Finally, genetic differences also cannot readily explain the near perfect correlation between use of pesticides and PD prevalence [29], the strong association between agricultural activities and its incidence […] For example, in France the increased risk of developing PD is not limited to farmers [39, 40] but extends to those living near farmland or vineyards [30]. Pesticide exposure may also lead to faster disease progression after the diagnosis has been established.
Although some older retrospective, case-control, and prospective longitudinal studies suggest that statins and LDL-C lowering are associated with cognitive impairment or dementia, the preponderance of observational studies and data from randomized trials do not support this conclusion, at least over the course of the trials that varied from a median of 1.6 to 6.0 years of follow-up. Additional studies are needed to ensure cognitive safety over longer periods of time. In the interim, contemporary guidelines recommending the risk-stratified attainment of lipid-lowering goals are reasonable.
Importantly, they did not include Parkinson’s in their assessment. Parkinson’s dementia and Lewy body dementia were not specifically explored but included as part of “all-cause dementia” I assume.
If we even assume some heritability, then the RR increase from using statins for 10 years must be very small, the total absolute risk. If the base rate is 2%, increases to 4% with genetic risk, 0.8% (20% of 4%) chance that PD develops before 50, or is my math off? Then you increase the 0.8% risk by whatever the RR increase is for statins which I don’t think we know. If we assume no heritability then it is half.
5 mg ezetimibe should reduce apo b by about 26%. Add in some fish (it may reduce omega 3 absorption) and you should be back jn the 60s.
Did your apo b rise due to rapamycin?
Thanks. I’m not even taking rapa so I don’t know the cause. As I got an incorrect result for another metric (PTH) from that lab I’ll first redo the test with another lab. But yes I’m not too worried, as there are available treatments.
Again, I would like to point out that methylene blue and photobiomodulation is useful in both treating and preventing brain disorders.
The first paper below has quite an extensive discussion on the use of MB in treating or perhaps preventing Parkinson’s disease
What is especially helpful about this paper is the plethora of citations concerning MB and brain and mitochondrial functions.
100% agree with the sentiment that we are all here to help each other.
I think that actually might have been what triggered me - I did not want the information and rationale that our discussion to lead to misunderstanding by anyone else reading the thread and then taking away incorrect ways of thinking about things.
I do truly believe you have always acted with good faith.
And - I do think you with your data and publication driven approach are one of the best contributors to the forum in recent months! So thank you so much for all your contributions.
Mitochondrial dysfunction plays a central role in the formation of neuroinflammation and oxidative stress, which are important factors contributing to the development of brain disease. Ample evidence suggests mitochondria are a promising target for neuroprotection. Recently, methods targeting mitochondria have been considered as potential approaches for treatment of brain disease through the inhibition of inflammation and oxidative injury.
@adssx have you thoughts about key thinks that sustain optimal mitochondria, like eg
I think that was discussed bought based on the worlds current data and understanding a few months ago on the forum?
Or let me know if there is any specific aspect(s) you think we should unpack further?
Otherwise perhaps ok to agree to disagree on how low optimal is in different contexts - and we can revisit as new studies, data and mechanistic understanding comes out?
Don’t you think optimal is different on case to case basis? Or you think someone with advanced ASCVD and someone with metabolic syndrome who smokes without signs of ASCVD and someone who’s genetics and phenotype is low risk for ASCVD should target same apoB?
Yes, fair point. I was really trying to soften the debate by reminding everybody that there’s much we don’t know, and there are other manageable factors that are important.
The experiment is a stretch. I don’t think there’s anything published on honeycomb derived policosanol. And the evidence for sugar cane policosanol is mixed. But i have the bees so I’m hopeful!
I think almost everything in medicine should take into account different case by case specifics
In this case goals and what resources are available and could be prioritized is the bigger driver.
The resource aspect is a real aspect here since “risk free” supply of some of the medicines (PSCK9i, Bemp Accid) are still crazy expensive (though that will chance as patents expire) - if one does not feel ok with getting via India or so of course.
When it comes to ApoB in the vast, vast, vast majority of people who are shooting for optimal longevity, the optimal is generally going to be to go at low as possible as long as an ok combination of diet and exercise and basically always one or more of the ApoB modulating medicines can be found to works - which in this unique part of medicine generally will be achievable.
There may be some theoretical corner cases of being allergic to all medicines or more commonly a person actually not want prioritize longevity optimization or may not even want to prioritize healthspan optimization, but if one does have a longevity goal, one will in my option - based on today’s totality of data - want to try and go after Apo B in a very, very hard way - even in cases where one is fit, metabolically healthy, etc.
Put yourself in the 80 apoB person’s shoes, which is scta123, what would make you comfortable to sustain that apoB at that level and not go up or down?
