Dr. Rocio Salas-Whalen: Do Weight Loss Medications REALLY Work?

Summary

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The Neuro Experience Podcast — Episode Summary

Episode Title: Dr. Rocio Salas-Whalen: Do Weight Loss Medications REALLY Work?
Host: Louisa Nicola
Guest: Dr. Rocio Salas-Whalen, Triple Board Certified Physician (Internal Medicine, Obesity Medicine, Endocrinology)
Date: January 10, 2024

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Episode Overview

In this comprehensive discussion, Louisa Nicola hosts Dr. Rocio Salas-Whalen, a leading expert in obesity, to demystify weight loss medications—especially Ozempic (semaglutide) and related drugs—and their role in tackling the obesity epidemic. The two delve into the origins of these medications, the biological complexities of obesity, the efficacy and limitations of pharmacological treatments, side effects, insurance and access issues, the evolving definition of obesity, and future directions in both medicine and societal perception.

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Key Discussion Points and Insights

1. Obesity: A True Epidemic

• Obesity is described as a global epidemic, with projections that by 2030, 50% of the world’s population will have obesity ([00:04], [20:12]).
  • "The WHO estimates that in the year 2030, 50% of the world population will have obesity." — Dr. Salas-Whalen ([00:07])
• Obesity is not just about aesthetics; it’s closely linked to all-cause mortality, Alzheimer's, dementia, and is a direct risk factor for over 30 types of cancer:
  • "It is a risk factor for all-cause mortality, Alzheimer's disease, dementias, more than 30 cancers." — Louisa ([00:16])
  • "Breast cancer, colon cancer, prostate cancer, stomach cancer, throat cancer, and the list goes on and on." — Dr. Salas-Whalen ([00:27])

2. Understanding Ozempic & Weight Loss Medications

What Is Ozempic?

• Ozempic is part of the “incretins” drug class, specifically synthetic versions of GLP-1 (glucagon-like peptide-1), a gut hormone.
  • Originally developed for type 2 diabetes, these drugs help the pancreas produce more insulin in response to high glucose and increase satiety ([03:54], [09:29]).
  • "Ozempic falls under an umbrella of a class of drugs called incretins... synthetic hormones we make on our own." — Dr. Salas-Whalen ([03:54])
• They suppress appetite by:
  • Reducing ghrelin (hunger hormone)
  • Increasing leptin (satiety hormone)
  • Reducing reward anticipation for foods/alcohol ([05:35]–[07:06])

How They Work

• Dual effect on eating: Target eating for fuel and the psychological reward from eating.
  • "I like to describe it to my patients in two ways. I say this drug targets the two reasons humans eat..." — Dr. Salas-Whalen ([04:40])
• GLP-1’s natural short half-life: Synthetic versions provide sustained action ([09:29]–[10:34])

Origin Story

• These were initially diabetes drugs, but unexpected weight loss in patients led to new applications.
  • "It was an unexpected side effect... we were seeing patients coming back not just with better glucose control, but losing weight..." ([08:09])

Other Drugs Discussed

• Tirzepatide (Mounjaro): “Twin incretin” (GLP-1 and GIP), showing greater weight loss and fewer side effects ([38:49])
  • "Tirzepatide is a twin incretin... we see more weight loss and I would say close to zero gastric side effects." — Dr. Salas-Whalen ([39:09])

3. Evolving Understanding of Obesity

• Not simply a lifestyle problem: Genetics, hormones, environment, and socioeconomic factors play significant roles.

  • "Obesity is not a lifestyle problem only. We know now that it's multifactorial..." — Dr. Salas-Whalen ([14:14])

• Childhood onset is common: Many patients struggle with weight from a young age and have tried sustained diet and lifestyle changes ([13:01])

• Socioeconomic and food industry factors:

  • Food industry’s role: Markets addictive, unhealthy foods, creating environments that foster obesity ([15:39])
    • "The food industry cares zero about your health...Healthy doesn't sell. Cheap addictive stuff sells." — Dr. Salas-Whalen ([15:42])
  • Low-income populations at higher risk: Access to healthy food, time for exercise, and medication affordability are all issues ([17:31], [18:35])

4. Diagnosis, BMI, and a Focus on Body Composition

• Dr. Salas-Whalen critiques reliance on BMI and scale weight:
  • “We were targeting weight loss or fixating in a goal according to a number in the scale or the BMI... they're losing muscle almost at the same speed as body fat...” ([21:25]–[22:44])
• Advocates for:
  • Measuring body fat percentage (goal: below 28%)
  • Assessing visceral fat
  • Encouraging muscle preservation and growth ([23:28], [24:43], [26:56])

5. Who Is a Good Candidate for Medication?

• Not only for “obese” by BMI, but also those with elevated body fat or visceral fat—even in “normal” BMI individuals.

  • “Somebody with a normal BMI doesn’t mean that they don’t need the medication... more common to see the opposite: a normal BMI with high body fat and low muscle mass.” ([25:49])

• Cautions about improper use:

  • The rise of off-label use and “skinny fat” phenomena due to muscle loss ([29:41])
  • Importance of physician expertise and proper body composition tracking ([28:52])

6. Medication Use: Process, Duration, Best Practices

Is It Forever?

• Medications work only while they're taken, like drugs for diabetes or hypertension; obesity is a chronic disease ([35:06], [36:18]).
  • “Obesity is a chronic multifactorial disease. Chronic. We categorize obesity as we categorize type 2 diabetes...” — Dr. Salas-Whalen ([35:06])
• Goal: Use the lowest effective dose long term, combine with lifestyle factors ([36:45])

Side Effects

• Semaglutide: nausea, dehydration, constipation. Proactively drinking water helps ([37:11])
  • “It suppresses your hunger. It somehow suppresses your thirst...” ([37:35])
• Tirzepatide: fewer gastric side effects ([39:28])

Safety & Patient-Doctor Relationship

• Proper education and follow-up are vital; the efficacy and safety depend on prescriber’s expertise ([42:36])
  • “The efficacy and the safety of the drug is dependent on the expertise on who’s giving you the drug.” ([43:13])

7. Addressing Stigma: Obesity as a Disease

• Changing language: “patient with obesity” rather than “obese patient” ([53:04])
  • “We are moving to first people language. So we don’t say the obese patient anymore. We say the patient with obesity.” ([53:04])
• Emphasizing the removal of guilt and bias from obesity treatment ([45:54])
  • “Bias, bias, bias. That needs to be stopped. People are not creating obesity on themselves.” ([45:54])

8. Beyond Medication: Muscle, Protein, and Lifestyle

• Muscle preservation and growth must be actively prioritized in treatment:

  • “Don’t count me calories, don’t count me carbs, don’t count me pounds—count me your grams of protein per day.” ([50:38])
  • Discussing exercise—especially reaching muscle failure for growth ([51:29])

• Distinction between weight/fat loss and liposuction:

  • Liposuction removes subcutaneous fat, not dangerous visceral fat ([47:39], [48:17])
    • "The subcutaneous fat is not what makes you sick. So you can have a liposuction, but you’re still at risk for type 2 diabetes..." — Dr. Salas-Whalen ([48:17])

9. Future Directions for Obesity Medicine

• New generations of drugs: More potent incretins, drugs that build muscle while reducing fat, and oral versions on the horizon ([60:57], [62:00])
  • “There are incretin plus a muscle activating protein. So you lose weight and you gain muscle...” ([61:23])
• Dr. Salas-Whalen predicts profound societal and healthcare changes:
  • _"I believe that this is the one of the biggest change that we in our generation will witness in regards to medicine. I think this is the biggest thing until the cure of cancer." ([58:17])

