"Obesity and its Management: What You Need to Know as a Sleep Medicine Physician/ Provider" Fatima Cody Stanford, MD, MPH, MPA (9.23.2020)

September 30, 2020

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00:0018 and a half us considered to be
00:03within normal weight status when
00:05their BMI is between 18 1/2 and 24.9,
00:08we get into a person having overweight
00:10when their BMI is between 25 and 29.9,
00:13and then we get into those
00:15three classes of obesity, mild,
00:17moderate or severe class,
00:19one Class 2 and Class 3A BMI of
00:2130 to 34.9 being mild obesity,
00:24BMI of 35 to 39.9 being moderate
00:26obesity and those that have severe
00:28remember not morbid severe obesity.
00:30A BMI of greater than or equal to 40.
00:33Now this is when we're going to really
00:35get down and dirty and looking at
00:37obesity because unfortunately in medical
00:39school and residency and fellowship
00:40we were not taught very much about obesity.
00:43But what we were taught was that it was just
00:46a simple simple energy balance equation.
00:47It's all about your calories you take
00:49in your food and beverage intake,
00:51and then the calories you put
00:53out your bodily functions,
00:54your physical activity and if we could just
00:57get this all balanced just the right way.
00:59We all should be just exactly
01:01the size that we want to be.
01:04But what we do know is that
01:05this is indeed a fallacy.
01:07This is false,
01:08and if we continue to support this notion of,
01:10this is how energy balance works.
01:12Will continue to fill.
01:13Our patients will continue to fill to make
01:15any progress with this disease process.
01:17So we'll learn about this disease process
01:19and want to tell you where to start it.
01:22Very elementary level.
01:22We're going to work our way up
01:24to very PhD level in terms of
01:26thinking about obesity disease.
01:28But don't worry,
01:28I'll bring it back down to 8th
01:30grade before looking at what we
01:32do individually for our patients.
01:34So here we are in Kindergarten
01:36School is in session,
01:37so on this left side of the screen
01:39you can see this slice of pepperoni
01:41pizza OK and on the right side of
01:44the screen we can see this much
01:46larger dental plate of quinoa.
01:47Chickpeas roasted red Peppers,
01:48carrots,
01:49tabouli,
01:49accelerate cetera and notice that
01:50the title of the slide says all
01:52calories aren't created equal.
01:54So I can tell you that every new
01:56patient visit I start off with this
01:58slide set and I asked them we have
02:00this slice of pepperoni pizza on
02:02the left side of the screen on the
02:04order of about 350 kilocalories.
02:06And on the right side of the screen,
02:08what we talked about a much, you know,
02:10maybe healthier set of foods,
02:11about 700 calories.
02:12I asked my patients which one
02:14would you eat and most people will
02:16correctly pick the right side.
02:17And then I say,
02:18well,
02:18what about the fact that I told
02:20you it was about double the amount
02:22of calories in every level?
02:23This this one is healthier and I
02:25asked him to explain why I think
02:27we can all agree that this is a
02:29healthier fear and so I can tell you
02:31that with none of my patients
02:32do I ever ask them about the
02:34number of calories there eating.
02:36What matters is whether they are processed.
02:37Or not, there was a lovely study that
02:40was run by Kevin Hall out of the NIH,
02:43where he looked at Adlib thieves and
02:45an adult humans and determined what
02:47happened to ones weight status with
02:49the use of idle process consumption
02:51of food versus a more virtuous
02:53fair like you see on the right
02:55side of the screen and what he saw
02:57overtime was that even though Clore
02:59consumption was about the same,
03:01the weight tended to go down and individuals
03:04that ate this fear compared to this,
03:06even though the chloric value
03:08was almost identical.
03:09So that's important for us to recognize.
03:12So we do know that obesity is a
03:15multifactorial disorder where genetics,
03:16environment,
03:17development and behavior all play
03:19a role in a person's likelihood of
03:22having this disease of obesity.
03:24Now this is when we get into the
03:26nitty gritty of really looking at
03:28the complexity of this disease.
03:30Let's look at how the body
03:32actually regulates food intake,
03:33and So what you're looking at,
03:35I'm going to look at be if we kind of
03:37took us a cross section of the brain
03:39and get to the central portion here,
03:42we will get to the hypothalamus right
03:44in the hypothalamus is getting signals
03:46from different parts of our body,
03:47which is governing our intake of
03:49food and storage of food is getting
03:51left in from our adipose tissue.
03:53Peptide YY from our large intestine.
03:55Cholecyst acain in from our
03:56small intestine insulin,
03:57of course,
03:58from the pancreas grilling from the stomach.
04:00Sending signals back via the
04:02spinous smile and vagus nerve to
04:04tell us not only how much to eat,
04:06but to tell us how much to store.
04:08Now let's look at these substances
04:11in a little more detail.
04:13So that we can see what the substances are,
04:15where they are being produced,
04:17and what their relevant effect
04:18on feeding are.
04:19So let's look at grilling so
04:21we can see Grill in.
04:22Here is being produced in the stomach
04:24in the fundus region of the stomach and
04:26also in the Inter and endocrine cells.
04:28It's also being produced in the
04:30neurons in the hypothalamus.
04:31You can see that it's relevant effect on
04:33feeding is that it is all rexha genic,
04:36which means it stimulates your appetite.
04:38Ananda mines,
04:38which are produced in the small intestine,
04:41also have a relevant effect on
04:43feeding for it to be over exigent
04:45to stimulate our appetite.
04:46Insulin, of course,
04:48we're talking bout endogenous insulin
04:50here producing the beta cells in the
04:52islets of languor hands in the pancreas.
04:54It's relevant effect on feeding
04:55is that it is anorexigenic,
04:57which means it promotes satiety.
04:59And of course,
05:00this responsible for both glycogen
05:01and lipid storage left in,
05:03which in the short term is produced
05:05in the stomach in the long term,
05:08and.
05:08The Alpha sights or fat
05:10cells is relevant effect
05:11on feeding is that it is anorexigenic,
05:13which means that it promotes
05:15satiety CCK or Cholecyst Acain and
05:17produced in the small intestine
05:18is responsible for early satiety.
05:20This is when you get full very
05:22quickly is also of course,
05:24responsible for the release of digestive
05:26enzymes from the actor can pancreas
05:28bile from the Gallbladder and then
05:30ask it from the bridal cells in the
05:32stomach and then finally peptide YY or
05:35peptide tyrosine tyrosine produced in
05:36the distal portion of the small intestine.
05:39In the ileum and then also in the colon.
05:41It's also relevant effect on
05:43feeding is that it is anorexigenic,
05:45which means that it promotes the tidy.
05:47Now we're going to focus on
05:49leptin in the subsequent slide,
05:50and we're going to look at the
05:52pathways by which left in controls
05:54food intake in food storage.
05:56What you can see here or there are two
05:58primary pathways in the hypothalamus,
06:00by which one may signal.
06:02We're going to focus on this
06:04right pathway here first.
06:05So left in,
06:06which is signaling from the
06:08adipocytes or fat cells.
06:09Binds to Receptor and stimulates
06:11what's called the Palm C or
06:13the proopiomelanocortin neuron.
06:15Here in the arcuate nucleus
06:18of the hypothalamus.
06:19When this neuron fires,
06:21Alpha Milana site stimulating hormones,
06:23then bind toward called Milan.
06:25According for receptors and you
06:27can see that this leads to the
06:30production of BDNF which is brain
06:33derived neurotrophic factor.
06:35This releases an anorexigenic
06:37signal and what happens to patients
06:40that travel down this pathway?
06:42As they have a lower intake of food
06:44and they have a lower intake of
06:47storage of the food that they do eat,
06:49so that's for patients that tend to
06:52be lean and we're very happy for them
06:54for travelling down this pathway,
06:56my patients exclusively have overweight
06:58and obesity and travel down an
07:00alternative pathway were left in
07:02bind to an alternative receptor and
07:04stimulates a different neuron in the brain.
