Obesity and Metabolic Syndrome | Clinical Medicine

what's up Ninja nerds in this video today we're going to be talking about obesity as well as metabolic syndrome which is usually a downfall of obesity again this is a part of our clinical medicine section if you guys like this video it makes sense it helps you please support us you can do that in a couple different ways one hit the like button comment down the comment section or subscribe also one thing that I really highly suggest is go down the description box below there's a link that goes to our website on our website we

have a lot of cool stuff we got really amazing notes illustrations tons of quiz questions and we're even developing exam prep courses so go check that out become a member and really enjoy a lot of that stuff let's talk a little bit about obesity within obesity the pathophysiology it really actually could be broken down pretty simply usually the problem with this disease is that the caloric intake I me there's a lot of different ways that you can look at this but often time it really boils down to this the caloric intake take is greater than

the caloric expenditure so the amount of calories that you are burning is less than the amount of calories that you're taking in when this happens what usually occurs is is it really stimulates a lot of lipogenesis so your adose tissue which is going to be this little guy here this atopos tissue is really going to amp up a lot of your Li your lipids so you're going to a lot of lipogenesis now with that you start building up more and more and more atopos tissue the problem with this is is that with more and more

and more atopos tissue becomes a problem as atopos tissue starts to accumulate as you start generating a lot more of this atopos tissue they start releasing lots of cyto kindes right that's usually one of the biggest problems here is you get lots of cyto from these cyto which there's a bunch bunch of different types but the most prominent ones are we call them adipo kindes so we have these things called adipo kindes and there's so many of them I'd say some of the biggest ones to remember uh usually consists of what's called leptin there's another

one called resistant and you even have other ones like cyto kindes like interlukin 6 and tumin acrtic Factor Alpha but there's all these different types of cyto kindes that are released from the adapost tissue when these adepo kindes are released due to lots and lots of adapost tissue which we see in obesity they have very profound effects on variable different tissues what are some of these effects well one of them is these adipo kindes they've been shown that you know the pancreas the pancreatic beta cells they make a hormone it's referred to as insulin now

insulin is supposed to act on these receptors here's an insulin receptor here's an insulin receptor what we've seen is that whenever there's high levels of O adoc kindes these these have been shown to inhibit the efficacy of insulin so now insulin is supposed to stimulate these channels on multiple different tissue cells in our body and what these tissue cells are supposed to do when they're stimulated is take glucose into the cell so glucose should be brought into the cell but whenever there is an inhibition or what we call an insulin resistant type of effect due

to high amounts of cyto kindes this process C is inhibited glucose is not taken up and therefore glucose builds up in the bloodstream and patients start developing hyperglycemia what's the concept behind this it's usually due to the the concept what we call insulin resistance so this is one really profound complication of obesity the other concept here which is actually really interesting I I don't really know how exactly this comes to effect but what it's been shown is adoc kinds have a very interesting effect on a ren Angiotensin ostrin system and on our sympathetic nervous system

whenever there's lots of these adipokines they may increase the activity of the Rin angens and ostrin system and the sympathetic nervous system if you guys know a little bit about your cardiovascular system what you'll know is is that when these two systems are stimulated and hyperactive this causes intense vasil constriction this causes intense lasal constriction what happens to your blood pressure as a result goes up and often times this is usually one of the big things is that these patients will develop hypertension so what we found with these adepo kindes is that they may be

a very profound trigger for an increase in blood pressure hypertension what else all right these adipo kindes have also been shown that they can act on the liver and they can do a couple different things with the liver you know there's a molecule it's called VL DL it's a it's a A lipoprotein that's produced by the liver and it primarily carries triglycerides what we've seen with these adoc kinds is they may stimulate the liver to increase the production of vldl if you increase the production of vldl you will increase the transport and release of triglycerides

and so often times these patients have very elevated triglyceride levels due to an increase in vld production what else the other thing is that HDL molecules may actually be destroyed by the liver so the other concept here is that sometimes these HDL molecules could be broken down if they are broken down and metabolized what happens to the HDL levels within the blood so this actually may get taken up in the liver and get broken down into different types of particles we may see a depletion in the HDL level so a lot of the time s