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Notable Quotes & Memorable Moments

• Obesity’s roots & stigma:
  • Dr. Salas-Whalen: “I haven’t met a single patient with obesity that fits in that category of lazy couch potato…” ([13:01])
  • Dr. Salas-Whalen: “Bias, bias, bias. That needs to be stopped. People are not creating obesity on themselves.” ([45:54])
• On weight loss drugs changing the paradigm:
  • “For the first time we have something that ... is going to help you maintain the weight loss ... but keep you there, that is the difficult.” ([36:18])
• Future outlook:
  • “We’re going to slow down the progression of all the diseases that we've built specialties for.” ([58:17])
  • Louisa: "This is exactly like Botox—to be honest, anyone can completely do the–but I was like, now know who is actually injecting your face?" ([60:02])

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Timestamps for Significant Segments

• [00:04] — Is obesity truly an epidemic?
• [03:54] — What Ozempic is & how it works
• [08:09] — The story behind weight loss as a “side effect”
• [13:01] — Debunking the “lazy” obesity myth, patient stories
• [14:14] — Understanding multifactorial causes of obesity
• [15:39] — Food industry’s role in the epidemic
• [20:12] — Obesity stats, risk factors, and impact
• [21:25] — Changing the metrics: beyond BMI to body composition
• [26:56] — Muscle loss concerns and the “skinny fat” phenomenon
• [35:06] — Chronic nature of obesity: do you need these drugs forever?
• [36:45] — Dosing and long-term use of medications
• [37:11] — Side effects, especially dehydration and nausea
• [39:09] — Tirzepatide (“the iPhone 14 of the iPhones”) as next-gen weight drug
• [45:54] — Destigmatizing obesity and patient experience
• [50:38] — Prioritizing muscle, protein, and resistance training
• [58:17] — How these drugs could change healthcare
• [60:57] — The next phase: muscle-activating and oral incretins
• [62:11] — Dr. Salas-Whalen on the future and patient resources

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Conclusion & Takeaways

• Obesity is a complex, multifactorial chronic disease, not simply a matter of willpower or lifestyle—and its prevalence is surging.
• New incretin-based medications such as Ozempic and Tirzepatide are game-changers, but proper use, expert guidance, and holistic approaches incorporating muscle and metabolic health are vital.
• The medical and societal understanding of obesity is rapidly evolving, including language, diagnosis, and therapeutic priorities.
• The future holds not just more effective drugs, but potentially a real decrease in obesity-related disease across generations—if barriers of access, education, and stigma can be overcome.

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Find Dr. Salas-Whalen on Instagram @Dr.SalasW
Host: Louisa Nicola @louisanicola_

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Summary compiled to assist those seeking in-depth understanding of this highly informative episode—without missing the nuance and critical guidance shared by leading voices in obesity medicine.

Transcript

[A]

So this obesity epidemic, you're saying, and is it an epidemic?

[B]

It is an epidemic.

[A]

Okay, what percentage?

[B]

So the WHO estimates that in the year 2030, 50% of the world population will have obesity. Yeah.

[A]

And see, that's scary because it is a risk factor for a all cause mortality, Alzheimer's disease, dementias, more than 30 cancers. 30 cancers, wow. I didn't know it was that specific.

[B]

Breast cancer, colon cancer, prostate cancer, stomach cancer, throat cancer, and the list goes on and on.

[A]

Yeah, so it is scary. Okay, and you're saying that, you know, large majority, 70% of that population is driven through more than just lifestyle factors. I'd like to take a quick moment to thank our first sponsor, inside tracker. InsideTracker is a personalized nutrition platform that analyzes data from your blood and DNA to to help you better understand your body and help you reach your health goals. Many of you are following me on social media and you would have seen that. I did a full blood panel, a very comprehensive blood panel with InsideTracker in September and let me tell you, it came back with some scary results. My vitamin D was extremely deficient, coming in at 24 nanograms per milliliter. I'm a long believer of getting regular blood work, especially as a woman. But a major problem with a lot of blood tests out there is that you get information back about metabolic factors, lipids and hormones, but you don't know what to do with that information. With Inside Tracker, they make it super easy because they have a personalized platform that allows you to see the levels of all of those things, metabolic factors, lipids, hormones, etc, but it also gives you specific directives that you can follow that relate to nutrition, behavioral modifications, supplements. And this can really help you bring those numbers into the ranges that are optimal for you. I highly recommend you do at least one of these blood panels per year. I do too. But if you'd like to try InsideTracker, you can go to InsideTracker.com Louisa to get 20% off any InsideTracker plans. That's InsideTracker.com L O U I S A Rocio welcome to the podcast. How you doing?

[B]

I'm doing good. Thank you for having me.

[A]

I'm so excited to be doing this with you. We connected on Instagram. I've seen so much of your work and you are dubbed one of the world's experts on obesity and everything we're going to be speaking about today. But just to be clear, you are a triple board certified physician. You what are internal medicine, obesity medicine and endocrinology Endocrinology. Damn. So where were you? Where did you go to school?

[B]

I was born and raised in Mexico and I went to medical school there. When I finished my school, I came the United States to do my USMLE boards and then I did my residency at Albert Einstein, my fellowship. I did one year at University of Maryland and one year in John Hopkins and then one year of obesity.

[A]

Oh, wow. And now you reside here, your practice is here?

[B]

I live in the city, in Manhattan and I. My office is on Park Avenue.

[A]

Wow. And you're primarily seeing who definitely, I.

[B]

Would say 90% of my patients are for weight loss.

[A]

Yeah, huge. And that's what we're going to get into today. Now, everybody listening has probably heard of this word ozempic, right? I've heard of it. But you know, over the last eight months, I think it's just become this thing that so many people know about everyone. I mean, I feel like everybody who everyone I know is like maybe associated with somebody who's taking Ozempic, maybe they're not. So we're going to get into that. But let's start off by, can you give us a broad overview of what ozempic is?

[B]

So Ozempic falls under an umbrella of a class of drugs called incretins. This class of drugs, they're synthetic hormones, gut hormones that we make on our own. So they're a synthetic version of it. And what incretins do they target the way that we eat, they target the way we think about food. They were initially developed for type 2 diabetes control. So they work in the pancreas by producing more insulin. When the glucose goes high, you actually have to have an elevated glucose to act as an anti diabetic drug. But if your glucose is normal, it doesn't touch the pancreas. That's why we don't see hypoglycemia in patients that don't have diabetes. And we're using this drug, right, and it doesn't cause hypoglycemia on patients with diabetes like insulin. So that's a big difference between what we find with these drugs in that it won't cause hypoglycemia. So for many patients that's always a concern if they're going to start eating like a low caloric diet and the way that they work in regards to weight loss. I like to describe it to my patients in two ways. I say this drug targets the two reasons humans eat. One, we eat for survival, for energy, for fuel. Right. And the other one is we eat for an anticipation of our reward from food, from alcohol, from smoking. Right. We anticipate a certain feeling from either the food or the alcohol for some. Right. So in the fuel part, what it does, it increases your satiety, your fullness hormones when you start eating. So you may get full with half what you normally would need to feel full before.

[A]

So what hormones are they specifically?

[B]

So it's ghrelin and leptin. Ghrelin is for. Increases your appetite, so it suppresses ghrelin.

[A]

So it suppresses ghrelin.