07:06This is called agouti related peptide neuron.
07:08This is here in the paraventricular
07:10nucleus of the hypothalamus.
07:12You can see that when the signals
07:14these agouti related peptides bind
07:16instead to the plan according receptors
07:18and inhibit the formation of BDNF
07:20or brain derived neurotrophic factor
07:22and what happens is these patients
07:24receive and or exogenic signal which
07:26not only increases food intake,
07:28it also increases storage so it's
07:30actually something wrong with the
07:32signaling of how the brain sees and
07:35that's what dictates the difference in
07:37how you could eat one meal and someone
07:39else can eat the same Milan they store.
07:42A lot more or less than you.
07:46Alright, so that may have been
07:48a little bit complicated,
07:50but you know we're all pretty savvy.
07:52So what we do know is that bring it
07:54back down inside the brain is getting
07:57signals about our diet quality?
07:59OK, so we want our diet to look more
08:02of like what you see on the screen.
08:04Lean protein, whole grains,
08:06fruits and vegetables as
08:07our predominant sources.
08:08I'm a strong advocate in
08:10duration of diet quality,
08:11not putting you on a fad diet that will
08:14last kind of with the blink of an eye.
08:17We want sustainability.
08:18Over the course of time,
08:20physical activity does play
08:21a role in weight regulation,
08:23but what we are often selling to patients
08:25is often the incorrect information.
08:27So we tell people to exercise and exercise
08:30is by far one of my favorite pastimes.
08:33But were telling the wrong thing in
08:35terms of what we expect with regards
08:38to weight regulation from exercise.
08:40One average exercise leads to weight
08:42stability, not significant weight loss.
08:44Now that's not to imply that someone
08:46or some people can't lose weight.
08:48From exercise itself,
08:49but on average for many of us,
08:51it helps us to promote weight stability.
08:54So we want to sell that as the
08:56accurate message of what physical
08:58activity does as it relates to wait.
09:00Of course,
09:00there's a lot of other benefits
09:02with physical activity,
09:03but we're talking about weight,
09:05particularly today.
09:06Now sleep.
09:06This is what you guys brought me here
09:09to talk about or think about is sleep
09:11quality and duration definitely plays
09:13a large role in how the body regulates.
09:15Wait there complete half ways that
09:17talk about how the suprachiasmatic
09:18nucleus interferes with hypothalamic
09:20control of feeding.
09:21That really is suggests that the quality
09:23of 1 sleep can be drastically affected
09:26an if the quality of sleep is affected.
09:29It affects the feeding behaviors,
09:31medications that we as doctors
09:33prescribe do cause weight gain.
09:35It is estimated that approximately 20%
09:37of the issues that we have in this
09:40country related to obesity are indeed
09:42do two things that we do is doctors.
09:45So medications that include
09:47everything from Lithium Deppe Coat,
09:48Tegretol, Celexa, Cymbalta,
09:50Effexor, Paxil, Prozac, Ambient,
09:51Transitive, Monistic Gabapentin,
09:52Library clip, cyclamen pride.
09:54Long term insulin.
09:55Long term.
09:55Prednisone beta blockers I VF medications.
09:58Just name a few antihistamines.
09:59These are medications that can cause
10:02considerable weight gain in our patients,
10:04so we want to be mindful of the
10:06contract contribution that we're
10:08making to our patients and their
10:10weight and weight regulation issues.
10:14This looks like another sweet picture
10:16and so you guys are sleep physicians.
10:18And so I wanted to make sure to indulge you,
10:21but this is a different sleeping
10:22or this is looking at a gentleman
10:24that sleeping during the daytime so
10:26circadian rhythm disturbances also
10:27can affect how the body regulates.
10:29Wait for some of us, we may be nocturnist
10:32and so we may have to work night shifts.
10:35Many nurses also.
10:35I'm in other professions.
10:37Unfortunately the brain doesn't like
10:38to really be awake in the middle.
10:40Then I prefer to be a wake when
10:42it's bright outside like it is now
10:44both in Connecticut here in Boston.
10:46I'm gonna sleep when it's dark outside,
10:48but when we turn the nail on his head,
10:51what we do know is the body wants to
10:53store more adipose and store more
10:55fat and so sometimes it's as simple
10:57as changing someone's work schedule
10:58that may lead to a change in weight
11:01status and then finally thermogenesis,
11:02which is how much the body burns
11:04at rest and with activity.
11:05A lot of this is genetically determined,
11:07but this does play a large role
11:09in how the central nervous system
11:11regulates weight and weight control.
11:13Now,
11:13I don't anticipate that you guys will
11:15internalize memorize this particular slide,
11:17but this is one of my favorite indeed,
11:20because it shows the complexity of
11:21obesity and all of the contributors
11:23that are outside of just calories
11:25in and calories out,
11:26which we disproved earlier.
11:27And So what you can see here are that
11:30there are things that are inside of a
11:33person that may lead to weight gain.
11:35Things that are outside of a person
11:37that may lead to weight gain.
11:38You can see here this top row.
11:41These things increase one's intake
11:42and then here in this bottom row.
11:44These are things that decrease
11:46expenditure and then here in the
11:47middle we have things that affect
11:49either intake or expenditure or
11:50we haven't yet figured it out.
11:52You can see,
11:53maybe unknown if you're looking
11:54at your screen very well now.
11:56For those of you,
11:57hopefully that aren't colorblind,
11:58there are different colors on the
11:59screen that actually means something in
12:01these are contributors or influencers
12:02to our weight and weight status.
12:04We're going to look at this in a little
12:06bit more detail in the next slide.
12:11So the contributors and influencers
12:12to obesity are as follows their
12:14biological or medical reasons.
12:16Why someone may struggle with their weight
12:18food and beverage behavior and environment,
12:20maternal and developmental,
12:21social, psychological,
12:21economic and environmental
12:22pressures on physical activity.
12:24We're going to pull out a few of these
12:26things from these categories just
12:28to get a sense of what's going on.
12:31And we're looking now at contribute
12:32obesity that happened within an individual.
12:34I couldn't pull out every single thing
12:37we'd be here for the rest of today,
12:39but let's just look at a few of these.
12:42Things that may increase intake are hyper
12:44reactivity to environmental food cues,
12:46so you pass by a pizza shop an
12:48all of a sudden you want pizza,
12:51and I passed by it and I'm like I don't
12:53really want pizza delayed satiety thing.
12:56You know,
12:56people take along time filling full
12:58and then disordered eating things that
13:00may decrease expenditure or issues
13:01like changes in the gut microbiota.
13:03What we do know is that the gut
13:05microbiota of those that are laying
13:07versus those that have obesity differ
13:09quite drastically in terms of the
13:11type of bacteria president once got.
13:13So much so that some of the studies
13:16that we're conducting here in MGH
13:18are really to ascertain exactly what
13:20this happened and we kind of deserve
13:22this from doing fecal transplants
13:24for patients that had refractory C
13:26diff when patients were receiving a
13:28fecal transplant from Uline Donor,
13:30they distorted to lose weight when
13:32they're receiving a fecal transplant
13:33from someone that had obesity,
13:35they started to gain weight and so
13:37one of our lead investigators on
13:39this particular topic here in GH
13:41is a woman by the name of Lane you
13:44who's studying this in more detail.
13:46To really figure out how we might be
13:49able to use this as Therapeutics when we
13:51look at the gut microbiota thermal Genesis,
13:54we talked about a little bit earlier,
13:56and then if someone has
13:58physical disabilities,
13:58obviously that decreases expenditure.
14:00Things that increase intake
14:01and decrease expenditure are
14:02genetic and epigenetic factors.
14:04And here I'd like to pause and say it's
14:06important for us to recognize that
14:08weight is more heritable than height,
14:11so I'll say that once again,
14:12wait is more heritable than height,
14:14so we know that the genetic contribution.
14:17From our parents.
