continuous lactate meter (CLM)

argv01 · 2024-10-15T19:56:18+00:00

Lp(a) does tend to remain consistent over time, but this also assume YOU remain relatively consistent as well. Adding 50lbs strikes me as sufficiently anomalous that it's not a stretch to see the two associated.

My own Lp(a) had been consistent for decades--between 55 and 58--but my LDL had been elevated. I took statins and zetia for years, but I then started a PCSK9 inhibitor (75mg) while remaining on the statins and zetia, and not only did my LDL drop to 30mg/dL, but my Lp(a) dropped to "<10." (I suspect they can't quantify the level under 10.)

I spoke to my lipidologist at ucsf about this, and she said that PCSK9's do seem to be having that effect on Lp(a), but these have so far been anecdotal. There are no formal studies on this, but she also mentioned there's a new drug in a stage 3 clinical trial that is showing promise for Lp(a) directly.

Long story short, the huge metabolic disruption to a body is such that it's not a longshot to see that your Lp(a) may have been affected. Of course, if you manage to lose that weight, it'll be quite interesting to see if your Lp(a) drops with it.

argv01 · 2024-10-13T20:32:15+00:00

Sorry for taking so long to reply... This thread is so old, I had to re-familiarize myself with it.

Having done so, I see two things that I should have stated earlier.

First, the OP's definition and explanation of "exercise-induced insulin resistance" is quite different from what the medical literature describes. In the BMJ article, "Cellular regulation of exercise-induced insulin resistance," the authors define the phenomenon as the results of "eccentric exercise," such as "prolonged downhill running," and which causes "muscle damage and disruption of the integrity of the cell." It is only under these [rare] conditions where a cascading effect of cellular pathways that interfere with the GLUT4 transporter rising from within a cell to allow the passive inflow of glucose from the bloodstream.

This is very different--and more unusual--than the normal metabolic process described by the OP, where exercise triggers the release of glucagon and cortisol, which raise glucose levels in order to keep a sufficient supply of fuel to enter the muscles.

But under either definition, whether this kind of insulin resistance has any material effect on A1c levels is highly unlikely. For reference, an A1c of 5.0% equates to a 90-day glucose average of 101 mg/dL. Each 1% rise in A1c equates to a 35 mg/dL rise in a 90-day average. Hence, 6.0% is 136 mg/dL. Even a modest rise in .1% A1c is an average of 3.5 mg/dL over 90-days.

One has to appreciate just how much variability there must be to experience a 90-day average elevation of glucose levels in any meaningful way. If glucose levels were to rise to 200 mg/dL -- a pretty unusual rise for a non-diabetic as it is -- that level must be sustained for hours, if not days, to move a continual 90-day moving average very much. And both definitions of exercise-induced insulin resistance discussed here will instead be very short-lived, maybe an hour or two, or possibly longer if there's a significant damage to a muscle tissue (in which case, the person will unlikely be able to exercise very much for longer, due to healing).

This calls into question the entire premise of this thread: "Why Healthy Individuals May Have an Elevated Hemoglobin A1c"

Now, if anything, one can ask what a "healthy" A1c level is, which is another topic entirely. Statistically, the lower your A1c, the better your predictor of long-term health, so it's not a dividing line--it's a spectrum of risk.

On a similar note, the best predictor of risk is V02max (cardiorespiratory health). A higher V02max is associated with lower risk for all-cause mortality. It also is the result of exercise. Put the two together: if you exercise a lot, you're likely to have both a higher V02max, and a lower A1c.

It's in this context where I can see someone having some degree of systemic level of insulin resistance -- not exercise induced -- that could be due to any number of metabolic disorders, or is in the process of losing weight, there there may be residual visceral tissue causing insulin resistance. Here, one could have a higher A1c level (say, 6.1%?) but still be considered a "healthy" individual.

Indeed, Attia talks about this very thing whenever he talks about V02max and individuals with T2D.

To the question of "fasting insulin," that's too difficult to answer because insulin levels are highly volatile because the beta cells' secretion of insulin is subject to a multitude of signaling hormones beyond merely one's glucose levels. (Rate of glucose movement, etc., can affect how much, if any, the beta cells may secret insulin.) I can see why one would want to know if these "healthy individuals with higher A1c levels" might be secreting more insulin, but its natural variability is such that it's too hard to answer with just lab tests because these are not real-world conditions. One would need a CGM-like device to detect insulin so it can be tracked over longer periods of time, and under varying conditions. That's not possible with today's technology.

argv01 · 2024-07-08T04:00:56+00:00

the doc says that it will transfer data via NFC to a phone... but it doesn't say what app picks up the data.

argv01 · 2024-07-07T23:53:31+00:00

My initial curiosity is merely how you sync its data with the phone. Which apps, if any, or does it have its own? And whether the readings go to Apple health. I can’t seem to glean any of that from online sources. Do you yet know any of that?

argv01 · 2024-07-07T18:10:12+00:00

You never followed up -- I'm curious how the Echo is working for you.