[B]

So it's ghrelin suppresses your appetite and increases leptide and your satiety, other satiety hormones. Right. So what it does is that you start eating and you get full with one third of half of what you normally would need. And then in between meals you don't feel hungry because it's suppressing your hunger hormone. So versus diet, when you're doing like a low calorie diet or any source of diet that decreases your caloric intake. Yes, you're eating small, but you're only thinking about food. You're thinking about your next meal. And for many patients, or for many people, the next meal and you blow it up. Right. Because of that hunger that you've been holding with this drug is you eat two meals a day for the majority of patients, feeling content through their meals. And then in the brain and the amygdala and the hedonistic eating, we have receptors for this drug or for this hormone. And what it does, it removes the anticipation of our reward from food. And again for some, for alcohol is actually being researched for alcohol abuse. Because it's that anticipation that you're going to feel when you have that drink.

[A]

Yeah, right.

[B]

You're going to feel, you anticipate that, you're going to get relaxed. You anticipate that in a social with your friends or certain food will make you feel better, special, not depressed. So when you're on these drugs because that, the habit, the routine is there, you reach for it, but then you try it and you feel zero reward from it.

[A]

That is.

[B]

So then you're like, I don't want it, I don't need it.

[A]

Yeah. So because, you know, a lot of the times, especially emotional eating, for example, you, you know, you'll eat the chocolate bar, the cake, whatever you turn to emotionally and you get something from it.

[B]

Exactly. You get a relief.

[A]

You get a relief.

[B]

Yeah. So it's, it takes it away. And it's not a negative thing. Many people like, oh my God, that's my happiness. It actually, for the majority of patients, I would say it's a really positive thing because they say for the first time in my life, I can think of a different source of relief. I can think of different things to do. I can exercise, I can go for a walk, I can call a friend. So they're not relying on food or beverage for that sort of relief.

[A]

Now, correct me if I'm wrong, you mentioned it was originally used for diabetes. Okay. And we know that insulin is a hormone primarily involved to lower glucose. Yes. Why now? All of it. Were they just seeing a lot of patients maybe losing weight on this drug and they thought, okay, let's, let's, you know, retarget the public and say that now it's a weight loss drug. Is that how it went?

[B]

It did, actually. It was, it was an unexpected side effect. An unexpected, an expected side effect. And the first that was approved of the class of incretins was called Bieta exinetide, and that was in 2005. It was a twice a day daily injection, 30 minutes before your breakfast and 30 minutes before your dinner. And what we were seeing, because I started using them when they came out, I was like, when I finished my training and they started happening. So we're like, oh, we have something new to use. And we were seeing patients coming back not just with better glucose control, but losing weight, which we rarely see that in diabetes treatment. Right. We rarely see some drug that's going to control your glucose and it doesn't promote waking up. Right. Because let's say insulin sulfonylureas, those medications can cause hypoglycemia and hypoglycemia makes the patient eat more. So there's always weight gain with insulin or sulfonylureas. So for the first time we have a drug that actually it was improving your glucose in a positive way and you were also losing weight and the weight loss was helping your diabetes get better. So it was a win, win situation because the majority of patients with type 2 diabetes had either overweight or have obesity.

[A]

So is, that's, that's incredible. What, so what's. Okay, so what is GLP1?

[B]

So GLP1 is a hormone that is produced in our small intestine.

[A]

Okay.

[B]

And it's produced in response to a meal. Right. So when we eat, that small gut where it's produced receives a message from distension of the stomach, it sends this message and then it gets released. And the function of that hormone is to improve insulin production. In your, in your pancreas to help you digest or to help your glucose normalize after a meal. Right. But it also controls some of your appetite. The problem with the innate GLP one is the, the half life of, of of the natural hormone. It's about one to two minutes. There's an insight. Yeah. There's an enzyme that, that degrades it very quickly. Dpp4 app4. Dpp4, that's the enzyme down innate GLP1.

[A]

Okay.

[B]

And. And it doesn't. And then the innate. It also doesn't cross the blood brain barrier.

[A]

Interesting. Oh, not many things cross that barrier.

[B]

Yeah.

[A]

Okay.

[B]

Thank God.

[A]

Thank God for that. So then you're saying that. So is ozempic just is Ozempic and GLP1, are they the same thing?

[B]

Yeah. Okay. It's a synthetic.

[A]

Synthetic GLP1. Okay. And now this. I, I guess you probably get asked this a lot and it focuses around why do we need this to begin with? Meaning why can't we just prescribe interventions for weight loss rather than injecting something synthetically? And this also goes into the second part of the question, which is what is the current state of this obesity epidemic here in the US to answer.

[B]

Your first question, we have to take a step back. Right. And we have to think about obesity and what we used to associate obesity with or as a result of and what it truly is. Right. And I think that helps to understand why we need the medication. So before, and I can tell you, even when I was in medical school, we got taught that obesity was self induced almost. Right. Like you were eating too much, you were not exercising. You had the idea of this, the, the couch potato eating bonbons and not moving. And that's why they were. Had obesity or were overweight. Right. If they wanted to change it, they could. Right. So you associated the patient of Lacey, not smart, not willing. Right. Not having self drive. But the reality and what we've discovered, and this I can tell you very personally after treating more than 2,000 patients with obesity, it makes me feel really sad and dumb for thinking that way, that it was what you're doing or you're not doing. Right. But what I've learned from my patients and what we know now is that patients were doing, we're following our recommendations, were eating less, we're exercising. Right. And they were not losing weight. Patients were trying. Many patients, I would say I haven't met a single patient with obesity that fits in that category of lazy couch potato, doesn't want to change the weight. What yeah. And then when you have this deep conversation with patients and you go further and further back in their story, most patients started at a very young age to struggle with weight.

[A]

Yeah, yeah, I've seen that. Especially when you look at, like, some of the documentaries they follow. I mean, I'm talking like morbidly, like huge people. If some of them are finding it hard to walk, they track them and they're like, you know, this was a picture of little Katie at age 10. And Katie is very big for.

[B]

Exactly. So they've struggled. Some patients tell me, my mom put me on my first day a date diet at 9 years old, or I went on my first diet or my first fat camp at 12. Right. So since that age, such, such an early age, they are aware of their weight. They are aware that they have to do modifications on the way that they eat. Right. Or the way they're going to move. So most patients have tried one way or another. Some patients have personal trainers, personal chefs, so they're following exactly what you're recommending. And they're still not losing weight. Because we realize that obesity is not a lifestyle problem. Only we know now that it's multifactorial obesity. One part, yes, could be lifestyle. There's genetics, family history. And in the, I would say in 70% of the patients, there's always some back family history of obesity or overweight. We have hormonal problems or hormonal changes, let's say PCOS in women, perimenopause, menopause and women. So that's going to promote weight gain, then aging.

[A]

Is that just due to estrogen?

[B]

Yeah, exactly. Lowering changes of estrogen or increased testosterone and pcos. Then we have aging, which is also not modifiable. Right. And then we have environmental causes. And environmental. It can go from stress of work, what you were exposed in utero, if you were exposed to bpa, endocrine, disrupting chemicals, the food industry. Right. All of these things can promote lack of sleep.

[A]

Lack of sleep, because I know with.

[B]

Lack of traveling for patients that are always in jet lag or moving from one place to being and on the airport. So those are environmental things that you may have some sort of control, but you would have to modify a lot of, like your work or your lifestyle where you live. Right. So really the only, only thing that the patient has truly control of is the lifestyle part. They're eating and they're moving. But then you have other four big factors that are going to be promoting weight gain, and that's why it has to become really non sustainable, very restrictive, that lifestyle change to see some weight loss, but it's not, not sustainable because then you're going to have all the other factors there promoting weight gain.

