Last week I shared a summary of the lipid panel results from my blood test following 30 days of eating nothing but ground beef, salt, and water.
This week I’ll be exploring my fasting blood glucose, liver enzymes, and kidney markers from the same blood test.
These are three things folks asked about following last week’s post, so I figured they’d make for a good follow up to last week’s exploration of lipids.
Similar to last week, this discussion will actually be more about my blood test results and what they may or may not mean than will be about my experience with a carnivore diet (which I’ll get to eventually).
I think you’ll find this article to be very enjoyable and eye opening, as I found it to be both of those while researching and writing it.
Oh, and I’m not a doctor so don’t make any decisions based on your own blood test results without consulting with a physician first 🙂
Fasting Blood Glucose
Glucose is the form of carbohydrate that our cells utilize and its level in the blood is strictly regulated.
When our blood sugar concentration rises above baseline, say, after a carbohydrate-rich meal, our pancreases release the hormone insulin to signal to other cells that glucose is available for use or storage.
When our blood sugar concentration falls below baseline, say, as we go about our day without eating, our pancreases release the hormone glucagon to signal to the liver to release its own stores into the bloodstream.
There are other mechanisms involved in blood sugar regulation in different contexts, but that’s the general gist of it.
Recommended fasting glucose levels vary, but generally hang around a minimum of 70-80 mg/dL and maximum 110-130 mg/dL.
I didn’t see too much of a change over the course of this experiment, as my fasting blood glucose decreased from 94 mg/dL to 93 mg/dL.
While this is below the maximum reference ranges mentioned above, it’s still a bit higher than I’d like, as either of these values indicate I could be at risk of Type 2 diabetes.
Prior to this experiment, my blood sugar had always been in the 80s, so I’m not entirely sure why it’s been up in the 90s for these past two tests.
Honestly, I don’t know.
Fortunately, there are a couple of other tests I can get done to get a feel for what my long-term blood glucose levels look like.
One popular test for long-term blood glucose levels is a measurement of hemoglobin A1c (hbA1c), or hemoglobin that’s been modified by glucose (glycated).
However, since hemoglobin might stick around longer on a low-carb diet I may get a false positive, as the longer-lived red blood cells have an extended opportunity for glycation.
Thus, I might consider looking at fructosamine, another marker of glycation.
Obviously, if insulin resistance is my concern, insulin concentration might be a good idea, too 🙂
Next we’re going to talk about two liver enzymes – alanine transaminase (ALT) and aspartate transaminase (AST).
Truthfully, I don’t have a clear grasp of what exactly these two enzymes do, so I won’t do you the disservices of acting like I do.
All I know is that they are considered to be two of the most reliable markers for evaluating liver health.
I also know that I’ve had elevated ALT and AST levels for the past couple of years, but they both saw marked decrease over the 30 days in which I ate nothing but meat, salt, and water.
My ALT decreased from 93 U/L to 68 U/L (reference range 7-56 U/L).
My AST decreased from 65 U/L to 36 U/L (reference range 0-35 U/L).
While it’s possible that their sharp decline is related to my diet, I suspect that their reduction is related strongly to my cessation of all coffee, tea, and alcohol.
The first two had been daily staples of mine for years, and the third is something that I would enjoy off and on – typically in a binging fashion on weekends (just being honest).
Regardless of why, the reduction in these markers appears to be a positive thing, even though they may still be elevated.
Elevated liver enzymes can also be a reflection of strenuous exercise, and I took this test a little over 12 hours after a heavy deadlift and front squat session.
One review I found suggested that, if asymptomatic, further evaluation becomes necessary when enzyme concentrations become double the normal range, which I’m nowhere near.
One thing I’d like to note is that my AST/ALT ratio decreased from 0.7 to 0.52.
One way this ratio is used is in differentiating alcoholic liver disease from non-alcoholic liver disease.
AST/ALT ratio greater than 2 can indicate alcoholic liver disease, an AST/ALT ratio lower than 1 can suggest nonalcoholic fatty liver disease (NAFLD).
Now, typically when people hear about NAFLD they think about carbohydrates and sugar.
