Why I Don't Recommend Ozempic Anymore (And What To Use Instead)

Watch the full video on Rumble: https://rumble.com/v7feba2-why-i-dont-recommend-ozempic-anymore-and-what-to-use-instead.html

If you searched for Ozempic, Wigoby, or Semiglutide, you found this video because you're trying to figure out whether this drug makes sense for you. It's the one everyone has heard of, it's what your doctor knows, and it's what insurance is most likely to pay for, which is exactly why it deserves a careful look rather than a reflexive yes.

None of this is medical advice, and you should talk to a licensed physician before you put anything into your body.

Before the comparison I want to make will land, you need the whole chain in front of you, because if you don't understand the mechanism the rest is just numbers.

Semiglutide is the active ingredient in Ozempic and Wigoby. It belongs to a class of drugs called GLP-1 receptor agonists.

GLP-1 stands for glucagon-like peptide-1, and it's a hormone that your gut releases naturally after you eat. Your intestinal L cells make it in response to food arriving, and it clears out of your blood in a couple of minutes because an enzyme chews it up almost immediately. That short half-life is the whole reason a drug version had to be engineered in the first place.

What GLP-1 does is it signals your pancreas to release insulin, slows down your stomach emptying so food sits in there longer, tells your brain that you're full, and reduces the amount of sugar your liver releases into your bloodstream.

So when you take Semiglutide, your body responds as if there's extra GLP-1 present.

The appetite effect comes from two places at once. There's the peripheral side, where food physically stays in your stomach longer so you feel full sooner and stay that way. And there's the central side, where the drug acts on hunger-regulating regions in your hindbrain and hypothalamus and changes how rewarding food feels, which is why the foods that used to call your name stop calling (Moiz et al., 2025).

All of that does one thing, which is that it makes it easier to eat less than your body burns.

Your body needs a certain amount of energy every day just to keep you alive and moving, and when you eat less than that, it has to pull the difference from stored energy, which is body fat. The deficit is what causes the fat loss, and Semiglutide's real job is making that deficit survivable rather than burning fat directly, so you're not white-knuckling hunger from noon until bedtime.

So what does the research actually show about Semiglutide? There was a major clinical trial published in the New England Journal of Medicine that ran for 68 weeks.

And at the end of it, the average person on Semiglutide lost about 15% of their body weight. The placebo group in that same trial lost 2.4%, and about 86% of the people on the drug lost at least 5% of their body weight compared to 31.5% on placebo (Wilding et al., 2021).

So for someone starting at 240 pounds, that's roughly 36 pounds of weight loss.

Then in December of 2025, the FDA approved a pill version of Wigoby for people who don't want to inject. And that showed about 16.5% weight loss for people who stuck with it. I cannot point you to a study on that oral number that I can hand you here, so treat it as what has been reported rather than something I am citing.

Blood pressure, cholesterol, liver fat, and blood sugar all moved in the right direction alongside the weight, and this drug demonstrated that the whole class works, a result that earned the attention it got.

Yet one detail gets skipped over more than it should, which is that the weight you lose on Semiglutide is not all fat.

Your body composition data from that same trial showed that somewhere between 39 and 45% of the weight people lost was muscle. That range lines up with what the broader body composition literature on these drugs reports, where lean mass typically accounts for a quarter to more than 40% of total weight lost depending on the population and the imaging method (Dubin et al., 2024).

If you lose 30 pounds on Semiglutide and 13 of those pounds are muscle, you've just damaged your metabolism in the process of trying to fix it. I have seen this play out often enough to say it plainly, though I cannot point you to a study that isolates lean mass loss as the cause of a lower resting burn rate, so take that as my read rather than settled science.

What I can tell you is how it looks. You hit the number on the scale and you're still soft, still weak, still wearing the same size in the shoulders and arms you were before.

Research presented at an endocrinology conference in 2025 confirmed that women and older adults are at even higher risk of this muscle loss, and that eating more protein helps protect against it, so the risk is manageable if you get aggressive about protein and training, though it remains a genuine constraint you have to plan around rather than something a supplement fixes on its own.

Coming off the drug brings its own reckoning. The extension data from that same trial showed people regained about two thirds of their lost weight within a year of coming off.

And a review published in the British Medical Journal in January of 2026 looked at what happens when people stop taking these drugs.

They found that weight comes back at a rate of about 1.8 pounds per month.

At that rate, you're back at your starting weight within about 18 months, except now you may be carrying less muscle than the day you started, since the drug only suppresses appetite while you're taking it and leaves the underlying metabolic wiring untouched.

