A disturbing must-see video for statin users such as myself.
# Statins Slash GLP-1 Levels: Human Controlled Trial
The same people who take this guy seriously also believe that cancer has been cured every time a popsci article says that X cures cancer because it worked in a petri dish.
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It’s a real issue. Obicetrapib + ezetimibe will solve that problem.
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Please - if anyone is posting a video now, include an AI summary (from here or other… Krisp | Free Youtube Video Summarizer with AI
Introduction to Statins and GLP-1 Levels
- The discussion begins with the speaker expressing a mix of excitement and annoyance regarding a recent scientific paper on statins, which are the most profitable drugs globally, generating over 20 billion dollars in annual sales.
- This paper highlights the role of statins in contributing to insulin resistance, increasing the risk of type 2 diabetes, and significantly lowering GLP-1 levels in humans.
- While the link between statins and insulin resistance is known, the impact on GLP-1 levels was previously unrecognized, raising concerns about the implications for current popular GLP-1 receptor agonists used for weight loss.
Lack of Awareness in the Medical Community
- The speaker expresses frustration that the findings of this important study, published in Cell Metabolism, did not gain the attention they deserved within the medical community or among the general public.
- During clinical rotations at Harvard Medical School, the speaker found that even among physicians, there was a significant lack of knowledge about the effects of statins on GLP-1 levels.
- In an informal poll of 12 physicians, including cardiologists, seven were unaware of the effects of statins on GLP-1 levels, highlighting a concerning gap in medical education and awareness.
Study Overview and Key Findings
- The study involved 30 patients starting treatment with Torvastatin, a common statin, alongside 10 control patients not on statins, followed for 16 weeks.
- Results indicated a significant increase in HbA1c levels, insulin levels, and insulin resistance in patients taking statins, along with a nearly 50% reduction in GLP-1 levels by the end of the trial.
- The speaker emphasizes that these findings should have been widely publicized, given the potential health implications for patients on statins.
Mechanism of Action: Statins and Gut Microbiome
- The research further explored how statins affect the gut microbiome, discovering that statin treatment altered the microbiome in a way that reduced the production of beneficial bile acids.
- A specific bile acid, ursodeoxycholic acid (UDCA), was found to be significantly reduced in patients taking statins due to the depletion of certain gut bacteria, notably Clostridium species.
- This depletion disrupted bile acid metabolism, leading to downstream effects including insulin resistance and decreased GLP-1 production.
Animal Model Confirmation
- To confirm the causative relationship, researchers conducted experiments on mice, which also exhibited insulin resistance and reduced GLP-1 levels when given statins.
- Transplanting microbiomes from statin-treated humans to non-statin-treated mice resulted in worsened insulin resistance, demonstrating the impact of the altered microbiome.
- Reintroducing the depleted Clostridium species or supplementing with UDCA reversed the metabolic damage, improving glucose metabolism and restoring GLP-1 levels.
Human Pilot Trial with UDCA
- A small pilot trial was conducted with five patients on statins for at least six months, who were given daily doses of UDCA at 500 milligrams.
- The results mirrored those observed in the mouse studies, showing significant improvements in blood sugar levels, insulin levels, insulin resistance, and restoration of GLP-1 levels.
- These findings suggest a potential simple and inexpensive solution to mitigate the negative effects of statins on metabolic health.
Broader Implications and Call to Action
- The speaker reflects on the deeper implications of the research, expressing concern about how the healthcare system often prioritizes profit over patient well-being, leading to gaps in patient care.
- The lack of discussion around simple and effective solutions, such as the use of UDCA, raises questions about the incentives driving medical practices and education.
- The speaker urges patients and clinicians to engage in conversations about these findings, share information, and advocate for better patient care and education in medical settings.
Conclusion and Recommendations
- The speaker concludes with a call to action for patients to share the information from the study and for clinicians to read the research and discuss its implications within their practices.
- The emphasis is placed on the importance of staying informed and questioning existing medical practices to better serve patient health.
- The overall message stresses the need for improvement in healthcare systems to prioritize patient outcomes over profit-driven motives.
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He has credentials: a PhD in Human Metabolism at Oxford and an MD from Harvard.
I will take his opinion any day over yours. What are your credentials?
At no point did he suggest that people should stop taking statins.
