Dr. Avinash Phadke and Dr. Manisha Talim in conversation with Ms. Ekta Batra, Anchor, CNBC-TV18,
- …..on Semaglutide and newer weight loss drugs: Where do we stand today?
Ms. Ekta Batra: Thank you, everybody, for joining in. I think I forgot to mention that we also have Dr. Phadke, who is my father-in-law, on the panel. So this is the first time in my career that I have the opportunity to interview him. We have a lot of conversations over the dinner table, but today it will be wonderful to hear his views as well as Dr. Talim’s views on what is probably one of the hottest topics in medicine today, which is basically GLP-1 drugs, weight loss drugs. Lots of people cannot pronounce semaglutide or tirzepatide, but they all know that they are weight loss drugs.
So I am going to kick off the conversation by asking the panellists to explain what these GLP-1 drugs are and why they are so useful to us.
Dr. Avinash Phadke: Thank you so much, Ekta.
These drugs have become the talk of the town. They have been called game-changers. They are among the most abused and the most lauded. The WHO, in September 2025, included them in the list of essential medicines. The essential medicines list already includes metformin and SGLT2 inhibitors, and now GLP-1 is also included in the list of essential medicines by the WHO.
Semaglutide and tirzepatide, as she said, have been available in India in oral form for two years. Then Mounjaro, which is tirzepatide, has been available in injectable form for six months, and Ozempic is only recently available. So experience is mainly with oral semaglutide and Mounjaro.
Having said that, before we come to why these drugs are game-changers, is there any potential for abuse? Is the corollary that these drugs are to be taken lifelong, just like a blood pressure medicine, the correct way to think about them? Is there a way one can start and then get off? Is it equal to a blood pressure medicine or a statin, where you take it for life, and you are sorted?
The answer is yes and no. They have to be taken for life for the benefit to persist, that is the first answer. But unlike your blood pressure medicine, if one drug does not work, for example, you are on an ARB (Angiotensin II Receptor Blockers) and it does not work, you have a calcium channel blocker; if that does not work, you have another diuretic, a mineral receptor antagonist, a sympathetic blocker. You have many other options.
Similarly, with diabetes, you have many other options. You have sulfonylureas, you have SGLT2 inhibitors, you have metformin, you have imeglimin, you have saroglitazar, and so many others. In other words, you have a backup plan.
Those of you who are businessmen always draft an agreement with an exit option. You may not read through the whole agreement, so long as the exit option gives you an opportunity to get out of the deal, because that is your safety wall that ensures that if things go wrong, you have some mechanism to exit safely.
Is there an exit option for these drugs in terms of diabetes control? Yes. The answer is unequivocally yes. You have an exit option. You can choose another anti-diabetic drug.
But, God forbid, if for some reason you have to stop it, and real-world studies show that 50% of people stop it within 18 months of taking it, then you are likely to regain all the weight back, and this time with less muscle and more fat. You will regain it at a faster speed than the weight loss happened.
So, in that sense, it is not exactly equal to taking a statin or a blood pressure medicine, except for the fact that it has to be taken for life, and the benefit persists only so long as you take these drugs.
Now, before we start the conversation, I will briefly explain the basic physiology of obesity, and then I will leave it to Ekta to proceed with the questions and answers.
We have hormones called leptin and ghrelin. Ghrelin is a hunger hormone, produced by the stomach. It makes you feel hungry. After eating, you have incretin hormones, which are essentially what we will be talking about GLP-1 and GIP. But in their natural form they last in the body for two to three minutes, and then they disappear. Their role is to delay stomach emptying and make you feel full.
Leptin is a hormone we often forget about, but it is important for energy balance. It is safe to say that most of us are not leptin-deficient. So there is no treatment for obesity by injecting leptin. Leptin injections are approved only in cases of lipodystrophy, which is a genetically inherited disorder. They are not approved for obesity management and are not available in pill form. The injection is also very difficult to obtain.
If leptin levels remain high, just as we talk about insulin resistance, the body tends to ignore the leptin signal, which is to make you feel full, because we can develop leptin resistance as well. So these are the three basic hormones.
