Today, we’ll examine an important debate in nutrition: whether skipping breakfast or skipping dinner is more effective for your health and metabolism. We’ll unpack what the research says, how your body’s internal clock affects metabolism, and why the timing of your last meal can make or break your weight loss—especially if you’re on a GLP-1 medication like semaglutide, dual GIP/GLP-1 like tirzepatide, or triple agonist like retatrutide.

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Let’s get into it.

Circadian Rhythms and Eating Windows

Our bodies are wired to follow a circadian rhythm—a 24-hour cycle that controls hormones like melatonin, cortisol, and insulin. One key thing to understand is that your body follows the rhythm of the day. When it’s light out, you’re naturally wired for activity—your metabolism is active, digestion works efficiently, and your body is more sensitive to insulin.

As daylight fades, melatonin levels rise, signaling it’s time to slow down, rest, and prepare for sleep.

Here’s the kicker: melatonin doesn’t just make you sleepy—it also reduces insulin sensitivity. That means when you eat late at night—say at 8 or 9pm—your body doesn’t handle sugar or calories as well. Instead of using that energy, you’re more likely to store it as fat.

So, a meal at 5pm when it’s still light out? Your body’s insulin response is stronger. You burn and use more of what you eat.

But a meal at 9pm in the dark? Your body’s gearing up for sleep, not digestion. Calories from that meal are more likely to go into fat storage.

Breakfast vs. Dinner Skipping—What the Data Says

Let’s talk about what the research shows when it comes to skipping breakfast versus skipping dinner. Several studies have looked at early time-restricted feeding, where you eat earlier in the day, like between 8 a.m. and 4 p.m., versus eating later, where you skip breakfast and stretch meals into the evening.

One of the most cited studies, published in Cell Metabolism. The study looked at men with prediabetes who followed an early time-restricted feeding schedule for five weeks. Even though they didn’t lose weight, they had significant improvements in insulin sensitivity, blood pressure, and markers of oxidative stress compared to those eating over a twelve-hour window. The takeaway? Eating earlier in the day improved metabolic function even without reducing calories.

Another study found that early eaters experienced lower evening hunger and better fat oxidation, meaning their bodies were burning fat more efficiently. By contrast, those eating later in the day had higher insulin and glucose levels after meals, signaling greater insulin resistance. And more broadly, research consistently shows that eating late at night, especially after seven or eight in the evening, is linked to increased body fat and higher risks of obesity and type 2 diabetes. The reason is straightforward: insulin sensitivity drops as the day goes on, so your body is less efficient at processing glucose at night, and those late calories are more likely to be stored as fat, especially around the belly.

So while skipping breakfast might be easier for some people, from a metabolic standpoint, skipping dinner—or at least finishing it earlier—tends to be more beneficial.

This connects directly to why fasting works for weight loss. Fasting gives your insulin a chance to drop, which signals your body to tap into stored fat for energy. Front-loading your meals earlier in the day aligns with your body’s natural rhythm: insulin sensitivity is higher, digestion is more efficient, and your body has more opportunity to burn fat overnight. People who eat earlier often report feeling more energized, less hungry in the evening, and sleeping better—all key factors in long-term weight control.

Now, if you’re taking medications like semaglutide, tirzepatide, or retatrutide, timing becomes even more important. These drugs slow gastric emptying, which helps you feel full longer but also means that eating a large dinner late at night can lead to bloating, nausea, heartburn, and in turn, poor sleep. Digestion naturally slows down as melatonin rises and your body prepares for sleep, so combining a late meal with slower gastric emptying can make it harder for your body to rest and burn fat overnight.

A good rule is to finish your last meal two to three hours before bed, ideally around five or six in the evening. This gives your body time to digest, allows insulin levels to drop, and lets you switch into fat-burning mode.

What’s the counter argument?

Of course, it’s important to remember that meal timing isn’t one-size-fits-all. While the research often favors early eating, some people naturally aren’t hungry in the morning, and skipping breakfast can actually be a helpful way to stick to a fasting window. 

Then there are the “night owls.” Some people’s circadian rhythms naturally shift later, and for them, eating later may actually align better with their biology. Forcing an early eating schedule might leave them tired, hungry, or unable to stick with it, which can actually be counterproductive for metabolic health. Research on chronotypes—the natural variations in our sleep-wake cycles—suggests that what works for a morning person might not work for someone who thrives later in the day.

Practical lifestyle factors also play a role. Work schedules, family dinners, or social events can make it hard to consistently finish dinner at five or six in the evening. For some, a slightly later meal, if it’s balanced and nutrient-dense, can be more sustainable over the long term than forcing an early window and ending up snacking late anyway.

Finally, metabolic flexibility matters. Some people can handle a later meal without negative effects on fat storage, insulin sensitivity, or sleep, especially if the meal is lighter or focused on protein and vegetables. The bottom line is that while early eating has clear metabolic advantages for many, especially those taking weight loss medications like tirzepatide, the most important factors are consistency, total calories, and the quality of your food, not just the exact timing.

So, whether you’re a morning eater, a night owl, or somewhere in between, finding an approach that fits your body and lifestyle—and that you can stick to long term—is often more important than following a strict rule about skipping breakfast or dinner.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend, please share this episode!

Until next time, be well, and as always, have a happy, healthy week.

Today, we’re talking about tesamorelin, a peptide that works through the growth hormone pathway and is especially effective when it comes to targeting stubborn belly fat.

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So, what exactly is tesamorelin? In simple terms, it’s a synthetic growth hormone-releasing hormone (GHRH) analog—basically, it signals your pituitary gland to release more growth hormone (GH). Why does that matter? Because GH plays a big role in fat metabolism, especially when it comes to visceral fat, the deep fat that surrounds your organs in your abdominal region.

Here’s how it works: when GH levels rise, your body starts breaking down fat for energy—a process called lipolysis. Visceral fat, in particular, is very responsive to GH. Reducing this type of fat isn’t just about looking better; it also improves metabolic health, boosts insulin sensitivity, and lowers inflammation, all of which support long-term health and reduce your risk of heart disease.

Why not just give GH directly?

Your body only produces a certain amount of GH naturally, and this declines with age. Giving exogenous GH can boost levels quickly, but it comes with higher risks like swelling, joint pain, and sometimes insulin resistance if overused. 

Tesamorelin, on the other hand, stimulates your own pituitary gland to release GH naturally, which tends to be safer and more physiologic over time. That said, GH injections might be preferred in certain clinical scenarios, but for most people, tesamorelin offers a more controlled approach.

What about side effects?

Some common ones include joint pain, swelling, and muscle aches. These happen because GH causes fluid retention and increased tissue growth, which can put pressure on joints and muscles. 

Also, tesamorelin can slightly increase blood sugar, so people with diabetes or prediabetes should be monitored carefully. But why does this happen?

Since tesamorelin works by boosting your growth hormone, it can have an impact on how your body handles glucose. Growth hormone naturally makes your body a little less sensitive to insulin, which means your cells don’t take up sugar as efficiently. So, some people might notice a slight rise in fasting blood sugar when they start using tesamorelin.

But here’s the interesting part: growth hormone also increases IGF-1, which has some insulin-like effects. In most healthy people, this helps balance things out, so blood sugar doesn’t spike dramatically. But if someone already has prediabetes or type 2 diabetes, it’s something to keep an eye on.

The takeaway? Tesamorelin can slightly raise blood sugar, but it’s usually manageable. Regular monitoring is smart, especially for anyone with a history of blood sugar issues. And compared to direct growth hormone injections, tesamorelin tends to have less of an effect on blood sugar because it stimulates your body to release GH naturally, instead of flooding your system with it.

Typical dosing of tesamorelin

For men, peptide therapy is often 1 mg at night to support natural GH peaks during sleep, and 1 mg in the morning before fasted cardio or exercise. Women usually do 1 mg daily. Tesamorelin can be expensive, so many people cycle it 5 days on, 2 days off to reduce cost, or just do 1 mg at night, which still supports GH production and can even improve sleep.

Typically, tesamorelin is cycled for 8 weeks on, then 8 weeks off, and most people start noticing results after 4 to 6 weeks. This cycling helps manage cost, reduce potential side effects, and allows the body to maintain responsiveness to the therapy.

My Final thoughts

Tesamorelin is a powerful tool for targeting visceral fat and improving body composition safely through your natural GH pathways. It’s not a cheap therapy, but if used strategically—especially timed with sleep or exercise—it can give great results while minimizing side effects.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend, please share this episode!

Until next time, be well, and as always, have a happy, healthy week.

I’m so glad you’re here today because we’re diving into a therapy that people are buzzing about—GLOW peptide therapy.

