GLP-1 drugs reduce cancer risk

Investment Analysis Clubs Macro Economic Trends and Risks
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This is a huge study. The effect is startlingly large. Many of the people are young – important because the rate of cancer in young people has been rising.

This will be a tremendous boost for the companies that manufacture GLP-1 drugs. About 40% of the U.S. population is obese but only 1% take GLP-1 drugs.

Weight loss drugs slash risk of 4 types of cancer by 50% or more, study finds

Medical News Today, 6/17/2026

  • The use of GLP-1 medications such as Ozempic and Wegovy for weight loss has been increasing.
  • Researchers continue to examine how GLP-1s might affect a person’s health beyond type 2 diabetes management and weight loss.
  • A new study found a potential link between taking GLP-1 medications and a decrease in the overall risk of developing obesity-related cancers in people without diabetes.

The use of glucagon-like peptide-1 (GLP-1) receptor agonistTrusted Source medications continues to rise, with a 155% increaseTrusted Source in the percentage of people with type 2 diabetes taking these drugs from 2018 to 2022.

The use of GLP-1s for weight loss is also increasing. The latest polls report that of the one in eight Americans who have taken a GLP-1 medication, about 38% have only taken them to help lose weight.

For this study, researchers analyzed the health data from a national database of more than 229,000 obese, non-diabetic people. [Now, that’s what I call “big data”! – W]

Between December 2014 and June 2025, 38% of study participants received a GLP-1 prescription, and the remaining 62% received diet and exercise counseling.

At the study’s conclusion, researchers found that participants who took GLP-1 medications containing semaglutide or tirzepatide had a 41% decrease in their overall risk of developing an obesity-related cancer.…

The most dramatic drops in risk, where this reduction was by 50% or more, also occurred in multiple myeloma, pancreatic cancer, and colorectal cancer, in addition to endometrial cancer…

GLP-1 receptors are expressed directly on certain cancer cells. That means the drug could be acting on the tumor itself, not just shrinking the patient… [end quote]

Holy Toledo! Most cancer drugs give such a small effect that the result has to be teased out by statistical analysis. (Like the aromatase inhibitor I took for 5 years after my bilateral mastectomy for double breast cancer.) But the GLP-1 result jumps up and bites you on the nose!

If I was obese and had a family history of cancer (which I do) I would immediately request a prophylactic prescription for GLP-1. I’m not obese so I think it’s not for me at this time but there are millions of people who would benefit.

Not to mention the shareholders. I have my eye on Novo Nordisk, an innovative company with a low P/E ratio and high dividend. And a lot of competition.

Wendy

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Yep. The reason NVO has a “low-PE” is because Eli Lilly is running rings around it.

intercst

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I ask Google…

Yes, your body naturally produces GLP-1 (Glucagon-Like Peptide-1). It is a hormone secreted by specialized cells in your gut that regulates appetite, blood sugar, and digestion. [1, 2, 3, 4]

How Natural GLP-1 Works

  • Source: GLP-1 is primarily produced by L-cells lining the lining of the small intestine (ileum) and colon. Small amounts are also made in the brainstem. [1]
  • The Trigger: When you eat, these gut cells “sense” nutrients (especially carbohydrates, healthy fats, and proteins) and release GLP-1 into the bloodstream. [1, 2]
  • The Effects: Once released, it signals your pancreas to release insulin, slows down stomach emptying, and tells your brain that you are full. [1, 2]

The Catch: Rapid Breakdown

While your body continuously makes GLP-1, the natural hormone has an extremely short lifespan. An enzyme in your blood called DPP-4 breaks it down within 1 to 2 minutes. This is why medications like semaglutide (Ozempic/Wegovy) and tirzepatide (Mounjaro/Zepbound) were developed—they are engineered to resist DPP-4, allowing the hormone’s effects to last much longer. [1, 2, 3, 4]

Boosting Natural GLP-1

Although medications create much stronger effects, you can support your body’s natural GLP-1 production through diet and lifestyle. Foods that stimulate L-cells include: [1, 2]

  • Dietary Fiber: Fermented by gut bacteria into short-chain fatty acids.
  • Lean Proteins: Trigger satiety signaling.
  • Healthy Fats: (Like olive oil and omega-3s) slow stomach emptying

Amazing, diet matters.