14:18In terms of our weight status
14:20determines our weight and such that
14:21if patients have severe obesity
14:23or parents have severe obesity,
14:24but likelihood that their offspring
14:26will indeed have severe obesity is on
14:29the order of 50 to 85% likelihood,
14:30even if we're virtuous and do all
14:33the right things once they get here
14:35breast feed for the first year of life,
14:37don't feed processed foods, etc.
14:39So it's important for us to
14:40recognize that age related changes.
14:42Age related changes are
14:43particularly important for women.
14:44There are three primary times
14:46doing a woman's life, by which.
14:48Should significant hormonal changes
14:49can happen that lead to weight changes,
14:52I'm Ethel instead of menses.
14:53Number 1 #2. If they decide to have
14:56children or get pregnant and then at
14:58the third stage of Life which is in
15:01the period post menopausal phase.
15:03When we see that decline in
15:05estrogen and that change from
15:06a gynoid distribution in fact,
15:08which is in the hip,
15:10buttock, and thigh region,
15:11typically in the subcu tissue
15:13to more of a central adipose
15:15tissue that happens with that
15:16down regulation of estrogen.
15:18Mood disturbances so
15:19depression anxiety for example.
15:21Julie to increase intake
15:24and decrease expenditure.
15:26Things that happen outside of a
15:27person that may lead to obesity or
15:30things that may increase intake are
15:32environmental toxins, pervasive food,
15:33advertising in large portion sizes.
15:35Those are things we've always heard,
15:37things that may decrease expenditure.
15:39The built environment, sedentary time,
15:40and labor saving devices,
15:42and then things that may increase
15:43intake and decrease expenditure.
15:45Things like stress with that chronic stress.
15:47Racism, for example.
15:48Weight cycling.
15:49Meaning if you go on a diet and
15:52then offer diet, wanted it off.
15:54The diet typically leads to the
15:56weight set point for an individual.
15:58Doing to climb.
15:59And as we mentioned earlier,
16:01maternal and paternal obesity.
16:03Now since we ended with maternal
16:05and paternal obesity,
16:06this is by design that I would begin
16:09to talk about fetal programming,
16:11and this is the concept is that
16:13of a mother goes into pregnancy
16:15with overweight and obesity.
16:17She is in a state where she has
16:19a higher level of inflammation
16:21so you can see that they have
16:24increased inflammation,
16:25increase insulin resistance,
16:26increasing like policies in VLDL Secretion,
16:29which leads to an increase
16:30in inflammatory markers,
16:31particular Interleukin one interleukin 6.
16:33Tina Falfa MCP.
16:34One what that does is then affects the
16:38fetus and the fetus is exposed to lipids.
16:41It reprograms their metabolic gene
16:43targets leading to fetal inflammation.
16:45An increase in hepatic lipids also issues
16:47in the skeletal muscle adipose tissue.
16:50The brain in the pancreas and this leads
16:53to childhood risk of disease so non
16:56alcoholic fatty liver disease resistance.
16:58Obesity Hyperphagia and Type 2 diabetes.
17:02So what has been done to study this?
17:05This is one of my favorite studies
17:07to show and demonstrate is the
17:09influence of a moms weight status
17:11in this generation on her offspring.
17:14In this particular study,
17:16they compared two sets of individuals,
17:18children's born to moms before she
17:20had metabolic and bariatric surgery
17:22in the form of a ruin Y gastric bypass.
17:25An after metabolic and beer at Ricks surgery.
17:28So BM S is before metabolic surgery.
17:31AMS after metabolic surgery.
17:32So we're comparing though.
17:34The child that was born before
17:35to the child that was born after,
17:37and so I want you to look at kind
17:39of a side by side profile of these
17:41children born before and after mom
17:43had bariatric surgery,
17:44same mom and Dad.
17:45'cause That's a question that comes up.
17:47So I want to make sure I'm clear about that.
17:50What you can see here appearing
17:51those children that were
17:53older compared to those were younger is
17:54that there an I want to look at these
17:57lovely P values that we're seeing over
17:58here that the wait was significantly less
18:00than those children born after surgery.
18:02There was a significant difference in
18:04the likelihood of Macrosomia Obviously
18:05there was a different age because this
18:07these kids were born after surgery,
18:09but BMI percentile was lower.
18:11The weights, lower body fat,
18:13slower and some levels are lower glucose.
18:15Lowering that child boring after surgery.
18:18So what we can see here when we
18:20look at this in kind of detail
18:23in that child born after surgery,
18:25there's a three fold decrease in
18:27the prevalence of severe obesity
18:29in those children.
18:30There's improved influence,
18:31and Acitivity improved lipid profile and
18:33an improvement in our inflammatory markers.
18:35So just with making that intervention
18:37in mom and often after surgery,
18:40mom still have obesity.
18:41But severity has improved,
18:42which means that likely the level of
18:45inflation is improved that this leads
18:48to an improved status for that child.
18:50Now let's look at the guidelines
18:52that we are currently following
18:53here in the United States,
18:55the most commonly used guidelines,
18:57or those from the American Heart Association,
18:59American College of Cardiology.
19:00In the obesity society,
19:01this was a joint venture
19:03between the three groups.
19:04It obviously starts with
19:05the patient encounter.
19:06We measure height, weight,
19:07and BMI.
19:08We determined that weight category is assess
19:10and treat cardiovascular disease risk factors
19:12and assess weight and lifestyle histories.
19:14Obviously these are things that
19:16we're all familiar with,
19:17but just to recap,
19:18we have our H&P that's done.
19:20We do our clinical laboratory
19:22assessments looking at blood pressure,
19:23fasting blood glucose,
19:24a lot of people would do
19:26a fasting lipid panel.
19:27We want to pay attention really,
19:29and I want to kind of push.
19:31Start here with the waist circumference,
19:33because it's not just adipose or fat,
19:35it's weird distributed.
19:36That really leads to higher
19:37likelihood of metabolic disease.
19:38So I do measurement with just a simple
19:41tape measure at umbilicus at every visit,
19:43to determine what waist circumference is.
19:45And you can see our target is less
19:47than 35 inches in women and less
19:49than 40 inches at men at them until,
19:51like his most men don't wear
19:53their pants there,
19:54they'll come in and they'll tell me why.
19:56I'm a 40 inch waist,
19:58but they are wearing their pants
19:59well below where we would measure
20:01for assessing Central Atapa City.
20:03We want to look at intensive management
20:05of cardiovascular disease risk factors,
20:06particularly hypertension,
20:07dyslipidemia, prediabetes,
20:07and diabetes.
20:08Obstructive sleep apnea,
20:09which is very germane to the work
20:11that you do and Sleep Medicine.
20:16We want to assess weight and lifestyle
20:18history when I ask questions about
20:20the history of weight gain and loss
20:23overtime that really has to do with
20:25that weight cycling question that we
20:27talked about a little bit earlier.
20:29We want to look at details of previous
20:31weight loss attempts, dietary habits,
20:33looking at quality over hyper,
20:35focus on any caloric value,
20:36physical activity,
20:37a family history of obesity is
20:39extremely important and any other
20:41medical additions or medications
20:42that actually may affect weight.
20:44As we talked about.
20:45And then we want to test with patients
20:47will be the need to lose weight advised,
20:50avoid weight gain and other risk factors
20:52assess their readiness to make change
20:54and identify barriers to success.
20:56Each person will have their
20:57own set of barriers.
20:58We want to determine weight loss and
21:00health goals and intervention strategies.
21:02I don't typically let my patients
21:04give me like I want to be.
21:06Ex.
21:06Wait, I mean,
21:07I guess that can let them tell me that,
21:09but I'd like to shy away from giving
21:12them any key number and the reason
21:14why that is is that sets up really.
21:16Tough expectations.
21:17I have no idea how patients are going
21:19to respond to whatever modality
21:21or therapy that I use and so we
21:23wanted to see what the body does.
