Metformin: Should You Still Be Taking It in 2026?

All right, let's talk about metformin. I'm Dr. Ahmet Ergin. I'm an endocrinologist at the Diabetes, Thyroid, and Hormone Center of the Treasure Coast and the founder of SugarMD. You can visit sugarmds.com for information, knowledge, supplements, et cetera, and my website for my clinic is tcmbo.com. Today, I'm going to say something that might surprise you coming from a physician. I have real concerns about how metformin is being used in 2026. Now, not because the drug does not work. It works, but because the way it gets handed out, sometimes as a first response, sometimes as the only response, and sometimes to people who genuinely do not need it yet. And that part concerns me deeply. So if you are on metformin, if your doctor just suggested it, or if you're just trying to understand what's happening in the diabetes world right now, stay with me. I'm going to give you the honest picture, the one that often does not happen in a 10 to 12 minute office visit. No fluff, no pharmaceutical cheerleading. Let's go. First, what is metformin and how does it work? Metformin is a biguanide, a drug class derived originally from a plant called French lilac, which was used in traditional European medicine for centuries to treat symptoms of what we now know as diabetes. Yes, one of the most prescribed drugs on earth started as an herb. Remember that. It'll be relevant later. Here's what metformin actually does in your body. It suppresses your liver's glucose output. Your liver constantly manufactures and releases glucose into your bloodstream, a process called gluconeogenesis. In people with type 2 diabetes or insulin resistance, the liver overdoes this dramatically. Metformin puts a partial break on that process. Fasting glucose comes down. A1c follows. It activates something called AMPK, a cellular energy sensor, sometimes called the metabolic master switch. Activating AMPK improves glucose uptake in muscle and reduces fat accumulation in the liver. Interestingly, this is the same pathway activated by exercise, which should immediately tell you something important about what else can do this job. It improves insulin sensitivity modestly, meaning your cells become somewhat more responsive to the insulin you're already producing. It doesn't fix insulin resistance. It nudges it. It also influences the gut microbiome. Newer research suggests metformin alters gut bacterial composition in ways that may contribute to its effects. This is still being actively studied, and it's genuinely interesting science. That's the mechanism. Now let's talk about why I have reservations, my honest concerns about metformin, and why I'm on the defensive here. I want to be very clear. I am not telling you to stop your metformin. That decision belongs to you and your physician. What I am telling you is that I think metformin is overprescribed, under-questioned, and far too often used as a substitute for a real conversation about root cause. Here's what I see regularly in my clinic. A patient comes in with a mildly elevated A1c, maybe 6.2, maybe 6.5, and they've been put on metformin. No one talked to them about what they were eating. No one asked about their sleep. No one checked their cortisol or their thyroid. No one assessed their visceral fat or their inflammatory markers. They just got a prescription and a, see you in three months. That is not metabolic medicine. That is metabolic paperwork. And here's what bothers me most. For a meaningful percentage of those patients, particularly those in the pre-diabetes range or early type 2, the lifestyle intervention alone would have done the same job or better without the side effects, without the B12 depletion, without the dependency on a medication that still doesn't fix the underlying problem. Let me walk through my specific concerns with metformin in detail. The real downsides. Not the fine print nobody reads. Gastrointestinal side effects are not minor for a lot of people. Nausea, diarrhea, stomach cramping, bloating. These are the number one reason patients stop metformin. And they are genuinely disruptive to quality of life. For some patients, it settles down after a few weeks. For others, it's a persistent misery. I've had patients lose weight on metformin, not because of any metabolic benefit, but because food became unpleasant. That is not a therapeutic win. The extended release formulation reduces gastrointestinal symptoms significantly. And taking it with a full meal helps. But the fact that we have to work around the side effects should at least prompt the question, is there a better option for this patient? B12 depletion. And this one genuinely keeps me up at night. Long-term metformin use interferes with B12 absorption