Ghrelin, the source of which is mainly the empty stomach, tells you to eat, that you are hungry. It peaks before eating and then drops after food intake.
Now, these are the hormones we discuss when we talk about GLP-1. These are naturally produced hormones in our own intestines. GLP-1 is produced by L cells in the intestine, and GIP is produced by K cells in the intestine. One is more proximal, one is more distal.
What is the difference? They tell the pancreas to produce more insulin. They suppress glucagon, which is a hormone that tends to increase blood sugar. They slow stomach emptying, and they make you feel full.
Now, if they are so good, then why do we put on weight? Because in their natural form, they last in the body for only two to three minutes, and then they disappear.
What we are talking about are the same hormones introduced in drug form, but modified in a way that makes them last in your blood for a period of one week, rather than two to three minutes. So every time you eat something, this increase in hormones will be sustained for a period of one week. They will last much longer, making you feel fuller, slowing your stomach emptying, and significantly suppressing your appetite. That is how you lose weight.
So do not think that these are abnormal hormones coming from somewhere else. They are based on hormones that your own body naturally produces. These are normally there in your body, produced by your own intestinal cells, but the signals are weak and not long-lasting.
Leptin, as a treatment, is not used for obesity. Nobody uses it. In cases of lipodystrophy, a genetically inherited condition, leptin injections can do wonders. There are cases which lose liver fat by 50% just on leptin injection, but leptin-deficient states are very, very rare. So, for most of us, leptin is not a management option, but it is a good hormone to understand.
What is the problem in obesity? It is how the WHO defines it. It is not something new. In 1948, the WHO defined it in some other way, they simply called it excess fat and a BMI of more than 30. Then they redefined it as a state of abnormal hormonal homeostasis with fat deposition and some degree of insulin resistance, which is the most common definition, though there are exceptions.
Now, the core problem in obesity is that your ghrelin signal is very strong. You tend to eat a lot because you are hungry. Each time you eat a carbohydrate meal, the insulin spike is very high. That spike of insulin also makes you more hungry, so you tend to eat again.
Suppose I have eaten cherries or strawberries with cream. My sugar spike is minimal because cream is fat; it does not produce a sugar spike. If I eat the same strawberries with curd, the sugar spike is a little more. But if I eat a slice of bread, just one slice of bread, it is like taking four teaspoons of sugar at one time. That kind of insulin spike will happen, and you will immediately get hungry again after a couple of hours.
The other problem in obesity is that the incretin signal is weak. So we have drugs called gliptins. Many of you must be on gliptins because they were considered among the safest drugs. They inhibit this enzyme called DPP-4, which degrades the incretin hormones that are naturally produced in our intestine. By stopping their degradation, instead of lasting for two minutes after a meal, they last longer but not like a week. With DPP-4 inhibitors, they last for a few hours. But when you take a GLP-1 receptor agonist or a dual GLP-1/GIP drug, the signals are much stronger, lasting for a week.
The weight reduction effect is not seen with gliptins, but it is seen only with GLP-1 and dual incretin drugs. Most importantly, the magnitude of sugar reduction is far greater with these drugs than with the earlier gliptin drugs.
If you are going to start them, you have to stop the gliptin because the pathways are the same, through the incretin hormone pathway. In other words, if somebody is taking sitagliptin or linagliptin and wants to take Ozempic, he or she has to first stop linagliptin or sitagliptin before starting Ozempic, because the pathways are common.
Why can’t the body fix this naturally? Because satiety is not under good voluntary control. The natural hormones that make you feel full, the incretins, do not last for a long time; they last for only two to three minutes and then they are destroyed. If you have a high-carbohydrate meal, it is very difficult to avoid the temptation of another snack a couple of hours later. Unless you have strong willpower and are guided by a physician about a lifestyle reversal programme, people find it difficult to lose weight, or they go through cycles of weight loss followed by weight gain again.
What these medicines essentially do is that they act at the brain level to suppress your appetite. They act at the level of the pancreas to produce glucose-dependent insulin release. In other words, insulin is produced only when you eat food, so there is no risk of hypoglycaemia, unlike older drugs called sulfonylureas. Some of you may be taking Diamicron MR or Amaryl. With this type of drug, even if you do not eat, insulin is still produced, and your pancreas is constantly stimulated. So if you skip a meal at night, you may have hypoglycaemia and need to have something sweet just to maintain your blood sugar. That is not the problem with these drugs, that is a very good safety feature.