21:25Always tell my patients their
21:26body is the answer key and we
21:28will use these different tools to
21:30find out how their body responds.
21:32We want to look at comprehensive
21:33lifestyle therapies alone,
21:34so we want to start there and in
21:36conjunction with adjunctive therapies.
21:38Now I started at the beginning
21:39of the lecture.
21:40For those of you that are coming in
21:43talking about the language that we
21:44use for patients that have obesity
21:46even need to not call patients.
21:48Obese,
21:48but rather they have the disease of
21:51obesity and there's a reason why I say that.
21:54It's not just for to make me feel
21:56warm and fuzzy inside is because
21:58actually weight stigma does lead
22:00to poor outcomes for our patients.
22:02So when patients experience weight
22:04stigma that leads to increased stress,
22:06that increased stress actually affects
22:08eating and physical activity behaviors
22:10where we see things such as binge eating,
22:12increased caloric consumption,
22:13maladaptive weight control,
22:14disordered eating in a lower motivation
22:16for exercise and less physical activity.
22:18That stress actually leads
22:19to physiological reactivity,
22:20and I think that's something that we're not.
22:23We're not maybe often clear about.
22:25So when people experience weight
22:26stigma that leads to stress at least
22:29a physiological reactivity which is
22:30demonstrated by increased levels of cortisol,
22:32CR, P,
22:33A1C,
22:33elevated blood pressure just to name a few.
22:36With regards to health care services
22:38when they experience weight stigma,
22:40there's poor treatment adherence.
22:42They don't trust us as health providers,
22:44they avoid it.
22:45Follow up care,
22:47there's a delay and preventative
22:48health screenings and poor
22:50communication between their physician
22:52an between us and them is patients.
22:54This, then in turn leads to weight gain,
22:57which then causes psychological
22:58health in distress,
22:59where we see depression,
23:01anxiety, low self esteem,
23:02poor body image, substance abuse,
23:04an A high level of suicidality.
23:07Finally, we see physiologic health in
23:08distress will receive poor glycemic control,
23:10less effective control of chronic
23:12disease with regards to self management,
23:14more advanced in poorly advance
23:16or poorly advanced advanced,
23:17I guess chronic disease and lower
23:19health related quality of life.
23:21So this stigma what we say to patients,
23:23how we're talking about them,
23:25how we're writing about them,
23:26does indeed lead to worse outcomes.
23:28So I really want us to be mindful of that.
23:32When we're looking at how
23:34we select obesity treatment,
23:35this is kind of just a grid to give
23:37you kind of how we're doing it.
23:40If we're using Villamizar primary criteria,
23:41it's important to note that many
23:43people are getting away from this,
23:45including Canada who just released their
23:47new guidelines for the treatment of obesity,
23:49in which they delete BMI categories
23:50really and just look at metabolic risk,
23:52which they're using.
23:53Things such as central adiposity
23:55and things to reflect.
23:56You can see here that across all levels,
23:58BMI that diet, physical activity,
24:00and behavioral therapy can be utilized,
24:02so that should be the.
24:03Cornerstone of our therapies.
24:04We can begin to introduce pharmacol
24:07therapy for the treatment of
24:08obesity when we get here to a BMI
24:11of 27 with comorbid conditions,
24:12which include things like obstructive
24:14sleep apnea, hypertension,
24:15and Type 2 diabetes.
24:16And then we're looking at metabolic
24:18and bariatric surgery.
24:19Really looking at those typically at
24:21the higher end of the weight spectrum,
24:23American Society of metabolic and
24:25bariatric surgery with encourage
24:26also mild obesity.
24:27But the typical guidelines are the
24:29test answer would be persons that
24:31have moderate obesity with comorbid
24:32conditions as previously noted.
24:34And those that have severe obesity.
24:36Now,
24:36do you want to put two stars by
24:38both pharmacol therapy and metabolic
24:40convergex surgery and indicate to
24:43you that only 2% of patients that
24:45meet criteria for the utilization
24:46of pharmacotherapy compared
24:47pharmacotherapy for the treatment of
24:49obesity actually receive such therapy?
24:51Here in the United States,
24:53only 2% that means we are failing at
24:55least 98% of our patients with regards
24:58to metabolic and Barack surgery.
24:59Only 1% of patients that meet criteria
25:02for metabolic emerging surgery receive it,
25:04so the numbers are actually relatively low.
25:06A lot of that I think has to do with
25:08our education and our willingness
25:10to acknowledge obesity for the
25:12disease that it actually is.
25:14I wanted to take this time to
25:16spend some time talking about
25:17the weight promoting medications.
25:19Sometimes people are reticent to
25:20consider anti obesity pharmacotherapy.
25:22The actual medications to treat obesity,
25:23but if you're not quite willing
25:25to move there,
25:26what I would say is maybe if need
25:28be thoughtful about medications that
25:30are known to cause weight gain so
25:33you can see here some of the just
25:35these are just a few representative
25:37medications antipsychotics,
25:37the answer depressants.
25:38All of our sleep agents,
25:40basically neuropathic agents,
25:41beta blockers, spirits,
25:42insulin, hypoglycemic agents,
25:43when you can find a more weight
25:45neutral drug within a class.
25:47That's the goal that you would
25:49try to utilize. So, for example,
25:51if you're looking at beta blockers,
25:52car vadal all by far is the most
25:55weight neutral of the beta blockers.
25:57All of the beta blockers
25:59will lead to weight change,
26:00but Corvetto law is the least likely.
26:03For example in that category.
26:04So our strategy of treatment
26:06for looking at weight,
26:07promoting meds as we want to investigate
26:10whether medications are a likely
26:11source of weight gain and patient.
26:13And if a weight promoting
26:15medication may be discontinued
26:16when it discontinued that agent,
26:18and if we can't consider
26:20or discontinue that agents,
26:22we do want to use consider the use
26:24of anti obesity pharmacotherapy
26:25for weight loss in conjunction with
26:28appropriate lifestyle therapies.
26:30So now let's look at these anti
26:32obesity pharmacotherapy agents.
26:33Even as someone who's completed
26:35a three year obesity Fellowship,
26:37Pyrdum GH had a strong interest
26:39in obesity medicine.
26:41I did not learn about these in residency,
26:44so hopefully.
26:44For those of you who aren't
26:47already untrained in obesity,
26:48these would be maybe knew or
26:51kind of new information.
26:52Most agents can be characterized
26:54into three primary groups,
26:56those that are centrally acting
26:58than pure dietary intake.
26:59Through those attack more peripherally
27:01to impair diety reabsorption,
27:03and then those that may
27:05increase energy expenditure.
27:06There is one that has been removed.
27:08I'll talk about that in a second,
27:10but these were the FDA approved
27:12medications currently available.
27:13The ones that have stars by them that
27:16you'll know those are approved by the
27:18FDA for long term use for the chronic,
27:20relapsing remitting progressive
27:21disease of obesity.
27:22So those ones that have stars by them
27:25were proved starting in 2012 and beyond.
27:27Anything that predates that,
27:28including Fenter mean,
27:29for example,
27:30which is the medication that was
27:32first approved for the treatment
27:34of obesity in the US back in 1959.
27:36None of those are approved for long term use.
27:39Interestingly enough,
27:40you can see that phentramin into pure
27:42mating combos approved a long term suit you,
27:45so maybe the FDA should reconsider how
27:47they think about these medications.
27:49One drive has been withdrawn with them
27:51from the market as early as this year,
27:53or at least later this year.
27:55I'm sorry and that forecast
27:57and it was a 5 HT 2C inhibitor
28:00for those that were around.
28:01And remember the Finn Finn era there
28:03was finter mean which was combined
28:05with fenfluramine that was FENFLURAMIN.