in the gut by disrupting a calcium-dependent mechanism in the ileum. B12 deficiency causes peripheral neuropathy. You know what else causes peripheral neuropathy? Diabetes. So here's the scenario I've seen play out in clinical practice. A patient with diabetes develops numbness and tingling in their feet. Their doctor sees it as diabetic neuropathy. The A1c is somewhat elevated. The natural response is to intensify diabetes management, possibly increase metformin. Meanwhile, the actual driver of the neuropathy is B12 deficiency caused by the metformin that's been running in the background for five years. This is not a rare edge case. This happens. And it happens because B12 monitoring in long-term metformin users is inconsistently done. If you have been on metformin for more than a year and your B12 has never been checked, that needs to happen. Non-negotiable. It manages the number. It does not fix the biology. This is perhaps my most fundamental objection to how metformin is used. Metformin brings your A1c down, but your insulin resistance, the underlying dysfunction, is still there. Your visceral fat is still there. Your liver is still fatty if it was fatty before. Your mitochondria are not suddenly healthier. Your inflammatory state has not improved. You have changed what the scoreboard shows. You have not changed the game. When patients stop metformin without having addressed their lifestyle, their numbers go right back up because the drug was managing the symptom. It was not treating the disease. It may blunt your response to exercise. This is newer and still somewhat debated in the literature, but there are studies, including research published in Nature Metabolism, suggesting that metformin may attenuate some of the mitochondrial adaptations that come from exercise training. Your muscles may not respond as robustly to physical training when metformin is on board. Now, the effect size is not catastrophic, and the research is ongoing, but the directional signal is not reassuring. Exercise is one of the most powerful metabolic interventions we have, possibly more powerful than metformin for many patients. If the drug is interfering with that, we need to weigh it carefully. It is not protecting your heart or kidneys in the way newer drugs do. This is the important context for 2026, the diabetes drug landscape has changed dramatically. We now have SGLT2 inhibitors, empagliflozin, dapagliflozin, with robust data showing they reduce heart failure hospitalizations and slow kidney disease progression. We have GLP-1 receptor agonists, semaglutide, terzapatide, with cardiovascular outcome data that is genuinely impressive, and significant weight loss effects on top. Metformin does not have that organ protective data. Some older trials suggested cardiovascular benefit, but the newer drugs have raised the bar considerably. For patients with established heart disease or chronic kidney disease, metformin is not the most important drug in the conversation anymore. So when is metformin reasonable? I told you I'm not dismissing it entirely, and I meant that. There are scenarios where metformin makes sense, and I do prescribe it, when lifestyle alone has genuinely been tried and hasn't been sufficient. If someone has been consistent, real consistency, not theoretical consistency, with diet, resistance training, sleep, and stress management for three to six months, and their numbers haven't moved enough, medication support is reasonable. Metformin can be a bridge when the A1C is significantly elevated and waiting for lifestyle-only results isn't clinically safe. If someone walks in at an A1C of nine or 10, with complications already developing, we need to bring glucose down now. Metformin plus other agents may be appropriate while lifestyle changes take hold. As part of a broader medication strategy in established type 2 diabetes, it's inexpensive, generally tolerable at lower doses, and can complement other agents. For the rare pre-diabetes patient with very high conversion risk, where lifestyle has not worked and other metabolic risk factors are stacking up. But notice the pattern in all of those scenarios. Metformin is a secondary consideration, not the automatic first response, and it should never be the whole plan. The natural alternative conversation, and this is where it gets really interesting. Let me tell you about berberine, and then let me tell you why regular berberine isn't actually the version you want. Berberine is a bioactive compound found in plants like barberry, golden seal, and Oregon grape. It has been used in traditional Chinese and Ayurvedic medicine for centuries. And here's what makes it pharmacologically remarkable. It activates AMPK, the exact same pathway as metformin. Multiple