In the stomach, they cause delayed emptying, so you do not feel hungry. In the liver, they reduce what we call glucose synthesis. Through all these mechanisms, they become very effective in glycohaemoglobin reduction, to the tune of anywhere between 1.5% to 2.3% reduction in HbA1c. A gliptin, which also operates through the same incretin pathway, reduces HbA1c by about 0.8% at best and has no weight loss benefit because the appetite suppression is not so strong, as the hormones are not retained for a full period of one week.
Having said that, I will hand over to Ekta, because this gives you the background to appreciate the discussion about the drugs; otherwise, it is only a chemical compound without understanding the physiology.
Ms. Ekta Batra: Thank you for that explanation. Without much further ado, I am going to kick off the conversation.
Dr. Talim, I am going to start with you. The statistics are that semaglutide results in 14% to 15% average weight loss in a person who takes it. Mounjaro is expected to be even better, at around 20% to 21%. We all know it is the top-selling drug in India right now. It has overtaken our favourite Augmentin in terms of sales as well. That is how popular Mounjaro is in the Indian market, and it was introduced just a couple of months ago.
From a doctor’s point of view, how transformative is this drug as compared to anything we have had before globally and in India?
Dr. Manisha Talim: In my opinion, it is very transformative. We know that even a 5% weight loss has benefits on blood pressure, sugars and lipids. If the weight loss is 10%, there are additional benefits on cardiac events. The greater the reduction in weight, the more organs are positively affected. For example, there are benefits for liver disease and benefits for osteoarthritis.
Therefore, having a drug that provides so much weight loss is definitely path-breaking. But these drugs have to be used under supervision and with monitoring.
Ms. Ekta Batra: Tell us about how many patients you are prescribing the drug to now, and what results or transformations you have seen in your patients.
Dr. Manisha Talim: The main thing that stops me from prescribing it more widely is twofold. One is the cost. I would have prescribed much more if the cost were lower. Secondly, there are some side effects that are of concern. We have safety data of four years, so I am cautious in using them. I would say I prescribe them to about 10% of my patients.
Ms. Ekta Batra: There was one doctor who told me that one in four prescriptions are now with either semaglutide or tirzepatide. That is not the case?
Dr. Manisha Talim: Not in my practice. I prescribe to around 10% of my patients.
Ms. Ekta Batra: But Dr. Phadke, Dr. Talim just mentioned side effects, and I think that is something of concern to anyone contemplating taking the drug. The common side effects are nausea, which occurs in around 15% to 30% of patients, and vomiting in around 5% to 10%, especially when the dose increases. How manageable are these side effects and how often do they result in stopping treatment?
Dr. Avinash Phadke: Here, you will see a huge discordance between clinical trial data and what we call real-world outcomes.
For example, with statins, the literature mentions that in clinical trials only 5% of patients had myalgia. In the real world, 20% of patients report myalgia with statins. Why does this discordance happen? Those who had muscle side effects were weeded out of clinical trials to begin with. Those prone to muscle issues were not continued in the trial programme. So it becomes a very biased population.
Similarly, if you look at real-world data, the latest one is from the Oxford group, who studied 9,300 patients in 37 clinical trials, published in the British Medical Journal in January 2026, over 18 months, 50% to 60% of patients on GLP-1 stopped it for one reason or another. Some stopped due to side effects, some due to cost, some due to vision issues or worries, some due to palpitations, which is a rare side effect, though there is an overall increase in pulse rate of four to five beats per minute, which people do not often discuss.
Most importantly, doctors advise that anybody on a GLP-1 should get an eye check-up done. All diabetics are prone to retinal issues, and they can develop retinal problems while on medication. Then what do you do? Do you withdraw?
The Oxford data showed that if 50% to 60% of patients have to stop the drug, their weight comes back at a faster rate than the loss of weight. They regained all the weight and the metabolic benefits disappeared. I am not saying this happens to all patients.