we see some type of dyslipidemia that's resulting primarily with an increase in triglycerides and a drop in the HDL last thing this one's actually weird the adepo kinds may also in some way shape or form cause fat distribution to occur most prominently in the central portion of the body in the abdomen you get those muffin tops right so often times these patients will have a lot of central obesity and if you have Central obes it what we will notice with this is that from this our waste circumference will increase so you know the one of

the biggest things here is that if I were to measure from here to here what would I see I would see that my waist circumference would really be increased and that's usually one of the big big signs here is that central obesity occurs it causes the waist circumference so that's going to be an increased waist circumference now with all of this being said this is the kind of process that we see in obesity what you have to notice is increase waste circumference decrease HDL increase triglycerides increase BP and hypoglycemia really kind of key you into

something there's a condition called metabolic syndrome now here's what I want you to know about metabolic syndrome metabolic syndrome is actually going to be a compilation of a couple different things it's usually you need at least three out of the five uh from the above requirements for this diagnosis what do I mean if I have a patient who has hypoglycemia so we say that this is whenever the blood glucos is greater than 100 at least fasting high blood pressure greater than 130 over 85 elevated triglycerides greater than 150 low HDL depends on if you're male

and female we'll talk about this in the diagnostic section and an increased waist circumference again depends on if if you're a male or female if they have at least three out of these five findings you can diagnose them with metabolic syndrome and so usually obesity is a prerequisite oftentimes for the presentation of metabolic syndrome which comes with a lot of complications that we'll talk about a little bit more in the next section let's finish up though we see this as really the end goal pathophysiology of obesity and metabolic syndrome the question that you have to

ask is and it may be super obvious but I thought let's talk about it the caloric intake Factor what's really causing this increased caloric intake there's a couple different things I think often times it's usually just whenever patients are eating high calorie foods high calorie foods that's usually the biggest thing so high food intake but often times this is going to be usually High calories the question that often times arises what's the trigger for the increased food intake it's not always is just the person just wants to eat more there could be particular triggers sometimes

one of the things that you have to remember for these patients is that increased food intake could be triggered due to often times maybe stress or depression so sometimes stress on the patient's life can really cause this depression may also do this another one is it actually could be due to medications so certain medications have been known to increase the patient's desire or the hunger activity and then that could be a very profound trigger what are some of medications that I would actually like want you guys to remember I think one of the big ones

is corticosteroids so steroids have really been shown to have a very profound effect corticosteroids things like prazone another one believe it or not is anti-depressants so you get depressed you take an anti-depressant and guess what you g you start having an increase in food intake so sometimes ssris are a very profound stimulator of this last one is anti an psychotics so certain antis psychotics may also increase the desire to have more food and eat more food so if the amount of intake due to these particular factors outweighs the caloric expenditure you see how this could

lead to this Cascade of events but it's often times an intermingling it's not usually always just increased intake at some point there's also a factor here where there is a reduction in the choric expenditure so when I talk about this one right off the get-go you can already identify that one of the biggest triggers is decreased physical activity if a patient has a sedentary lifestyle this will definitely not lead to as many catabolic activities that are going on you're not going to break down fats you're not going to break down carbohydrates so you're not going

to burn the amount of calories that you should be that's pretty obvious the other one though may be actually due to a metabolic disease so this actually could be due to disease disease states that are altering our metabolic activity so what if I have diseases that actually decrease my metabolic activity so you know that metabolism is a process that can definitely be influenced by hormones right what are some hormones that if reduced could actually lead to this well I'll tell you what one of them is it could be due to hypothyroidism so hypo thyroidism has