So is there something better? The answer is yes, and it comes down to receptors.

Semiglutide binds a single receptor, while Terzepotide, which you might know as Monjaro or ZepBound, hits two.

It activates GLP-1 and something called GIP. What GIP does is it improves your insulin response and something called nutrient partitioning, which basically means your body handles the food you eat more efficiently.

GIP is the other major incretin hormone, released from the upper small intestine, and it acts on fat tissue and on the pancreas in ways GLP-1 does not, which is why combining the two produces effects neither gets alone (Nauck et al., 2021).

So with terzepotide, you get the appetite suppression from GLP-1, plus better handling of nutrients from GIP. Now we actually have head-to-head data comparing these two drugs directly.

There was a clinical trial published in May of 2025 in the New England Journal of Medicine where they gave one group semiglutide, another group terzepotide, and tracked them for 72 weeks to see who lost more weight.

Terzepotide produced 20.2% average weight loss against semiglutide's 13.7%. That's 47% more weight loss on terzepotide.

About 32% of the people on terzepotide lost at least 25% of their body weight, compared to only 16% of the people on semiglutide.

The body composition data from terzepotide trials showed that only 25% of the weight people lost was muscle, compared to semiglutide's 39-45%.

So roughly three quarters of what comes off is fat. You end up leaner and stronger instead of just lighter, and that difference is what changed my recommendations more than the headline percentage did.

There's one more compound worth knowing about, and it isn't approved yet. Retitrutide activates three receptors: GLP-1, GIP, and glucagon.

Glucagon is the addition that changes the math, because it tells your liver to mobilize stored fat and it raises the calories you burn at rest, and where every drug before it worked only on the intake side of the equation, this compound reaches into the expenditure side as well.

And the Phase 3 trial results from December of 2025 showed 28.7% average weight loss at 68 weeks, which is roughly 71 pounds lost on average. Thirty-nine percent of people in that trial lost 30% or more of their body weight.

There's a side effect that comes with it. About 21% of patients at the highest dose experience something called dysesthesia, which is an abnormal skin sensation or tingling.

I have seen it firsthand, since I went through it myself, and the sensation is genuinely unpleasant to sit with. It didn't push many people out of the trials, including me, but you should know it's there before you start.

There is a lot more of this inside the free community, and it is genuinely free, so if you want somewhere to ask the follow-up question the men's group is here: https://www.skool.com/jh-iron-forge-brotherhood/about

Research: Wilding et al., N Engl J Med 2021; Moiz et al., Am J Med 2025; Dubin et al., Diabetes Obes Metab 2024; Nauck et al., Diabetes Obes Metab 2021; Liu et al., Drug Des Devel Ther 2025.

References:

Moiz A, Filion KB, Tsoukas MA et al.. Mechanisms of GLP-1 Receptor Agonist-Induced Weight Loss: A Review of Central and Peripheral Pathways in Appetite and Energy Regulation. Am J Med. 2025. https://pubmed.ncbi.nlm.nih.gov/39892489/

Nauck MA, Quast DR, Wefers J et al.. The evolving story of incretins (GIP and GLP-1) in metabolic and cardiovascular disease: A pathophysiological update. Diabetes Obes Metab. 2021. https://pubmed.ncbi.nlm.nih.gov/34310013/

Liu Z, Yu S, Jin X et al.. The Clinical Application of GLP-1RAs and GLP-1/GIP Dual Receptor Agonists Based on Pharmacological Mechanisms: A Review. Drug Des Devel Ther. 2025. https://pubmed.ncbi.nlm.nih.gov/41312047/

Wilding JPH, Batterham RL, Calanna S et al.. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021. https://pubmed.ncbi.nlm.nih.gov/33567185/

Gu Y, Sun L, Zhang W et al.. Comparative efficacy of 5 sodium-glucose cotransporter protein-2 (SGLT-2) inhibitor and 4 glucagon-like peptide-1 (GLP-1) receptor agonist drugs in non-alcoholic fatty liver disease: A GRADE-assessed systematic review and network meta-analysis of randomized controlled trials. Front Pharmacol. 2023. https://pubmed.ncbi.nlm.nih.gov/36992825/

Dubin RL, Heymsfield SB, Ravussin E et al.. Glucagon-like peptide-1 receptor agonist-based agents and weight loss composition: Filling the gaps. Diabetes Obes Metab. 2024. https://pubmed.ncbi.nlm.nih.gov/39344838/