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Now, you’ve probably heard me talk about individual peptides before, but this one’s a peptide stack—a combination of three peptides that are designed to work together. And honestly, the name says it all. People who use this blend often say they recover faster, their skin looks healthier, and they just feel better overall. That’s why it’s called GLOW.

So today, I’m going to walk you through what GLOW peptide therapy is, what’s actually in it, how each of these peptides work, typical dosing, cycles, side effects, who should avoid it, and finally—I’ll go through some of the most common questions people ask.

The Three Peptides in GLOW

GLOW therapy combines BPC-157, TB-500 or thymosin beta-4, and GHK-Cu. Each one does something unique, but when you put them together, you get this synergistic effect that’s bigger than the sum of its parts.

Let’s start with BPC-157. This peptide is naturally derived from something we all have in our stomach lining—it’s literally called the body protection compound. And the name fits. It helps protect and repair tissue, calm down inflammation, and even support gut health. A lot of people first hear about BPC-157 because athletes use it for muscle strains, tendon injuries, or joint pain. But it’s also been studied for gut issues like ulcers and leaky gut. The magic is in how it helps new blood vessels form so your tissues can actually heal faster and stronger.

The next thing I want to touch on is that the GLOW peptide stack sometimes lists TB-500 or Thymosin Beta-4 (TB4) as if they’re interchangeable. And while they’re closely related, they’re not exactly the same.

Both of them are best known for their role in healing and recovery. They guide cells to the site of an injury, help reduce scar tissue, improve blood flow by encouraging new blood vessel growth, and calm down excess inflammation so real healing can happen.

Where they start to differ is in their scope of action. Thymosin Beta-4 is the full-length, naturally occurring peptide — the master version, if you will. Because it’s the entire chain, it interacts with more pathways and has been studied in a wide range of areas: wound healing, heart repair after a heart attack, corneal healing, brain and nerve protection, even immune system regulation.

TB-500, on the other hand, is a synthetic fragment of Thymosin Beta-4. It contains the “active core” that drives cell migration and blood vessel growth. That makes it very effective for tissue repair, tendon healing, wound closure, and circulation. But it doesn’t have all the extra regulatory sections that give the full peptide those broader effects on the heart, brain, or immune system.

What’s good to know, is that in practice, most formulations use TB-500 because it’s more stable (both in the body and for storage), widely available, and it’s cost-effective. Some clinics may use the full Thymosin Beta-4, but that’s far less common due to the cost of production.

From a user perspective, both serve the same purpose in the stack: recovery, regeneration, and repair. However, TB-500 does not have all the broader effects that the full-length Thymosin Beta-4 peptide has. Think of it this way, TB-500 tends to be seen as more targeted — very good at tissue and tendon repair, wound closure, and improving circulation, but without the same wide-ranging effects on the heart, brain, or immune system that you see with the complete TB4 peptide.

Okay, moving along to the last component of the GLOW peptide stack: GHK-Cu or the copper peptide. You might’ve already seen this one in the skincare world—creams and serums often brag about having copper peptides because they boost collagen, smooth wrinkles, and improve elasticity. But GHK-Cu is more than just cosmetic. Inside the body, it promotes wound healing, reduces inflammation, fights oxidative stress, and even supports hair regrowth. This is the peptide that really brings the “glow” to GLOW therapy. People notice their skin looks fresher and healthier, their hair feels stronger, and they just have that rejuvenated look.

Now, each of these peptides—BPC-157, TB-500 or TB-4, and GHK-Cu—can be prescribed and given separately as a subcutaneous injection, and sometimes that’s the right approach depending on someone’s goals. But for convenience, they’re often combined into a single formulation or vial, which makes daily use a lot simpler. Instead of juggling three different injections, you’re working with one balanced blend that delivers the same benefits in a more streamlined way.

Why Combine Them?

So, why put these three together? Well, BPC-157 is like the fire extinguisher—it calms down inflammation and starts the repair process. TB-500 or TB4 is like the construction crew—it moves the right cells into place and helps the tissue heal in a well-organized way. And GHK-Cu is like the finishing touch—it strengthens the structure, adds resilience, and brings back that youthful skin and hair quality.

Individually, they’re great. Together, they have synergistic power.

Typical GLOW Dosing

Alright, let’s get practical and talk about dosing for the GLOW peptide stack. For BPC-157, the sweet spot is usually somewhere between 200 and 500 micrograms a day.

When it comes to TB-500, most people land in the range of about 2 to 5 milligrams per week. If the formulation uses full thymosin Beta-4 instead, the dosing is usually a little lower since it has those broader effects on things like the immune system. In that case, you might see 1 to 2 milligrams per injection a couple times a week, or sometimes smaller daily doses depending on the goal.

And then there’s GHK-Cu, which typically runs in the 100 to 300 microgram per day range.

So while the exact numbers can shift depending on the protocol, those ranges give you a good sense of what’s common in practice.

For convenience, GLOW formulations that contain all three peptides usually come in a single vial with 10 milligrams each of BPC-157 and TB-500, and 50 milligrams of GHK-Cu, so you can draw your doses from one vial rather than juggling three separate injections. Of course, these are just general guidelines—the exact dose and frequency really should be tailored to your specific needs and always prescribed by your provider.

Side Effects

So, what about side effects? Most people tolerate these peptides really well, but there are a few things to know.

The most common side effect is some redness, irritation, or swelling at the injection site. With GHK-Cu, a lot of people notice a brief burning sensation when they inject it. It doesn’t usually last long, but it can be a bit uncomfortable, especially the first few times.

Other mild side effects that sometimes get reported include fatigue, headache, or dizziness. Very rare, but worth mentioning.

Typical Cycles

A question I get all the time is: how long should I stay on GLOW therapy?

This isn’t meant to be taken nonstop forever. A common approach is a 4 to 12 week cycle, depending on your goals. After that, people usually take a break for 1 to 2 months to let the body reset. 

For example, someone recovering from an injury might just do one cycle and be done, depending on the severity. While someone with chronic pain or inflammation (e.g., arthritis or degenerative disc disease, Crohn’s) or someone using it for skin and anti-aging might do multiple cycles per year. It’s really individualized.

Who Should Avoid It

So, who should not be on GLOW therapy? Because these peptides promote healing and blood vessel growth, anyone who is pregnant or breastfeeding or with a history of cancer should avoid GLOW therapy. And of course, if you’ve had any kind of allergic reaction to peptides before, that’s a clear “no.”

Frequently Asked Questions

Alright, let’s wrap up with some FAQs because these usually come up.

1. How soon will I notice the results?

It really depends on what you’re targeting. For joint pain or muscle recovery, some people notice improvements within a week or two, especially if the inflammation is mild or the issue is more recent. More chronic or long-standing injuries can take a little longer. When it comes to skin and hair benefits from GHK-Cu, those changes usually take a couple of months to become noticeable, since collagen production and hair growth are naturally slower processes.

2. Do I have to stay on this forever? No, that’s where cycling comes in. Most people use it for 4–12 weeks, then take a 1-2 month break.

3. Is GLOW only for athletes or injuries? Not at all. Athletes use it for recovery, but many people use it for gut health, skin rejuvenation, hair regrowth, or even surgical recovery.

4. Can I stack GLOW with other treatments? Yes, but it should be coordinated with your provider. It’s often combined with hormone replacement therapy, PRP, or even cosmetic treatments, but the plan should be individualized.

5. Can I use GLOW peptides if I’ve had cancer in the past?

Even after someone has been treated for cancer and is considered “cancer-free,” not all cancer cells may be completely eliminated from the body. Some microscopic cells can remain dormant for months or even years. Because BPC-157 and TB-500 or TB4 promote tissue repair, cell growth, and new blood vessel formation, there’s a theoretical risk that these dormant cells could be stimulated. That’s why these peptides are generally avoided in anyone with a history of cancer unless a doctor has carefully reviewed the risks and given explicit clearance.

Final thoughts

So that’s the full picture on GLOW peptide therapy. It’s a blend designed to help your body heal, repair, and restore—whether that’s from an injury, surgery, or just the natural wear and tear of life. And while the “glow” is real, it’s not magic—it’s science-driven, and it works best when used thoughtfully and safely.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend—because we all could use a little GLOW up.

Until next time, be well, and as always, have a happy, healthy week.

Welcome to The Peptide Podcast.

In this episode, we’re unpacking the latest on retatrutide and how it measures up against semaglutide and tirzepatide. 

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We’ll look closely at what the studies tell us so far — from overall weight loss to reductions in visceral fat and how much lean muscle mass is preserved. We’ll also talk about where the evidence is solid, where it’s still developing, and why cross-trial comparisons should be made with caution.

What is retatrutide?