So they should not be used at random. As Dr. Talim said, she prescribes them to about 10% of patients, there is a reason for that. If you are grossly obese, have obstructive sleep apnoea, fatty liver, uncontrolled diabetes. But suppose you are a lean patient at risk of losing a lot of muscle mass, would you use them? If somebody already has glaucoma or retinal issues, would you use them? Somebody with a history of pancreatitis? A history of thyroid cancer? You would not.
Not only that, in cases of severe dehydration, many patients develop acute renal injury, not because of the drug per se, but because they vomit a lot. There may also be concomitant antihypertensives, which can precipitate renal injury. These things are seen.
I am not painting a picture that these drugs are not game-changers; they are. They are on the essential medicines list. Provided we choose the patient population judiciously, keeping in mind the side-effect profile, the risk-benefit ratio must favour the benefit and not the risk.
Ms. Ekta Batra: So who is the person, or who is the patient, who should be prescribed a drug like this? Dr. Talim.
Dr. Manisha Talim: If you have a patient who is obese, that would be a BMI of more than 30, or more than 27 with comorbidities and they do not have various complications such as existing gastrointestinal issues or eye complications, then that kind of patient, who is stable and would follow instructions, monitor regularly and come for follow-up, would be the ideal patient for it.
Ms. Ekta Batra: Have patients come back to you with side effects?
Dr. Manisha Talim: Not yet, but we have just started, so it is still early. It is a relatively new drug, and when we start it, we increase the dosage in a gradual, stepwise manner. That does reduce the likelihood of complications. However, it takes time for complications to occur, so I would still be careful and cautious.
Ms. Ekta Batra: What do you tell a patient who walks into your clinic? What is the first line of treatment that you give them, and when do drugs such as these come into play? Is this a second line of treatment or a first line? Hypothetically, if a patient walks into your clinic, what kind of treatment would you give them?
Dr. Manisha Talim: Every treatment has to be customised. It is individualised. Earlier, we used to focus on sugar control; it was glucose-centric. Now therapy is complication-centric.
We assess the patient’s weight, blood pressure and other parameters, and see what kind of complications they have. Suppose they are at risk for atherosclerotic complications affecting the heart or the kidney, then we would consider it.
The first drug that we generally use is metformin. After that, we would consider these newer drugs. If they have a high risk of complications, we would think of a GLP-1, but again, only after looking at the patient profile, whether they would be regular with follow-ups, whether they already have gastrointestinal issues. Everything has to be individualised. There is no one particular plan for everyone.
Ms. Ekta Batra: And metformin with food control, diet control and exercise?
Dr. Manisha Talim: Lifestyle modification would be the first thing. In fact, even when a patient is on GLP-1 analogues, lifestyle management is extremely important. They must maintain adequate protein intake; otherwise, there would be muscle mass loss. They also need strengthening exercises for the same reason. You cannot think that this is a miracle drug that does not require lifestyle modification. That has to be a part of the therapy as well.
Ms. Ekta Batra: That is what I was going to say, for all the ladies and for myself, it is not a miracle drug that you just take and the kilos melt off.
But Dr. Phadke, I wanted to come to that Oxford study where it says that people regain 9 to 10 kilos in the first year and are back to their original weight in the next 18 to 24 months. So how much sense does it make to actually take the drug in the first place? Do you then need a lifelong dosage in order to maintain your weight?
Dr. Avinash Phadke: Yes, the answer is yes. You need it lifelong.
I will compare it to something many ladies here may relate to. For osteoporosis, suppose you are taking denosumab, what we call the Prolia injection. Ask any patient how long they would take it and what happens when they stop. First of all, they are told to finish any dental procedures beforehand because there is a risk of jaw complications.
But what is not always emphasised is that if you stop it, then there can be severe rebound osteoporosis. Patients are not always clearly told that it is probably lifelong therapy. And if you develop dental issues or other complications, there is no fail-safe backup plan. Even if you migrate to bisphosphonates, rebound osteoporosis can still occur.
Prolia is justified in metastatic bone cancer, for example, in carcinoma of the breast with metastasis or advanced prostate cancer because in those cases the risk–benefit ratio clearly favours its use.