Your main contribution seems to be trolling.
I take statins and rapamycin, both of which raise my A1C, and I can’t tolerate metformin.
So, yes, I am going to take TUDCA for at least 30 days and monitor what it does to my fasting glucose levels and A1C.
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Can we move these discussions somewhere else than the flozin thread? We have a UDCA & TUDCA thread by the way: UDCA (ursodiol) / TUDCA for healthspan and lifespan?
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Every single statin denialist I’ve interacted with has also been an LDL cholesterol denialist, without fail. Really remarkable.
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I might change my statin (currently atorvastatin) to a less glucose/insulin impacting version. My fasting blood glucose levels have been hovering around the 95 to 105 level and I’m wondering if changing statin might lower these…
ChatGPT Query: are some statins better than others in terms of contributing to insulin resistance, increasing the risk of type 2 diabetes, and significantly lowering GLP-1 levels in human?
Yes — different statins vary in how much they affect insulin resistance, type 2 diabetes (T2D) risk, and GLP-1 levels. Here’s a breakdown based on the best available clinical and mechanistic data:
1. Insulin Resistance & Diabetes Risk
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Higher risk (more likely to impair insulin sensitivity and increase T2D incidence):
- Atorvastatin (especially 40–80 mg)
- Rosuvastatin (20–40 mg)
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Simvastatin (at higher doses, e.g., 80 mg)
→ These are “high-intensity” statins and show the clearest signal for increased diabetes risk in trials and meta-analyses.
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Lower risk (neutral or sometimes beneficial for insulin sensitivity):
- Pravastatin – may even improve insulin sensitivity (WOSCOPS trial).
- Pitavastatin – considered metabolically neutral or slightly favorable; marketed in Asia with this distinction.
- Fluvastatin – limited data, but generally seen as lower-risk.
2. GLP-1 Levels
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Evidence (still limited, mostly small human studies + animal work):
- Simvastatin & Atorvastatin – associated with blunting GLP-1–mediated insulin secretion after meals, possibly by altering gut L-cell function.
- Rosuvastatin – some studies suggest mild GLP-1 reduction, but evidence weaker than atorvastatin/simvastatin.
- Pravastatin & Pitavastatin – appear to have little to no effect on GLP-1; some data suggest neutrality.
- Fluvastatin – minimal data, but not strongly linked to GLP-1 suppression.
3. Mechanistic Takeaways
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Statins impair glucose metabolism through:
- Reduced insulin sensitivity in muscle and liver.
- Impaired pancreatic β-cell insulin secretion.
- Decreased adiponectin (insulin-sensitizing hormone).
- Possible direct suppression of GLP-1 secretion in the gut.
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Potency, dose, and lipophilicity matter:
- Lipophilic statins (simvastatin, atorvastatin) penetrate tissues more widely → higher chance of affecting insulin/GLP-1 pathways.
- Hydrophilic statins (pravastatin, rosuvastatin) have more liver-targeted action → rosuvastatin still increases diabetes risk at high dose, but pravastatin seems protective.
Bottom Line
- Most diabetogenic / GLP-1 lowering: atorvastatin, simvastatin, rosuvastatin (high dose).
- Least diabetogenic / GLP-1 neutral: pravastatin, pitavastatin (possibly fluvastatin).
- Middle ground: lovastatin, moderate-dose rosuvastatin.
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If it’s diabetes risk you care about, atorvastatin is better than rosuvastatin. Just like with other side effects, testing around.
Use CGM’s as well before and after swapping. Do a OGTT before and after. Peter Attia knows a lot about this.
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My LDL-C is extremely low right now - around 46 I think at last measure, so I’m thinking of moving to pravastatin to see how it impacts my fasting glucose levels. I don’t worry if my LDL-C / APO-B goes up a few points.
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That’s what Brad Stanfield did. Not something I think is future proof. I’m suspecting we will learn that lower is better for sure. It’s not going in the other direction.
Fasting glucose is not that informative on its own, that I know. But if you can keep your glucose lower while apoB the same that’s better of course.
It’s an interesting question… which is more damaging to the body, 5 or 10 points on LDL-C or fasting Blood glucose measurements? I don’t think we have an answer yet do we?