28:07That was a 5 HT 2B Receptor,
28:10So what they tried to do was come
28:12up with the five HT 2C Receptor
28:15because that combination of
28:16Phentramin and conforming was such
28:18a great combo in terms of weight,
28:20but not the degree comment
28:22combo in terms of Health,
28:24it caused heart valvulopathy this was
28:26withdrawn for the presumption that this
28:28may cause an increase in cancer risk.
28:30When you looked at the studies
28:32when they were looking
28:33at Post hoc analysis of those individuals
28:36that had undergone clinical trials.
28:38The persons that were on location 7.6%
28:40of them developed some type of cancer,
28:43whereas those that were
28:44not on low caster in 7.0%.
28:46So there's a little bit of discrepancy
28:48as to whether or not it was
28:51really statistically significant,
28:52but I think because of caution FDA did
28:55ask them to move that from the list.
28:58You can see we have CNS stimulants
29:00and Anorexia.
29:01It's into depressants and
29:03dopamine reuptake Inhibitors,
29:04along with opioid antagonists.
29:05And then finally our GI
29:07agents such as Orlistat.
29:08And our GOP one agonists like
29:10Liraglutide Horse extended the
29:12treatment dose to 3 milligrams
29:13for the treatment of obesity.
29:15Other agents that docs may use
29:17you seen some of these in the
29:19previous slide in combination
29:21with certain drugs such as tapir,
29:23mating soon as my both for Witcher
29:25anticonvulsants bupropion,
29:26which many of us know and probably
29:28are more familiar with for the
29:30treatment of either depression
29:31and or for smoking cessation.
29:33Metformin or amulet agonists
29:34in RSG LT2 inhibitors,
29:36which of course are utilized for
29:38the treatment of type 2 diabetes.
29:41The criteria for metabolic
29:42and bariatric surgery.
29:43Just a reminder, won't belabor this point.
29:45BMI greater than or equal to 40,
29:47so those have severe obesity.
29:49BMI of 35 to 30 point,
29:519.9 with a serious comorbid condition,
29:53and then it's important to know.
29:55Kind of this next bullet so the main bullet,
29:58three prior unsuccessful
29:59weight loss attempts.
30:00So we don't just send people
30:01to surgery because they meet
30:03criteria we want to first try
30:05are more conservative measures,
30:06but if they are continuing to have
30:09resistance in terms of their body responding.
30:11We do want to use the appropriate
30:13treatment tool and we do know is the
30:16best tool for the treatment of obesity
30:18anywhere in the world currently
30:20is metabolic in Berwick surgery.
30:22You can see acceptable operative
30:23risk is important,
30:24the ability to producing treatment
30:26and long-term following an ability to
30:28understand that this their success,
30:30significant lifestyle changes that
30:31are necessary for the life course.
30:34It's important to know that your notes
30:35also when you're working with patients.
30:37The most common procedures that are
30:39performed here in the USI do want to
30:41let you know that the most common procedure,
30:43hands down,
30:44is the Sleekest recta me almost
30:4570% of all cases performed in the
30:47United States now are the sleep
30:49distract me and you can see here.
30:51I'm a large portion of the
30:52stomach is removed.
30:53A lot of people call these both restrictive
30:55and or malabsorptive procedures,
30:56and that is not the primary
30:58mechanism by how these act.
30:59If you can remember when we talked
31:01about hormones such as ghrelin,
31:03which we know is housed here
31:04in the fundus of the stomach.
31:06Removing this portion of the
31:07stomach then reduces grilling.
31:09It reduces hunger for example,
31:10especially in that immediate postoperative
31:12course and the postoperative course
31:14that lasted till about 12 months.
31:15Those hormones can then resume.
31:17Remember they were also pregnant president,
31:18for example, grilling in the
31:20neurons in the hypothalamus.
31:21So, but this is the most common procedure.
31:24It's important for us to know
31:25which procedures being done because
31:27the side effect profile does
31:28vary for the different surgeries,
31:30so make sure when you're either referring
31:32out or are getting referrals in.
31:34That's been correctly noted in the chart.
31:36I'm the room.
31:37I gastric bypass is still by far the most
31:40efficacious in terms of weight loss.
31:42Comparing the two does have
31:44a significant difference.
31:45I guess side effect profile in
31:47terms of dumping syndrome.
31:48For example,
31:49if you need something that's
31:50sweet or concentrated,
31:51sweet feeling like you're going to pass out,
31:54you can see that you bypass a large
31:56portion of the stomach an the proximal
31:59portion of the small intestine.
32:01So I'm going to go into a few
32:03cases just to see how this works
32:05in real life with my patients,
32:07because a lot of this is kind
32:09of just like facts and figures.
32:11It doesn't really mean anything until
32:12we see how it works in real life.
32:15So I'm going to present a few of
32:17my patients and then open it up for
32:19questions so we have a 54 year old
32:21woman here that's coming in with the
32:23past medical history of untreated
32:25hypertension, migraine headaches.
32:25Gastroesophageal reflux is these
32:26IDs metabolic syndrome.
32:27She tells me she's retained 20 pounds
32:29with each of virtue president pregnancies.
32:31So like 40 pounds up from
32:33what her baseline was free.
32:34Having children,
32:35she's tried many commercial
32:36programs which led to 20 pounds.
32:37That seems to be the magic number
32:39of unsustainable weight loss.
32:40Each attempt she tells me, hey,
32:42you know I lost some significant weight,
32:44but that Finn Finn back in the 90s
32:46I lost £50 over the course of six
32:48months and so she comes into me
32:50interested in weight loss medications
32:51and in behavioral therapies.
32:53So I'm going to show you her graph
32:55and I wanted to just take a little
32:57bit of time explaining what you're
32:59seeing on the screen.
33:00Here we have this weight in pounds
33:02on this axis and we have BMI which
33:04stands for body mass index.
33:05Of course on this axis.
33:07And then we have time.
33:08So you get a sense of what's going on.
33:11Notice how if you're looking at a
33:12graph at 20 pounds that she tells
33:14me she keeps losing and gaining that
33:16actually happens and it happens overtime.
33:18But she comes into me with a BMI of 40,
33:21so she's definitely coming into
33:22me with severe obesity.
33:23You could maybe recall what she
33:24told me she was interested in,
33:26and notice she did have a pretty lovely
33:28response. She comes down to BMI of 31.
33:30If I were there in person,
33:32I'd ask you what happened and you lies
33:34will respond with a resounding she
33:36had surgery because I just finished
33:38talking about that and I would say.
33:39That makes sense,
33:40but that was not what happened.
33:42She participate in our twelve week program
33:44here called healthy habits for life.
33:46It's run by or dietitians.
33:47I was indeed as astonished as you
33:49probably are looking at this being her
33:51response to behavioral modification,
33:53because this differs so drastically
33:54from her attempts previously,
33:55and that program we do not teach
33:58anything about calorie counting or
33:59point counting or any of these things.
34:01We teach things such as volume
34:03metrics like what foods are
34:04going to improve hunger satiety,
34:06how not to hyper focus on things
34:08such as calories, and so this did.
34:10Make a huge difference for
34:11this particular patient.
34:13What I want you to notice
34:14that the patient stabilizes,
34:16which is exactly what we do.
34:17Many patients will reach their
34:19nadir with either behavior,
34:20medication or surgery,
34:21and then they'll begin to rebound back as
34:24the body tries to defend its set point.
34:26But notice she began to
34:27continue to trickle down here,
34:29and that was when I added an phentramin,
34:31which I told you is the drug
34:33that's been around the longest.
34:35Notice how she comes down here
34:37and then rebounds just a smidge,
34:38but stabilizes and BMI of about 28.5 and
34:41then notice using another downward trend.
34:43That was when I added her second agent.
34:45Show pyramid so mimicking the phentramin
34:47topiramate improved under combination
34:49under the trade name of Kissimmee
34:50am I like to use these dictionaries
34:52from many different reasons.
34:53First of all I try to use the lowest
34:56number of medications that I can.
34:58I do recognize that these patients
34:59will need to be maintained
35:01indefinitely on these medications for
35:03chronic treatment of their obesity,
35:04and so the least number of drugs
35:06I can use is always great.