The Captain

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Indeed. Over the past five years NVO is up 5% (with dividends reinvested). For LLY the increase is 380%.

DB2
Long LLY

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At the study’s conclusion, researchers found that participants who took GLP-1 medications containing semaglutide or tirzepatide had a 41% decrease in their overall risk of developing an obesity-related cancer.…

Well, wouldn’t the fact you are no longer obese lead to a reduction in obesity related cancer? No really the drug, and just the weight loss?

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And exercise supports glp1 function:GLP-1 agonists and exercise: the future of lifestyle prioritization - PMC

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This is an important question which will require a lot more research.

Wendy

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Those using GLP-1 drugs were statistically matched with participants using diet/exercise. For example, those with a BMI < 40 showed a 37% reduction in cancers between the two treatments.

The authors write that “use of GLP-1RAs for weight management was associated with a significantly lower cumulative incidence of OACs [obesity associated cancers] compared with diet or exercise consultation alone.”

GLP-1 receptor agonist use and cancer risk in obese nondiabetic adults
Hsu et al.
https://www.annalsofoncology.org/article/S0923-7534(26)00157-2/fulltext

DB2

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Well, that’s kind of hard to predict since most of the large, longer term studies are in…the obese. The increasing numbers of folk who’re using GLP-1 receptor agonists for what’s dismissively called “vanity pounds” (which I call pre-pathology pounds) might start to shed light on this question and possibly stimulate funding for studies to find a reasonable answer.

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My initial thinking was that obesity was the cause of the problem. As I learned more it was visceral, not subcutaneous fat that was the problem. The science of it is complex, way above my pay grade, but humans existed before we invented science and science was not needed to keep us from being obese. Conclusion, we need a healthy life style, specially in what we eat.

The Captain

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@Volucris …so, at great inconvenience (actually, not…awake at 2 am, so I needed something snore worthy) and out of the goodness of my heart, I had a stab at the primary document. It’s a looong , dreary read, with statistical analysis and a wordiness that had me a bit flummoxed. However, I couldn’t find a table in all the confusing hyperlinks that compared body weight/body composition/body fat between the two groups. That’s the sort of detailed information that you need in order to be making grand statements about the medication used (rather than its commonly accepted outcome of weightloss) …and is almost always missing in these big data studies.

Seems to me that GLP-1 receptor agonists, when compared head to head with diet and exercise (and, as far as I can tell, it wasn’t supervised diet and exercise …like, say, in metabolic ward studies where subjects only get to eat what’s provided … but more the “advice to”) are way superior in producing “weight loss”. It’s pretty hard to isolate the anti cancer effects of GLP-1 RAs in obesity related cancers from the effects of not being obese.

What it does suggest, though…at least for the folk who aren’t obese yet, but maybe headed there in spite of their best efforts…intervention with these drugs might be indicated at a far earlier stage than waiting for the inevitable. That’s what I’m betting would be a winning strategy…much like early invention with a good many other ailments.

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That seems crucial. GLP-1’s effect is basically calorie limiting, since you eat less when on it.

Can one quit GLP-1 once their weight goal is attained? Or, is it a lifetime maintenance dose?

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Essentially nothing new here. Caloric restriction has been shown to reduce some cancer rates for years. Some studies going back to the 1940s. The only thing different is the method, i.e., a shot vs. gastric bypass surgery vs. diet.

Yes, if you are truly morbidly obese these drugs can be a lifesaver. If you are taking them to loose 5 pounds for your Instagram photo you are asking for trouble.

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I guess it’s a bit like any energy restricted diet…with or without pharmaceutical enhancement. If you stop and return to something like the eating habits that caused the problem in the first place, weight gain is inevitable.