To answer your question: if somebody has tried multiple cycles of weight loss and lifestyle modification without success, I would look at it this way, even if the success rate is 50%, it is still better than 0%, because that person has already exhausted other options. They have exhausted lifestyle modification and appetite control through willpower.
These drugs do not modulate your basal metabolic rate. They do not alter your body’s energy requirement. What they modulate is appetite, the sensation of stomach fullness, delayed gastric emptying, appetite suppression and sugar control.
There is one important distinction I want the audience to know. Officially, semaglutide that is, Ozempic, was approved for diabetes control. In September 2025, it received approval for two additional indications: reduction in cardiovascular disease and reduction in kidney disease. That is not the case with Mounjaro.
Mounjaro produces greater weight loss and has approval for diabetes and weight loss, but it does not have approval for kidney or heart protection.
The highest-dose semaglutide, what we call Wegovy, is also approved for non-alcoholic steatohepatitis, what we conventionally call fatty liver, specifically advanced stages with grade 2 fibrosis. Trials have shown significant reduction in progression in patients who might otherwise have ended up with cirrhosis. It has reduced risk by 50% to 60%.
So, in that sense, semaglutide has additional benefits over Mounjaro. While Mounjaro offers better glucose control and greater weight loss, the cardiovascular, liver and kidney risk reductions are proven with semaglutide and not yet with tirzepatide.
Ms. Ekta Batra: Dr. Talim, one of the points regarding these weight loss drugs is dose escalation. You start with the smallest dose, but the body seems to become resilient to that dose. Either weight loss stagnates or weight returns, and then the dose is increased. Explain that to us.
Dr. Manisha Talim: The smaller doses are not capable of producing significant weight loss. Weight loss is dose-dependent. We start low and go slow to avoid side effects, because the most common side effects are nausea and vomiting. About 15% of people stop using the drug because of these effects.
So gradual escalation helps improve tolerability.
When patients stop the drug, there is rebound weight gain. The metabolic rate changes, the set point changes, and different people have different gut flora – all these factors influence weight regain. Those who have diabetes, thyroid disorders or depression tend to have a higher likelihood of regaining weight.
Therefore, when building up the dosage, it should be gradual. And even when someone wants to stop the drug, that too should be gradual, because the metabolic set point and related factors need to adjust slowly.
Ms. Ekta Batra: Dr. Phadke, I just wanted our audience to understand what happens when you stop the drug. Why does the weight come back like a rubber band — almost in full force and you tend to eat much more, resulting in weight regain? At least that is what the Oxford study has indicated.
Just explain what this hormone is and why this happens. Is it suppressed with the medicine, which then results in it bouncing back more strongly?
Dr. Avinash Phadke: As I have already discussed, both GLP-1 and GIP are endogenous hormones. That means they are naturally produced in your own body from intestinal cells called L cells and K cells. The problem is that the signal is very short-lasting, it lasts for only two to three minutes.
If you take a DPP-4 inhibitor, which is a gliptin, the signal lasts a little longer. But with GLP-1 receptor agonists or dual incretin drugs, the signal is much stronger and lasts for an entire week. There will be newer drugs where the signal may last for one month.
In other words, appetite suppression is much more prolonged compared to your naturally produced incretin hormones, which suppress appetite only briefly before disappearing. If the hormone action is sustained for a whole week, then appetite suppression, the sensation of stomach fullness, hunger management and sugar control are all more effective.
As I mentioned earlier, these drugs do not cause hypoglycaemia because they do not constantly stimulate the beta cells of the pancreas. They stimulate insulin secretion only when you eat food. If you are not eating, they do not cause hypoglycaemia on their own. So that risk is not there.
Now, regarding the Oxford study, it can be interpreted another way as well. Yes, 50% of patients stopped the drug and regained weight. But out of 100 patients, if they had not started GLP-1 therapy at all, many of them had already failed multiple lifestyle modification attempts. Earlier, their success rate may effectively have been zero. At least with GLP-1, 50% succeeded in keeping the weight off and maintaining metabolic control.
If you look at it from that perspective, it does not appear as discouraging. That is one reason why the WHO has included them in the list of essential medicines because they are essential in the management of morbid obesity.