So let’s start with the basics—what is retatrutide? Retatrutide is a new type of weight-loss medication called a triple agonist. That sounds fancy, but what it really means is that it targets three hormone receptors in the gut and pancreas: GLP-1, GIP, and glucagon. Each of these plays a slightly different role in metabolism and appetite regulation.

To break it down: GLP-1, which you might already know from drugs like semaglutide, mainly slows digestion, helps you feel full, and improves insulin sensitivity. GIP, which tirzepatide targets along with GLP-1, also helps regulate blood sugar and may improve how the body stores and burns fat. Retatrutide adds glucagon receptor activation on top of that, which seems to further boost fat burning.

So how does this compare to semaglutide and tirzepatide? Semaglutide is a GLP-1-only drug, so it mainly works by reducing appetite and slowing gastric emptying. Tirzepatide is a dual agonist, hitting GLP-1 and GIP, which gives it a slightly stronger effect on blood sugar control and fat metabolism compared to semaglutide. Retatrutide goes one step further by adding glucagon activity, potentially giving more total fat loss.

In other words, you can think of it like a spectrum: semaglutide hits one target, tirzepatide hits two, and retatrutide hits three—each additional receptor seems to enhance metabolic effects and fat loss in clinical trials. That’s why people are excited about retatrutide, though it’s still early, and we’re waiting on larger studies to see exactly how it compares head-to-head with the others. And that’s going to be key, since right now we don’t have direct comparisons to other advanced therapies like semaglutide or tirzepatide in the published Phase 2 data.

How does retatrutide compare to semaglutide and tirzepatide?

Total body weight loss:

Now let’s put these three medications side by side and look at what the trials actually tell us about total body weight loss.

Starting with retatrutide: in its Phase 2 obesity program, the numbers were unusually large, especially given the relatively short trial window. In the 48-week study, people on the higher doses—8 or 12 milligrams weekly—lost about 22 to 24% of their body weight on average. That’s the result that really made headlines. It’s worth noting that some trials report slightly different averages depending on the group studied—people with obesity but no diabetes versus people with type 2 diabetes—but across the board, that 48-week signal is consistently very strong.

For comparison, let’s step back to semaglutide at the 2.4 mg dose, which was tested in the pivotal STEP-1 trial. Over 68 weeks, participants lost about 15% of their body weight on average. That was a landmark finding when it was published in the New England Journal of Medicine—it essentially set the modern benchmark for what a GLP-1 monotherapy could do.

Then we have tirzepatide, the dual GIP and GLP-1 agonist. The SURMOUNT-1 trial, which ran for 72 weeks, showed dose-dependent results: about 15% weight loss at 5 mg, 19.5% at 10 mg, and 20.9% at 15 mg, compared to only around 3% with placebo. Other obesity studies with tirzepatide have backed this up, especially at the higher doses. And in head-to-head comparisons with semaglutide, tirzepatide has consistently come out on top.

So if we zoom out: retatrutide’s Phase 2 data suggest the greatest average reductions—over 22%—in less than a year. Tirzepatide follows closely behind with around 21% over 72 weeks. And semaglutide shows very meaningful, but smaller, weight loss of around 15% over a similar time frame.

The big caveat here is that these aren’t perfect apples-to-apples comparisons. The trials differed in their length, the types of patients enrolled—some had type 2 diabetes, some did not—their baseline weights, and even the way results were reported. Plus, retatrutide is still in Phase 2 for obesity, whereas semaglutide and tirzepatide already have large Phase 3 programs and real-world data backing them up.

Visceral fat reduction:

Next, let’s talk about visceral fat reduction—that’s the deep fat that surrounds organs like the liver, pancreas, and intestines. It’s particularly important because high levels of visceral fat are strongly linked to cardiometabolic disease.

Starting with retatrutide, one of the Phase 2 substudies used DEXA scans to measure body composition in detail. At the higher doses—8 and 12 milligrams per week—participants saw visceral fat drop by about 29 to 31% over 48 weeks. That’s a very large relative reduction in under a year and one of the reasons people are excited about retatrutide’s potential not just for weight loss, but also for improving long-term metabolic health.

How does that compare to the other drugs? With semaglutide, we also have DEXA and imaging substudies from the STEP program and follow-up mechanistic work. These consistently show meaningful visceral fat reductions, along with improvements in the ratio of lean to fat mass. The difference is that semaglutide studies typically report VAT changes as “significant and clinically relevant,” but they don’t always publish one clear headline number that’s directly comparable to retatrutide’s ~30%. In other words, semaglutide definitely lowers visceral fat, but depending on the study and population, the exact percentage looks different.

For tirzepatide, we also have imaging-based data from the SURMOUNT trials and related body-composition studies. These show that the majority of weight lost is fat mass—including a significant portion of visceral fat. Some analyses report reductions on par with what’s seen with GLP-1 therapies, while others suggest tirzepatide may push a bit further. But again, the actual percentages vary depending on whether the study used DEXA, CT, or MRI, and on who was enrolled.

The big caveat here is that we don’t yet have a head-to-head imaging study comparing all three drugs in the same population with the same methods. Retatrutide’s ~30% visceral fat drop is certainly eye-catching, but without that kind of standardized comparison, it’s hard to say definitively whether it’s truly better than semaglutide or tirzepatide.

Lean muscle mass preservation:

Now let’s shift to lean mass preservation, which is just as important as total weight or fat loss. Across all of the modern obesity drug trials, one thing has been consistent: most of the weight people lose is fat, but some lean tissue is lost too. That’s expected whenever you’re in a sustained calorie deficit. The question is how much muscle is preserved, and how the proportions break down.

With retatrutide, the DEXA substudy showed something reassuring. Even though people lost a lot of total weight and fat, the proportion of lean mass lost compared to total weight loss was similar to what we see with other therapies. In other words, the drug seems to drive large fat reductions without causing disproportionate muscle loss. Interestingly, the absolute amount of lean tissue lost in kilograms was pretty stable across different doses, even though fat loss varied quite a bit. That suggests the extra weight loss with higher doses is really coming from fat, not muscle.

Looking at semaglutide, the STEP trials with DEXA scans reported the same general pattern. People lost more fat than lean mass, and when you adjust for the total weight loss, body composition actually improved. In fact, some analyses showed a slight increase in the percentage of body weight that was lean tissue, even though the absolute lean mass in kilograms went down. So again, it’s not that muscle isn’t affected—it is—but fat loss makes up the majority of the change.

For tirzepatide, the SURMOUNT body-composition studies found that about 75% of the weight lost is fat and about 25% is lean mass. That split is very similar to what was seen in the placebo groups, which means the drug isn’t shifting the balance unfavorably. It preferentially reduces fat, while lean mass preservation is in the same ballpark as semaglutide and retatrutide.

Now, here’s the important nuance: lean mass on a DEXA scan isn’t just skeletal muscle. It includes water, organ tissue, and other components. So if someone loses 3 or 4 kilograms of “lean mass,” we don’t know how much of that is functional muscle versus water or smaller organ size. That’s why these numbers can be misleading if you take them at face value.

And this is where lifestyle comes in. Resistance training and adequate protein intake are critical alongside medication. Lifting weights or doing bodyweight resistance work helps preserve functional muscle, while getting enough protein—typically somewhere in the range of 0.8 to 1 gram per pound per day depending on age and activity—supports muscle repair and maintenance. Every trial we’ve seen shows that the best outcomes, in terms of maintaining strength and function, come from pairing these drugs with exercise and nutrition strategies. That way, the unavoidable lean mass changes have far less impact on long-term metabolic health and performance.

Limitations, biases, and what’s missing (the critical context).

1. No large, peer-reviewed head-to-head trials (yet) comparing retatrutide with semaglutide or tirzepatide for the same endpoints using identical imaging protocols. Most comparisons are cross-trial and therefore imperfect. Retatrutide Phase-2 was often compared to placebo or dulaglutide (in the T2D DEXA substudy) rather than to semaglutide or tirzepatide. A head-to-head (planned/registered) study vs tirzepatide is listed on ClinicalTrials.gov but results are not published yet.

2. Different populations & durations. Some retatrutide data come from cohorts that include people with T2D or NAFLD; semaglutide STEP trials were often in people with obesity (without diabetes) and run longer (68 weeks), while tirzepatide SURMOUNT trials ran to 72 weeks. These differences change the absolute and percent outcomes.

3. Funding and reporting bias. Many of the early retatrutide analyses are industry-funded (Eli Lilly), which is standard for drug development, but it requires us to carefully read methods, endpoints, and completeness of reporting. Independent replication and Phase-3 confirmation matter.

4. Imaging method variation. VAT reported by DXA vs MRI vs CT are not directly interchangeable. Some trials report VAT area, others percent change; that complicates cross-trial percent comparisons. 

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend. Until next time, be well, and as always, have a happy, healthy week.