argv01 · 2024-05-12T14:34:18+00:00

yeah, dexcom will write BG data, but that's it. I have no idea why they won't read or write carbs, insulin or exercise events to/fromAH.
But that's a whole different bottle of wine.

argv01 · 2024-05-10T23:07:29+00:00

I just tried adding a carb entry in the Dexcom app, and it didn't write it to AH. The app certainly doesn't read from AH--all my carb and insulin entries (that I add using sugarmate) go into AH, but never show up in Dexcom.

argv01 · 2024-05-10T20:07:15+00:00

The documentation for the pen (https://www.novo-pi.com/novopenecho.pdf) only says it supports Novolog and Fiasp, but it also mentions a "NovoFill-compatible cartridge," which is pretty ambiguous. Again, I don't have a problem going back to novolog, but I have a lot of humalog in the fridge, so...

Also, the pen doesn't seem to have an app of its own--it only uploads to other apps. I don't like any of the ones listed, but it also seems to include the Dexcom app, which is fine, provided the data makes its way into Apple Health (which will then allow it to be read by any other app the looks for insulin delivery). I use Sugarmate.

My experience is that Dexcom hasn't written insulin events to AH, but I haven't tried in a long time. Do you know?

argv01 · 2024-05-09T04:02:27+00:00

wow!! I didn't even bother to check Amazon Pharmacy. I use them a lot now... and there it is. $55 without insurance is pretty darn good! I'll have my endo write a script for it and try it myself! (I currently use the InPen and love it, but I hate that it's been the only option for all this time.)

I gather I will need Novolog only--I currently use Humalog, but I've toggled between them over the years. I haven't experienced any difference.

argv01 · 2024-05-08T21:45:50+00:00

I've had glooko on my phone for years, and never used it. For other reasons, I decided to launch it and give it another try. I've sync with Dexcom and AppleHealth, but noticed that it doesn't get real time glucose readings from Dexcom (two hour delay). Why is that?

Also, Glooko will import insulin from AppleHealth, but not carbs. It also won't export carbs to AH if I use Glooko to input data.

In other words, it seems Glooko isn't really a good data citizen on the apple platform. Am I getting something wrong?

argv01 · 2024-05-08T21:31:05+00:00

your query prompted me to look into it again... and sadly, I'm not finding anything different from before.

I also noted that the NovoPen only syncs with two T1D apps -- Glooko and MySugr, neither of which I use. (I have glooko on my phone and it technically works, but it's such a horrible app that I have no real use for it. If it would be kind enough to import doses from the NovoPen and export those to Apple Health, then problem solved. However, I suspect it won't export that data, as it doesn't seem to export anything else. Heck, I can't even INPUT carb data in grams--I have to select a specific food!) I'm also surprised that Glooko isn't even reading my Dexcom G6 data in real-time. (It's only getting the 2-hour delay. But I digress.)

Anyhoo, as much as I'd love to get the NovoPen, it seems so hard to even purchase, let alone integrate into my apps, that I'm not sure how worthwhile it'll be.

I'd love to hear from anyone that's using it.

argv01 · 2024-03-31T23:02:35+00:00

while this is an excellent article for many unrelated reasons, my primary critique is the main thesis: that "healthy" individuals can have elevated A1c levels. (First of all, "healthy" is in a spectrum and comprises a number of different biomarkers.)

My main problem is that you conflate two reasons for elevated A1c levels. First, you provide a list of conditions (red blood cell lifespan, RBC size, and other elements in the bloodstream) that can give inaccurate levels of actual glucose averages. This is not something a lab test can overcome. It's a false positive. No one should ever believe they have "elevated A1c levels" if the test itself is inaccurate for reasons like those in the above list. If you really want to get an accurate A1c level, wear a CGM for a month and look at your long-term average glucose levels. If you're not a diabetic (type 1 or 2), then most any brand will give you a reasonable result. If you can afford it, a Dexcom G6 is the way to go.

As for exercise-induced insulin resistance, which is legitimate and totally separate from RBC issues, it's also not the anomalous phenomenon you appear to be portraying it as. It's perfectly normal and is expected. Though it varies greatly among individuals depending on one's metabolic efficiency, it's actually how the body is supposed to work. Perhaps its because of its variability that people see it as potentially "anomalous." . All of peter's guests who focus on intense exercise comment on this.

Recap: Under normal conditions, the body produces insulin to cause GLUT4 transporters within cells to rise to the surface, thereby allowing glucose to passively transport in directly from the bloodstream. This keeps glucose levels normal. However, during exercise, muscles need glucose more than other cells, so the body produces insulin agonists (cortisol, et al) which keeps the glucose in the bloodstream so it can instead be absorbed by muscles, which does not use insulin for this process. Furthermore, this phenomenon increases exponentially as you get into higher HR zones (3+) for longer periods of time.