35:08And if I start medications in combination
35:11also I'm not able to control for
35:13what caused what in terms of side effects.
35:15So let's say I put her on the
35:17combination at the outset.
35:19And she developed some significant
35:20side effect.
35:21Was it due to the finishing move here mate?
35:23May I could probably try to guess,
35:25but I might eliminate using two
35:27potential drugs that could be used.
35:28Keeping in mind that we don't
35:30have alot available currently.
35:32This is one of my favorite case actually
35:34saw this patient today and clinic
35:36which I'm doing via zoom so not really.
35:38She was on the vineyard when
35:40we did our appointment,
35:42so there's a 57 year old woman who's the
35:44past medical history of dyslipidemia,
35:46breast cancer,
35:46hypertension,
35:47depression and pernicious anemia give
35:48you a little bit more information
35:50here about her diet.
35:51For some reason she likes Brown
35:53rice in the morning cashews and
35:55goat cheese for lunch she's doing
35:56fish sandwich with vegetables.
35:58She may do some cheese and
36:00crackers or some cashews,
36:01and for dinner she's doing more
36:03like a spinach salad with some
36:05lovely vegetables added in.
36:06She's pretty active.
36:07You can see here she's doing
36:09exercise class three times a week,
36:10two videos a week for 1/2
36:12hour to doing yoga tonight.
36:13She's getting 8 hours of restful sleep,
36:15so I know you guys are sleep
36:17position is wondering about what's
36:18going on with the sleep and for her
36:21she was doing a pretty good job.
36:22So here again we have another one of
36:24these graphs they're drawing to skill,
36:26so weight in pounds again to remind
36:28you on this axis, BMI or body mass
36:30index on this axis and then time here,
36:33but I want you to see is that this
36:35patient had very severe obesity.
36:36BMI is greater than 50 or above, very severe.
36:39Sometimes you'll hear this.
36:40To a super obesity,
36:42she comes down quite nicely.
36:43I think we can agree to a BMI of 33,
36:46which is quite quite dramatic
36:48in terms of weight lost.
36:50150 pounds of weight loss.
36:52An I would ask you know what
36:54happened and that you might be like.
36:56Well, she didn't do surgery for the last one,
36:59so the likelihood this is surgery from
37:02an obesity medicine position is probably
37:04low and you probably right with that.
37:06So this was phentramin,
37:08a tapir mating combination.
37:09I wanted to put this up because some
37:11people have very very very pronounced
37:13responses to these medications.
37:15I want you to notice is
37:16that she began to regain.
37:18And so she comes back up to this BMI of 40,
37:22which is severe,
37:22but nowhere near where she started.
37:24But notice we were very sharp increase
37:26and you might wonder what happened.
37:29So at that time her physician
37:31stopped her medications because,
37:32oh,
37:32you don't keep these medications
37:34on long-term,
37:34or that was the mantra at the
37:36time and she quickly began to
37:38regain obviously an intervention,
37:40a curd, and we were able to bring
37:43her back down to BMI of 33.
37:45But this time she underwent a bypass.
37:47I think that we can all agree
37:49here that her response to bypass.
37:51Compared to response to phentramin
37:53into appear,
37:54Maine comma knows significantly different.
37:55You might say, OK, well,
37:57actually for she was much to
37:58have much more to lose here.
38:00Be up,
38:01but like that's not the response to bypass.
38:03Not really that great, you know.
38:05Maybe we would expect you to bring more
38:08to the line now she comes in to see me.
38:11Of course, here when she's begun to
38:13regain and notice kind of gradual gain.
38:15Overtime.
38:15Sorry guys.
38:16Anne,
38:16she comes here with the BMI
38:1944.5 comes down nicely here.
38:20Notice this is a much lower point
38:23than she initially got back in 2004
38:25or even after her surgery in 2006,
38:27and so the question I would ask
38:29you is what did I do for this
38:31lovely lady who is on the vineyard
38:33hanging out an at this time.
38:35I just reintroduce what was working for her,
38:38which was the Phentramin and that
38:39appear mate so I would have argued
38:41that she didn't need the room.
38:43Why that that was not a
38:45necessary procedure for her
38:46as much as I am a proponent for the
38:48use of metabolic in Berwick surgery,
38:51even in children.
38:52Which I do send to surgery,
38:54but for this particular patient we've
38:56already proven that she had done well
38:58with pharmacotherapy and she needed
39:00to remain on such pharmacotherapy.
39:02This case resonate with
39:04you asleep physicians.
39:05A 46 year old woman coming in with the
39:07past medical history of hypertension,
39:10anxiety, and depression.
39:11She has asthma, fibromyalgia.
39:12She's a history of bipolar disorder,
39:14gerd, and metabolic syndrome.
39:15She's history being on several
39:17way promoting medications,
39:18including Disapper Acetone,
39:19Quote Typing Deluxe Attan
39:21Deluxe 18 satala pram,
39:22fluoxetine does openemr transitional
39:24attend law pre gabelein nortriptyline
39:26I think if this medicine thing doesn't
39:28work out for me will be an auction ear
39:31postpartum weight retention of £20 and.
39:33Notice she has poor sleep.
39:34She has daytime hypersomnolence
39:36she's snoring, his morning headache,
39:37and so this is my favorite case
39:39for this particular presentation.
39:41She comes in with mild obesity,
39:43a BMI of 33.5,
39:44and she comes down quite nicely here.
39:46I think we can say to a BMI of 26.
39:49There are few clues as to what we're kind of.
39:52My treatment strategy for this particular
39:54patient and the clues are as follows.
39:57She did have undiagnosed
39:58obstructive sleep apnea,
39:59did get seen by one of you.
40:02Lovely sleep positions
40:03shouldn't hi index of about 30.
40:05Three when I sent her so she was started
40:08on C Pap and the only other treatment
40:10that I gave to her was metformin.
40:13So metformin is the first line
40:15agent for the treatment of
40:17psychotropic induced weight gain.
40:18You could see that she had been on
40:21several psychotropic agents for the
40:23treatment of her bipolar disorder.
40:24This response not with traditional
40:26pharmacotherapy but with good old C Pap.
40:28Can metformin notice how I told
40:32you they will?
40:33Respond with a little bit of a bounce
40:35up from where they can stabilize it.
40:38A different set point.
40:39Don't buy those product hands
40:40at the lowest setpoint.
40:41Wait until your body kind of recalibrates OK.
40:44Keeping their.
40:48Alright, so this is where she stabilized.
40:51This is a 34 year old woman passed
40:53with migraine headaches, asthma,
40:55Hypothyroidism, Depression,
40:56generalized anxiety disorder,
40:57history of anorexia nervosa is also
40:59important to note that patients that have
41:01a history of either anorexia nervosa,
41:04bulimia and of those there,
41:05or binge eating disorder have about a 40
41:08to 50% likelihood of developing obesity.
41:10If not already struggling with obesity.
41:12Obviously, Anorexia would not
41:14be those of binge eating.
41:15An orderly Mia may have obesity,
41:17gerd Chondromalacia of the
41:19Nitches vitamin D deficiency.
41:20She has a history of suicidal ideations
41:22Which we talked about a little
41:24bit in that weight stigma piece.
41:26I'm sure the history beyond
41:27fluoxetine for depression.
41:28I do want to note the fluoxetine
41:30or Prozac is by far the most
41:32weight neutral of SSR eyes,
41:34but I still like to capture.
41:35Some people may have experience in
41:37weight gain but not typically the issue.
41:41So in this particular case,
41:43we have this woman that came in
41:45with initially a BMI of 37 comes
41:47down nicely with the BMI 25.5.
41:49This was with behavioral means,
41:51so she did Weight Watchers here.
41:53Notice she creeps up gradually,
41:55so the body wants to defend that set point.
41:57She came to me with a BMI of 32.