Today, I want to shine a light on a fascinating, little-known peptide called Pancragen. 

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Now, if you’ve been following the world of anti-aging and metabolic optimization, you probably know about GLP-1 medications, metformin, and other mainstream therapies—but Pancragen is something a bit different. It’s a tiny peptide with a big mission. That is rejuvenating your pancreas and restoring metabolic function. And trust me, the science behind it is pretty remarkable.

What is Pancragen?

So here’s the story—Pancragen was developed by a team of Russian researchers led by Professor Vladimir Khavinson in St. Petersburg. These are the same minds behind legendary peptides like Epitalon and Thymalin.

What they discovered was pretty fascinating. In the bovine pancreas, they found a tiny tetrapeptide—just four amino acids—that acts like a molecular switch for keeping your pancreas youthful. The full sequence is Lysine, Glutamic acid, Aspartic acid, and Tryptophan.

Now, in biochemistry, we usually shorten these with a one-letter code, so Lysine becomes K, Glutamic acid is E, Aspartic acid is D, and Tryptophan is W—which is why this peptide is known as KEDW. Pancragen was created to mimic that exact peptide. 

And over decades of studies in both animals and humans, the results have been honestly amazing.

How Pancragen Works

Here’s where it gets really exciting. Unlike most medicaitons that act broadly and non-specifically in the body, Pancragen is precise. When you inject it under the skin, it travels through your bloodstream straight to the pancreas. And get this—it can even enter the nucleus of pancreatic cells and interact with the DNA that controls key genes for insulin and enzyme production, like Pdx1, Ptf1a, and Pax6.

Pdx1 is essential for insulin production, Ptf1a helps pancreatic cells make digestive enzymes, and Pax6 keeps the insulin-producing cells functioning properly. 

Basically, Pancragen flips these genes back on, helping pancreatic cells survive, grow, and work efficiently. The result? Better insulin regulation, improved enzyme production, and a pancreas that behaves years younger—think of it like updating your pancreas’s software to the latest version.

What the Studies Show

Let’s talk numbers. 

In aging patients with type 2 diabetes, Pancragen reduced fasting blood glucose by 20–25% and improved post-meal glucose even more. Even better, patients needed up to 35% less insulin for the same level of glucose control—meaning their cells became more sensitive to insulin rather than being forced to overwork.

In primate studies, old monkeys treated with Pancragen actually outperformed those on glimepiride, a standard diabetes medication. Pancragen restored normal insulin and C-peptide rhythms without forcing the pancreas into burnout—and these effects lasted for weeks after treatment ended.

And here’s a bonus: Pancragen also normalizes melatonin secretion, which helps improve sleep, circadian rhythm, and overall metabolic health. So it’s not just about blood sugar—it’s a full-spectrum metabolic reset.

Safety and Benefits

Pancragen has been on the market in Eastern Europe for over a decade with no reported toxicity or adverse interactions. It simply breaks down into regular amino acids when its job is done.

Users report:

• More stable blood sugar and fewer hypoglycemic events

• Reduced insulin requirements

• Better digestion and enzyme function

• Increased energy and fewer “hangry” moments

• A general feeling of metabolic youthfulness/health

And because it works at the gene-expression level, these benefits can last for weeks or months after a cycle of Pancragen.

Who Should Consider Pancragen?

So, who is Pancragen for?

• People with type 2 diabetes or prediabetes: Pancragen helps restore normal pancreatic function, improving insulin production and glucose control instead of just masking symptoms.

• Those with chronic pancreatitis or enzyme insufficiency: By supporting pancreatic cells and enzyme production, it can help the pancreas work more efficiently, which may ease digestive issues.

• Older adults looking for metabolic anti-aging support: Pancragen can rejuvenate pancreatic function, improve insulin sensitivity, and support overall metabolic health—essentially helping the body act younger.

• Athletes or high-performers wanting optimal metabolic efficiency: Better pancreatic function means more precise insulin and enzyme regulation, supporting energy, recovery, and performance.

• People looking to prevent a plateau from GLP-1 therapy: Over time, some GLP-1 users hit a point where their progress stalls. Pancragen may help “reset” the pancreas so therapy stays effective.

But keep in mind, if you’re just after a quick appetite suppressant, Pancragen isn’t for you. But if your goal is true pancreatic rejuvenation and long-term metabolic health, it can help.

How to Use Pancragen

The typical approach is to take 2 mg of Pancragen per day—either under the skin or into the muscle—for about 30 to 60 days (1 cycle).

Most people repeat this course two to three times a year to keep the pancreas functioning at its best. 

Which brings me to a good point. 

If you stop taking Pancragen, nothing dangerous happens—it’s not like suddenly quitting a medication. What you’ll likely notice is that your pancreas gradually returns to its baseline function over time. The improvements in insulin regulation, enzyme production, and overall metabolic efficiency may slowly taper off, which is why most people do repeat courses a couple of times per year to keep those benefits going. Think of it like hitting “pause” on a fitness program—your gains won’t vanish overnight, but staying consistent helps maintain them.

You also don’t need any complicated stacks to see results, though Pancragen can work well alongside GLP-1s and other anti-inflammatory peptides like BPC-157 or thymosin beta-4, if you’re already using them.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend.

Until next time, be well, and as always, have a happy, healthy week.

Today we’re tackling a question I hear all the time: What’s the difference between thymosin beta-4 and TB-500? These two names often get tossed around like they’re the same thing — but they’re not. I’ve touched on this before, but because it can get pretty confusing, I want to break it down in more depth today.

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We’ll break down how each peptide works, the potential benefits and side effects we know about, what their half-lives look like, and why dosing often ends up being two to three times a week — even though technically you could dose daily at lower amounts. 

I also want to note that we’ll talk specifically about subcutaneous use, since that’s how these peptides are most often used in practice.

What is Thymosin beta-4 and TB-500? 

Let’s start simple.

Thymosin beta-4, or Tβ4, is the full-length natural peptide — it’s 43 amino acids long, and your body actually makes it. You’ll find it in platelets, white blood cells, and tissues all over the body. It helps with wound healing, new blood vessel growth, reducing inflammation, and keeping cells moving where they need to go.

On the other hand, TB-500 is a synthetic (man-made) fragment of Tβ4 — basically, chemists figured out that a small part of the Tβ4 sequence, specifically the section that binds actin, or the 17-23 fragment, that seemed to carry a lot of the healing and regenerative activity. 

The tricky part is, TB-500 isn’t always just that one fragment. Let me try to explain this very confusing concept. 

Most of the time, when people say TB-500, they’re talking about the 17–23 fragment — the piece linked to actin binding and tissue repair. But full-length thymosin beta-4 can actually break down into several different active fragments, like Ac-SDKP, the 1-4 section, the 4-10 section, and even the 20–35 region — and each of those has its own unique effects on healing, inflammation, or fibrosis. Something we can discuss in another podcast. 

The focus today will be on the full-length, naturally occurring 43-amino acid peptide and the common N-acetylated 17-23 fragment often referred to as TB-500.

So think of it this way: Tβ4 is the whole book, TB-500 is one powerful chapter.

How does thymosin beta-4 and TB-500 work?

Both thymosin beta-4 and TB-500 are best known for their role in tissue repair and recovery — but the way they work isn’t identical.

They both help guide cells to where they’re needed after an injury, a process called cell migration. They also help prevent or limit scar tissue, improve blood flow by encouraging angiogenesis — the growth of new blood vessels — and help settle down excessive inflammation so healing can happen.

Where they start to differ is in their scope.

The full-length thymosin beta-4 is like the master version. Because it’s the entire 43–amino acid chain, it has more binding sites and interacts with more pathways. That gives it a broader range of effects — it’s been studied not just for wound healing, but also for heart repair after a heart attack, corneal healing in eye injuries, nerve and brain protection after trauma, and even immune system modulation.

TB-500, on the other hand, is a synthetic fragment that contains the ‘active core’ sequence responsible for actin binding. This means it still boosts cell migration and new blood vessel growth, which are huge for recovery, but it doesn’t have all the extra regulatory sections of the full Tβ4 molecule. Because of that, TB-500 tends to be seen as more targeted — very good at tissue and tendon repair, wound closure, and improving circulation, but without the same wide-ranging effects on the heart, brain, or immune system that you see with the complete Tβ4 peptide

Half-Life and Dosing

 Okay, let’s talk about half-life, because this confuses people all the time.

Tβ4 has a short plasma half-life in humans — about one to two hours after IV dosing. That sounds super quick, right? But here’s the kicker: just because it clears from the blood doesn’t mean the effects are gone. Once it gets into tissues, it kicks off repair programs that can last for days.

