An instance where Mike is being interviewed… and a very good overview of his scientific approach to longevity; with a focus on testing to validate the things you are doing and taking are actually working for you (which I think is something we can all learn from). @ConquerAging has a great YouTube channel here: https://www.youtube.com/@conqueragingordietrying1797
@ConquerAging , Mike - can you share a little bit of your thought process as far as moving to try out rapamycin?
You’ve been so fervently focused on diet for many years, so I’m surprised you’re moving in this direction. Very interested in how it goes for you. I look forward to hearing about how it impacts you and all the metrics you track.
I think Mike’s biomarkers are going to go ‘crazy’ relative to previous interventions, widely change in all directions, it would be interesting to see if any potential net longevity benefit could be picked up in blood tests.
Indeed Mike has been quite adamant about getting all of his nutrients from food whenever possible, and has resorted to supplements only reluctantly.
But incorporating prescription pharmacueticals is a whole new chapter in the longevity strategies evolution (if I recall correctly, previously Mike only took - and still takes - some compensatory drug for a thyroid condion).
To be completely honest, I can’t say I’m deeply shocked. If your aim is to extend health and lifespan to the greatest degree possible, inevitably at some point you’ll need to step beyond the naturalistc diet, exercise, lifestyle - once you’ve maximized along that axis, pharma is your next stop. I suspect a lot of people agree, and were only held back by a relative paucity of agents which provably can accomplish that - with the ITP results, we now at last have candidates with at least confirmations in mammals, and rapamycin is the early undisputed champion with the biggest scientific support so far… now there’s an explosion of candidates, but rapa has the most robust track record and a relatively good safety record for the risk/reward ratio.
It also makes sense, because rapa can be initiated later in life, so perhaps it might be easier to observe positive effects sooner and more distinctly compared to a young person in excellent health.
I’d also be interested in the sourcing of the rapa, if possible.
Stunning. A major change in direction. I’ve been thinking that Mike had run into limits to his long-standing approach. I admire his willingness to change his mind when necessary to continue making progress. I look forward to learning from him on this addition to his approach.
This morning’s 57-43 isn’t great news [first number is HRV and second is nighttime pulse, he is generally quite a bit higher on the HRV and often a bit lower on the pulse], but is an improvement over the past 2 days (52-45, 51-46). Yesterday, there was additional resolution for the work stress that triggered these changes, so I’m expecting a big improvement for HRV and RHR over the next couple of days.
57-43 may also be good news because I was (and still am) wondering if rapamycin may be bad for HRV and RHR. This morning’s data suggests that they can improve while taking rapa-we’ll see how this story plays out over the next few days.
Isn’t this a clssic short term vs long term effect? We have to wait longer term to draw conclusions, same as exercise messes up a ton of biomarkers short term, but improves long term. Or it could be a geniune effect like rapa on glucose and lipids.
62-43 is a small improvement over yesterday’s 57-43 (higher HRV, but the same RHR), but might be better news than expected when considering that Thursday was an active day, with a daily HR (55 bpm) that was almost as high as on a workout day (56 - 57 bpm), but without a workout. With that in mind, 62-43 would be decent data relative to post-workout induced alterations to HRV and RHR.
Today, I can take as close-to a full rest day as possible, which should help push HRV and RHR towards better values on Saturday. If not, is rapamycin bad for RHR and HRV? Nonetheless, I’m committed to taking rapa until next Thursday, to see if it can reduce Candida IgG.
I meant that his approach might both work and that CR itself.
Because CR is expected to work in animal models, and now both method and CR validated in N=1 according to human epidemiological data (ACM). I might be thinking incorrectly on the CR validation part though.
7 or so biomarkers improve on ACM, 1 negative, that means his method in itself might be valid and that’s important.
It was long ago but I will take a look, I think important is to have the correct method of evaluating strategies.
Wonder if the benefits in human CR studies were on biomarkers showing a net benefit on short term ACM risk.
I don’t have any studies per se, what I meant was:
Mike has a method he believes will improve his longevity.
This method of optimizing biomarkers according to ACM epidemiological or youth data show that CR works really well for him with lots of biomarkers going in the right direction.
Is his method good? I’m thinking that his one actually works and there’s signal in the epidemiological data for ACM and youth because it shows that CR works well. Which validates his approach.
Does that make sense? If so:
Next would be to see if short term studies on calorie restriction improves biomarkers for better epidemiological ACM, including ones he saw improvement in.
I might be missing something here, but I feel like it shows that it works? Unless we believe CR to not work in humans, thus we can’t determine how valid his method is based on it. I might be confusing myself here, though.
For anyone interested in CR studies in humans and the associated research, you should look at the work of professor Luigi Fontana. He’s the primary investigator behind the CALERIE trial. He’s done a ton of CR work in humans over the decades, and if you google around you’ll find his work everywhere.
@AnUser and any anyone else interested in this topic (@adssx what is your latest thinking), here is one thread that also references several other recents ones