definitely been shown that if a patient has low amounts of thyroid hormone they will have a reduced basil metabolic rate their amount of calories that they'll burn is lower that's one big thing the other concept here that could alter the metabolism but it really does it through a a weird process where there's lots of lipolysis with redistribution of fat particularly in the central portion of the body is Cushing syndrome so watch out for Cushing syndrome as another very profound trigger here of a patient having an altered metabolic State either way in these two scenarios what

we see is is that the patient is not being active that's often times the most common trigger and having a lot of caloric intake this will lead to this whole pathophysiological process that leads us to the next question if a patient is obese right we have different ways of defining that often times the most common utilization for obesity is BMI we'll talk about that more in the diagnostic section and use it as a way of classifying the severity another way is waist circumference we talked a little bit about that it's definitely more appropriate for uh

determining the the relative incidence of comorbidities that the patient may face and again we'll talk about them more in the diagnostic section with metabolic syndrome what I want to do now is talk about what are the long-term complications of remaining obese all right my friends so now when a patient comes in they have obesity we already kind of have an understanding that again more caloric intake than expenditure we talked about all the kind of pathophys and causes behind that we talked about the kind of the downstream Cascade from having lots of adapost tissue in a

depoc kind release which was the again insulin resistance the high blood pressure the H dyslipidemias The increased waste circumference we talked about how at least three of those five particular categories would fulfill the diagnosis of metabolic syndrome well when a patient becomes obese as their BMI goes up and up and up or their waist circumference particularly more specifically that waist circumference goes up up up it's more of a predictor that they could experience complications and comorbidities along the line what are some of those that you have to be on the look for one of the

things with obesity is that they can definitely develop hypertension the concept behind this we already kind of talked about a little bit that adapost tissue as you have more and more and more of it especially around the central portion of the body you have more depoc kindes they stimulate an increase in the Ren otens and AER system Rin otens and ostrin system and increas in uh the activity of the sympathetic nervous system so having lots of adoc kindes increase here and increase here what's the end result of this well I kind of briefly talked about

it before that this will lead to the increase in angot tensin too what will otens and two doe to your blood vessels squeeze the heck out of them right so your systemic vascular resistance will go up and therefore your blood pressure will go up so that's going to be one effect is that they'll act on the otens and 2 receptors squeeze the heck out of the blood vessels so your svr will go up you'll have intense vasil constriction and your blood pressure will go up sympathetic nervous system may increase your heart rate but it also

will act on the alpha 1 receptors and when it acts on the alpha 1 receptors that'll squeeze the heck out of the blood vessels increase your svr and increase your blood pressure so as a result this is something that we can see with the addition just to remember you also can see particularly from the sympathetic nervous system a profound stimulation of the beta 1 receptors in the heart which can increase the heart so you can see Tac cardia sometimes in profoundly obese individuals as the blood pressure goes up we utilize the diagnosis of hypertension whenever

you at least two out of two readings on separate occasions where the blood pressure is greater than 130 over 80 for stage one or greater than 140 over 90 for stage two so again high blood pressure and again to make the diagnosis you need at least two readings and then again depending upon the stage that you're at is really really important at least two high blood pressure readings greater than 130 over 80 for stage 1 greater than 140 over 90 for stage two this is a big complication that we see in obesity the second one

is aosc orotic cardiovascular disease it's actually again pretty straightforward whenever you have lots and lots of atopos TI especially on the central portion of the body lots of adipokines adipokines what we know are problematic and one of the reasons why is that they may act on the liver and when they act on the liver they have been shown to increase vldl production and lead to a consumption of HDL and so one of the things that these patients have is lots of vldl which leads to lots of triglycerides and lots of HDL consumption so at the

end result here is that they have high vldl low HDL and lots of triglycerides what else lots of adoc kinds also will inhibit the effect of insulin on the insulin receptors and so this will lead to that concept of what we talked about before insulin resistance my friends with increasing insulin resistance what do you do to glucose can you take it in you can't take it into the cell and so because of that glucose won't be able to be brought up into the cell and as a response to that since it can't be brought into