TB-500 hasn’t been studied as thoroughly in humans, so we don’t have published plasma half-life numbers you can point to. What we do know from animal and lab studies is that the fragment is also cleared pretty quickly, but the biological effects last much longer than the detectable levels in blood likeTβ4. That’s why protocols often use two or three injections per week rather than daily.

Now, could you take either one every day? Technically, yes — especially at lower doses, and that’s actually been done in clinical research with the full-length thymosin beta-4. But in the peptide therapy world, particularly with TB-500 where we don’t have as much human data, most providers stick with two or three injections a week. It’s a sweet spot that keeps the benefits going, avoids overdoing it, and makes things easier and more affordable for patients.

Let’s talk about subcutaneous dosing for TB-500 and Tβ4. Most of the time, these peptides are injected under the skin, usually in the abdomen or thigh.

For TB-500, people commonly use 2–5 mg per injection, two to three times a week. The exact dose can really vary depending on what you’re using it for — tendon repair, muscle recovery, or general tissue healing.

Tβ4, the full-length peptide, is similar, though sometimes the dose is a little lower because it has broader effects, including immune modulation. You might see protocols using 1–2 mg per injection, a couple times a week, or even lower daily doses for certain situations.

BPC-157 is often called synergistic when used with (stacked with) peptides like TB-500 or Tβ4 because it enhances and complements their healing effects. TB-500 and Tβ4 mainly help with cell migration, tissue repair, and reducing fibrosis, which is great for muscles, tendons, and ligaments. BPC-157, on the other hand, is especially effective at protecting and repairing the gut, blood vessels, and connective tissue.

When you use them together, you’re essentially covering multiple layers of healing: TB-500 or Tβ4 move cells to the injured area and support repair, while BPC-157 helps stabilize blood flow, supports angiogenesis, and promotes stronger tissue remodeling. The result is often faster, more complete recovery than using either peptide alone — that’s why people talk about them as being synergistic.

What Are the Benefits of Tβ4 and TB-500

So what are people actually using these peptides for?

Tβ4 has a wide range of uses when it comes to healing and recovery. It’s been studied for soft tissue repair, chronic injuries, and general recovery, and in surgical settings, some researchers and surgeons have even used it intra-operatively to help tissues heal faster and reduce scar formation. It’s also been applied post-procedure to speed recovery and calm inflammation. On the musculoskeletal side, Tβ4 shows promise for tendon and muscle repair, helping reduce fibrosis, boost new blood vessel growth, and support regeneration of muscle and  tissue. Beyond that, it’s been explored for corneal injuries, dry eye, heart ischemia, neuroprotection, and inflammation control — making it a very versatile peptide with effects across multiple systems.

TB-500 is popular for tendon and ligament repair, muscle recovery, post-surgical healing, and sometimes even athletic performance support.

More on inflammation… Mast cells are immune cells that release chemicals like histamine when they get activated. This can cause redness, swelling, or itchiness — the classic signs of inflammation. But this isn’t all bad. Mast cell activation actually helps start the healing process by bringing other immune cells to the area and signaling the tissue to repair itself. In a controlled way, this early activation can help resolve inflammation faster because the tissue heals properly and swelling eventually goes down.

This is also why full-length Tβ4 can sometimes cause more side effects than TB-500. Tβ4 interacts directly with mast cells and other parts of the immune system, so it can trigger more of these early inflammatory responses. TB-500, being a fragment, mostly focuses on tissue repair and cell movement, so it tends to cause fewer immune-related side effects.

And speaking of well-tolerated, I want to talk about potential side effects next. 

Side effects tend to be mild, but people have reported injection site irritation, redness, or mild swelling. People have also reported headache, fatigue, or a “flu-like” feeling in some users.

What Are My Final Thoughts?

Tβ4 is the natural, full-length peptide, and it has the broadest range of effects. There’s even some human trial data supporting it, especially for things like eye and wound healing.

TB-500 is a shorter, synthetic fragment — it’s more targeted, easier to produce, and widely used in peptide therapy, but it doesn’t have as much human clinical data behind it.

Both peptides leave the bloodstream quickly, but their effects last longer in the body. That’s why most people dose them two to three times a week with subcutaneous injections. That said, at lower doses, they can also be taken daily if needed.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend.

Until next time, be well, and as always, have a happy, healthy week.

 

 

Today we’re diving into a topic that a lot of people struggle with quietly but don’t always feel comfortable talking about: food anxiety.

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Maybe you’ve felt nervous about going to a party because you weren’t sure what kind of food would be there. Or maybe you’ve found yourself planning your entire day around what you’ll eat and how to control it. Perhaps you’ve even finished a meal only to have guilt set in right away.

That’s what food anxiety looks like—and you are definitely not alone.

Today we’re going to talk about what food anxiety actually is, why it shows up, what you can do to calm it, and even how some of the newest medications—things like GLP-1s and dual GIP/GLP-1s—may actually help by quieting some of the mental “food noise.”

What is food anxiety?

At its core, food anxiety is stress or fear around eating. And the thing is, it doesn’t look the same for everyone. For one person, it might show up as constantly worrying they’ll overeat. For another, it’s that lingering guilt after eating something they feel they “shouldn’t have.” And sometimes it’s more subtle than that—like a constant hum in the background of your mind where you’re thinking about food all day, even when you’re not hungry.

I often describe it like having a radio station in your brain that’s tuned into “food talk.” Sometimes it’s background noise, sometimes it’s blaring, but either way, it’s draining. And over time, that stress around eating chips away at both your mental and physical health.

Why does food anxiety happen?

So why does this happen in the first place? A big part of it is the culture we live in. For decades, we’ve been bombarded with messages that carbs are bad, fat is bad, sugar is the enemy—and the list keeps changing. That constant labeling of food as “good” or “bad” teaches us to feel guilty when we eat the so-called wrong thing.

For others, food anxiety starts when they get a medical diagnosis. If you’ve been told you have diabetes, heart disease, or that you need to lose weight for health reasons, suddenly every single bite can feel like a math problem. You’re not just eating—you’re calculating, you’re worrying, you’re second-guessing.

And then there’s the way dieting itself messes with our natural signals. When we spend years restricting, counting, and controlling, we often lose touch with our body’s hunger and fullness cues. Instead of trusting how we feel, we rely on rigid rules. And when those rules get broken, the anxiety hits hard.

And finally, we can’t ignore biology. Food, especially highly processed food, lights up reward pathways in the brain. For some people, those signals are incredibly strong—stronger than for others. That means more cravings, more urges, and unfortunately, more guilt when they give in.

What can you do about food anxiety behaviorally?

Now, here’s the good news. There are things you can do to reduce food anxiety, and you don’t need to overhaul your entire life to start seeing changes.

One of the simplest but most powerful tools is mindful eating. And I know that phrase gets thrown around a lot. But at its heart, mindful eating just means slowing down. 

It means actually tasting your food, noticing the textures, and checking in with how your body feels. When you slow down enough to notice satisfaction, you’re much more likely to stop eating when you’re comfortable instead of stuffed—and that takes a lot of the stress out of the meal.

Another shift that helps tremendously is dropping the “good” and “bad” food labels. Health isn’t decided by one cookie, just like it isn’t guaranteed by one salad. What matters is your overall pattern, week by week, month by month. When you start to see food as neutral—as fuel, as enjoyment, as part of life—it loosens the grip of guilt and allows you to be more flexible.

And speaking of flexibility, having a loose structure around meals can be calming. Instead of rigid dieting rules, like “I can never eat after 7 p.m.,” focus on balance. A meal that has some protein, some fiber, and a little healthy fat is naturally stabilizing. It helps keep blood sugar steady, which means fewer spikes and fewer crashes. And when your body feels stable, your brain feels calmer, too.

It’s also worth paying attention to your personal triggers. For some people, weekly weigh-ins, keeping a food log, or using a nutrition app can be helpful. But for others, they actually fuel the anxiety. If you notice those things making you more stressed rather than less, it’s okay to step away from them. You can still eat intentionally without logging every single bite.

And while we are on the subject of personal triggers like daily or weekly weigh-ins, I want to talk about this a bit more. It’s really important to remember, your body weight naturally fluctuates from day to day. Daily weight changes are completely normal and can happen for a bunch of reasons. 

Your body might hold onto water from salty foods, hormones, or just changes in hydration. What you’ve eaten recently can also temporarily add weight, and when you eat carbohydrates, your muscles store them along with water, which can make the scale go up a bit. For women, hormonal changes during the menstrual cycle can cause water retention that shows on the scale as well. On top of all that, if you’ve been exercising more, you might be building muscle even while losing fat. Because muscle is denser than fat, the scale might not move—or could even go up slightly—while your body is actually getting leaner and stronger.

Because of these normal variations, seeing a slightly higher number on the scale one day can feel discouraging—even if you’re making great progress.

