I lost 80 pounds from just removing
sugar from my diet. Great for them. Excellent. But just because
it worked for you, doesn’t mean it’s going to
work for the next person. And so I have to tune into
what works for that individual, and use the right tool
for that individual. And recognize that
that’s malleable, meaning what tool
may have worked today may not always
work continuously, and I get to keep adding. Much like– I can’t remember
the individual that said, oh we have to keep trying– where’s that lovely– you. You’re like, we have
to keep doing things? Yes, you have to
sometimes keep trying. It’s nice when I can
just do one thing, and then I solve their
problem, which means that I didn’t really solve it. I’m just treating the problem. But often, it requires
a lot of different steps that I’m having to take. And working through
all of the motion that goes into this person
struggling with weight. So yeah. She’s one more. I can hear you, you can talk. – [INAUDIBLE] – Go on. OK. – OK, I’d like to suggest
that another indicator– cause– might be
growing up feeling silenced for political reasons. And therefore, eating. And even after one works on
its ramifications in therapy, I don’t think it’s necessarily
easy to then just kind of lose the weight off, right? I mean, after dealing
with emotional issues, if one has been obese
all their life– – Has obesity. You don’t never classify it. You have the disease. You’re not classified by it. It does not govern you. – Yeah. So how does that work? – I think the question is
surrounding– and just, you can tell me if I’m right– is if you’ve had a life– because I’m going
to kind of group it into people that have
had lifelong struggles. I have people that
are Syrian refugees, for example, if they’ve
dealt with a big struggle of that sort, how do you
deal with emotional issues. I think it’s a lifelong process. It’s not something I
anticipate that I will get over in three sessions with you. And that’s why most of these
people do remain in therapy. People that came to our center
when it first opened in 1999, who are still seeing
our psychologists today, means that we’re not
fixing it in one session. And it may never be fixed. Maybe just we’ve improved
upon these issues. So I think it requires lifelong
treatments with regards to the psychological issues. And for some people, maybe
lesser therapy than others. And we just have to tailor
it to fit the individual. – [iNAUDIBLE]. – No, it doesn’t become easier. And even after patients lose
tremendous amounts of weight, they may still
have significantly disordered thinking
as it relates to how they’re
perceived, and how they navigate their daily life. Yes. So I think that I
am departing now. But it’s been a delight. So yes. Well, thank you guys. Thanks for coming. I really appreciate it.

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