We identified 291 incident PD cases during 6 years of follow-up. Users of ibuprofen had a significantly lower PD risk than nonusers (relative risk [RR], adjusted for age, smoking, caffeine, and other covariates = 0.62; 95% confidence interval [CI] 0.42–0.93; p = 0.02). There was a dose–response relationship between tablets of ibuprofen taken per week and PD risk (p trend = 0.01). In contrast, PD risk was not significantly related to use of aspirin (RR = 0.99; 95% CI 0.78–1.26), other NSAIDs (RR = 1.26; 95% CI 0.86–1.84), or acetaminophen (RR = 0.86; 95% CI 0.62–1.18). Similar results were obtained in the meta-analyses: the pooled RR was 0.73 (95% CI 0.63–0.85; p < 0.0001) for ibuprofen use, whereas use of other types of analgesics was not associated with lower PD risk.
The pooled risk ratio of PD with NSAID use was 0.95 (95% CI 0.80, 1.12). The pooled risk ratio of PD with high-dose or long-duration NSAID use was 0.91 (95% CI 0.78, 1.05). The pooled risk ratio of PD for aspirin (acetylsalicylic acid) users was 1.08 (95% CI 0.93, 1.26). The pooled risk ratio of PD among ibuprofen users was 0.76 (95% CI 0.65, 0.89). The pooled risk ratio of PD in men using NSAIDs was 0.79 (95% CI 0.69, 0.92), and in women using NSAIDs, it was 0.72 (95% CI 0.45, 1.15).
You’ll have to explain why many papers found that ibuprofen users had a lower risk of developing Parkinson’s disease.
The ORs of PD occurrence in patients who took NSAIDs, Ibuprofen, and non-aspirin NSAIDs were 0.88 [95% CI (0.8–0.97), p = 0.01], 0.73 [95% CI (0.53–1), p = 0.05] and 0.85 [95% CI (0.75–0.97), p = 0.01]. Meanwhile, the risk of PD in patients who took aspirin was not statistically significant.
Other papers found no difference, but none found an increased risk:
A total of 18 studies were included in the analysis to assess the overall effect of NSAIDs on the risk of PD (Figure 2). The RR with a 95 % CI was 0.96 (0.83–1.11), with a p-value of 0.57. This suggests that there is no statistically significant association between the use of NSAIDs and the risk of PD.
If your theory was correct, we would expect that NSAID users would have an increased prevalence of PD. That’s not the case. It might even be the opposite.
The situation with antibiotics is complex. Like NSAIDs, it’s not a homogenous class: some antibiotics might be detrimental while others might be beneficial:
The role of small intestinal bacterial overgrowth in Parkinson’s disease 2013: “Patients with small intestinal bacterial overgrowth were treated with rifaximin and were clinically and instrumentally reevaluated 1 and 6 months later. The prevalence of small intestinal bacterial overgrowth was significantly higher in patients than in controls (54.5% vs. 20.0%; P = .01), whereas the prevalence of Helicobacter pylori infection was not (33.3% vs. 26.7%). Compared with patients without any infection, the prevalence of unpredictable fluctuations was significantly higher in patients with both infections (8.3% vs. 87.5%; P = .008). Gastric half-emptying time was significantly longer in patients than in healthy controls but did not differ in patients based on their infective status. Compared with patients without isolated small intestinal bacterial overgrowth, patients with isolated small intestinal bacterial overgrowth had longer off time daily and more episodes of delayed-on and no-on. The eradication of small intestinal bacterial overgrowth resulted in improvement in motor fluctuations without affecting the pharmacokinetics of levodopa.”
Antibiotic Exposure and Risk of Parkinson’s Disease in Finland: A Nationwide Case-Control Study 2019: “After correction for multiple comparisons, exposure to antianaerobics and tetracyclines 10 to 15 years before the index date, sulfonamides and trimethoprim 1 to 5 years before the index date, and antifungal medications 1 to 5 years before the index date were positively associated with PD risk.”
Effects of antimicrobial exposure on the risk of Parkinson’s disease 2024: “In a large UK-representative population, the risk of PD was modestly lower among adults who had previously received multiple courses of penicillins in the last 15 years and modestly higher among those exposed to antifungal medicines in recent years.”
Thank you, Antoine, you are doing the Lord’s work here. I saw Viktor’s post and was going to respond, but didn’t have the energy, there are so many of such, and responding to each is like fighting weeds, soon there’s a new one. Life is too short to have to repeat the same things over and over again. I posted a study in another thread showing that NSAIDs were helpful in dementia, so whatever impact on leaky gut, it’s net positive - and this is a brand new one from this month:
Long-Term Exposure to Non-Steroidal Anti-Inflammatory Medication in Relation to Dementia Risk
And Viktor recommended a book by S. Gundry. That’s a red flag. Gundry is a notorious money spinner peddling discredited conspiracy theories to generate cash. He’s all over yt and in ads all over the net, the guy is a misinformation industry. Anyone who thinks that guy has any credibility really has done no research. The moment I saw that name, I could’ve stopped reading. It’s like you want to discuss astronomy and somebody starts the discussion by recommending a flat earth book - this is not going to go anywhere.
I was wondering if perhaps we could have a pinned post or FAQ where the most common talking points surrounding useless recommendations for conditions like PD and cholesterol denialism are dealt with citing studies, and whenever a poster comes along repeating one of those, one could send them to the FAQ/pin, instead of trying to deal with the same points over and over again. If we could do some kind of wiki here we could cut down on noise quite a bit?
It’s not my theory, but I fully support it. Since I don’t see a clear explanation for many diseases.
The gist of it: damage to the intestine (leaky gut) and subsequent inflammation, with increased levels of calprotectin in the feces and this is a marker of inflammation.
There is a lot of work supporting this theory: https://www.nature.com/articles/s41598-023-45929-z
Exploratory analyses indicated that calprotectin levels were also associated with cerebrospinal fluid markers of AD, and with lower verbal memory function even among cognitively unimpaired participants. Taken together, these findings suggest that intestinal inflammation is linked with brain pathology even in the earliest disease stages. Moreover, intestinal inflammation may exacerbate the progression toward AD.
Benefit of this review was to elucidate that high fecal calprotectin level in PD patients indicated gut dysbiosis and intestinal inflammation. Early increment of fecal calprotectin indicates the development of gut dysbiosis and/or gut-barrier injury which may precede motor symptoms by decades. Thus, fecal calprotectin could be a diagnostic and prognostic biomarker in PD. preclinical and clinical studies are warranted in this regard to emphasize the potential role of fecal calprotectin in PD neuropathology.
I can’t agree, but here’s another book that completely confirms the information in the first one:
David Perlmutter BRAIN MAKER
Or is Perlmutter also a red flag?
I agree, there’s no clear solution.
There are hypotheses, and this hypothesis seems to me the most plausible.
Here are a couple more videos on the subject:
I’d love to say goodbye to you, too
Your level of narcissism is off the charts.
You say that A causes Parkinson’s and dementia. We show you many high quality papers showing that A is protective against Parkinson’s in animal models and that the more you use A the less likely you are to develop these conditions. When asked to explain the discrepancy your only answer is “It’s not my theory, but I fully support it.” and you send some YouTube videos.
It’s OK but it’s just that here we’re trying to be a bit smarter when it comes to health. You better go to Reddit r/Supplements where you will find your crowd.
I don’t say there is no clear solution. I say that I have a hypothesis here
Which explains the cause of the various sorts of Parkinsons and gives an opportunity to manage the consequences and to some extent reverse it (although reversing is really hard and there a limits on regrowing neurons).