[A]

Okay, so when it comes to the obesity epidemic per se, who do you think is to blame? Is it the food industry?

[B]

I think the food industry has a big, big part of responsibility of where we are as a society and obesity. Right. The food industry cares zero about your health. Right. It's an economic, it's a business. And healthy doesn't sell. Cheap addictive stuff sells. So their main goal is to make money and not for you to be healthier. Right. That's, that's going to be our, our part of our responsibility as a consumer. But definitely I feel like there's going to be a point where the food industry will be held accountable as the tobacco industry was. Right. That we know. But at one point they cannot hide it anymore. And at one point we're going to be healthy that we don't want that food anymore. Right. That we don't crave that food that is not goes with our vibe right now being healthy, lean and fit. Because this medication is letting us get to a point that we might have never gotten personally without the medication. Right. In a healthy state. So I feel the food industry is going to really feel a hit in regards to what they sell.

[A]

Well, I read that the food industry, let's just look at PepsiCo for example, may has like a marketing budget of like a billion dollars.

[B]

Exactly.

[A]

Yeah.

[B]

But whenever a drug gets approved, their stocks drops. So they, they're feeling.

[A]

You think they'll lobby against Ozempic?

[B]

I feel like I, I mean I don't want to do conspiracy theories, but definitely the food industry, the restaurant industry are going, the alcohol industry are going, are noticing already the, the effects of being on these drugs and having a healthier lifestyle.

[A]

But then again you also have to question socioeconomic status, you know, families who may not be able to afford fresh food, etc. And then so they see the marketing of this, you know, industrialized food and corn and whatever it is and they think okay, I'll just buy this for the kids. And that's how it, it adds up.

[B]

Yeah, exactly. And that's, I think that has to be, we have to blame the food industry for that. Right. Because they're making unhealthy food for the masses when they're not taking any responsibility of what they're causing. Right. And if you talk about the low income population, then they're more risk of developing obesity, chronic Disease because of what they're eating, because they don't have time to work out if they have two jobs. Right. And then you make these medications for the ingredients very inaffordable. So they will be having to have changes because we're not going to make only the rich ones healthy and the poor more unhealthier. Right.

[A]

But how would the socioeconomic, the low income earners benefit from WeGovy if there is a huge price tag on there?

[B]

Well, unfortunately, either insurance, they will have to get some sort of insurance. Right. Medicaid covers Ozempic. So I would say don't, don't assume that it's not going to be covered by whatever type of insurance has you. We're surprised many times like oh wow, we got covered. Great. It's an investment, Right. I will always say this is a, this is an investment that is going to really give you results because it's going to be your health. What of use if you are a single mom with two jobs and then you get sick. Right. So I always see it as, and people spend money on diets independent of the socioeconomic status. So I feel like we also have to change the way that we see to this drugs. Right. If you're telling me I'm going to buy a drug to make me skinny because I want to go to a wedding, then you can say, yeah, that's, that's insane. Right. But I'm going to invest on this medication that overall is going to improve my quality of life, how, how I feel physically and mentally. Right. Because obesity has a great toll in mental health. Then you can see it as an investment too. Right. So I don't want people to say, oh, I can't afford it. No, but what are you investing in? What can you invest now in regards to your health?

[A]

Yeah. So this obesity epidemic, you're saying, and is it an epidemic?

[B]

It is an epidemic.

[A]

Okay, what percentage?

[B]

So the estimates that in the year 2030, 50% of the world population will have obesity. Yeah.

[A]

And see that's scary because it is a risk factor for a all cause mortality. Alzheimer's disease, dementia is more than 30 cancers. 30 cancers. Wow, I didn't know it was that specific.

[B]

Breast cancer, colon cancer, prostate cancer, stomach cancer, throat cancer, and the list goes on.

[A]

Yeah. So it is scary. Okay. And you're saying that, you know, large majority, 70% of that population is driven through more than just lifestyle factors.

[B]

We know now that what the mother's BMI pre pregnancy can impact the weight of the offspring, what they do or how Much they gain in the first trimester can have an impact on predicting the weight of the offspring. Right. So even before we were born, it can determine how our weight is going to be just by what our mother did, who was probably not aware. Right. Of. Of what choices she was doing or eating or drinking that or even if she had family history and she was struggling with weight on her own. Right. So even that we know that can impact a person's weight.

[A]

I've heard you speak about BMI and you're not. It's not something that you really like anymore. Okay. So how are you diagnosed or what is an obese person? Because according to a BMI, I mean, I haven't done my BMI actually.

[B]

Good.

[A]

You don't need it early 20s, but yeah, I haven't done it.

[B]

It. So again, weight loss medicine is evolving. Right. It's relatively new. And what we're learning is that we were targeting weight loss or fixating in a goal according to a number in the scale or the bmi. Right. But really we didn't know what the patient was losing. Right. They could have. Now that we're doing body compositions on patients, I can really see what is it that the patient is losing. And many of the times they're losing muscle almost at the same speed as body fat. And what. And that's happening that if they're losing body fat and muscle at the same rate. Yeah. They're going to be £50 less. But be sarcopenic obesity, which is what we call a skinny flat, skinny fat, meaning that you're still at risk for metabolic diseases, you're still at risk for those 30 cancer, you're still at risk of type 2 diabetes. Yes. You were in size 2, but we didn't improve your body composition.

[A]

Yeah. Your body fat percentage maybe still higher. Okay.

[B]

And I see that every time if a patient loses weight, losses muscle, they may gain percentage body fat even though they lost ten pounds. Right. And the patient is so happy. And I'm like, oh, well, not because of the muscle loss. Right. So I think we've been seeing weight loss very different from what we should. And it's more concentrating in muscle mass and fat loss and not total body weight loss. Right. And if you just go by the scale of the bmi, we're going by total body weight loss, but we're not knowing what's happening inside the patient. Right.

[A]

Yeah. So then. Okay, then what would be a classic measurement of, you know, giving a diagnosis of obesity then?

[B]

So we go by percentage body fat, visceral Fat. Right. So those are my. Those are the markers that obesity specialists use to categorize a patient with overweight or obesity and levels of obesity. And those are our targets to improve in the weight loss. Right. And the gold standard to do a body composition is an mri. But we're not going to be doing MRI on patients every visit. Right.

[A]

Is that a DEXA scan or is.

[B]

It an actual mri?

[A]

Wow.

[B]

The second is a DEXA scan and the third is an impedance machine. Yes, Embody. And there's other brands right out there. So the easiest to use and the safest to use every vest. Every Is going to be an impedance machine. Right. But let's say some doctors that don't have this machine set at the office. Right. I would suggest measuring waist circumference, doing other body. Yes, the weight, but doing waist and then going by that more in regards to weight loss. Right.

[A]

So you're generally looking at, I mean I. You can't even go by age or anything. It's really dependent on you. So are we looking at what a 30 body fat? Are we looking at 40 body fat?

[B]

So ideally or normal is below 28. Equal or below 28.

[A]

Okay, so anything above 28 body fat, regardless of if it's visceral fat.

[B]

Well, regardless of bmi, regardless of visceral fat, we consider that.

[A]

And then having obesity, that would make that individual a perfect candidate.

[B]

Yes.

[A]

For medication for Ozempic, which is a. Once a week.

[B]

Once a week subcutaneous injection.

[A]

Yeah.

[B]

Very small needle.