42:00We bring her down to about 26.5
42:02and this was with the introduction
42:04of two medications be propri,
42:06on which many of you may
42:08be familiar with doses.
42:09Onus money may be less familiar
42:11with its anticonvulsant.
42:12That combination,
42:13I think will be a drug that becomes
42:16approved in combo by the FDA.
42:17It was first really published
42:19in the literature back in 2007,
42:21which is the citation you see
42:23at the bottom of your screen.
42:26I think we're getting to the end
42:28of the cases 60 year old man Dino,
42:31that I've only presented women so I
42:33wanted to make you men fill included
42:35here so we have a 60 year old man
42:38with hypertension type 2 diabetes,
42:40dyslipidemia, hypogonadism,
42:41secondary juice, obesity, and depression.
42:42You can see what he eats is
42:44not quite as virtuous.
42:46Is what we've seen previously.
42:48Fiber one bar bagel with cream cheese.
42:50Chicken Salad Sandwich,
42:51which is just basically mayonnaise and bread.
42:53Chicken Caesar.
42:54Similar hot dog pizza he eats.
42:56Chicken vegetable salad in
42:57the evening and he's toast.
42:59Tells me he's recently illuminated
43:00rice and pasta he's doing about an
43:02hour and a half of daily walking,
43:04and he's doing some afternoon calisthenics.
43:06This is his graph which shows you that
43:09he started off with me with a BMI of 57.
43:11I really thought with the degree of
43:13weight that he had that he would be
43:16a great surgical candidate and also
43:18in light of his comorbid conditions,
43:20which you can see here is that he did not,
43:23and I can tell you that almost
43:25every patient that comes in.
43:26With very severe obesity does
43:28not want surgery.
43:29But after a year he had only come
43:32from a BMI of 57 down to 52,
43:34which was still very severe.
43:36He did undergo a sleeve gastrectomy
43:38which is the VSG that you see
43:41here and you can see that he
43:43stabilizes here and a BMI of 37.
43:45He did pretty well.
43:46This is 58% of his excess body
43:49weight loss which is average
43:51response to a sleeve as between 55
43:53and 60% of excess excess would be
43:55everything above this BMI of 25.
43:57So we did pretty low.
43:59But I added to pure made.
44:00After he stabilized,
44:01you can see that it is stabilized
44:04over the course of about six months
44:06to appear mate was added and we were
44:08able to drive him down to a BMI of 30.
44:11I published the largest studies to
44:12date on the use of pharmacotherapy
44:14as an adjunct to metabolic and
44:16bariatric surgery with pull data
44:18here from GH in combination with
44:20the data that was provided by
44:22Cornell Anlu erroneous group there.
44:24And so you can see that he has done quite
44:26well with his response, very final case,
44:29and then I will have a few minutes.
44:31I think for questions 36 year old woman
44:33past medical history of hypothyroidism
44:34to stymie allergic rhinitis,
44:36chronic back pain migraine headaches,
44:37you can see that her diet is pretty virtuous,
44:39pretty active at the gym, as you can see,
44:42you can see that she does 6 to 7
44:45hours a night of restful sleep.
44:47When she comes in to see me,
44:49she comes in at a BMI of 36.
44:51She is moderate obesity and she comes
44:54down here to BMI of 29.5 but it takes
44:57us two years for us to get her there.
44:59Notice how she comes back.
45:01That's what century do appear.
45:02Make who's back to a BMI of
45:0436 and you might wonder.
45:06OK, well what happened?
45:07There are few clues on the slide
45:09so she's a 36 year old woman.
45:11She did decide that she
45:12wanted to have children.
45:14All of the medications with an exceptional
45:16metformin are contraindicated during the
45:17use of pregnancy and or breastfeeding.
45:19So we took her off of these medications
45:21an it took four months to regain the
45:24weight that it took two years to lose.
45:26So the chronic use of these medications
45:28isn't even important outside of the
45:30context of someone who is trying to conceive.
45:32She was able to successfully conceive,
45:34but responded with that weight response.
45:36So if you take home points,
45:38we want to track weight loss
45:40in terms of excess body weight.
45:42We want to listen to those patient cues.
45:44I ask my patients every single
45:46visit about their hunger, satiety,
45:48and side effects of medications.
45:50If there one medications we want to
45:52encourage healthy lifestyle behaviors,
45:53I will not start medications without
45:55a baseline of physical activity at
45:57least 150 minutes of moderate intensity
45:59activity per week with high dive quality.
46:01If a patient does have a superior
46:04response to.
46:04Pharmacotherapy which is 5 to
46:0610% of total body weight loss.
46:08We do want to continue these medications
46:10indefinitely and we do want to advise
46:12women of reproductive potential about
46:14discontinuing medication prior to conception.
46:16I wrote a book here at MGH.
46:19As you can see published by the MGA
46:21Psychiatry Academy on facing overweight
46:23and obesity which is published with
46:25some of my psychiatry colleagues here,
46:27our goal was to kind of pull together
46:30information for both clinicians and
46:31for patients with regards to obesity.
46:34If you are interested,
46:35this is available free for those
46:37that have Kindle Unlimited.
46:38On Amazon,
46:39and if not this still available
46:42in the Amazon.
46:44This is me doctor Fatima Cody from thank
46:46you each for your time and attention.
46:49Hopefully you got a chance to see
46:51how patients respond to multiple
46:53forms of therapy.
46:54And I would love to take any questions
46:57at this time. Thank you so much.
47:01Thank you doctor Sanford,
47:03that was really just fantastic
47:05overview that was filled with so much
47:07information useful to all of us.
47:08If anyone has questions you can take this
47:11opportunity to please unmute yourselves
47:13and ask your question on your own.
47:15Or if you prefer to put it in the chat,
47:18I'll read it out for you.
47:20Yes, so I'd like to ask a question.
47:22This is Mayor Krieger. OK. Right,
47:27so 70% of our of the patients that we see,
47:31the routine patients we see with
47:33with sleep apnea have obesity there
47:36obese and don't use that word right?
47:39We got rid of that.
47:41They have obesity.
47:42I got you.
47:43They're bigger than they would like
47:45to be an an an and we start them on
47:49C Pap and we and most of the time we
47:52don't do anything about their weight
47:54and and they're not necessarily,
47:56you know, they don't necessarily
47:58have a huge BMI or average patient.
48:01Probably has a BMI between 33 and 35.
48:03OK, should we be starting to?
48:06Maybe treat them with some of the
48:08medications that you mentioned absolutely.
48:10So if you're finding that
48:12they've maximized lifestyle?
48:13Remember, I said that I don't ever as.
48:16You know, if you just think about it,
48:18the clinical trials that were done
48:20on pharmacol therapy agents, right?
48:22You had Group One.
48:23Let's say that was on a placebo
48:25but had died and lifestyle kind of
48:27maximize and then group two that
48:29got the actual the pharmacotherapy
48:30agent with that same diet and
48:32lifestyle really kind of managed.
48:34I don't like to start the medications
48:36without that being maximized,
48:37especially since we know that we're
48:39going to use these medications indefinitely.
48:41So after maximizing that Doctor Krieger,
48:43if you're noticing that Oh my goodness,
48:45my patients are still struggling.
48:47The addition of pharmacotherapy can
48:48have significant could be a significant
48:50benefit for the patient with regards
48:53to proving what it sounds like to be
48:55more mild to very moderate obesity,
48:56but we that's those are the patients that
48:59the medications are really suited for,
49:01almost ideally because those
49:02patients that have severe obesity,
49:04often with an exception of that patient,
49:06that I showed you that was by
49:08far an exception,
49:09aren't going to get the the average
49:11weight loss which five to 10% is
49:13what many of the agents will produce.
49:16So I definitely would think about the
49:18introduction of these medications and
49:19kind of putting that in your wheelhouse.
49:21So which one would would you pick?
49:24It depends on the person,
49:26so I always personalize it to the person
49:29based upon what they're presenting with,
49:31right?