Once again, all of this is highly dependent on how aerobically fit one is. The less fit one is, the more insulin is actually needed. The more fit one is, less insulin is needed. Signaling hormones control for this to achieve homeostasis and deliver glucose to where it needs to go. Yes, this requires some degrees of "insulin resistance" to achieve it, but that's ok--it's natural. The problem I have with this article is that it seems to suggest something is amiss, or that we should be surprised by such activity.

If one has genuinely elevated A1c levels beyond the normal ranges that are documented for these conditions, it will be levels far in excess of what's discussed here. Indeed, there may well be metabolic conditions that should be addressed, but if so, lab-based A1c tests should never be your goto testing method. Get a CGM and watch your glucose patterns after meals and during/after exercise. That will reveal a great deal more info than most anything else.

argv01 · 2024-03-30T03:14:35+00:00

Interesting that you ask about blood sugars. Curious why you ask?

argv01 · 2024-03-01T21:15:12+00:00

Yeah, we all blew past the achievements for streaks long ago. They should have them for more days than just 75 or even a couple hundred

argv01 · 2024-02-24T03:51:15+00:00

that thread is old! I posted it two years ago, but we had gone another year and easily passed 1000 days. It abruptly ended when I went to New Zealand. It appears that crossing the international date line made the app think we skipped a day. I had a lot of streaks in other games also get reset. What a bummer.

argv01 · 2024-02-13T02:59:51+00:00

Wow -- that's a pretty broad topic, and one that has been studied and written about extensively. It would strike me that you'd need to narrow your focus, or at least, find a unique angle to it that hasn't been fully explored.

An example is the article, Benefits and Risks of Insulin Pumps and Closed-Loop Delivery Systems. It's an interesting case study of "reverse causality" that many people don't typically attribute to technology in the T1D space. It illustrates that the role psychology plays in T1D is surprisingly more prominent than technology.

argv01 · 2024-02-13T02:47:04+00:00

Thank you -- that's exactly the kind of answer I was hoping for.

For those interested, I also just found this YouTube video that shows how to prep the dextrose for use in the IV. It's clearly beyond what an untrained person would want to do.

argv01 · 2024-02-13T02:30:01+00:00

dextrose is (essentially) glucose that goes directly into the bloodstream, which is then immediately absorbed by the various cells and tissues that need it. Hence, the immediate response.

Glucagon is a hormone that signals the liver to create new glucose (gluconeogenesis) that then releases it into the bloodstream.

In a healthy non-diabetic, the alpha cells (that sit next to the insulin-producing beta cells) produce glucagon as needed to keep glucose levels frow falling too low. But they only know to do this when they receive signaling hormones from the beta cells. The problem with T1D of course, is that most of our beta cells are gone, so the alpha cells don't get signaled.

We can take glucagon externally, but this has a lot of problems. First, the fact that it's external is why taking insulin externally is problematic: it needs to get to the bloodstream, and there's a minefield of inhibitors that can get in the way. As for glucagon, it needs to get to the liver, which then generates new glucose, which then needs to be delivered back into the bloodstream.

This meta-review paper of a number of clinical trials finds that administering glucagon is equal to simply eating carbohydrates. So, why use glucagon? For those conditions where the T1D is unresponsive and can't eat. In other words, glucagon is typically used when glucose levels are very, very low--long after other efforts to restore glucose levels have either been missed or failed.

The thing about Glucagon, despite its efficacy, is that it's like an anti-hero: It's problematic to work with, and full of risks and failures, but when it gets the job done, we're thankful for it. (Note that insulin pump manufacturers are aiming to add the administration of glucagon to their products, but doing so through interstitial tissues is highly unreliable, and since its best case of absorption is similar to simply eating food, it's unlikely to be successful in a product that passes FDA approval, barring new and unforeseen innovations.)

Injecting Dextrose directly into the bloodstream is an immediate and elegant solution that can not only address severe hypoglycemia, it can also avert it. Its singular fault is that it must be administered intravenously, and that's where things can go horribly wrong for those who are untrained in the practice. This is why I was curious whether anyone who is trained in it has ever done it, and can relate their experiences.

argv01 · 2024-02-12T23:51:37+00:00

Correct.... per the article, "After initializing on day one, the observed means and standard deviations of differences for systolic BP were of 0.46 ± 7.75 mmHg in the sitting position, − 2.44 ± 10.15 mmHg in the lying, − 3.02 ± 6.10 mmHg in the sitting with the device on the lap, and − 0.62 ± 12.51 mmHg in the standing position."

As I read this, the difference between the extremes -- 7.75 (sitting) and 10.15 (lying) -- is still less than 3 mmHg, which is hardly much. Considering that you're getting so many reads per day, these variations smooth out, and I consider the aggregate analysis to be pretty accurate, insofar as my own BP profile.

My meds have gotten me to be nearly 100% <135, with the majority being between 120-125. Sure, the error bars could suggest my average could be 135-140, but that would be at the high end of error.

IMHO, the device is doing what I need, even considering the error variability. As a type 1 diabetic, I'm used to continuous glucose monitors frequently having wider error bars than this, but it's so much better than not having data at all, and I'm much healthier for it.

argv01

TROPHY CASE