Instead of focusing on daily fluctuations, a better approach is to look at your net overall trend over a month. Tracking the weekly or monthly average gives you a more accurate picture of real progress and helps reduce stress or obsession with the number on the scale

And lastly, support makes a big difference. Whether that’s working with a dietitian, talking with a therapist, or joining a group, sometimes having someone else in your corner makes it easier to change both your habits and the way you think about food.

Where medications may help: GLP-1s and dual GIP/GLP-1s

Now let’s shift gears for a moment, because in the past few years, there’s been an exciting development in how we treat weight and appetite. Medications like GLP-1 receptor agonists—semaglutide is one example—and the newer dual GIP/GLP-1 agonists, like tirzepatide, have been game changers.

So what do they actually do? GLP-1s mimic a natural hormone your gut makes after you eat. That hormone tells your brain, “Hey, you’re full.” It also slows down how quickly food leaves your stomach and helps keep you fuller, longer. They also cause your pancreas to release insulin when there’s too much sugar from food in your bloodstream. This lowers your blood sugar and helps your cells use glucose (sugar from the food you’ve eaten). This is helpful because extra sugar your cells don’t use for energy is stored as fat, which is why high blood sugar can cause weight gain. 

The dual GIP/GLP-1s do all of that, plus they act on another hormone called GIP, GIP improves how your body uses sugar AND fat (storing less of both by breaking them down to use for energy).

Now, here’s where it gets fascinating for food anxiety. People who take these medications often report that the “food noise” in their head finally quiets down. Instead of thinking about food all day, the volume on that radio station turns way down. Meals feel more manageable. A normal portion actually feels satisfying. And for many, that overwhelming urge to snack or binge just isn’t there anymore.

When your hunger cues are more predictable and less intense, you don’t feel like you’re constantly fighting your own body. That alone can dramatically reduce the anxiety around eating. And by calming the physical side—the cravings, the urges—it gives you more space to work on the mental and emotional side of eating without feeling like you’re swimming upstream.

Of course, these medications aren’t a magic fix. They don’t erase years of learned guilt or change the culture we live in. But they can be powerful tools, especially when paired with mindful eating practices and professional support.

My Final Thoughts

If you take one thing away from this episode, let it be this: food anxiety is real. It’s not about weakness or lack of willpower. It’s shaped by culture, by biology, by personal history—and it can be incredibly challenging.

But there are ways to reduce it. Slowing down and being more mindful at meals, letting go of the “good food versus bad food” mindset, building flexible eating habits, and getting support are all steps in the right direction. And for some, medications like GLP-1s or dual GIP/GLP-1s can make the process easier by quieting the biological noise that drives anxiety in the first place.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend and please remember you’re not alone. Many people struggle with food anxiety, and there is nothing wrong with reaching out for help—whether that’s behavioral support, medical treatment, or both.

Until next time, be well, and as always, have a happy, healthy week.

 

Today we’re talking about something every woman deserves straight talk about—perimenopause and menopause and the many changes that happen as estrogen and progesterone begin to decline.

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Now, most of us have heard about hot flashes, but very few people explain what’s actually happening inside our bodies, why it’s happening, and what we can do to feel better. And yes, that includes some really interesting therapies like peptides.

What is happening?

Let’s start with the transition itself. Perimenopause is that phase leading up to menopause, which is officially defined as twelve months without a menstrual cycle. It usually starts in your 40s, though some women notice changes earlier. The reason it can feel like a rollercoaster is all about hormones. 

Estrogen is our multitasker—keeping our bones strong, our skin glowing, our brains sharp, and even helping with vaginal lubrication. When estrogen dips, it’s not surprising that hot flashes, vaginal dryness, and mood swings start showing up. 

Progesterone, on the other hand, is what I like to call our “chill hormone.” It helps us sleep and keeps our cycles balanced. When progesterone drops, insomnia, irritability, and mood swings can sneak in. 

And let’s not forget testosterone, which fuels energy, muscle, and libido. As testosterone slowly declines, it’s no wonder sex drive can take a hit. When these three hormones are fluctuating or dropping during perimenopause, it can touch nearly every part of the body, making this phase feel intense and, at times, overwhelming.

Brain fog

Then there’s brain fog. You know, that feeling when you walk into a room and can’t remember why you’re there. Estrogen actually plays a big role in keeping our brain sharp by influencing neurotransmitters like acetylcholine, which manage memory and focus. When estrogen levels fall, those neurotransmitters aren’t as efficient, and poor sleep from night sweats can make brain fog even thicker. 

What helps? Regular exercise, consistent sleep, omega-3s, and even brain-training games can make a difference. And peptides can play a role here too. 

Nootropic peptides like Selank and Semax support neurotransmitter balance, helping with focus, memory, and mental clarity, while also helping the brain manage stress and fatigue.

Weight gain

Let’s talk about one of the biggest frustrations women bring up during perimenopause and menopause—weight gain. You may notice that even if you’re eating the same and moving your body the way you always have, the scale starts creeping up. This isn’t your imagination. As estrogen levels drop, metabolism slows down, muscle mass tends to decrease, and fat starts redistributing—especially around the belly. On top of that, poor sleep, more stress, and shifting insulin sensitivity can all make it harder to keep weight steady.

The good news is there are ways to manage this. Resistance or strength training helps preserve and even rebuild muscle, which keeps your metabolism active. Prioritizing protein with every meal can support that muscle, too. Managing stress through mindfulness, yoga, or simply better boundaries can help with cortisol—the stress hormone that encourages belly fat storage. And paying attention to blood sugar balance, by choosing more whole foods and fewer processed carbs, can really make a difference. For some women, hormone therapy can provide extra support by improving sleep, mood, and metabolism, making it easier to maintain a healthy weight.

And now, we also have GLP-1 agonists—like semaglutide—and even newer dual GIP/GLP-1 agonists, such as tirzepatide. These medications work by improving satiety, slowing digestion, balancing blood sugar, and supporting insulin sensitivity, all of which can make weight management during menopause more achievable. They’re not magic, but when combined with lifestyle changes, they can be powerful tools to help women feel more in control of their weight and overall health during this stage of life.

Hair changes

Hair changes are another big one. Estrogen helps keep hair thick, strong, and healthy by promoting follicle growth and prolonging the growth phase. When estrogen drops, hair can start thinning. 

At the same time, shifts in androgen levels like testosterone and its potent form, DHT, can trigger hair growth in places we really don’t want it, like the chin or upper lip. 

Collagen supplements, checking iron and vitamin D levels, stimulating the scalp, or even low-level laser therapy can all support healthier hair. 

Peptides like GHK-Cu, a copper peptide, stimulate hair follicles by promoting cell growth, increasing blood supply, and supporting collagen production. Thymosin Beta-4, or TB-500, also helps by reducing inflammation and encouraging tissue repair, creating a better environment for hair growth.

Skin changes

As estrogen dips, natural moisture throughout the body also decreases. This can mean dry eyes, crepey or itchy skin, and new sensitivities popping up seemingly out of nowhere. 

Support can be as simple as artificial tears, omega-3s to support tear production, gentle fragrance-free moisturizers, or running a humidifier at night. 

Peptides like Epitalon reduce oxidative stress, support collagen production, and promote cellular repair, which can improve skin elasticity. BPC-157 helps reduce inflammation and supports healing, making the skin less reactive and more comfortable.

Bladder issues

And then there are those bladder surprises. Ever sneeze, laugh, or cough and suddenly wonder if you should’ve packed a spare pair of underwear? Dropping estrogen weakens the pelvic floor and thins the bladder lining, which can make those little “oops” moments more common. 

Kegel exercises, pelvic floor physical therapy, vaginal estrogen creams, and avoiding bladder irritants like coffee or alcohol can help. 

Peptides like BPC-157 support tissue healing in the bladder and pelvic area, and KPV may help calm irritation in urinary tissues.

Mood changes

Mood changes are another challenge. Shifts in estrogen, progesterone, and serotonin can trigger anxiety, irritability, or low mood seemingly overnight. 

Things like therapy, mindfulness, regular exercise, and making sure you get enough vitamin D and magnesium can really help. 

Peptides give an extra boost too. Selank is a gentle anti-anxiety peptide that won’t make you drowsy, DSIP (Delta Sleep-Inducing Peptide) helps improve deep sleep, naturally stabilizing mood, and Semax works on dopamine pathways to lift energy, focus, and motivation when you need it most.

Sex drive

Finally, let’s talk about something we don’t discuss enough: libido. Vaginal dryness, fatigue, and shifting hormones can all make desire dip, and this is very much physiological, not just in your head. 

Lubricants, vaginal moisturizers, hormone replacement therapy, and open communication with your partner can all help. 