The newer drugs, which may become available within the next year, are expected to produce weight loss approaching that seen with bariatric surgery to the tune of 30% of body weight. They are game-changers. They are not the answer for everyone. But for the morbidly obese, heavily diabetic patient with multiple complications who is unable to lose weight and who may not be willing to undergo bariatric surgery. They can be an ideal solution.
However, for someone who simply wants to lose three or four kilograms, reduce some abdominal fat or fit into a particular dress for a function, this is not the answer.
Ms. Ekta Batra: I just wanted to understand, we have Oprah Winfrey who has taken the drug, Karan Johar who has taken the drug, Venus Williams who has taken the drug. She has lost significant weight and said that although she works out eight hours a day as a professional athlete, she was never able to lose that weight before this drug.
But the drugs they have taken, semaglutide and tirzepatide, come with the serious side effects we have discussed. I am not talking about nausea, but about risks such as thyroid cancer, suicidal thoughts or eye issues. What makes them comfortable taking on those risks, Dr. Phadke?
Dr. Avinash Phadke: The Oprah Winfrey show has certainly created a lot of publicity in favour of these drugs, almost projecting them as a solution fully within the patient’s control. It also sends a signal, the book titled Enough, that enough of lifestyle advice; this is a hormonal issue, not a matter of willpower.
When that narrative is endorsed by high-profile personalities, including professional athletes, it has a major impact. However, any clinician would agree and there are many doctors here, that these drugs should not be marketed in that way. It is also important to note that there may be financial interests involved. These aspects are not always fully disclosed to the audience.
If you look at such programmes, everyone appears glamorous and fit, and there is not a single person discussing serious side effects. You hear only success stories ,15 kg lost, 20 kg lost, 30 kg lost. That is one side of the picture. If the Oxford study presents one perspective, these celebrity endorsements present a more glamorous, pro-drug version. The truth lies somewhere in between.
Ms. Ekta Batra: Dr. Talim, what about prescribing the drug for issues other than diabetes, for example, cardiometabolic issues and other expanding indications?
Dr. Manisha Talim: That is precisely the point, we should view this as a metabolic drug, not a cosmetic one. With that perspective, studies have shown benefits in cardiac complications, kidney complications, brain health and liver disease. That is why these drugs are included in treatment algorithms for diabetes patients, and in some cases even for non-diabetics with metabolic risk.
For example, in NASH – non-alcoholic steatohepatitis, which is a liver disease, these drugs have shown benefit. So we need to shift our focus from merely trying to look good to actually being healthy from within.
Ms. Ekta Batra:
Okay. All right. Well, just before we wrap up, I have a couple of questions under rapid fire. So I’m going to ask both of you, and if you could just answer in one short sentence, that would be helpful. Dr. Phadke, I’m going to start with you. The biggest misconception about GLP-1s?
Dr. Phadke : That it will make me look good without addressing my metabolic issues. I think my first concern should be that it addresses my metabolic issue and also makes me look better.
Ms. Ekta Batra: Okay, Dr. Talim, one patient who should not take these drugs.
Dr. Talim: Someone who has a personal or family history of medullary thyroid cancer or multiple endocrine tumours should not be taking this drug.
Ms. Ekta Batra:
Okay, Dr. Phadke, one thing you wish every patient understood before starting these drugs.
Dr. Phadke: I think they have to understand that it’s a lifelong journey and very few can manage to wean off and successfully maintain their weight loss. The patient has to be told by a clinician that this is a lifelong journey. The dosage could be altered or reduced in some cases, but you cannot completely do away with medication and maintain the same metabolic benefits and weight. The metabolic benefits and weight last only so long as you take the medication.
Ms. Ekta Batra: Okay, Dr. Talim, a red flag in a patient history that makes you pause.
Dr. Talim: That would be if they already have GI complications. In diabetes, we get something known as autonomic neuropathy, so they already have a tendency towards gastritis. I wouldn’t use this drug in such patients. It would be a red flag.
Ms. Ekta Batra: Okay. Dr. Phadke, who worries you more – someone obese or someone just chasing cosmetic weight loss, or both?