[A]

Interesting. I mean now given that, you know, 28, like as you know, we were speaking offline, you know, we include the DEXA scan in when we bring for everyone. And I'm generally looking at bone density, to tell you the truth, and lean body mass. I'm very interested in that. Rarely do I see actually over 28%. But I'm working with us, you know, select population group who are extremely active, extremely excited. Most of the men I'm seeing at around 12 because they're athletes. Probably because they're athletes. So that's great. Yeah. So none of them would be, you know, I might not have to send any your way.

[B]

And looking at a different view. Right. Somebody with a normal BMI doesn't mean that they don't need the medication. Because in a patient with a normal bmi, maybe it's normal because they have low muscle mass compared to body fat. So I've seen so much being normal BMI 20, 21 with high percentage body fat and it's normal or low BMI because of the muscle. They don't have muscle. Yeah, right. So those patients still require medication. So really I feel we under diagnosing patients instead of over diagnosing with the bmi. Yeah, we're missing out a lot. It's very rare the patient that will have a high BMI due to high muscle mass. Right. It's more common to see the opposite. A normal BMI with high body fat and low muscle mass.

[A]

Yeah, absolutely. So then what would be the down like? Because right now you're selling this drug to me, it's like, you know, I'm seeing a lot of people taking it off label who are, you know, I look at them and maybe to me, I don't know, I don't walk, I'm not an MRI scanner.

[B]

Exactly right.

[A]

But I look and I do know many people. I've got a lot of girlfriends who are like, yeah, I'm taking Ozempic, I'm like, why would you do that? You're so, you look great. So there's just been this uprise, I think personally in the last three months of people just taking it and it just seems like everybody is now.

[B]

Yeah. So there's different things to discuss that in particular one is, as you mentioned, we don't have MRI vision. Right. So even if you see somebody who may look slim or to you, or not overweight or don't have obesity, you don't know their visceral fat, you don't know their percentage body fat. Right. You don't know their muscle mass, you don't know what's their body composition. So many times somebody may look normal to the eye, but once you do a body composition I, they do require medication or you have this patient that may be maintaining a somewhat normal ideal weight, but up to what level does it disrupt their life to maintain that weight? Right. Because if you have a patient that's counting every calorie that is working two hours a day, that it becomes a full time job, then that patient may benefit from the medication. Right. Because it's going above normal sustainable measurements to maintain a normal weight. But if you take all of that, the patient will be prone to have a busier waking. Yeah, Right. So those patients also benefit. Now there's more people that need it than providers that know how to prescribe it at this moment.

[A]

Yeah. So you're an obesity specialist, ladies and gentlemen, it's not just a PCP here.

[B]

And I can tell you, even as an endocrinologist that I didn't learn as when I did Obesity medicine. Right. So even as endocrinologists are the ones, ones deal with metabolism, we're still better than a non endocrinologist in regards to metabolism, but not enough to be treating obesity.

[A]

Well, that's why we have different specialties now in medicine.

[B]

Excellent. So if a physician, a provider, a nurse practitioner, a pa, a med spa are trying to prescribe these medications, I would say do it responsibly. Get educated. Right. If you want to start prescribing Ozempic to many patients because it's going to bring your patients, buy yourself a body composition machine or test. Right. Do things responsibly because all those bad things that we're hearing now, the stomach paralysis and all those, the vomiting is I think it's provider, provider costs or related because they're not following what the patient, the guidelines. Right. They're just concerned about the drop in the number on the scale. You lost £10 in a week. Great. No, you lost muscle actually. Right.

[A]

So that's what I'm hearing, a lot.

[B]

Of muscle loss and it's. And then we're creating an obesity, a skinny fat population.

[A]

Yeah.

[B]

Right. So that's not going to be healthy either. So we, we're learning and medicine is an evolving science so we, we need to apply what we're learning. Right. Not do things as we always used to do. I think that's a big challenge for many doctors.

[A]

I'd also like to thank the second sponsor of today's episode, which is Mud Water. I've been drinking mud water as a coffee alternative for I would say around three months now. I got into it as soon as the weather started getting cold in New York City. So if you are looking for a coffee alternative, then look no further. Mud Water is the solution. It's basically having your chocolate hot coffee without the caffeine, the crash and all the jitters that come along with having a coffee. The best thing about it is it's got four functional mushrooms in each, which they've actually been specifically chosen for the purpose of making you perform better. It has cacao and chai and that kind of gives you a hint of caffeine and chocolate taste. It's got lion's mane for focus, cordyceps to promote natural energy coffee. It's got both chaga and reishi which helps support a healthy immune system. It's 100% USDA organic, kosher, vegan and gluten free. So if you are looking for a delicious alternative to your morning coffee, this is where to start. And right now you can save $20 plus get a free sample of creamer and a free frother by going to the link link in the description below or heading to mudwtr.com Louisa so go on, get your free frother, free samples of coconut creamer and sweetener. Go to mud water that is mud wtr.com Louisa on that link you'll get all of those samples for free. A good way to actually think about this is just what I'm thinking is it's the same thing as taking a supplement. If you'll. Even though this is an FDA approved product which requires a prescription, it's this, it's not a take this supplement and that's it. Just sit on the couch. It is, it's a, it's something to be added into a lifestyle just to help you.

[B]

Well, I can prescribe chemo drugs. Yes. Do I, I don't because I don't know how to use them. I don't know I'm going to cause most more harm on my patient than improving, right? Same with these drugs. It's not just because you can prescribe it, you should. So again if, if some people want to venture and we need more and more of we, we are not enough obesity specialists, but just get educated on it. Get a, do an online course, see beyond the the scale, right? Make your patients healthy at the end. So my goal for my patients is to make them strong, fit and lean, right? And it's, I can tell you it's amazing when a patient comes and they say, well I want to wear a size 4 again and I'm a size 16, this is not my body. They're concentrating on an external and that's granted, that's okay, right? But once we go into it halfway, concentrating on muscle, lowering percentage body fat, the patient feels different, they just don't look different. It's now they like how they feel. They say, oh, I feel stronger, I feel more flexible, are more agile, I can do this, I can do that. And then they get hooked. Then they get hooked. Feeling that way, not only they don't want to look like before, but they don't want to feel like before. Then it becomes part of their DNA, right? And then they apply it. They want to build muscle, they want to feel strong and at the end they want to end up fit. Which is, that's the main goal in all the patients, right, Is to talk about muscle, to talk about protein. So there's many things that you have to, to talk about and not just let's count how Many pounds you've dropped per week?

[A]

Yeah, I, you know, I, I was a. I was a triathlete. I raced for Australia. And so I was part of a team. And we were training anywhere. I was training seven days a week. I would say average six hours a day. Six, seven. And I was, too. I was, I was in university. So I struggled. I have to tell you, I'm not naturally a small build, so I, I struggled. And you think, like, I, I was, like, constantly hungry because swimming made me hungry. So I was, I was big. And I remember during race season, so during the winter where we would train really hard, I maybe gained a, you know, a few extra kilos. Then during my cutting season, we'd have to get really, like, lean to be faster on the bike, to be faster on the road, to run. And it was so hard for me mentally to stop. Stop eating or. Because I was just constantly hungry. And I remember I just, I went through a phase, was my last season, and I just stopped eating dinner because that's where I. And I just was like, losing weight, Losing weight. Go. And it was, it was actually at the detriment, I ended up really skinny. And I just think back now, like, with all the things that I know, I think, oh, my God, what if. Imagine if I had this information. You know, my concern here is that once you're on it, do you have to be on it for the rest of your life?

