Yes, I’d ask her to provide scientific studies instead of speculative hearsay. We need to go hard on the science here and from what I’ve seen, Ms. Glorioso’s evidence is observational at best and hearsay at worst. If someone can provide some scientific studies, I’d be interested.
It could be that diabetics overcome their diabetes with Metformin, live longer but then develop PD because of the diabetes. That’d make more sense to me.
I would posit there’s a simple reason why smokers don’t develop PD. It’s not the nicotine preventing PD. It’s the cancer from smoking killing you before PD can develop.
No, diabetes is protective against PD. If you give a high sugar diet to PD models, their PD symptoms decrease. (But they die earlier of CVD ) And metformin is only associated with PD at high doses. At low doses metformin is protective (some people are even studying low-dose metformin as a disease-modifying treatment for PD). No one knows why. One assumption is that PD may be caused by toxins (such as pesticides) crossing a leaky gut over time and then reaching the CNS and the brain. And (low dose?) metformin and smoking both reinforce the gut barrier. But that’s just one assumption.
A few years ago, I took two Viome tests, six months apart.
The methods for self-collecting blood samples was laughably poor. Each time, I ended up getting blood drawn at a local lab, but even these failed at the Viome Lab and required a second sample. I also supplied stool samples each time, and they also failed. One of the samples failed after a very long wait of approx. two months after arriving in their lab.
The Website and App look great but overall it felt like an expensive approach to sell expensive supplement subscriptions.
If anyone has used a gut test that they regard as reliable, please let me know.
Yes but that trial enrolled people with very early PD, just after diagnosis. So early that they were not even on meds. But we know that their prodromal PD started 10+ years before. And nicotine did not slow down the progression of their symptoms. So it’s hard to imagine why it would have slowed down the progression a few years before.
Dr. Glorioso suggests starting nicotine at age 80+. But by that age many/most people already have the Parkinson’s disease prodromal markers. It’s just that they die before developing the symptoms.
So if there’s a case for nicotine (and I’m not sure there is) it is not at age 80yo that it should be started but way earlier. The average PD patient is diagnosed at 60yo. Pre-PD symptoms start 10 to 20y before. So, if you have a higher than average PD risk, you could start nicotine at 40. And maybe low-dose selegiline (which seems to have similar PD protective properties) is more efficient
Different papers say different things but it looks like below 0.3g/d is for sure safe. And above 2g/d is for sure unsafe. Between these two extremes Also, the total exposure may matter as much as the daily dose.
Anyway, I have an elevated risk of PD, that’s why I not using metformin but SGLT2 inhibitors (SGLTi slash the PD risk by 5 and even reverse PD in animal models). Someone with a family history of severe UTIs would probably make the opposite decision. [btw, same reasoning for beta blockers (linked to high PD rates, even though it might not be causative) VS some CCB (isradipine) and some ARBs (telmisartan/candesartan) that seem to be able to slow down PD]
You’re welcome. Your profile says that you take “Metformin Canagliflozing (or other SGLT2 inhibitor) Acarbose”. How do you combine them today?
GLP1 agonists (exenatide, semaglutide, etc.) can be a good alternative to metformin as well. They have not been tested in the ITP, but they look better than metformin in longitudinal studies to prevent or delay neurodegenerative diseases.
I find I can learn more from any of these “experts” from listening to their podcasts / YT interviews, provided their interviewer is good, than reading their books. They delve more into nuances and details over a live interview which preemptively answers some of my questions or otherwise helps me make up my mind on what I think of their take compared to the relatively dry /
sterile book material.
I find Attia impressively knowledgeable on exercise issues, like he would make the world’s best personal trainer — with a focus on what you need to be fit in your old age, such as foot strength / stability. I’m recovering from a sprained ankle and learned a lot from his interviews promoting the book, which has already helped in my recovery.
Outside this subniche my opinion of his expertise does take a downward slide. When it comes to diet I think I’m honestly better informed. And I don’t think I have such a big head.
Either way, someone worth learning from, not gospel material, but then again who is?
I just started and don’t take it with every meal but rather when I eat whole grains like oats, buckwheat for breakfast or fruit and berries. My glucose is the same with Acarbose or without and stays in the range 92-97 in the morning after 12-14 h night fast. I would like to see it lower and that’s why I’m trying Acarbose. I don’t take Metformin.
You may need more real time data like from a CGM to see the differences because it’s more that acar decreases the spikes and variability than the average or morning after fasting levels.
Would be nice to get a CGM, but my insurance wouldn’t cover it bc I’m not a diabetic. Instead I poke my finger a few times a day to get a better understanding how it moves.
) And metformin is only associated with PD at high doses. At low doses metformin is protective (some people are even studying low-dose metformin as a disease-modifying treatment for PD). No one knows why. One assumption is that PD may be caused by toxins (such as pesticides) crossing a leaky gut over time and then reaching the CNS and the brain. And (low dose?) metformin and smoking both reinforce the gut barrier. But that’s just one assumption.
