Probably less. Coffee is non negotiable.Spoken like a true 99% carnivore
You should start a log in the strong food logs sub forum, that way you don't have to wade through the rest of the posts in this thread.Carnivore Day 1
Breakfast: 4 fried eggs & 5 strips of bacon
Lunch: 3 hamburger patties with pepper jack cheese & a splash of tabasco on each
So far, so good, but dinner awaits.......maybe I will have to hit Wendy's and grab 4 more hamburger patties.
That’s actually very interesting. I’m curious of your observations.Currently wearing a continuous glucose monitor. I was going to wait until next time I saw my doc, but then a friend offered to prescribe me one and I couldn't pass it up. I'll post an actual write up here in about a week, but for now I just want ya'll to know that I have quantifiable proof that a toddler tantrum is more stressful than heavy snatches. That is all.
Currently wearing a continuous glucose monitor. I was going to wait until next time I saw my doc, but then a friend offered to prescribe me one and I couldn't pass it up. I'll post an actual write up here in about a week, but for now I just want ya'll to know that I have quantifiable proof that a toddler tantrum is more stressful than heavy snatches. That is all.
Pretty cool analysis Matt. Thanks for sharing.Data: Food and Fasting
Take a look at the following two blood glucose tracings. Specifically, the first 18 hours of each one. One of them is of a normal day, one of them is the last 18 hours of a 26 hour fast (the asterisks just note an actual blood draw).
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The bottom graph is the fasting day. Both graphs have two exercise inflections in it (I jog about a mile to/from class), and the general trends are about the same. This was one of the really neat things I saw. There’s not that big of a difference between a fed or fasted state for me, assuming stress and activity levels remain constant. The biggest difference I did see was that my glucose didn’t get quite as high in response to exercise. My AM jog to class didn’t cause as much of a jump, and I did a bit of an experiment right after I got home. I did three sets of 15 kettlebell swings. Normally that kind of work would give me a sensor reading up around 110 mg/dl, but I only got up to 102 on the sensor. I imagine this is what things would look like if I dropped my protein intake and did more of a keto approach. Less of a glucose response to stressors. I think the extra protein allows my body to be a little more generous with the glucose. Maybe that’s good, maybe it’s not.
I will point out, based on the fact that I can reliably get my fasting blood glucose over 100 (granted, that’s in response to exercise), I could qualify as pre-diabetic. I don’t know how many doctors would give that diagnosis when my average blood glucose is 87 and my normal fasting glucose is around 80-85, but it still technically meets the diagnostic criteria. That being said, that diagnostic criteria assumes that a measured fasting glucose >100 indicates a fasting glucose that is consistently >100, and is based on the study of a population that is very insulin resistant and, by definition, has poor blood glucose control. I don’t see my own blood glucose response as being pathological. I think it’s kind of neat that my body can just turn my glucose levels up or down as needed, assuming I ate some time within the last day.
So why did I want to get a CGM in the first place, besides general nerdiness? Because I wanted to figure out what the deal was with my HbA1c. I’m going to explain how the HbA1c test works, so if you already know, skip the next two paragraphs.
Hemoglobin (Hb) is in your red blood cells (RBC’s). Glucose floats around in your blood, and gets into your RBC’s, where it chemically interacts with Hb. Essentially, the glucose sticks to the Hb. This is a normal, random chemical reaction called glycation. Glycation happens at a very reliable rate. It happens to pretty much all the proteins in your blood. Theoretically, we could measure glycation of albumin, sex hormone binding globulin, or any other protein. The two ways to affect glycation rates are 1) increase or decrease glucose levels, and 2) increase or decrease the amount of time the protein spends in the blood (if a protein is in the blood longer, it will react with more glucose molecules and get more glycated). If a protein is highly glycated, we know it’s been in a high-glucose environment for a normal time, it’s been in a normal glucose environment for a long time, or some mix of the two.
We measure the glycation of Hb because your RBC’s live for about 90-120 days. There are plenty of other proteins that live for predictable lengths of time, but 90-120 days is useful for diabetes monitoring. You get your HbA1c every three months when you see your doctor; simple. We’ve collected enough data that we can look at how glycated your Hb, assume that we’re looking at your 90 day average, and work backwards to see what your average blood glucose levels have been. Now, it’s not ideal. If you’re a poorly controlled, insulin dependent diabetic with a lot unhealthy highs and lows, your HbA1c can look alright. But anyone on insulin should also be checking their blood sugar multiple times a day, anyways. It’s usually a good lab test for telling us how someone’s doing in a very general sense.
So what’s the big deal with my HbA1c? Well, my last one was 5.5. The one before that was 5.4. The one before that (pre-carnivore) was 5.0. Now, 5.0 gives me an average blood glucose of 97. Not bad. I was doing 16:8 time restricted feeding, with one large serving of starch per day, and otherwise keeping carbs to a minimum (with the exception of an irresistible sugary treat 2-3x/week, because sugar is like crack and starch is a gateway drug, at least for me). I go carnivore, and my “average” jumps up from 97 to about 110. What the hell!?!? Having a HbA1c of 5.7 (average blood glucose=117) meets diagnostic criteria for pre-diabetes, for crying out loud!! So what happened? Did the near total elimination of carbohydrate from my diet result in occasional bouts of raging hyperglycemia?