clinical trials have compared berberine directly to metformin in people with type 2 diabetes. A study published in the journal Metabolism showed comparable reductions in fasting glucose, post-meal glucose, and HbA1c between the two. The berberine group also showed improvements in triglycerides and LDL cholesterol, areas where metformin doesn't really move the needle. Other trials have shown berberine reducing A1c by 1 to 1.5 percentage points over three months. That is clinically meaningful. That is not a supplement doing supplement things. That is a compound with genuine pharmacological activity. But here's the problem with standard berberine, bioavailability. Berberine is poorly absorbed in the gut. Your body doesn't take it up efficiently, which means a significant portion of what you swallow never actually reaches systemic circulation. You're essentially leaving a lot of the benefit on the table. This is where dihydroberberine changes everything. Dihydroberberine is a reduced form of berberine. It is absorbed significantly better. Studies suggest roughly five times more bioavailable than standard berberine. Your gut absorbs it more efficiently. And once it's inside your cells, it gets converted back to berberine, where it activates AMPK and does its work. What that means practically is that you get a much stronger effect at a lower dose with less of the gastrointestinal irritation that some people experience with high-dose standard berberine. Superberberine by SugarMD contains dihydroberberine, not standard berberine. That distinction matters a lot. The formulation exists specifically because I wanted a tool that actually delivers what the research promises, not a watered-down version that gets mostly destroyed in your gut before it does anything useful. If you are in the prediabetes range and looking to avoid medications, this is one of the most evidence-supported approaches available to you. If you're already on metformin and working to reduce your pharmaceutical dependence under physician supervision, dihydroberberine is absolutely worth a conversation with your doctor. If you are managing your metabolic health holistically and want additional evidence-backed support, superberberine is a meaningful part of that toolkit. Again, do not make medication changes unilaterally, but do have these informed conversations with your physician. Bring the research. Be an active participant in your own care. The medication landscape in 2026, full picture. Let me give you a brief, honest tour of where metformin sits relative to other options because context matters. GLP-1 receptor agonists, semaglutide, terzepatide. These are the drugs everyone is talking about right now, and for good reason. They lower A1C substantially, drive meaningful weight loss, have cardiovascular protective data, and reduce appetite in ways that make dietary changes more sustainable. Downsides? Expensive, nausea, and gee, eye side effects, especially initially. Muscle mass loss, if not paired with resistance training, and we don't yet have the decades of long-term safety data we have with metformin. Stopping them without a plan almost always means regain. SGLT2 inhibitors, empagliflozin, dapagliflozin, canagliflozin. These lower glucose by making your kidneys excreted in the urine. They also reduce heart failure hospitalizations. And slow kidney disease progression in a way that's genuinely impressive. Downsides? Genital yeast infections, urinary tract infections, and a rare but serious condition called diabetic ketoacidosis, particularly in people who are restricting carbohydrates significantly. Also relatively expensive without insurance. Metformin. Cheap. Decades of data. Doesn't cause hypoglycemia on its own. Modest weight neutrality. Downsides? Gee. Eye side effects. B12 depletion. Doesn't fix the root cause. Possible exercise adaptation blunting. No organ protective data matching the newer classes. The honest hierarchy for 2026. If you have established cardiovascular disease or significant kidney disease, an SGLT2 inhibitor or a GLP-1 agent is likely more important than metformin. If you have obesity driving your diabetes, a GLP-1 agent addresses more of the root cause. If you're in prediabetes with a motivated patient who's committed to lifestyle change, metformin may not be necessary at all. None of these drugs. Not a single one is a substitute for fixing the lifestyle factors that created the problem. What actually moves the needle long term. The part we never skip. Here's what I know after years of seeing real patients with real outcomes. Resistance training changes your metabolic destiny. Skeletal muscle is your body's primary glucose disposal site. Building muscle creates glucose storage capacity that operates