I agree with others - there is not a mechanism for a “false high reading” - it is instead a real elevation. It is pretty common and varies individual to individual. My. Personal HbA1C went from 4.7 to 5.5% with adding Rapa 8 mg q8days, which is my regimen.
Lipids also may go up a bit. This is why we measure.
Irrespective of whether a diabetic or not, I see a high rate of individuals on the board also being on SGLT2-i, Acarbose, GLP1/GIP agonists, and/or Metformin.
Some of these agents also have the advantage of likely slowing cognitive decline, possibly due to improving insulin sensitivity in the brain. Irrespective - if doing a general longevity protocol, it would be common to be on medications that will blunt/reverse this anticipated effect.
In general, best way to track these things is through a continuous glucose monitor to see in real time impacts of behavior and interventions on glucose. I’d generally think that after 3 weeks of your final dose, would be a good time to look at your glucose to get an idea of what the effect will be, and then talk with your doctor about ways to mitigate any increase, generally with a strategy that has benefits of improving longevity and improving insulin sensitivity in the brain.
I wore a CGM last April and posted the results here:
There is one subtlety about HbA1c in that there are two ways of measuring it either just ketoamine or aldimine and ketoamine glycated haemoglobin.
Thanks to all for responses so far. I’ll see if I can find the article again and try to find out what was meant by “artifically high.” I’m not ignoring all the data about blood sugar/A1C elevations; but I found the info. interesting and wanted to see what the consenses is. Not that it matters but FWIW: I made a typo in my original post, I did my 8mg dose today, not 7mg. No side effects that I can tell so far on my ramping up to 8mg/wk.
If the red blood cells lived longer or shorter on average, that would “artificially” change the meaning of the HbA1c (vs a change in the average blood sugar levels). Is there any mechanism for rapamycin or anything else we do for longevity impacting the turnover of red blood cells?
The average RBC survives around 100 days. But the HbA1C isn’t really going to massively change if your RBC’s survive 90 vs. 110 days. I believe Rapamycin only makes a difference on RBC production - such that you are likely to decrease your hemoglobin level a little. This is actually a good thing for a lot of people - and works synergistically with men who are needing Testosterone replacement, where we worry about Hb increasing.
I don’t know of any information that RBC survival is impacted by Rapamycin. There are individuals who destroy their RBC’s more rapidly, and I’ve not seen any literature indicating that the HbA1C isn’t accurate in those individuals - however, the impact would be over what period of time you have the average - which should match the days the average RBC survives.
well if my A1C/blood sugar goes up like most people seem do; there’s not a whole lot I can do about it other than maybe take a low dose metformin? My last labs in Jan my A1C was 5.4. I excercise 5-6 days a week for a min of 1 hr ea. day. (I swim laps, 4.5 miles on treadmill and the rowing machine on different days and do a few different nautalis machines each day) and I watch carbs (but don’t completely avoid them).
Some of us are taking acarbose and / or an SGLT2 inhibitor like Canagliflozin or Empagliflozin.
Even though I take Metformin, I would recommend an SGLT2I like empagliflozin for HBA1C control. If it can keep your HBA1C at normal levels, there’s no need for Metformin. I’ll be taking a low dose empagliflozin starting this summer.
I receive no hbA1c benefit from my sglt2 inhibitor (Farxinga). I don’t know why. Akkermansia is the only thing that made a big impact for me.
Just a thought. Should we keep our dosages low enough not to have a significant impact on blood sugar without ancillary medications? Raised blood sugars seem to come from mitigation of mTORC2 which we are trying to avoid.
That’s kind of where I am at this point. I still use acarbose with meals that have carbs because it is supposed to boost mtor2. Only other way to boost it is fasting. I also use metformin some for a day or two after Rapa dose.
is a day or two enough? if sugar only rises for a day or two I wouldn’t think that’s really that harmful. I would be more worried if it was continously high. (I dose 8mg once per week)
I didn’t want to take the common TR treatment meds so my Urologist suggested Clomi. He said it was very safe and hardly any side effects. I take 25 mg daily (he initially prescibed 50mg but I wanted to see what a 1/2 pill did) My testosterone went from high 100’s to 480’s on 25mg. After I got my results and told him I was only doing 25mg, He said stay on the 25mg! 
This is a common treatment, as is HCG, if your body has the ability to build testosterone. Currently, I will try this in those <55 years with other lab values looking likely to have this be successful - but the success rates go way down in the mid 50’s. Not that it never works. With Clomid, there are a significant number of people who get side effects - but also a significant number who don’t. HCG is the stand in if you don’t tolerate clomid and you can build Testosterone.
I’m 65 and started Clomi a little over a yr ago. My Urologist said there were few side effects and I haven’t seen any since I started. My labs are normally very good. (CMP, CMP, PSA, Tsetosterone, Vit B, Mg) My Mg was critically low due to long term PPI use and started giving me heart issues. Mg Supplements wouldn’t bring it up so I stopped the PPI. You would think your Gastro would tell you about Mg and PPI use…but Nooooo. I had to figure it out on-line…sigh. My PCM says he wishes his Labs looked like mine. 
Mg supplements will bring it up… it is dose and formulation. Irrespective, these drugs (PPIs) are harmful, and wildly overused. Never indicated, beyond 4 weeks.
Mess up B12 and endogenous NO, increase risk of dementia and osteoporosis.
Not on my list of things to take unless I’m trying to expedite my wife collecting on my life insurance!
In regard to the clomid, monitor, you are in the minority in your age group that this works for, but this is superior for several reasons when it works over giving testosterone.
( dose and formulation). I did not get into the normal range on supplements. Close but not normal. Initially I was told to use oxide which is the cheapest but it didn’t budge my numbers. I then tried a few different types as I found that most have lousy uptake. (You may make take 1000mg but only uptake 10mg). I ended up using a combo that had magnesium glycinate, magnesium malate, magnesium taurate & magnesium citrate for uptake and bioavailability. This was the one that brought it close to normal. But it was expensive so I ended up quiting the PPI. (and then the Mg suppl as my Mg went into normal range after stopping PPI use.)
Good thing to be off the PPI in general. As an aside, magnesium oxide has ~4% absorption … so cheap — but not a good source.
Yes. I believe the best forms of magnesium are Magnesium glycinate, threonate, or citrate depending on your needs… 
I suppose but then my stomach acid wasn’t being controlled. I already had barrett’s stage 3 when I went on the PPI. I have had a number of times the past 9 months where I had food getting stuck on the way down. The last time about 3 weeks ago it hurt so bad I thought I was having a heart attack! I have an EGD this friday to see what’s up… (then my colonoscopy the following week). That’s why in an earlier Post I was asking about stopping my sirolimus dosing. My Gastro said there’s a new medicine out that shut’s down acid production like a PPI but doesn’t have the side effects. We’ll have to put in paperwork for my insurance to pay for it because it’s Non-Formulary??; (depending on what the EGD looks like.)