the cell it'll build up in the bloodstream when patients have high triglycerides to some degre degree it can increase the risk of atherosclerosis but way more so low HDL is a very profound stimulator so I'm going to put two pluses here for this one this is a very profound stimulator of atherosclerosis having high glucose is actually another really bad one too because what glucose does is is it can actually add a glucose onto LDL and it can glycate it when you glycate LDL molecules you make them really really increase risk of forming plaques so this

is a very profound stimulator as well and then highy triglycerides these more cause problems with pancreatitis but they still can cause atherosclerosis so here we see how all of these factors are really causing this nice chunky plaque inside of the actual Lumen of the blood vessels it's really narrowing the blood vessels why is this a problem well if it Narrows some of the blood vessels inside of the brain or near the actually coming into the brain what can happen you cannot get enough blood supply to the brain tissue especially if this plaque ruptures and so

what may happen is sometimes patients may experience infarcts so now there's some dead tissue there what could this be called we can call this a TIA if it's transient or a CVA if it's a permanent type of infarction or a permanent neurological deficit as a result they may also have poor profusion to The myocardium so if they have poor profusion to The myocardium because the plaque ruptures udes the blood flow then they can end up with death of the myocardial tissue sometimes it may be enough that it actually just reduces the profusion to some of

the tissue sometimes it may infar the tissue if they just have reduced perfusion this may cause coronary arter disease which can present with angena but if they present with very profound angen and on top of that ST segment depression or ST segment elevation or troponin elevations that's an MI because of infarction and then last but not least if the atherosclerotic plaque blocks up the blood flow to the lower extremity it may reduce some of the blood flow to the muscles that whenever you're walking it causes claudication pain and that's called intermittent claudication which is classic

of Pad but if you rupture the plaque and olude the entire blood flow to the muscle and then you get so much pain that it even occurs at rest or you get ulcers because of like necrotic tissue of the skin or Gang Green now we're talking about like critical limb eskey this is the big thing that you have to watch out for patients who are obese they're high risk of stroke high risk of heart attack and high risk of P or critical lisia along with hypertension all right another thing that they're super high risk for

is type two diabetes the concept is actually pretty straightforward we already kind of hit a little bit of it here as you release lots of these Ado kinds leptin resistin and then on top of that there's even less production of another hormone called adiponectin which is a really problematic issue but we'll talk about that in the future again adipokines when these are released in high amounts what they can do is again we said that they'll particularly act to block if you will the effect of insulin so insulin is supposed to go and work on these

insulin receptors and when they go to work on these insulin receptors they're supposed to help in shuttling in glucose into the cell but if adoc kindes are present it will inhibit this effect of insulin it'll inhibit the glucose uptate and glucose will build up in the bloodstream now if glucose builds up enough that it actually starts causing complications polyurea polydipsia polyphasia we start seeing signs of diabetes so one of the things that you have to watch out for with high glucose levels is those classic three PS I'm just going to put down the three PS

and what is this again we'll talk about this more in diabetes polyphasia polydipsia poly areia you pee too much eat too much and you're thirsty too much the other thing that you need is as glucose levels go high you need lab values to support diabetes because there is a difference between metabolic syndrome and Diabetes Type 2 metabolic syndrome the glucose only has to be greater than 100 fasting but if the A1C is greater than or equal to 6.5% if the fasting blood glucose is greater than equal to 126 mg per DL or if the oral

glucose tolerance test usually it's a 2hour one is greater than or equal to 200 milligrams per DL this is usually diagnostic of Diabetes Type 2 that you would not see in anabolic syndrome so again you're kind of changing the direction there so you need labs to be present as well as symptoms to be present to really trigger the diagnosis of diabetes okay now we come over to this guy here as patients develop obesity right one of the complications that can arise is that some of this fat tissue that's around the neck area they can start

getting like a lot of thickening here and there can start to develop compression of the upper Airway so with obesity comes upper Airway compression the problem with upper Airway compression is when you're sleeping so as you sleep you compress the Airways you won't ow for air to naturally flow via the Nars down into the trachea or from the oral cavity down into the trachea this will be compressed so you see how I'm kind of including the air flow at that point what happens is with that upper Airway compression you lead to nocturnal hypoxia so periods