That would be one good reason for earlier intervention, I reckon. It must surely be easier to maintain a weight loss than wasn’t that great in the first place. The longer a person spends with eating habits that build and then support a large weight gain, the harder to overcome the habit part, I suspect. If a person is accustomed to eating upwards of 3,500 Cals a day, a paltry 1800 or so Cals…or fewer…necessary to stay lean is going to feel pretty unsatisfying. I can attest to this even, though this is my customary allowance.

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If you go back/continue your bad habits, you’ll put the weight back on. What is not known, and what is more concerning, some of the side effects are not going away. I’ve seen reports of people still having bad side effects after being off the drug for a year. The problem is, we just don’t know because people haven’t been on it for that long nor have they been trying to get off it for long.

Again, for morbid obese it can be life saving. For vanity weight loss, you’re asking for trouble.

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What sort of bad side effects…and what sort of reports, come to that? A serious question, not JAQing off, BTW

The precautionary principle always seems to favour non intervention when cast iron guaranteed long term “safety” cannot actually be guaranteed (look at the arguments of the cholesterol denialists/statin phobics, for instance)

I think the concept of early intervention in disease prevention is still a bitter pill to swallow for many (so to speak)when the particular disease has a long lead in time with no apparent measurable symptoms in the here and now.

I bet a good many 300+lb behemoths experienced a period when they didn’t look too bad hefting around that first 20-30lbs of weight gain. They can’t all have not cared as the extra adiposty…and underlying irreversible patholgy …grew with every extra 10 lbs. Hence, pre patholgy vs vanity pounds is probably a more worthwhile way of looking at it.

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The main ones: pancreatitis, acute kidney damage, bowel obstruction, intestinal paralysis, muscle loss, and hair loss to name a few.
Again, people haven’t been on them for long nor have enough tried stopping the medication yet to know the full effects.

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Ahhh…so conditions that mostly are not related directly to the drugs themselves, but rather the consequences of rapid weight loss. Along with gall stones…a condition that is quite strongly related to being obese in the first place. One side effect that can be attributed directly is xerostomia. They do, apparently, cause reduced saliva production…hence the “Ozempic Mouth” squawks. Seeing as many of the other medications that get prescribed for the obesity related maladies cause this same condition, it’d be hard to tease out numbers.

Many of these side effects are dose related, though and are likely increased when dosage needs to be ramped up (from, say, the starter .5 mg). Possibly more likely a scenario with the higher poundage than at the pre-pathology (or “vanity”, if you must) end of the scale?

Anecdotally, my daughter’s weight gain due to stress eating during the the last year before she split from the wankertron …and then his post separation vendetta … plus the documented side effects of her migraine meds would fall into this category of pre pathology pounds. Thankfully, she was/is vain enough to want to lose it …and, in truth, a good many folk couldn’t see why she wanted to take such a “dangerous” drug when she “wasn’t fat” (a sign of the times with growing acceptance of overfat bodies as the norm…well I guess they are these days :frowning:) None of the above applied. She actually continued to build strength and muscle mass. Never experienced xerostomia (I did warn)

We’re all free to put our own interpretation on daughter’s experience but one perfectly plausible explanation is that, because she intervened at a very early departure from healthy homeostasis in fat gain, she avoided the common unpleasant side effects that are oftentimes cited. Reversing the trend at the pre pathology stage rather than waiting until predictable adaptations to excess adiposity have taken hold.

A conundrum not dissimilar to early intervention in ASCVD before the disease state requiring more aggressive treatment strategies and polypharmacy. Or recognizing that prediabetes is not without pathology in and of itself.

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One thing that did occur during her so called vanity pounds weight gain was an increase in visceral fat per the bio impedance analysis on the scanner at our gym. Worth noting here as, per her lipid panel done at the last physical before her weight loss (including measuring her Lp(a) and Apo-b…seeing as I might’ve gifted my dodgy genes), everything was well within the current guidelines for healthy. Yep…just a couple of years or so with the extra bodyfat that so many folk seem willing to tolerate but a much higher activity level than so many folk seem willing to tolerate also and she’d developed enough visceral fat to qualify as well into the unhealthy range. This dropped almost more rapidly than overall bodyfat.

I’ll stick with prepathology pounds as a moniker, I think.