#182

I heard it from Peter Attia, but I haven’t done more research than that since he typically is often right about things. I didn’t like berberine and it is a dirty drug so I don’t bother looking for pro/cons.

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#183

Are you taking Acarbose for sugar control? I just started a 25 mg dose.

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#184

Ok so no reliable evidence. Traditional medicines have been taken for many years. Some such as ashwagandha have a record of bad side effects. Others dont. French lilac (metformin) has its functions. The evidence does not substantiate its use by non diabetics. My HbA1c is below 5, lowest 4.18% (probably after a real bender).

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#185

On reading @RapamycinCurious well written post, something about his mention of rotenone triggered a thought/memory so I thought I’d add it.

There is a belief that Parkinson’s may be caused by exposure to environmental toxins, if that is true….

Epidemiological studies link exposure to environmental toxicants – like rotenone, paraquat and trichloroethylene – to increased risk of PD , even though the exposures may have occurred decades before the emergence of symptoms

Transient exposure to rotenone causes degeneration and progressive parkinsonian motor deficits, neuroinflammation, and synucleinopathy | npj Parkinson's Disease.

….then metformin should have a protective effect on dopaminergic neurons.

Metformin has a protective effect on DA neurons against rotenone-induced neurotoxicity through inhibiting neuroinflammation and ER stress in PD mouse model.

Protective effect of metformin against rotenone-induced parkinsonism in mice - PubMed.

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#186

A lot of it is metabolic. I say this in a pub in the UK having drunk 4 pints of Old Peculiar (that’s me) and on my third 100ml of port. If my CRP is unmeasurably low i must have got the biochemistry right. Hic!

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#187

I am neutral on Berberine supplementation.

After reading several articles, it appears berberine at clinically useful doses has a wide safety margin. I can find no articles concerning what the maximum safe dose is.

Most studies that I have read have used dosages between 900-1500 mg per day, split into 3 doses. “The optimal dose of BBR was 1 g/day for TG, TC, and weight, 1.8 g/day for insulin and HOMA-IR, and 5 g/day for HDL”

The cytotoxicity is dose-dependent.

I have been taking Berberine on and off for decades with no apparent ill effects.

Now that I am older, I don’t want to take any supplement that might be damaging.

I was taking berberine as a supplement because I quit taking metformin. I did a self-experiment with metformin. After cutting metformin for a few days my whole gut and digestive system felt better. I tried metformin on and off a few times and found indeed metformin was affecting my digestive system.

Oddly enough my doctor prescribed metformin based only on one blood test that showed a higher than normal reading.

After quitting both metformin and berberine my fasting and HEMOGLOBIN A1c levels are normal. Probably because I am on a low-carbohydrate diet.

That said, I believe in metformin both as glucose-lowering and life extension benefits.
If you can tolerate metformin I would take it over Berberine.

Berberine attenuates mitochondrial dysfunction by inducing
autophagic flux in myocardial hypoxia/reoxygenation injury
https://sci-hub.se/10.1007/s12192-020-01081-5

Biological properties and clinical applications of berberine
https://sci-hub.se/10.1007/s11684-019-0724-6

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#188

FYI, it is widely studied. It’s just that it failed:

(but yes, for sure, smoking is protective against Parkinson’s, like diabetes by the way)

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#189

I’m curious about using Metformin or berberine for short bursts to improve akkermansia. There seems to be reasonable evidence for both, and it would seem to be easier than sourcing probiotics.
Have you ever had a gut microbiome test?

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#190

But sometimes that doesn’t make them any less “dirty”. In case of metformin vs. berberine that are both “dirty” drugs and just cause one is pharmaceutical does not make it less “dirty”. And poor man’s is just for entertainment purposes I suppose, as metformin is one of the cheapest drugs probably. I picked up a pack of 100 x 500mg pills for a little over 2 EUR, but do not take it for the same reason as I don’t take berberine, they are both “dirty” and mitochondrial toxins plus metformin seems to blunt exercise benefits which berberine does not.

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#191

Of course. I was comparing Cana with Berberine, but I don’t know how clean it is.

#192

That trial is the latest amongst many small trials of similar design, almost all of which have failed. To be fair to Dr. Glorioso, an important caveat is that all of these trials were for treatment of people with existing PD, whereas the epidemiology suggests that smoking may reduce the risk of developing PD. This would require an extremely long trial in many subjects (since PD is not common and there aren’t really any high-risk groups if you leave aside people with genetic cases and maybe some agricultural workers), and based on the trials, you’d likely get a high dropout rate due to side-effects.

#193

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.

#194

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 :joy:) 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.

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#195

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.

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#196

Good to know.

What were the doses for high and low Metformin in regards to PD?

#197

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 :man_shrugging:

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#198

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 :man_shrugging: 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]

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#199

Thank you that.

I take, what would qualify as a ‘high dose’ of metformin and what you’ve just posted has give me something to think over :blush:

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#200

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.

#201

No, I have never had the test. From what I have read, supplementing with oral pro-biotics is not very effective.