Dr. Phadke: I think real obesity is now classified as a medical illness, whether it’s a form of insulin resistance, whether it’s a hormonal disturbance, or whether it’s a lifestyle issue. There are multifactorial reasons. Even NASH — non-alcoholic steatohepatitis, there is no universal agreement that it’s a metabolic disorder of single origin. It’s not only glucose control or lipid control or insulin resistance. It includes gut microbes, lack of sleep, and many other factors. So the diseases are multifactorial, and the answer to these diseases cannot be a single medicine. In other words, even if you go on medicine, you cannot do away with lifestyle modifications while you are on medication.
Ms. Ekta Batra:
Okay, and Dr. Talim, lastly, are these drugs being overused in people who don’t medically need them?
Dr. Talim: Possibly, yes. For the same reason, they don’t understand the implications of use. They don’t understand the side effects that can happen. They might think it’s just about weight loss. But as we have discussed, it can have serious side effects on the eye. It can have serious side effects on the pancreas or elsewhere. So we have to be very careful and not jump to conclusions.
Ms. Ekta Batra: All right, Dr. Phadke as well as Dr. Talim, thank you very much for joining and speaking to us about the GLP-1 drug.
ROTARIANS ASK
I brought my semaglutide with me because I’ve just started it. And it’s only been a month, but I haven’t lost any weight and I’ve had no nausea, no side effects. I just wanted to know, the first time my sugar came high, the first medicine they gave me was this, not metformin or anything else, and only in the morning on an empty stomach once a day. Why on an empty stomach and only one sip of water? You’re always told to drink a lot of water with medicine. She said one sip, one tablet.
Dr. Phadke: So, you must be on oral semaglutide. Semaglutide, right? Yes. So that is Rybelsus in India. Oral semaglutide is to be taken on an empty stomach with only 50 ml of water and no other medication for the next one hour or so. That is because it has the potential for drug interaction and reduced absorption if taken simultaneously with other medication. Secondly, the weight loss with oral semaglutide is not going to be as much as with injectable — that’s the reality. They have now come out with the latest version of oral semaglutide, 25 mg.
How would you compare bariatric surgery with these kinds of drugs, and what would be the pros and cons?
Dr. Phadke: I don’t think I am qualified, that’s the first qualifier, I would say. But bariatric surgery has proven outcomes. To me, it’s almost an 80–90% success rate. What is heartening in those patients is that the metabolic benefit starts much before the weight loss benefits. So if somebody undergoes bariatric surgery, the fatty liver changes, sugar control, and blood pressure control precede the actual weight loss. So there is something more to metabolic surgery, we don’t call it bariatric anymore, we call it metabolic surgery, where there is a hormonal interplay and the remissions of obesity are to the tune of 80-90% for a period of 10 years. So somebody who is morbidly obese and wants to avoid all this I don’t think this drug will reduce the number of bariatric surgeries, but I think there will always be a place for bariatric surgery in spite of these drugs.
And then there is no continued requirement to take drugs and the side effects are far more limited.
Yes. At the same time, it’s major surgery. Of course, they now give statistics that the mortality rate and complication rate are similar to hernia surgery, that’s the latest data. But we have seen cases of peritonitis and many complications can happen because it’s major intestinal surgery. But in good hands, in 99% of cases, bariatric surgery gives fantastic metabolic as well as weight loss benefits.
You mentioned Mounjaro having an effect of reducing appetite, reducing weight, and taking care of sugars. What happens if the contrary happens with Mounjaro that you don’t lose weight, you gain weight, and your appetite doesn’t get suppressed? Is it possible?
Dr. Talim: No. What can happen is it depends on what dosage it is started with, and that is why it is stepped up. Your doctor would increase the dose strength gradually. Ideally, the patient should lose about 1% of weight per week. So if that’s not happening, then the dosage would be increased. Secondly, it’s not enough to only take the drug. As I said, there has to be lifestyle management. There has to be adequate protein intake. There have to be strengthening exercises. It has to be a complete programme and also include counselling. If all these things are done together, then there’s a higher chance of success with the programme.
So what you’re saying is it’s not the drug alone.
Dr. Talim: Yes. You have to have the whole package.