49:31So if it's a patient that has
49:34let's say maybe pre diabetes,
49:36hemoglobin A1C is 6.4.
49:37I'm concerned about them with regards
49:40that I might start a GOP one agonists if
49:43their insurance allows me to cover it.
49:45Getting over the idea of a daily
49:48injection can be a barrier to
49:50some patients in addition to.
49:52The prior the problems with
49:54getting this improved by insurers.
49:55We do have decent coverage for many of the
49:58private insurers here in Massachusetts,
49:59but not from mass health.
50:01Which of core at least 1/3 of
50:03my patients or masshealth,
50:04which don't have that same level of coverage?
50:07If it's a patient,
50:08that's maybe a younger patient.
50:10Very active patient might consider
50:11the introduction of finter mean,
50:13but with Phentramin it requires a
50:14little bit more work on the side of
50:17the patient because phentramin can
50:18increase blood pressure and heart rate.
50:20I have them take their blood
50:22pressure and heart rate.
50:24Try my stark phentramin
50:25or increase their dose.
50:26I have them taken Monday morning,
50:28Wednesday midday and Friday evening
50:29and send that through our what we call
50:31our patient gateway in epic so that I
50:33can see how the patient is responding.
50:35Not just regards to their way.
50:37That's great.
50:37If they lose weight obviously,
50:39but I want to make sure that I'm
50:41not causing any elevations of blood
50:42pressure systolic or diastolic,
50:44and or Tachy Cardia,
50:45so there's a little bit more work
50:47on that side is the cheapest of
50:49everything that we talked about
50:50because we can get that pretty
50:52cheap if you're using good RX.
50:53For example, the tablet is covered.
50:55Very, very inexpensive for some reason.
50:57Also, if you use your AAA card,
50:59yes,
50:59the Carthage use of your car breaks
51:01down on the side of the road.
51:03It gives you 1/2% off.
51:04I'm are half off of phentramin
51:06so that just depends.
51:07I try to personalize it by patient
51:09and many patients will end up
51:11on multiple agents which I will
51:12gradually introduce overtime,
51:14but I never start more than
51:15one agent at a time.
51:17So just to give it just to
51:19give you some thought process.
51:21Thank you hi, this is Chuck.
51:24Also wanna sleep dot.
51:25Thanks for a wonderful talk freely
51:28and perspective on how complex this
51:31diseases and so one of the questions
51:33I have is mechanistic and it has
51:36to do with leptin and sort of near
51:39and dear to us as a sleep positions
51:43because leptin does have some.
51:45Function in restaurant control.
51:47Another error muscle tone and
51:49there's been some recent studies,
51:50at least in animals and mice,
51:53showing that at least some hypothesis
51:55that perhaps it's really the resistance
51:57to left in the central resistance to leptin,
52:00that's causing some of the weight gain,
52:03and even some of the
52:04sleep disorder breathing.
52:05So I was wondering,
52:07based on what you know,
52:09how much of the contribution of
52:11leptin is due to resistance in the
52:13sent from the central nervous system.
52:16And you know you've shown very nice
52:19diagram of the two mechanisms by which
52:21left and could act within the CNS.
52:24And whether that differs by
52:26resistance status for each patient?
52:27Well, so it's you know,
52:28I think that's a great question,
52:30and one of the things that's was.
52:32I guess the reason why I'm
52:33going to be able to give you a
52:36convoluted answer is that we don't
52:37know. I think is the answer to that.
52:40A lot of it is because we're not really
52:42measuring leptin in most patients, right?
52:44Like that's not one of our standard labs.
52:46When I even showed you guys the lapse to ask,
52:49you know like we can measure
52:50insulin resistance, right?
52:51If someone has hyperinsulinemia
52:52or hyperinsulinism present,
52:53we can order fasting insulin level
52:55to couple their other fasting labs.
52:56We don't really know for individual
52:58patients what's happening,
52:59and I'm sure that there's differences
53:01in how patients would look.
53:03I mean, we have patients,
53:04for example,
53:05that have BMI's that are in
53:07these kind of higher 5060 range
53:09that come in with no evidence,
53:10for example of hyperinsulinism and then
53:12patients that have very mild to moderate
53:14obesity that have hyperinsulinism in.
53:16I would assume the same is
53:18true with left and right,
53:20so that there's probably
53:21variations that don't directly
53:22correlate to one's weight status.
53:24I think just having an understanding
53:26of the complexity.
53:27Of this disease process,
53:28and how there's often a lot of trial and
53:30error in terms of of utilizing therapies,
53:32I think is kind of my thought process,
53:34and even with you guys asleep physicians,
53:36you know that people respond in
53:38terms of to see pap in different
53:40ways in terms of how you set your
53:42settings based upon their hi and
53:44all of these types of things that I
53:46would not be able to do very well
53:48because I'm not trained in that way.
53:50So I think that that so I gave you a
53:52convoluted answer because there's not
53:54a direct like clear cut answer, but.
53:57Hopefully that gives some guess
53:59response to the question.
54:02Sure, yeah, absolutely.
54:03Just maybe a comment to for mayor.
54:06One of the drugs,
54:07Unison light is very similar to
54:09a suit is olamide at my actually
54:12improve some of the sleep,
54:14disorder,
54:14breathing something that is delightful
54:16so I Love Xena semide alot of so for
54:19patients that so tapir made us better
54:22studied in obesity I would say the
54:24best of the two anticonvulsants studied.
54:26But for patients that develop significant
54:28issues with cognitive issues,
54:30word finding difficulty for example
54:31with tapir made or paresthesias
54:33that are persistent.
54:34I will switch them over to zonisamide.
54:37The typical starting those frozen
54:38is my math published this letter.
54:40I can send this over to unlearn,
54:42kind of like my stepwise approach
54:44if I'm using to appear meters in
54:46this amide and surgery for obesity
54:48and related diseases.
54:49So as soon as my starting those typically
54:51would be 100 in the evening time,
54:54I just those anticonvulsants,
54:55even the evening time,
54:56because many of the patients
54:58will say they sleep better.
54:59Having taken that either
55:00at dinner or at bedtime,
55:02that equivalent dose for to appear
55:04mate would be approximately.
55:0525 milligrams for the two appear
55:07made two of 100 milligram dose
55:09of zonisamide for my patients
55:11that maybe order 65 plus I am a
55:13little bit more gingerly in
55:15Amazonas amide and may start at a 50
55:17milligram dose which was just introduced
55:19in the market about three years ago or so.
55:22So just to give some perspective,
55:24Max dose for the treatment with zonisamide
55:26will be 400 milligrams in the evening
55:29that before castles on the Max dose that
55:31typically will use for the treatment of
55:33obesity with to appear mate would be.
55:36About 1:50, although most people will
55:39unfortunately develop some side effects when
55:42they cross that 100 milligram threshold.
55:44So much, I think super a few
55:47minutes over the hour.
55:49We will end tier,
55:51but thanks for writing your contact
55:53information and I can get a copy of your
55:57book and maybe send a link out to that.
56:00Basically there's only one Fatima,
56:02Cody Stanford, so if you Google that
56:04you will find my step one review book,
56:06but you guys have all passed step
56:08one so don't buy that one.
56:10Like this, never do later.
56:13If you great,
56:14thank you so much again and for everybody.
56:19Let me highlight next week talk.
56:22We're going to have a talk by Caroline
56:24Okorie who is a clinical assistant
56:27professor of pediatric pulmonary
56:28and Sleep Medicine at Stanford.
56:30She's going to be speaking about
56:32sleep concerns in pediatric
56:34populations with special needs.
56:36So Mark your calendars for that.
56:38And also.
56:51Well, I guess I think we're leaving.
56:53I think more may have left.
56:54Thanks so much for attending and
56:55I wish you guys a wonderful day.
56:56Thanks so much.
56:58Bye bye take care thank you.
57:01Thanks for good question. Right?