Ozempic keeps wowing: trial data show benefits for kidney disease

It is fine to be sceptical, but I think you should have taken a few minutes to read the method chapter in the study, seeing as that possibly could have eased your doubts. The first sentence cites the previously published design of the study. In the method chapter it is reported to be an "international, double-blind, randomized, placebo-controlled trial" with 3533 participants and a mean median follow-up of 3.4 years[0]. The cited article on the study of the trial states that "Participants were enrolled from 418 trial locations across 28 countries." [1]

[0]: https://www.nejm.org/doi/full/10.1056/NEJMoa2403347#sec-1

[1]: https://pubmed.ncbi.nlm.nih.gov/36651820/

> Many clinical trials are controversial when they are positive.

Which isn't the same as being "faked".

> Most clinical trials are subcontracted.

They are not subcontracted, clinical trial sites are identified. They are basically doctors interested in running a trial. Usually done at academic hospitals.

> The subcontractor has a deep interest in pleasing his client.

No they don't. They have no vested interest beyond their own careers and publications. Doctors only put a few hours into a clinical trial each month, usually their own patients. Most of the work is done by clinical trial staff. The costs of the trials are paid for by the sponsor, but that money doesn't go into the doctor's pocket, it's the hospital.

> You can select patients at the beginning of the trial, or during the trial you can report that a patient with a "bad" result, just dropped out of the study.

But pretty much every trial is triple blinded. The company, doctor and patient don't know if the patient got the drug or the placebo. Placebos are chosen to pretty much be identical to the drug (people get injections, take pills that look exactly the same).

And no, you can't just "say a patient dropped out". There is a predefined set of criteria that the doctor needs to follow. The patient needs to agree to follow them as well. But again, the doctor doesn't know who received what so how they can they "tweak" the results?

Plus if a patient drops out, the results are penalized. The data doesn't just disappear. All data needs to be reported to the FDA for every patient, including all follow ups.

> And indeed in most clinical trials there is no strong adverse effects (just weak) reported except when patients die.

This is 100% false. All adverse events need to be reported, whether caused by the drug or not. This is why relatively innocuous drug have weird side effects like "diarrhea, constipation". The top adverse events have to be reported, even if it's 0.01% who had them.

> Moreover, the hospitals that implement the trial often only do the minimum to satisfy the principal investigator

No, the hospital doesn't know which patient received the drug or not. If the patient needs a blood test, they get a blood test like any other patient.

And again, the process needs to be followed or else the deviation reported. All of that is reported to the FDA. If enough deviations happen, the FDA can say they won't approve the drug.

> Just look at the field of neurodegenerative diseases or ask patients how negligently they have been treated.

What are you talking about? Can you provide a source?

You've already made many statements that are clearly false, which you would know if you had done even basic research into the field using google. You clearly don't know the field very well, so I'm not sure why you feel like your "ideas" of how trials are run are of any value.

No there isn't. There's no serious debate and no evidence for the carbohydrate insulin model of obesity.

There absolutely is not. There is raging internet debate, not scientific debate.

There are books for every theory, this isn't one that any scientist in the actual field takes serious.

But fringe theories are always popular among certain people, same as conspiracy theories.

It's not the only drug that suppresses appetite, but GLP-1 agonists (Ozempic, Zepbound, etc) appear to work for a larger percentage of the population, and significantly outperform previous appetite suppressants.

There's also findings that suggest that it goes beyond simply suppressing appetite, but also manipulates the "reward" center in the brain. Individuals who take it to lose weight find that they have reduced desire to drink or smoke, suggesting it's less that they struggle with appetite and more the medicine helps overcome addictive behavior.

> Ozempic is not the only drug that suppresses appetite

If there were a drug that is equally as effective with the same or fewer downsides, then it would've been just as popular for that use case already.

Someone else mentioned nicotine. There are still a lot of "unsuccessful" nicotine users compared to Ozempic.

Funding tends to be a constraint with larger studies, and it's best to keep studies focused anyway — less confounding variables.

Here, I'll pontificate a bit. For instance, study 1 finds that Ozempic is associated with a reduced risk of X. Study 2 is now funded to see if the association can be experimentally reproduced to establish a causative relationship. Competing institution gets Study 3 funded to test competing drug Mounjaro, reaches same conclusion. Study 4 by another institution finds same conclusion with a drug that acts in an entirely different manner, Buproprion. Study 5 by yet another institution finds similar results with amphetamines. Study 6 is funded on the premise that there's an underlying mechanism that needs to be explored, gets funding to study caloric restriction, gets similar results. Meanwhile, study 2 finds a causative relationship between Ozempic and X, concluding experimentally that Ozempic achieves X by inducing calorie restriction, which concurs with study 6.

I'm oversimplifying. But you see where I'm going with this. Much easier to both control and fund the smaller studies than a giant one, and you develop more knowledge in the process.

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Also, I'm not an academic, so I could be wildly off base. Would appreciate a gut check by someone who actually does this for a living.

That GLP-1 agonists are as successful as they are and appear to modulate the reward center of the brain (per the latest research on the same class of drugs and smoking/alcohol cessation) suggests that it's certainly not just a psychological matter.

That's why I made the heroin comparison. People underappreciate the addictive properties of refined sugars.

Edit: people also looked at the opiate angle too, apparently. https://pennstatehealthnews.org/2024/04/qa-can-weight-loss-d...

You’re right in your argument about “just do this” suggestions without considering how hard it can be based on intrinsic factors.

I feel there is a point in the thread you’re commenting on though. It would be scientifically interesting to know whether the desired(positive) outcomes of this drug can be replicated by consciously controlling the quantity or quality of food without the use of the drug(by those who can). Still, presenting the result in a useful way rather than stating the drug is useless.

If you had a way to get the same results without any pharmaceutical intervention, and you’re a lucky one that _can_ do it, wouldn’t you want to know how?

And not just genetic luck, but luck of childhood circumstances. Lots of people were given a deranged relationship to food as a child by their parents, leading in many cases to actual metabolic derangement as well.