If you’re making that same connection, you might be wondering how I could possibly be developing NAFLD if I’m eating a zero carb diet.
Remember in my last post how I suspected my elevated triglycerides and remnant cholesterol were related to my sustained caloric surplus?
Well, get this – NAFLD is also associated with excessive caloric intake.
Additionally, a lower AST/ALT might be an indicator of metabolic syndrome.
Thus, my AST/ALT ratio dropping further and further below 1.0 might be an indication of my energy status (as if I needed liver enzymes to tell me what the scale already has been).
Now, there are plenty of other markers associated with liver health, but they were all either within normal ranges or didn’t change significantly, so I’m not going to comment on them for now.
Creatinine is a byproduct of the breakdown of creatine phosphate in the muscles.
Urea is produced in the liver as a byproduct of protein metabolism.
Both are filtered by the kidneys through what are called glomeruli, and then excreted.
Blood creatinine and blood urea nitrogen (BUN) concentrations can be used as measures of kidney function.
My creatinine concentration jumped from 1.12 mg/dL to 1.52 mg/dL (reference range 0.5-1,2 mg/dL).
My BUN concentration increased from 34 mg/dL to 46 mg/dL (reference range 3-20 mg/dL)
At first glance, both of these suggest I may have kidney issues.
Thus, my high protein diet and my training could certainly be playing a role in these elevated values.
Oh, and since you may be wondering, while a high protein intake might be a bad idea for existing kidney disease, it does not appear to cause kidney disease.
Additionally, there’s a measure called glomerular filtration rate (GFR), which is a measure of the blood that passes through tiny filters in the kidneys called glomeruli.
I didn’t get this measured, but we can use my BUN and creatinine levels to estimate it (eGFR).
My eGFR dropped from 86 mL/min/1.73m2 to 60 mL/min/1.73m2.
I didn’t get my urine tested, but I do have a couple of signs of kidney disease – I have been a bit more tired and I have had a poor appetite.
However, considering that I’ve been eating a zero carb diet, training hard, eating a caloric surplus, and may not be getting enough salt (I’ll elaborate on this on a future post), there are plenty of other variables that could be contributing to the low energy and poor appetite.
Also, at least one review suggests that eGFR is not a reliable replacement for measured GFR (mGFR).
I’m definitely glad to have this on my radar, and depending on what trends I observe moving forward with my blood markers and symptoms, a urinalysis and mGFR might not be a bad idea.
On a side note, I observed that my uric acid concentration increased from 4.9 mg/dL to 6.8 mg/dL (references range 3.5 – 7.2 mg/dL).
As mentioned above, though, I plan to write about the whole salt thing a bit later on after I have some time to play around with it a bit.
Does this increased uric acid concentration mean that I’m going to develop gout?
While it’s generally accepted that uric acid and purine-rich foods like beef contribute to gout, one paper mentions that only 5% of individuals with uric acid levels higher than 9.0 mg/dL develop gout and that other factors play a role.
This suggests to me that it might not necessarily be the high levels of uric acid that are the issue, but perhaps impaired clearance, prolonged residence time, or other factors contributing to crystallization within joints.
Might be a good subject for another blog post.
The two things that most caught my eye were my fasting blood glucose of 93 mg/dL and my AST/ALT ratio of 0.52.
These markers, along with the fact that my TG:HDL ratio and remnant cholesterol both increased over their previous readings, might indicate an underlying developing insulin resistance or metabolic syndrome.
While you might think that insulin resistance is odd on a zero carb diet, I’ll reiterate that I am eating at a caloric surplus, which (as mentioned last week) is a driver of insulin resistance.
Aside from that, the kidney markers definitely caught my eye, but I’m going to hold off on looking into that further until my next physical in a couple of months unless I see any progression of symptoms.
I’m not quite done with this experiment, as there are a couple of small tweaks I’ll be making over the coming months to see how they affect my labs.
Next week I’ll wrap up my exploration of this set of blood test results, and will then move on to other subjects I’ve had on my “to write about” list for quite a while now.
Until then, have a most excellent week!