Peptides like PT-141 (bremelanotide), work on melanocortin receptors in the brain to boost sexual desire. It’s an on-demand injection, usually taken a few hours before intimacy, and many women feel it helps restore that spark that seemed long gone, though side effects can include flushing or nausea.

So here’s the big takeaway: menopause is much more than hot flashes. It’s brain, body, skin, mood, and sexual function all shifting at once. But you don’t have to just “tough it out.” From lifestyle shifts to targeted peptides, there are tools to help you feel like yourself again. And the most important thing to remember is that you are not alone. Every chin hair, every laugh-leak, every brain fog moment—you’ve got millions of women nodding right along with you.

Thanks for listening to The Peptide Podcast. If today’s episode resonated, share it with a friend—because if she’s in her 40s or 50s, she’s probably going through the same changes and wondering if she’s the only one.

And if you want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. 

Until next time, be well, and as always, have a happy, healthy week.

 

 

 

Thank you for listening to The Peptide Podcast. If you enjoyed the show and want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. 

Today, we’re diving into one of the most talked-about topics in health and weight loss right now: GLP-1 medications like semaglutide and the newer dual GIP/GLP-1s like tirzepatide. You’ve probably seen the headlines, scrolled past a few TikToks, or heard a friend mention it — but with all that noise comes a lot of confusion, half-truths, and flat-out myths.

Today we’re breaking it all down. What’s real? What’s hype? And what do you actually need to know if you're using these medications — or thinking about it? Let’s separate science from scare tactics and get to the truth, one myth at a time.

Myth #1: GLP-1s Cause Dangerous Muscle Loss

The claim:  “GLP-1s cause massive muscle loss.”

Truth: This is an overstatement.

Some loss of lean mass is normal with any kind of weight loss — whether it’s through diet, medication, or surgery. What studies show is that with medications like semaglutide (Wegovy) and tirzepatide (Zepbound), about 20–25% of the total weight lost comes from lean mass, and the rest is fat — which is exactly what we’re targeting in obesity treatment. That 20–25% figure isn’t unique to these meds; it’s actually pretty typical in weight loss without focused resistance training or optimized protein intake.

You may also hear “You’ll lose all your muscle and become frail on GLP-1s.”

Truth: You won’t “lose all your muscle.” In fact, muscle loss is preventable by maintaining adequate protein intake, resistance training, and managing weight loss pace. Furthermore, many patients gain strength and mobility as excess weight comes off.

And lastly, my favorite myth is “You can’t preserve muscle on GLP-1s.”

Truth: That’s completely false — muscle loss isn’t inevitable on GLP-1s if you take the right approach. You can absolutely preserve muscle by making a few intentional choices: aim for enough protein each day (a good goal is around 0.8 grams per pound of body weight), include some strength or resistance training a couple times a week, and avoid losing weight too quickly. These simple steps go a long way in protecting your lean mass while still getting all the benefits of weight loss.

One study on semaglutide showed that people lost an average of about 15% of their body weight, and only around 3–4% of that was lean mass. So if someone drops 30 pounds, maybe 6 to 8 of those pounds might be lean mass—not ideal, but definitely not disastrous either, and very manageable with the right lifestyle habits. 

The truth is, while some lean mass loss is expected with any type of weight loss, research shows that most of the weight lost on GLP-1s is actually fat, not muscle. For example, in the STEP 1 trial, about 80% of the weight lost on semaglutide came from fat, and only about 20% from lean tissue (as we mentioned earlier). 

The SURMOUNT-1 trial with tirzepatide showed similar results—significant fat loss with relatively preserved muscle, especially when paired with resistance training. And that’s important, because preserving muscle during weight loss helps protect metabolism, strength, and overall health. With good nutrition and movement, GLP-1s can lead to healthier body composition—not just a lower number on the scale.

Okay, moving along to the next myth …

Myth #2: GLP-1s Can Cause Blindness

The truth: This myth stems from concerns about diabetic retinopathy worsening, which is tied to how quickly blood sugar drops, not to the drug itself.

In the SUSTAIN-6 trial (Marso et al., NEJM, 2016), a small subset of patients with pre-existing advanced diabetic retinopathy saw transient worsening—but only in those with rapid improvements in A1c.

No increased rates of blindness or new-onset retinopathy have been found in non-diabetic patients using GLP-1s for weight loss.

The bottom line is that those without advanced diabetic eye disease, there’s no increased risk of blindness. Patients with diabetic retinopathy should be monitored closely—but this is about glycemic management, not a direct effect of the medication.

Myth #3: GLP-1s Cause Kidney or Liver Damage

The truth: This is false. In fact, GLP-1 agonists may protect kidney and liver function—especially in patients with diabetes or fatty liver disease.

The most recent notable study showing kidney‑protective effects of a GLP‑1 receptor agonist is the FLOW trial, which evaluated semaglutide in people with type 2 diabetes and chronic kidney disease (CKD). This double‑blind, randomized, placebo‑controlled trial included 3,533 participants followed for a median of 3.4 years and found that semaglutide reduced the risk of major kidney‑related events—including kidney failure, substantial eGFR decline, and death from renal or cardiovascular causes—by 24% compared to placebo.

A 2025 meta-analysis of multiple randomized controlled trials (11 studies, 85,373 participants) concluded that GLP‑1 receptor agonists reduced the risk of composite kidney failure outcomes by 18%, kidney failure by 16%, and all‑cause death by 12%.

And let’s not forget the SMART trial, involving obese patients with kidney disease but without diabetes, found that semaglutide protected kidney function in this non‑diabetic, CKD‑affected population. 

When it comes to the liver, there's actually growing evidence they’re actually helping reverse non-alcoholic fatty liver disease (NAFLD).

The STEP 1 MRI substudy and SURPASS-3 MRI substudy have shown people on these medications can reduce liver fat by 30 to even 50% and in some cases, completely resolve liver inflammation — that more serious form called NASH, where fat is combined with inflammation and early scarring.

The LEAN trial found that nearly 60% of people taking semaglutide had resolution of NASH, without worsening their liver scarring. That’s huge.

And even better, we’re seeing these effects even in people who don’t have diabetes. Just losing weight helps fatty liver, but these meds seem to do more than that — they actually target inflammation and fat storage in the liver itself..

The bottom line is GLP-1s are not nephrotoxic or hepatotoxic. In fact, they may be organ-protective—especially for people with underlying metabolic issues.

Myth #4: These Drugs Lead to Bone Loss

The claim: “You’ll get osteoporosis from losing too much weight!”

The truth: While extreme weight loss can affect bone density, GLP-1s themselves do not cause bone loss, and may even have neutral or protective effects on bone.

A 2022 study in Bone found no significant change in BMD (bone mineral density) in adults treated with semaglutide for obesity. While the SUSTAIN and PIONEER programs found no increased risk of fractures in semaglutide-treated patients versus placebo.

Truly, concerns about bone loss are more relevant in extreme calorie restriction or eating disorders—not evidence-based GLP-1 treatment with appropriate nutrition.

Myth #5: Everyone Gets Gastroparesis

The claim: “These medications paralyze your stomach”

The truth: GLP-1s slow gastric emptying, which is part of how they work—making you feel full longer. But this is dose-dependent and typically reversible.

A 2023 FDA safety review found that true gastroparesis is extremely rare and resolves when the drug is stopped.

Reality check: Nausea, early satiety, and mild bloating are common but manageable side effects. True, lasting gastroparesis is not typical, especially when doses are titrated gradually.

Myth #6: GLP-1s Make Your Hair Fall Out

The claim: “You’ll lose a ton of hair—just like with crash diets”

The truth: Hair shedding is not directly caused by GLP-1 medications. Instead, it’s often a temporary, non-scarring condition called telogen effluvium, which can happen with any rapid weight loss, regardless of the method.

A 2023 analysis from the American Academy of Dermatology emphasized that telogen effluvium is common with surgical or medical weight loss, especially if patients lose more than 10% of their body weight within a few months.

In clinical trials like STEP and SURMOUNT, hair loss was not listed as a common side effect, but patient-reported data show it occurs occasionally—likely tied to nutritional stress, not the drug itself.

So why does hair loss happen? We’ve talked about this before, but I don’t want to leave this important information out. 

Hair follicles are sensitive to internal stress. Rapid changes in caloric intake, nutrient levels (like iron, zinc, and biotin), or hormone balance can push hairs into the shedding phase. This is a delayed effect, often showing up 2–3 months after weight loss begins, and it typically resolves within 6–12 months.

What helps is slower, sustained weight loss, prioritizing protein intake, supplementing iron, zinc, and biotin if deficient, and avoiding very low-calorie diets and over-restriction.