independently of insulin through GLUT4 transporters activated by muscle contraction. This is free medicine. Two to four sessions per week is enough to see meaningful A1C improvement. Every patient I have who has built consistent muscle mass has better metabolic numbers. Every one. Visceral fat is the enemy. The fat around your organs. Not the fat you can pinch. The fat you can't see. Is metabolically active tissue that drives inflammation and worsens insulin resistance directly. You cannot spot reduce it. But as insulin sensitivity improves through all the interventions we're discussing, visceral fat gets preferentially mobilized. It shrinks. And when it shrinks, everything else gets easier. Sleep is not optional medicine. I've said it before and I'll keep saying it. Chronic sleep deprivation raises cortisol. Cortisol triggers gluconeogenesis in the liver. The same process metformin is working to suppress. You can be on metformin. Eating well. Exercising. And poor sleep will undermine all of it. Seven to eight hours is the prescription. It doesn't come in a bottle. Chronic stress is biochemical. Not just psychological. Sustained cortisol elevation causes your liver to dump glucose. Drives insulin resistance at the receptor level. And shows up directly in your blood sugar. I've had patients with stubbornly elevated A1C doing everything right. And when we dug into their stress load, that was the missing piece. Stress management is metabolic intervention. Not soft. Not optional. Dietary quality over everything. Not calorie counting. Not macro obsession. Quality. Eliminating ultra-processed food. Increasing fiber to 30 to 50 grams per day. Prioritizing protein at every meal. These changes improve glucose stability even without deliberate calorie restriction. The NIH's Kevin Hall showed that people eating ultra-processed diets consumed 500 more calories per day without even trying to overeat. The food was doing that to them. Whole food does the opposite. The thyroid and hormone piece that most doctors miss. As an endocrinologist, I see this constantly. Subclinical hypothyroidism worsens insulin resistance. Low testosterone in men is strongly associated with metabolic syndrome. Unaddressed hormonal dysfunction can make glucose management feel like pushing a boulder uphill. You need someone looking at the whole endocrine picture, not just your A1c in isolation. What I actually tell my patients. Here is the conversation I have when someone comes to me on Metformin wanting to understand their options. First, don't stop your medication because of a YouTube video, including mine. Have this conversation with your physician. But be an informed patient. Ask questions. Push back where appropriate. Second, get your B12 checked immediately if you've been on Metformin for over a year. If it's low, supplement. If you have neuropathy symptoms, this is urgent. Third, ask whether your Metformin is actually necessary right now or whether a structured lifestyle intervention first would be appropriate. Not everyone who gets prescribed Metformin actually needed it in that moment. Fourth, look at dihydroberberine as part of a comprehensive approach, particularly in prediabetes. Superberberine from SugarMD was formulated specifically for this. Enhanced absorption, evidence-backed dosing without the limitations of standard berberine. Fifth, understand that if your goal is to come off medications over time, lifestyle is the only path there. Not a better drug. Not a smarter supplement stack. Lifestyle. Building muscle. Reducing visceral fat. Sleeping. Managing stress. Eating real food. That is the only exit ramp from long-term pharmaceutical management. Sixth, get a full picture from an endocrinologist who looks at thyroid, hormones, inflammatory markers, gut health, not just the A1C number. You are a complete biological system. Treat yourself like one. You deserve better than a prescription and a wave goodbye, right? The patients I have seen achieve genuine long-term reversal of prediabetes, remission of early time prediabetes, and dramatic A1C reductions. They didn't get there because we found the right pill. They got there because they treated their health like a system. Sleep, stress, muscle, food quality, hormone balance, gut health. All of it together with intelligent medical support alongside. Not instead of the lifestyle change. Now, that is the practice of medicine I believe in. And it is the only approach I have seen that actually lasts. Now, if you want help building that system with someone who specializes in exactly this, you know where to find me. I'm Dr. Ahmet Ergin. I practice in Fort St. Lucie, Florida. And obviously, see you in this channel at SugarMD. And please visit sugarmds.com. See you in the next one.