[B]

So let's talk about what medication that we have works when you don't use it, right? So drugs have an effect while you're using them, while you're taking, and once you stop them, you don't have the effect anymore, right? Let's talk about. Have. Let's talk about type 2 diabetes, right? We can give you medication to lower your glucose. It's lowered because of the medication, but if we stop the medication, most likely your sugar is going to go back up. We can do this with high blood pressure, we can do this with cholesterol, right? We control it. Obesity is a chronic multifactorial disease. Chronic. We categorize obesity as we categorize type 2 diabetes, as we categorize hypertension, hyperlipidemia. Chronic diseases that we don't cure. We control them, right? So obesity is in the same category. And I always tell my patients, this is something positive, this is something that we should be happy about, because for the first time in history, we have something that is going to help you maintain the weight loss, because everybody can take you to the, to the weight loss goal, but keep you there. That is a difficult. Right.

[A]

Because everyone's struggling. Most, A lot of people, I mean.

[B]

Most people, yeah, most. I mean, I would say the majority. So for the first time we have something that not actually is going to be safer to use for weight loss, but it's going to get you to the goal and then that is going to maintain you at your goal. The difference what I do in my patients is I may max a dose for to reach the goal. Once I'm at the goal, I pull back as low as I can. So Michael for my patients is at the lowest dose possible long term.

[A]

And does that have like, do they get used to it and then end up needing more?

[B]

Not, not no. Actually once you reach your goal, once you maintain that weight, you don't need more and more. It's just mind, we don't need any more weight loss, we just maintaining. Now I always tell my patients too, the medications don't replace exercise and eating healthy. Eating healthy and exercise doesn't replace the medication. Right. So they work together.

[A]

Okay. Now with every up, there's got to be some downs. I would love to talk about some of the side effects. Some of the ones that I have heard that have been reported are headaches. I don't know if that's a, if that's just individualized or if that's an actual side effective drug. Nausea. They're the two that like I've fatigued. Fatigue, is that another one?

[B]

Right. So the headache and the fatigue and dizziness, sometimes people think, oh my sugar is too low, I haven't eaten eight hours, I'm hypoglycemic. No, it doesn't cause hypoglycemia, number one. And we can be without eating for days, without us sugar or glucose dropping. Right. It's dehydration. Right. So because normally we drink when we eat. Right. In every meal you drink, so you're going to having less meal, so you're going to be already drinking less. It suppresses your hunger. It somehow suppresses your thirst so you can be dry as a bone. Your thirst effect is not going to kick in. So you proactively need to be drinking and keeping track of how much you should be. You drink it throughout the day, so about a liter and a half to two liters per day. When you're on this drugs to prevent the fatigue, the headache, the constipation also is from the hydration. Right. The nausea. Definitely. With semilutite, it happens especially after we go up every time on a dose. You may feel the Nauseous and. And the nausea is more like a fullness feeling that you need to get used to it. Right. Many people are not used to feeling full or feeling full with small amount. And then they may overeat and they're like, you feel not good. Right. With Terceptide, which is our newest of the bunch, Appetite.

[A]

Yeah.

[B]

It's like the iPhone, 14 of the iPhones right now. It's improved, better debug, less side effects.

[A]

It's like the plus plus. Oh, okay.

[B]

What differentiates tirsepatite from semaglutide is that it's a twin Incretin. So semalotide is a 1 incretin GLP1, tirasepatite is 2 incretins and one is GLP and GIP.

[A]

GIP. So tirzepatide is the increment plus the GIP, GLP.

[B]

Yes.

[A]

Okay. Wow.

[B]

So with this drug we see more weight loss than semaglutide and I would say close to zero gastric side effects.

[A]

Oh, wow.

[B]

I don't even have to talk about nausea. I don't even like in my patients with Dystar on their sepatide, I don't even mention nausea because it's inexistent.

[A]

Yeah.

[B]

But with semaglutide, the majority of patients will have nausea at one point in the, in the drug. Right. What's the best drug for me? Right. If you, if you're going to ask me like what's what's best to sepitide or Somalia, what's best is what you're going to be able to maintain long term. Meaning what's best may be what your insurance covers. Right.

[A]

Is tiride is a different.

[B]

So Tir Appatite right Now is approved FDA for type 2 diabetes only. But middle of December, they're coming with SEP Bound, which is terepatite, branded for weight loss independent of diabetes. We have OIC, which is for type 2 diabetes exclusively. And then they came out with Wegovy, rebranded, same drug, same pharmaceutical as Wegovy for weight loss. So FDA approved for weight loss if you don't have diabetes but you can lose weight or you have obesity, overweight, then they'll approve the Wegovy or the.

[A]

Sepa and can even. Because you mentioned pregnancy earlier, is this safe for pregnant women?

[B]

No. And I think, I think at one point in the future it will be. What I think we're going to have to study is the caloric intake, that it doesn't affect fetal growth.

[A]

Yes.

[B]

Right. Because that's very important because Definitely very important. So there's going to. And it can be done with a. Maybe with a 0.25 of ozempic that they're still eating, but maybe not as much. They're still providing calories for the baby, but not enough for the mother to gain weight during the pregnancy or regain some of the weight. But we're not there yet. That's what I anticipate that is going to be a problem is we don't want to decrease the caloric severely. The caloric intake like in a first trimester in the development of the baby. Right.

[A]

Yeah. If somebody came to you and they were misusing it, for example, have you ever had an incident of that or have you heard of that misuse?

[B]

Well, misuse. What I would say that I see more often, not on my patients, is going up too fast on the doses. Auto injecting double or higher doses.

[A]

Is that because they're maybe not feeling.

[B]

It's because they want to lose quick? Yes.

[A]

That's always, you know, just keep running.

[B]

They have a wedding coming up. They have this come. No, I always. It's not a sprint. This weight loss journey is a marathon. Right. If you are targeting to lose five pounds per week, you are losing muscle and you're going to end up skinny and frail and sick looking. And that's when people say, oh, you stop losing weight. It's because they're losing the muscle. Right. So. And they don't want. And they're not going to feel great. So I feel like there's a misuse there and patients auto medicating themselves. Hmm.

[A]

I think, I think the education part is probably the most important when it comes to this. Like it's, it's educating the patient on how best practices of use, which is obviously with every pharmacological intervention, but it's also about the, you know, how do you manage taking this and not lo. And keep going to the gym and keep doing what you're doing.

[B]

See, the key here is the patient doctor relationship. You're not going to have all discussions that I'm mentioning to you in 15 minutes. It's humanly impossible. So you're gonna reduce the service to take this. Come back in four weeks, you may have nausea. Bye. They're not gonna have time to talk about muscle. They're not gonna have to talk about how to avoid the headaches, the fatigue. They're not gonna have time to talk to you about what exercise you need to do, what you should expect. I have a very clear here, the efficacy and the Safety of the drug is dependent on the expertise on who's giving you the drug.

[A]

What is this one called in Europe?

[B]

Terceptide is not available in Europe.

[A]

No, there's something similar to Europe, because when this was very big, I was in Europe with my parents in around April, May, and there was. It wasn't Ozempic.

[B]

Where Colby.

[A]

No, it's. Okay. Maybe it's. I thought it was eccentric or something like this, and I heard a lot of people taking out. No, I'm not sure. But I was asking, and they said it's basically Ozempic, but it's called Wiggleby.

[B]

That's the commercial name. And it was approved for Europe. I mean, it's been approved a while, but they're just been holding it because they cannot provide enough for the United States. They cannot make enough to also give in Europe. Mounjaro tersepatite is currently available in the US and the Emirates, Dubai, Saudi Qatar, Abu Dhabi.