where you're not ventilating at all that nocturnal hypoxia is terrible because these patients often times what happens is they wake up in the middle of the night maybe from snoring or they'll you know they wake up you know like because they get woke up from the profound hypoxia or snoring sometimes one of the big things is that your partner May witness the snoring or the apic events often times from Osa these patients have profound daytime somnolence and fatigue but often times to really make the diagnosis of obstructive sleep apnea really to make the diagnosis of

obstructive sleep apnea you need to have what's called A polysomnogram and A polysomnogram would have to look at the Ahi which has to be at least greater than or equal to five to make the diagnosis of mild and again we'll talk about that more in the pulmonary Sleep Disorders but this is one of the big things for Osa is obesity particularly right around this vicinity of the neck could lead to Osa in patients who have obesity hypoventilation syndrome what happens is you really have a lot of fat tissue around the chest wall or around the

area of the abdomen which kind of hikes up the diaphragm so you're either hiking up the diaphragm right so let's kind of represent the diaphragm here you're either hiking up the diaphram which kind of impairs the makes the lungs smaller or you have this large fat tissue around the chest wall which reduces the chest expansion so you have two effects here you have a hiked up diaphragm so we'll write that down either a hiked up diaphragm and a very large chest wall That's reducing chest expansion all right either way with both of these particular scenarios

it really reduces the ability of the lungs to expand and if you can't expand the lungs you won't be able to ventilate and so patients usually get reduced lung expansion and then as a result they develop hypo ventilation you know the big thing that's really different here is is that this happens during the day and it could happen at night so sometimes patients who have Osa may also have what's called obesity hyperventilation syndrome but one of the characteristics ways of diagnosing OHS from Osa is they have hyperventilation during the day and the night and whenever

patients have hypoventilation what we know is is that their CO2 levels really shoot up CU they don't exchange the CO2 properly so if it ever gets to the point where it's greater than 40 5 and you've excluded any other reason why they could have a respiratory acidosis you have now clinched the diagnosis of O HS but you have to exclude any other reasons for them having a respiratory acidosis or a hypoventilatory disorder like COPD so that covers Osa and Ohs again need a polysomnogram need an ABG and exclusion of other diagnosis and a patient who

has obesity to diagnose OHS what about this last one this is actually becoming the most common it's really starting to develop as one of the more common causes of therosis in the United States population and this is non-alcoholic fatty liver disease as you start to develop more and more and more atopos tissue you release lots of those Depo kinds and I already told you before that what this does is this leads to that insulin resistance type of effect well one of the things is that insulin resistance can have a very profound effect on our liver

so whenever patients get insulin resistant let's actually write that down they develop that insulin resistance that means that the insulin is not working as well on multiple different peripheral tissues the problem with this is is that insulin if it's resistant it stops kind of you know helping with glucose uptake in carbohydrate metabolism you know up that kind of triggering what it does is it stimulates a lot of free fatty acid uptake into the liver so now these free fatty acids get shuttled right into the liver heavily you know when you take a lot of free

fatty acids into the liver you know what can happen it can start causing the liver to become super fatty and you start getting all these like fat globules that kind of accumulate into the liver this big big fat globules you know what they call this steatosis so we actually refer to this this kind of state here as it's called nonalcoholic um ST steatosis nonalcoholic steatosis which is just kind of a fat Laden liver okay then what happens is the steatosis the fat molecules they trigger reactive oxygen species which is unfortunate so then what happens is

you get lots of reactive oxygen species and oxidative stress as this occurs this increases the inflammation of the liver tissue so now you have a liver tissue that's filled with fat filled and filled with fat tissue but on top of that the reactive oxygen species from all these fat molecules that are accumulating in there triggers the inflammation of the liver now the liver is getting all hot and heavy now if you have steatosis on top of inflammation of the liver what do we call that Stato hepatitis this is abbreviated often times what we refer to