No. Obviously. As I stated my average blood glucose over 2 weeks was 87, which translates into a HbA1c of 4.6. Definitely not pre-diabetic. What gives?
Let’s go back to the formula. What causes glycation to increase? Either an increase in glucose levels, or an increase in time spent at those glucose levels. I feel pretty confident in saying that my glucose levels decreased. That means that the time must have increased. In other words, my RBC’s are hanging around for considerably longer than expected, allowing the Hb to get more glycated than usual. Why would that be?
It could be for a variety of reasons. For instance, the spleen is primarily responsible for clearing out old, beat up RBC’s, so maybe my spleen shut down (people without spleens have terrible HbA1c’s). Doesn’t seem likely. There’s another explanation, though. Oxidative stress. RBC’s are exposed to pretty high levels of oxidative stress. This is one of the ways that they get beat up (besides getting smashed through capillaries). Theoretically, if we reduce systemic oxidative stress, we could extend RBC life span, and “artificially” elevate HbA1c. How would we know if we reduced oxidative stress? Well, the most obvious way would be to look at inflammation. Oxidative stress is a major cause of inflammation, so if it’s reduced, inflammation ought to come down, too. Well, we know the carnivore diet reduces inflammation in most people…So now things are coming together. Carnivore diet -> reduced oxidative stress -> longer RBC life span -> more time for Hb to get glycated -> artificially elevated HbA1c.
To be fair, I’m not hating on the HbA1c test. It was made for use in diabetic patients, who have notoriously high levels of oxidative stress. The assumed RBC life span for someone with metabolic dysfunction is pretty solid. The test is totally valid when applied to the patient population it was designed for. Turns out, context matters. Who knew!?!?
So what can I pull from this?
That’s what I got. But what do I know, I’m just a pre-diabetic knucklehead who’s going to die of colon cancer any day now…
- Stress matters for metabolic health. A lot.
- My levels of oxidative stress likely went down when I changed my diet. Either that or my spleen turned off. Because, despite my average blood glucose levels going down with the carnivore transition, and my HbA1c went up. This indicates a significant increase in RBC life span, for some reason or another.
- I need to watch out how I apply HbA1c to healthy people in the future (you know, when I grow up, and have patients). I mean, I don expect an error of XXXXX in everybody, but if someone looks healthy, has otherwise good labs, and has an HbA1c of, say, 5.4? Maybe I shouldn’t sweat it. A 5.4 in someone who obviously isn’t healthy, on the other hand, is something I’m going to keep an eye on. Again, it would appear that clinical context is an important part of individualized treatment. Who woulda thunk?
- Not sure when I’ll get another sensor and run through the process again, but when I do:
- I think I’ll spin up my Elite HRV app again and see what connections I can draw
- If I get a Keto Mojo monitor from Santa this year, I would also like to take a look at what my ketones are doing
- I would like to do the next run at a time when I’m at my normal, healthy baseline for the majority of the two-week period, instead of hacking like a smoker and abnormally stressed out over school for a large portion of it
Very cool stuff and tons of food for thought...Glycation happens at a very reliable rate....This indicates a significant increase in RBC life span, for some reason or another.
Interesting that you can correlate a stressor and subsequent release of glucose like that going about general events in your life.Stress matters for metabolic health. A lot
I think so. I think CRP can be a very useful marker to track, and it can be an early indicator that things are not as they should be. I've had mine done for my last two blood draws, and it wasn't measurable (less than .2) either time, which is right where I want it. I didn't have the foresight to get a pre-carnivore CRP, so I don't know what it was before. If it had been higher, that would really have supported my theory about reduced oxidative stress, but who knows. CRP is a little tricky, though. It tells you if you have inflammation, but not why. If you're developing a cold, healing from an injury, or otherwise dealing with some sort of physical insult, CRP will likely be elevated. In other words, having a low CRP when you "feel normal" is a good sign. Having a single high CRP, especially if there's something else going on, doesn't tell you much. If you have five elevated CRP's in a row, then maybe you can't blame it on the colds anymoreMatt - if you paired your HbA1c test with a C-reactive protein test would that add any insight?
1) There have been quite of few cases of people managing autoimmune issues, in part or in full, using a carnivore diet, nearly carnivore diet, or animal based keto diet with lots of fasting.Jordan Peterson credits a beef only diet (and really that means 100% beef) as causing remission of autoimmune diseases in his family, although I've not seen a sensible scientific analysis of why that might be the case
You bring up a good point that I should probably explain a little more clearly. The glucose that get stuck to Hb doesn't end up getting used as fuel. Glucose is floating around freely in the blood plasma, ready to get pulled in by whatever cells need it (ketones are the same way). The RBC's are bathed in the glucose-rich plasma, and take up glucose to use for fuel. Think of a RBC as a sack of water that's floating around in more water. The concentration of glucose inside the RBC ends up being very similar to the concentration of glucose outside (in the plasma). Most of the glucose that goes into the RBC's gets used to fuel cellular processes, but some of it sticks to the Hb. That's the glycation that we measure.Is it even possible that RBC glycation has an efficiency rating based on number of chemical reactions the particular cell has experienced?
Are ketones transported in a similar manner?
Is this the only way glucose is transported to working muscle?