[A]

Do you feel as though this is something that should have been implemented and introduced into the US Population years ago? If we had the science?

[B]

Yeah, because for us Endocrinologists, it's not something new. Again, we've known about them since 2005. You know, the first incretin that was able to be produce in a Lab was in 1994 on Mount Sinai in the BA Hospital in the Bronx by a endocrinologist and researcher who saw the Gila monsters, which is a lizard, in its victims. When they. When they bite them, they produce pancreatitis in the victims, and that's how they die. So him being an endocrinologist and a researcher said, what is it in the venom that attacks or works in the pancreas? And how can this. We use this for glucose control. And that's how he discovered exenatide, which is the first one that came out, and then commercialized us by ERA by Eli Lilly. So we've known for this drug since. Since 2005, 1994. Right. For weight loss. I started using them in 2010. So for us endocrinologists, it was like, oh, you finally cut. Cut up with it. Right. Because we've been using them.

[A]

Okay. I kind of feel like you'd probably get a lot of pushback. Do you think with this drug, like, there'd be maybe a population that might say, why do you need that? Why can't you just be mentally strong and just stop eating and just be on. Do you see that?

[B]

Of course. And. And I can see that on. Sometimes patients don't want to talk about being on the medication because of that.

[A]

Yeah.

[B]

They're going to be, oh, you could have done this on your own.

[A]

Yeah.

[B]

Again, bias, bias, bias. That needs to be stopped. People are not creating obesity on themselves. And I've had grown men cry in my office when they understand this. And you remove that guilt and pressure that been carrying since they're eight. Right. When you tell them it's not your fault, actually. So we have to understand obesity for what it is. It's a multifactorial chronic disease, is not self induced. Right. So when you take that out, then you remove the bias of having to do it on your own because we know it's not going to happen. And then there's more acceptance as medication, as a treatment.

[A]

Yeah. I was, I mentioned to you earlier, I was talking to Dr. Guillenay, Stephen Guillenay, and he, he's doing a lot on the neuroscience of obesity and he was the one that actually first introduced the idea in my head, or the topic of a mother and what she eats during fetal development, which can actually lead to obesity. That was a real light bulb moment for me. I thought, oh, my gosh, it goes.

[B]

Even back then when you even had a choice of what to eat.

[A]

Yeah. And goes back to their mother, her mother and her mother.

[B]

It's transgenerational, it's generational.

[A]

What's your take on. I was actually looking and so the reason why I brought him up is because he taught me. I said to him, well, why not just get liposuction? You know, and he was telling me the difference between, you know, actually removing the fat cells and then if you actually lose weight and not removing the fat cells and they just shrink. And that's. And so we were just going to. So many different ways to solve obesity. We never talked about.

[B]

I love this. And I love this because it's. There's places for both. Right. They can take 10 pounds out of fat and liposuction and you can still have visceral fat. The liposuction doesn't go into your abdominal.

[A]

Visceral fat is fat surrounding the organs.

[B]

The organs is your intra abdominal fat that's attached to your liver, your pancreas, your gut. Right. That can lead to fatty liver, insulin resistance, type 2 diabetes. That fat is internal. It won't. The liposuction machine won't touch it. They remove subcutaneous fat.

[A]

Yes.

[B]

Right. The subcutaneous fat is not what makes you sick. So you can have a liposuction, but you're still at risk for type 2 diabetes or if you had type 2 diabetes going in the liposuction, it's not going to improve, it's not going to change. Your numbers are not going to change. Right. So it's very different what we're doing as a weight loss treatment than liposuction. So there's no. They cannot be compare comparatively as a treatment for obesity.

[A]

Okay. This visceral fat. Let's just say somebody presents with visceral fat, you know, fatty liver or the fat is wherever it is on the organs. How does that naturally. Like, how does that naturally. Like, how do you lose that?

[B]

It's. That's a very phenotype predisposition. Right. So it's like you're almost calm. You almost. You're born with a DNA on how you're going to store food fat. So for many patients, we can tend to store fat more centrally is what we call like the apple shape that the people that are more Predisposed of type 2 diabetes versus the purple, the people that are like the pear shape, they're more predisposed to cardiovascular diseases. They don't. They're not. They don't not. They don't store so much body visceral fat. But some population tend to store more central body fat. And that's visceral fat.

[A]

Yeah. Okay.

[B]

I was thinking like African American, Hispanics, Asians, we tend culturally cultural, centrally to. To store. To. To store centrally and store body fat centrally. And that's why there's higher rates of type 2 diabetes in Hispanics and African American people and Asians.

[A]

I love that you're treating this disease, which, by the way, I'm now calling obesity a disease, which.

[B]

Thank you.

[A]

Is, you know, and I love that you're fighting for this. I was speaking to, To Gabrielle today. We spoke about her, our friend that we have in common. And she's like, Louisa, you know that there's no one actually prescribing anything for muscle, you know, because she loves muscle. And she's like, you know, you can get these weight. You love muscle.

[B]

And.

[A]

But this is. You're not giving an intervention to grow more muscle.

[B]

I do.

[A]

Oh, what. What?

[B]

I do, of course. Oh, my goodness.

[A]

Is it a pharmacological?

[B]

No, that's what we go over. Well, well, yes, for some patients it could be testosterone.

[A]

Okay. Yeah.

[B]

Right. But not everybody that comes to my office, I put in my testosterone. Right. There's patients that benefit from testosterone beyond muscle growth that will be on testosterone. But for the majority of patients, it's just having a discussion about it. Right. I mean, but again, you need time to do this. So I discuss with my patients grams of protein. I tell my patients, don't count me calories, don't count me carbs, don't count me pounds, count me your grams of protein per day. Right. So there needs to be an increase in protein intake. When somebody goes in any weight loss program to preserve muscle, and then we're talking about building muscle. Then I go over my patients, what exercise they need to do, how much they have to exercise. So definitely weight training. Right. Weight bearing exercises. They need to reach failure. I teach them how to reach failure when weight training. So there's muscle growth. If the muscle doesn't reach failure when you, your weight training, you won't have growth. You maintain it, but the muscle actually has to tear when it reaches failure. And when it gets together is when it grows right. With the protein there. So my goal for my patients and I, and you know, when the patient comes and tells me how do I do a muscle, it's like music to my ears. Like they got the message, I'm happy. Or we're following this, or I don't see any muscle loss in their next visit. So that's what I'm saying. If you're going with somebody who's not talking to you about muscle, about protein, doing body composition. Patient, go somewhere else.

[A]

Yeah. And do inform your patients that you can have fat in your muscle as well.

[B]

Yeah. And that a lot of the muscle in patients with obesity is not healthy muscle.

[A]

Okay. So that means that they're. They're like a wagyu steak.

[B]

Exactly.

[A]

And the marbling is the fat, just like in a steak. But can you get rid of that?

[B]

Yeah, you can, you can.

[A]

Obviously when you lose fat, body fat.

[B]

And when you increase protein intake. Yes. I mean, and as you're losing body weight, percentage body fat, visceral fat, that's going to come down too.

[A]

Something I forgot to ask you earlier is what's the. Like, can you give me. Like, this is so interesting. The, the lipid profile of an obese patient. Does it matter? Like, is that, are you looking at lipids? Are they, are they generally coming to you with a high ldl, high apob?

[B]

Not necessarily. And before we move forward, something that I want to share with you is that we are moving to first people language. So we don't say the obese patient anymore. We said the patient with obesity.

[A]

Wow.

[B]

As we don't say the diabetic patient, we say the patient with Diabetes. So we're removing the disease as a label for the patient. So it's the human with the disease.