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I’ve not really heard people talk about fasting glucose in isolation, it’s always relative to insulin levels taken at the same time for HOMA-IR calculation, and even better is OGTT according to Peter Attia. Of course there are association studies of the optimal levels but it might be a separate issue.
As he wrote, it’s the non-HDL-C and apoB that matters, not lowering to a specific triglyceride level (which is e.g a marker of insulin resistance/diabetes).
AI answer:
An isolated +10 mg/dL rise in apolipoprotein B (apoB) with a simultaneous –10 mg/dL drop in fasting glucose is generally more harmful than the opposite change (‑10 mg/dL apoB, +10 mg/dL glucose), especially when the glucose change stays within the normal range.
Why a 10‑mg/dL increase in apoB carries more risk
Factor What the number means Typical risk per 10‑mg/dL change (approx.) Why it matters apoB Each 10 mg/dL rise reflects ≈10 % more circulating atherogenic particles (VLDL‑apoB, LDL‑apoB, Lp(a)‑apoB). ≈6–9 % higher risk of major atherosclerotic cardiovascular disease (ASCVD) events in prospective cohorts, independent of LDL‑C. apoB is the direct count of atherogenic lipoprotein particles; every extra particle can enter the arterial wall, become oxidized, and trigger plaque formation. Fasting glucose A 10‑mg/dL rise is ≈0.55 mmol/L. In a person whose glucose is already in the normal range (e.g., 85 → 95 mg/dL) this is still well below the diabetic threshold (126 mg/dL). ≈1–2 % higher risk of ASCVD (if glucose stays <100 mg/dL) and very modest impact on microvascular risk. Glucose‑related damage is largely a function of chronic hyperglycemia (≥126 mg/dL fasting) or sustained elevations that raise HbA1c >6.5 %. A single 10‑mg/dL bump rarely pushes a normoglycemic person into that high‑risk zone.
It makes sense, as long as you’re not diabetic or becoming so and harming the arteries with excess glucose, it’s better.
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The FDA approved Repatha for primary prevention. https://www.medpagetoday.com/cardiology/dyslipidemia/117148
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Unfortunately there are always tradeoffs.
“Compared with baseline values, patients treated with atorvastatin had no change in atheroma burden, whereas patients treated with pravastatin showed progression of coronary atherosclerosis.”
Of course this paper’s subjects had a higher BMI, and the dosages were not adjusted so it’s not exactly apples to apples.
As I previously posted, I will give TUDCA a trial.
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That is a really interesting question!
This suggests there are threshold effects for hba1c
" There was a non-linear relationship between mean HbA1c during follow-up and the risks of macrovascular events, microvascular events and death. Within the range of HbA1c studied (5.5–10.5%), there was evidence of ‘thresholds’, such that below HbA1c levels of 7.0% for macrovascular events and death, and 6.5% for microvascular events, there was no significant change in risks (all p > 0.8). Above these thresholds, the risks increased significantly: every 1% higher HbA1c level was associated with a 38% higher risk of a macrovascular event, a 40% higher risk of a microvascular event and a 38% higher risk of death (all p < 0.0001)."
Association of HbA1c levels with vascular complications and death in patients with type 2 diabetes: evidence of glycaemic thresholds | Diabetologia)
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I guess so. End of the day, we are not chimps or lions and I just don’t think we should be setting them up as any sort of comparison. Lion diets consist entirely of red meat and they don’t get heart attacks. Weirdly the horse has high cholesterol, but they are cardiovascularly extremely fit. I think every organism has unique physiology.
Yep, and honestly, I think these lipidologist people are also making a mistake of getting into the weeds on this sort of argument. The whole “appeal to nature” thing is bullshit. I also think that “20-40mg/dl is normal” is a stupid statement. It’s trying to hijack the natural = best argument. It would simply be better to say 20-40mg/dl is optimal for ASCVD prevention, without trying to make appeals to nature IMO.
The key word here is “potential”. As far as I know, the actual evidence still massively favours using statins. To get excited about changes in GLP-1 or bacterial metabolites is maybe putting the cart in front of the horse. It’s academically interesting but I don’t think it’s worth the “hype”. As @desertshores says, there are always trade-offs. The important thing is overall outcomes. You take a statin to address one thing, which causes something else to change, and then something else (like TUDCA) is taken to address that. But TUDCA itself has drug interactions, so the cycle will never end haha.
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