• GLOW Peptide Therapy
    Oct 2 2025
    I’m so glad you’re here today because we’re diving into a therapy that people are buzzing about—GLOW peptide therapy. 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. https://pepties.com/partners/ 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 ...
    Show More Show Less
    14 mins
  • How Retatrutide Compares to Semaglutide and Tirzepatide
    Sep 25 2025
    Welcome to The Peptide Podcast. In this episode, we’re unpacking the latest on retatrutide and how it measures up against semaglutide and tirzepatide. 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. https://pepties.com/partners/ 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 ...
    Show More Show Less
    15 mins
  • Pancragen
    Sep 18 2025
    Today, I want to shine a light on a fascinating, little-known peptide called Pancragen. 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. https://pepties.com/partners/ 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...
    Show More Show Less
    7 mins
  • TB-4 vs TB-500 — Clearing Up the Confusion
    Sep 11 2025
    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. 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. -> https://pepties.com/partners/ 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 ...
    Show More Show Less
    12 mins
  • Food Anxiety and GLP-1’s
    Sep 4 2025
    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. 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. 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...
    Show More Show Less
    10 mins
  • Peptides for Perimenopause and Menopause Wellness
    Aug 21 2025
    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. 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. 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 ...
    Show More Show Less
    10 mins
  • MythBusting GLP-1s: TRUTH About Weight Loss Medications
    Aug 14 2025
    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 ...
    Show More Show Less
    17 mins
  • Beyond Blood Sugar: Metformin’s Surprising Promise
    Aug 7 2025
    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 ...
    Show More Show Less
    6 mins