[A]

Funny you said that just recently. I think they changed this as well for suicide. Instead of saying this boy committed suicide and died, it's he died by suicide. I just, that was a. Yeah, you're.

[B]

Taking, you're taking the label out of the person itself. Right, but what was the question? I got out of the tangle.

[A]

Yeah, no, I love that it was do obese.

[B]

Oh, the lipid profile.

[A]

Yes.

[B]

Not necessarily. You know, many patients, especially young patients with obesity in their 20s, female, they may have completely normal levels. Right. Then we go into the metabolic healthy obesity. Right. That metabolically healthy means that they don't have high blood pressure, they don't have elevated cholesterol, they don't have pre diabetes, that they just have obesity. Right. But we know there's studies that those metabolic healthy patients with obesity, they will develop eventually metabolic disease. Right. So maybe now at that moment the weight, the obesity hasn't created enough damage. Doesn't mean that it won't. So those patients should still be treated it. Yeah. Okay.

[A]

I feel like for myself I went all over the place with this episode. People know I come here with like a set of questions and I've just gotten through one. I do want to. I'd be remiss if I didn't ask you if you knew of any studies that are done on the correlation between Ozempic. This is actually a question. I, I put it out on Twitter and I told everyone else interviewing you. And one did ask if there's any correlation between Alzheimer's disease and this drug.

[B]

Yeah. So obesity, the fat tissue, the adipose tissue, is a pro inflammatory tissue. Those fat, excess fat cells promote inflammation. Right. They promote release of all the cytokines, tumor necrosis factor, all the things that cause inflammation. We know Alzheimer is also an inflammatory disease. Right. Of the brain. So we are seeing a lot of improvement, not just in weight and glucose control. I think patients feel better even before the weight loss starts happening. And it's because of the decrease of inflammation, so there is less inflammatory factors. This, this is what happened with COVID Right. We were telling patients with obesity, in 20 years you're going to get this. If you don't lose weight, you're going to develop this and that and that. 20 years, I'll worry when I have to came COVID Patients with obesity, highest mortality, highest ICU stay, highest risk of complications from COVID And it was found because of that inflammatory process that the Fat tissue is going. It was using all the, the inflammatory process that could have been used to com. To fight the virus is being occupied by the fat tissue and that's why the virus had a party in those patients. Right. So I feel also like patients really got the message that having obesity, even if your numbers are good right now, it's not good.

[A]

Yes.

[B]

Right. So I think it was a positive broad light into this and the obesity. Right. And I think because going back to Alzheimer's, so we know, know that GLP1 or incretins improve the vascularity, increases vascularity. So there's less risk of fat in your arteries. Right. That's one reason. Also increases.

[A]

It increases vascularity.

[B]

It increases endothelial cells. Wow. Yeah.

[A]

Well, we talk, everyone knows about this. We talk about vascular, the vasculature of the brain. And the brain being the most vascular rich organ in the body, it provides, you know, nutrients and oxygen. And if, and we know that the smallest ones, which are the capillaries, they die off during hypertension per se, which means that we have less blood flow evidently going to the brain. But now what you're saying is we can, this increases GLP one can increase.

[B]

Vascularization, elasticity of the vessels too. Right. So this is just the, this is just a tip point because we have so many diseases, there are, are caused by obesity that will improve once we start treating more patients with obesity. Right. So I feel as we know now, it improves kidney function, cardiovascular function. Right. So because it's improving overall, everything. Right. I think we got used to as a medical society, as a, as a healthcare, we got used to treating all the complications of obesity. Right.

[A]

Isn't that what medicine is pretty much.

[B]

Not anymore. It will change this. I, I believe that this is the one of the biggest change that we in our generation will witness in regards to medicine. I think this is the biggest thing until the cure of cancer. But otherwise why? Because we're going to slow down the progression of all the diseases that we've built specialties for. Right. So we're going to have less patients. It's going to take about probably two generations, but we'll have less type 2 diabetes, less hypertension, less cardiovascular disease. We hope we will, we will lessen oncology cases, less development of cancer. Right. So I feel it will take a few gen, like one or two generations, probably two generations for us to see the results. Right. That we're decreasing chronic disease. And I think Alzheimer's, dementia is going to be definitely one of them.

[A]

So, so where do you see the Future of this field. Let's just say we, we take a magic pill and we jump 10 years into the future. Do you see more people actually on Ozempic? Yes, almost. I mean, I mean you're pretty much pretty saying to me, you've pretty much saying said to me this is a completely safe drug. Almost anyone and anyone. Oh, is it age restricted?

[B]

Like 12 and above?

[A]

12 and above. Okay. Can take it. It doesn't matter even.

[B]

What about 85 and take it now? I. I don't want to say it's free of side effects. Right. Because even if you take an Advil that can have a side effect. It depends the supervision that you're having on this drug that will be. It will be a good result or negative result or a good experience or a negative experience. Right. It's depend who is guiding you through the journey.

[A]

This is exactly like Botox, to be honest. Anyone can completely do the.

[B]

But.

[A]

And I was like now know who is actually injecting your face?

[B]

I have a friend, Lara Devgan. I don't know if you know her, she's a plastic surgeon and she saw me, I don't know, like six months ago and she's like, oh my God. She's like, I just thought of you as me. That everybody's starting putting Botox and everybody's starting giving a bad reputation and having all these complications. Botox is going to toxic the oic. And I said yes. And I even tell people like if you could buy Botox in the pharmacy, would you apply it yourself? No. Why would you do the same with this drug? Yeah, right. It's the same thing.

[A]

Yeah.

[B]

Everybody wants a piece of it, but you have to do it responsibly.

[A]

Of course. Can people get it without going to.

[B]

A doctor in some countries.

[A]

Oh, in some countries.

[B]

Not here.

[A]

Not here.

[B]

No, thank God.

[A]

But I mean Mexico, you can pretty much get anything there.

[B]

No. Yes. I didn't want to say it, but yes.

[A]

Okay, where's that's. I just want to know where do you think. Do you think many people are going to be taking this in 10 years?

[B]

So let me tell you what's coming up, right, so we have a. A3 incren coming up at the beginning of the year. So even we're seeing even more weight loss than on terepatite. We're seeing currently in study in phase two. There are an incretin plus a muscle activating protein. So you lose weight and you gain muscle with.

[A]

No way.

[B]

Yes way.

[A]

Oh my gosh.

[B]

Yes. So believe me, the possibilities are endless. What's the.

[A]

What's the ink? What is it?

[B]

I'll give. It's a. It's still like in the. It's like. It's like a BPRC looks. It's still in that study. But they already presented in the obesity conference. Obesity Week over the Obesity Society and they presented the results and so this is just getting better.

[A]

Yeah, we're just. Safer seat at the table and. Better, safer, better disease free. Everyone knows.

[B]

Right before we went from twice a day day to once a day to once a week now.

[A]

Brilliant.

[B]

The oral versions are coming out too. So for patients that don't want to bend the needle, now they can do oral. So again, this is just, this is just the beginning of what it's going to be.

[A]

Wow, I love this. And we can, you know, anyone listening who may feel like they're a bit lost on this journey, if they are on this journey, they can come and see you. You're located here in New York City. You are the, you know, you are the expert on this. And we're going to link everything below and you have a wonderful Instagram page where you share a lot of knowledge and we can go there to. What's your Instagram handle? Is Dr. Salas W. Okay, we'll link that too. Thank you so much for being part of the neuro experience.

[B]

Thank you for inviting me.