Probably many more than that but I didn’t chase down all the references.
So when I got afib from (most likely) low magnesium and I was referred to the best heart doctor around. That clinic was very nice and so were all the members of his team. I asked what caused it and asked several specific questions about cause. He said it didn’t matter what I eat and never mentioned dental hygiene either. These papers aren’t brand new, they act like this is common knowlege, just going by the language in the papers. The bacteria cause the infection that starts the ball rolling.
Why don’t I get a test for my microbial burden at my next checkup? If it’s high then what do I do? Ozone?
As someone with both a degree in medicine as well as dentistry I think I can safely say that MDs are completely clueless about anything related oral health…
If you want your teeth to rot out of your mouth eat many small meals throughout the day with plenty of carbohydrates and fruits and what do doctors recommend…
I’ve been chewing Spry gum which is sweetened with xylitol. I don’t like to chew, but it works muscles and is supposed to be good for you. Probably end up swallowing the pathogenic bacteria. So I start every day with a small piece of aged cheddar which is supposed to have enough spermidine to close all the loose junctions in the gut.
Peach kernel safflower is high in luteolin. I love fruit–it’s pretty much the only carb I eat–but try to always take some luteolin with it when I eat it.
The article on statins is well done because it looks at the two factors that matter most. Absolute risk reduction and total mortality rates. In those most important factors statins mostly strike out. The sole exception being males under 65 with a history of heart attack. Most rapamycin users don’t fall into that category.
Blagosklonny posted a study today from 2013 which supports the notion that the metabolic effects of short term rapamycin are in direct contrast to the long term effects.
This was also seen in marmosets where lipid dysregulation was transient.
In this study we see in mice that the adverse insulin resistance at the beginning of treatment switches to the preferred insulin sensitivity over time. The same was seen with lipids.
Maybe patience is all that’s required after all.
Isn’t 20 weeks a long time for a mouse? If it dies in 100 weeks that’s 20% of its lifespan. I’m not sure I want to wait that long for things to normalize!
Fair point. I’m not certain that the translation from mice to humans actually works that way, but it might. The encouraging thing is that a similar transient metabolic effect was also seen in marmosets.
Also, according to the posted study, they make the claim that the “ metabolic switch “ from the unfavorable to the favorable occurs in renal transplant patients as well.
Perhaps I have been doing myself no favors by taking a washout period.
Do you think a steady dose and not doing periodic washout periods might be the better strategy to normalize our lab panels while on rapamycin?
It’s really hard to know and I debate this with myself frequently. I also don’t think that anyone really knows the answer to it.
So right now I’m straddling the fence, keeping my rapamycin dose reasonably low on a weekly basis while incorporating in flax and taurine to keep the lipids at bay.
As I’ve stated before, metformin messes with my exercise, so I’m seriously considering berberine for insulin sensitivity. I realize that it works via a similar AMPK mechanism but I’ll see how my stamina responds.
In the meantime, I do think that the metabolic effects will sort themselves out over the long run. I’m very skeptical that any drug could consistently give significant longevity while inducing long term metabolic dysfunction.
So I’m optimistic, but cautiously so.
Statins did not reduce major cardiovascular events in non diabetics even in those with a baseline high atherosclerotic burden.
In those with CAC of zero, statins may actually increase risk.
I have read many studies similar to this and I am now going back to a lower dose, 5mg/week of rapamycin with EVOO. This time I will not be taking any “washout” periods.
This will give rapamycin a chance to revert lipids to normal.
I will have blood work done every two months to track lipid changes. My diet is pretty regular except for the holiday season when I will be eating out more and having dinners with friends and relatives. If my lipids stabilize, I will keep doing the 5 mg/weekly with EVOO, which translates roughly to 7.5 mg/week.
I interpret recent articles to suggest that there is a u-shaped dosage curve with the sweet spot being roughly 5 - 10 mg/weekly for humans
I do believe that I read that a fatty meal enhances the absorption of rapamycin by about 30% - 50%. I take rapamycin with a shot of EVOO along with a high-fat meal. Maybe I am wrong, I just want to be somewhere between 5 and 8mg