as nonalcoholic Stato hepatitis Nash now if this continues to happen continued inflammation from consistent obesity adipokines insulin resistance free fatty acid influx lipogenesis theosis inflammation eventually this will trigger fibrosis and as you go to the fibrosis limb then what happens is this patient can start getting lots of fibrotic tissue which starts leading to the actual liver becoming nonfunctional what is this called especially if it starts getting nodular like so you start getting nodular type of appearance and you still have fatty tissue there this is called therosis so often times in patients who have non-alcoholic fatty

liver disease what happens is they start off with just some fatty liver we call this a fatty liver then they end up with an inflamed inflamed fatty liver and then they can end up with therosis how could this often present they may present in the the farther stages of therosis often times so they may present with jaundice aites so features of portal hypertension and maybe some changes in their lfts you know non-alcoholic fatty liver disease one of its claimed to fames is that you need to have a negative uh serotic workup so you need to

have a negative sorosis workup but the other thing is that you often times have to have the uh the ratio like the a to alt ratio less than one and sometimes that's some of the things that may help you to think about this patient having nonalcoholic fatty liver disease okay that's the complications of obesity and metabolic syndrome now let's go into the diagnostic approach it's often times for obesity looking at their BMI if it's 30 to 35 it's technically considered to be class one because anything greater than equal to 30 is obesity as you go

up above 35 and you get to 35 to 40 it's Class 2 anything greater than 40 is considered to be severe class 3 obesity the next thing is for metabolic syndrome is you do have a patient who's likely going to be obese so they're going to have an elevated BMI but what we look for is more particularly those factors the weight pneumonic that I told you guys about so do they have impair glucose a glucose greater than 100 do they have an elevated BP greater than 130 over 85 do they have triglycerides that are greater

than 150 do they have a waste circumference of greater than 40 for male 35 for female do they have an HDL less than 40 for males and then less than 50 for females if they have three out of these five they have the diagnosis of metabolic syndrome the question here is how do we treat these patients is oftentimes going back to the root cause it's kind of reducing food intake and increasing physical activity and often times that's the simple thing that we try to go about here is just lifestyle modifications try to restrict some of

the calories within your diet um try to increase your physical activity and see if that helps with weight loss often times if patients do that they may improve they may actually start seeing a decrease in their glucose a decrease in their blood pressure a decrease in their triglycerides and increase in their HDL and potentially even a redu a reduction in their waist circumference and even BMI however in some patients that don't respond to these particular physical activity changes and dietary changes we may have to progress so if they're still persistently above 30 or more um

with their BMI even if they don't have any comorbidities we should still consider Pharm mological therapy so what does that really consist of there's a bunch of different medications one is orat this is used to be commonly used but I would say it's not as commonly used as much as it used to be um one of the mechanisms behind this is that it's basically going to inhibit the light Paces inside of our intestines so light Paces are designed to be able to break down triglycerides into fatty acids so that they can be absorbed but if

I do this I'm not going to be able to break down the triglycerides and the fatty acids and therefore I won't absorb them so I'm going to lose a lot of fat in the St stol that was one potential downside it can lead to some slight vitamin deficiencies it can lead to some foul smelling and greasy appearing stools the other one's fenine into pyramid um fentam is actually going fine is going to be one of those drugs that we use to uh increase in pathetic activity and to actually U improve satiety and then appetite suppression

uh to pyramid is going to be one of those anti-seizure medications but it has been shown to potentially provide benefit and appetite suppression stide l atide these are basically your glyp Agonist these are becoming the big things that to use today um because they have multi- system effects they can do so many things to be able to improve weight loss um so a couple of those mechanisms one is they have been shown to potentially affect the hypothalamus and improve Satine suppress appetite they also have been shown to increase insulin production and reduce glucagon production which