Myth #6: GLP-1s Cause Dehydration

It’s a common myth that GLP-1 medications cause dehydration — but that’s not exactly true. The medication itself doesn’t directly dehydrate you. What can happen is that some people experience nausea, vomiting, or a reduced appetite early on, which can lead to drinking less water without realizing it. That’s where the dehydration risk comes in.

A good general rule for staying hydrated is to aim for half your body weight in ounces of water per day. So, for example, if you weigh 160 pounds, try to drink around 80 ounces daily — more if you're active or live in a hot climate.

Electrolytes can also be really helpful, especially if you’re feeling tired, dizzy, or crampy. I like LMNT packets — they’re a clean option with no sugar and a good balance of sodium, magnesium, and potassium. The sodium in LMNT packets helps keep you hydrated by pulling water into your cells and helping your body retain the fluids it needs to function properly. Just one a day can make a big difference in how you feel.

Myth #7: You Have to Stay on GLP-1s Forever or You’ll Gain All the Weight Back

The claim: “As soon as you stop taking it, all the weight comes back”

The truth: Yes—some weight regain is likely after stopping GLP-1 medications. But that doesn’t mean they’re ineffective or that you’re doomed to rebound completely. The same pattern happens after any type of weight loss intervention, whether it’s a diet, surgery, or medication.

The STEP 4 trial (Wilding et al., 2022) showed that participants who stopped semaglutide after 20 weeks regained an average of 6% of their weight loss over the next year. But it’s important to note that they still weighed less than at baseline—and many continued to experience improvements in blood pressure, cholesterol, and insulin sensitivity.

Similarly, in SURMOUNT-4, patients who stopped tirzepatide also regained weight, but less than they lost.

So why does this weight gain happen?

I feel like the answer to this is obvious, but I’ve found that it’s not. 

GLP-1s change your appetite and hunger cues. Once the medication is stopped, your body’s baseline hunger signals return—and often with increased intensity, due to metabolic adaptation. But this isn’t unique to GLP-1s. The same thing happens after crash diets, keto, intermittent fasting, or bariatric surgery if long-term changes aren’t made.

The real issue isn’t the drug—it’s the lack of a plan after the drug. To help make results sustainable, we need to use the medication as a tool, not a crutch. We should use it to help us lose weight and understand our hunger cues, while transitioning to a whole foods, protein based diet coupled with resistance training to help preserve and build muscle. 

Just remember, if you're coming off a GLP-1 and want to keep the momentum going, the key is to approach it thoughtfully. Tapering slowly under medical supervision can help your body adjust and reduce the chances of weight regain. At the same time, this is a great moment to double down on the habits that helped you feel your best while on the medication. Think ongoing support—like working with a health coach, joining a support group, or even doing behavioral therapy—to help reinforce those long-term lifestyle changes. It’s not just about what you stop; it’s about what you keep doing that matters most.

You don’t necessarily have to stay on GLP-1s forever—but if you stop without a plan, some weight regain is very likely. Think of them like glasses: they help you see clearly while you build the habits to eventually navigate without them. For some, that may mean staying on a lower maintenance dose long-term—just like with blood pressure or cholesterol meds.

What are my final thoughts?

I want to be clear—GLP-1s aren’t magic. But they are powerful tools when paired with education, support, and smart lifestyle changes. 

Myths like ‘you’ll go blind,’ ‘you’ll lose all your hair,’ or ‘you’ll be stuck on these meds forever’ aren’t just misleading and downright false—they discourage people from getting real help. 

So if you’re thinking about these medications, get informed, ask the hard questions, and make your decision based on science—not fear.

Thank you for listening to The Peptide Podcast. If you enjoyed the show and want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. 

Until next time, be well, and as always, have a happy, healthy week.

Thank you for listening to The Peptide Podcast. If you enjoyed the show and want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. 

Today we’re switching gears a bit to talk about a medication rather than a peptide — metformin. If you’re someone who’s interested in peptides for metabolic health or inflammation, you’ve probably heard metformin mentioned alongside them. It’s been around for decades as a diabetes medication, but recently it’s gaining attention for its potential benefits beyond blood sugar, including longevity, inflammation, and neuroprotection — even in people who don't have diabetes.

Let’s get into it.

Metformin and Longevity

Can metformin really help us live longer?

One of the biggest sparks came from a 2014 study published in Diabetes, Obesity and Metabolism, where researchers found that diabetics on metformin actually lived longer than non-diabetics not taking the medication. 

The authors suggested that metformin may offer protective benefits beyond glucose control, possibly by reducing oxidative stress and slowing cellular aging.

This inspired the launch of the TAME trial—short for Targeting Aging with Metformin—which is designed to test whether metformin can delay the onset of age-related diseases like cancer, cardiovascular disease, and cognitive decline. While results are still pending, it’s the first large-scale effort to study aging as a treatable condition, not just a process.

Inflammation and Immunometabolism

Next up: inflammation. Chronic low-grade inflammation is at the root of so many health issues—heart disease, dementia, even depression.

Metformin appears to blunt systemic inflammation by activating AMPK. Think of AMPK as a metabolic master switch that lowers inflammatory signaling.

A 2021 review published in Pharmacological Research found that metformin can inhibit NF-κB, a major pathway that drives inflammation. It also helped lower levels of CRP—a protein made by the liver that rises when there’s inflammation from things like infection, injury, or chronic disease—and IL-6, another immune system protein commonly elevated in chronic inflammatory conditions.

Because of these anti-inflammatory effects, researchers have been exploring metformin’s potential in conditions beyond diabetes, including autoimmune diseases, multiple sclerosis (MS), PCOS, and even COVID—where it’s been linked to lower mortality in patients with diabetes.

Brain Health and Neuroprotection

What about the brain? Can metformin help protect against cognitive decline?

There’s some promising data here too. A 2017 study in Aging Cell found that metformin improved neurogenesis in the hippocampus of aged mice—basically, helping old brains grow new neurons.

In 2019 a cohort study in JAMA Network reported that people with type 2 diabetes taking metformin had a lower risk of developing dementia compared to those not taking it.

Mechanisms may include reduced insulin resistance in the brain, less oxidative stress, and—again—AMPK activation, which promotes mitochondrial health and energy production.

Still, human trials are mixed, and more controlled research is needed before we can call it a “smart drug.”

Lower Cancer Risk

So, here’s an interesting one—can metformin actually lower the risk of cancer? Well, the short answer is: maybe. People with diabetes tend to have a higher risk of developing certain types of cancer, so part of metformin’s benefit could just come from better managing blood sugar and insulin levels. But what’s really exciting is that researchers think metformin might do even more than that.

There’s evidence suggesting it could have direct effects on cancer cells—like slowing down their growth or making the environment less friendly for tumors. Some studies have found lower rates of cancers like breast, colon, and prostate in people taking metformin.

Now, this isn’t a magic bullet or anything, but it’s a promising area of research that’s getting a lot of attention. So metformin might be pulling double duty: managing diabetes and potentially helping reduce cancer risk through other mechanisms we’re still learning about.

Metabolic Health for Non-Diabetics

Now here’s where it gets controversial—should healthy people without diabetes be taking metformin?

Some researchers argue yes, especially for people with metabolic syndrome, prediabetes, or high inflammation. Metformin improves insulin sensitivity, reduces liver glucose production, and may even support modest weight loss.

That said, there are tradeoffs. Metformin can cause stomach-related side effects (e.g., nausea, gas, heartburn, and diarrhea) and vitamin B12 deficiency (which may lead to nerve damage). It can also cause extreme fatigue. 

Metformin may sometimes cause sexual side effects, like erectile dysfunction in men. Some studies suggest it might lower testosterone, which we know is important for male sexual health. But interestingly, other research points to metformin actually improving blood flow to the penis, which could help with erectile issues. So, it’s a bit of a mixed picture—and it really depends on the individual.

And although rare, it can cause lactic acidosis (a life threatening condition where lactic acid builds up in the blood) in older adults, people with advanced kidney disease, or those who drink excessive amounts of alcohol. So it’s not a free pass. 

So what are my final thoughts and who should you take metformin for longevity?

Metformin isn’t a one-size-fits-all solution, and it’s definitely not something to start just because you heard about it on a podcast. We still need more research—especially in people without diabetes—to really understand who benefits most. But it might make sense for some people, like those with prediabetes, PCOS, metabolic syndrome, or even older adults looking to support healthy aging. 

As always, it’s something to talk through with your healthcare provider. 

The science is exciting, but it’s all about finding what makes sense for you.

Thank you for listening to The Peptide Podcast. If you enjoyed the show and want to support what we do, head over to our Partners Page. You'll find some amazing brands we trust—and by checking them out, you're helping us keep the podcast going. 

Until next time, be well, and as always, have a happy, healthy week.