definitely has it also a very significant impact on again appetite suppression and improved satiety the other thing is it reduces gastric emptying so if you think about this it's going to take a longer time for you to push things out of your stomach into your duodenum that means that the stomach stays a little bit more distended and whenever you have a distension of the stomach that activates the vagus nerve and then helps to be able to again trigger satiety and improve and act as an appetite suppressant so these are multi-stem mechanisms that you can see

how glyp one Agonist stide lorag there's many more now that have been shown to be very beneficial in weight loss but they do carry some risks such as meary thyroid cancer as well as pancrea itis buproprion and nxone is one of those that are often times beneficial for patients who have underlying depression um maybe some type of addiction problem um the concept here is if a patient's on an anti-depressant buproprion has anti-depressant properties however it has more of a sympathetic effect it has more of that appetite suppressant effect and so it may provide weight loss

in the combination of treatment for depression now treone may actually act as more of an opioid antagonist and help to alter some of the misol limic pathways that are involved with the with the reward of food but again these are medications that can be considered in patients who maybe have underlying depression or some type of addiction problem these are becoming the more highly utilized uh pharmacological interventions in patients with metabolic syndrome and obesity however in patients who have a persistently elevated BMI despite changing your diet increasing your physical activity taking a gpol and Agonist and

they're still having a high BMI you should then kind of consider a consultation for bariatric surgery because these may be alterations and the potentially the way that food is restricted or absorbed and we'll talk about that in a little bit of a second here another indication to go straight to a bariatric consultation may be going in a completely different direction what if the BMI is pretty high greater than equal to 35 and they already have a comorbidity maybe they have hypertension maybe they have obstructive sleep apnea obesity hyperventilation syndrome type 2 diabetes atherosclerotic cardiovascular disease

in the form of a TIA CAD or pad and and then non-alcoholic steatitis or non-alcoholic fatty liver disease in these particular scenarios you should go right to a bariatric consultation because the complications from the metabolic syndrome are becoming very bad the other one is is we don't even care if they have comorbidities their BMI is greater than 40 or at least equal to it these patients have a very high risk of complications we need to consult consult them for a bariatric surgery and really help them to lose some of this weight now how does bariatric

surgery help with weight loss particularly there's a couple different mechanisms one is called a sleeve gastrectomy basically what you're doing is you're kind of reducing the size of the stomach which helps to restrict the amount of intake that you can bring in your stomach will stretch a lot earlier it'll produce more of an early satiety and more of an appetite suppressing effect so that you don't allow yourself to eat more food because if you do you get nauseous and potentially vomit so again you're kind of cutting down the actual stomach into a small little sleeve

which acts as a restrictive type of mechanism for food intake the other one's gastric banding same thing it's just basically you're taking a band and you're kind of inflating it and compressing and squeezing around the actual stomach and this helps to be able to again reduce the intake of food into the stomach which may produce early satiety and again an appetite suppressing effect the last one that's actually become a little bit more commonly utilized because it provides not only a restrictive effect but it also provides a malabsorptive effect is what's called a ruiny gastric bypass

basically what you do is you take the stomach and you cut it into a small little pouch and then this other big pouch does nothing right and even the the dadum here which is where a lot of nutrients get absorbed does nothing so what you do is you take the pouch and you take this tiny little segment here and you kind of move it past the dadum here and then you're going to reattach it at this part here here the concept behind this is very interesting the reason why is if food comes down I'm going

to have a very small little pouch that's going to cause the stomach to stretch really quickly if the stomach stretches really quickly I'm going to have appetite suppression early satiety all right cool that will help me to potentially reduce my intake on top of that any food that does kind of make it through here it's going to bypass the dadum that means I'm going to not absorb as many nutrients as potentially possible because a duum absorbs a lot of our nutrients and so this will not only provide a restrictive effect but also prevent me from

absorbing as many of the calories as I'm intaking and so that's the benefit of a gastric bypass surgery there is another one called a dadal switch procedure and it's kind of similar to this one we're not going to talk about it all right my friends that covers obesity and metabolic syndrome I really hope it made sense I hope that you guys did enjoy it and as always thank you love you and until next time [Music] for