I have to confess that I don’t get my bloodwork done as often as I should. For type 2 diabetics, HbA1c is supposed to be done every three months and annual testing is recommended for lipids and kidney function as is an annual eye exam for signs of diabetic retinopathy. In my case, nine years post-diagnosis, I get my A1c done along with lipids and kidney function every 18 – 24 months, at best. My last eye exam was three or four years ago and I don’t test my fasting sugars at all. Is this irresponsible? Am I setting a poor example? Perhaps. But, before you judge, have a look at my most recent results:
Fasting glucose 5.7 (3.3-5.5) mmol/L
HbA1c 5.7 (4.5-6.0) %
Sodium 141 (134-145) mmol/L
Potassium 4.5 (3.5-5.0) mmol/L
Urea 6.5 (2.5-9.0)
Creatinine 73 (70-120) umol/L
Estimated GFR 97 (>60) mL/min
ALT 21 (<60) U/L
AST 23 (<35)U/L
CK 102 (<300) U/L
Total Cholesterol 5.82 (2.00-5.19) mmol/L
LDL Cholesterol 3.49 (1.50-3.39) mmol/L
HDL Cholesterol 2.05 (>0.90) mmol/L
Chol/HDL ratio 2.84 (<4.9)
Triglycerides 0.62 (0.45-2.29) mmol/L
Apolipoprotein B-100 0.95 g/L
TSH 2.4 (0.38-5.5) mU/L
C Reactive Protein 0.5 (<5.0) mg/L
What does it all mean? Well, according to the guidelines, my fasting glucose being slightly elevated means I am at risk for type 2 diabetes. This, coupled with the fact that my HbA1c is also on the high side of norma, if I were a non-diabetic, would indicate risk of diabetes and mandate further testing like an oral glucose tolerance test. In my case, however, since I am already diagnosed with type 2, those results are actually pretty good. The target for HbA1c in diabetes management is <7%, far higher than what is considered normal. Why is this? My opinion is that this reflects a tendency to move the goal posts when we can’t get better values with the conventional therapies. For people who use drugs and/or insulin, to get better values than that is difficult and possibly dangerous. In the ACCORD trial, where they threw the pharmaceutical kitchen sink at people to try to get better values, they actually ended up killing more people than with the conventional more relaxed approach. So, there is a tacit admission of defeat in this target in my opinion with physicians now believing that it is perhaps even dangerous to try to get down to normal HbA1c values in their patients. For those who understand that diabetes can be managed quite well by carbohydrate restriction, the achievement of normal HbA1c values is not surprising at all and certainly not dangerous.
My elevated fasting glucose suggests that I still have hepatic insulin resistance but not too severely. It certainly isn’t leading to an elevated HbA1c and I don’t think I am experiencing hypoglycemia, at least that I can detect subjectively, so I am not too concerned with that one abnormal value.
As you can see, my kidney function is fine. My creatinine, which tends to rise if kidneys are diseased, is actually at the low end of the range, which is good. My glomerular filtration rate is also well into the normal range. That is good to know as kidney failure is a common complication of type 2 diabetes. Mine appear to be perfectly fine.
Ditto my liver. Based on these liver function test results, my liver does not appear to be under any kind of stress. So far, so good.
Now the interesting part, the lipid profile. Here is where I deviate a bit from the norm. My total cholesterol, LDL (so-called bad cholesterol) and HDL (good cholesterol) are all elevated. The numbers for cholesterol and LDL are not terribly high but if I were being managed according to the book, I would be a candidate for statins based on these results alone. In case you didn’t already know, I am not a big fan of statins, for myself or anyone else. I find the science is full of contradiction and I suspect that the evidence that statins are beneficial may be due to their anti-inflammatory effect rather than their effect on LDL.
Let’s look a little closer at my lipid results. My HDL is way up there, which is good because it turns out that the best predictor of cardiovascular risk is actually the Cholesteral/HDL ratio. In my case, I am well down into normal territory with that value. And my triglycerides are in the basement. This is good and is a common result of carbohydrate restricted dieting. Some argue that the ratio of HDL to triglycerides is a better predictor of CVD risk than the cholesterol ratio. If that is the case, I am in excellent shape here.
I also got an ApoB done for the first time. On it’s own, ApoB is supposed to be a marker of CVD risk. The ratio of ApoA to ApoB is supposed to be as good or better than the cholesterol/HDL ratio as a predictor. I didn’t get that done. Perhaps next time. ApoB also tells you something about the particle size of your LDL. Smaller particles are thought to be more dangerous. The lab didn’t report a normal range for ApoB but, digging around in the research literature, it is apparent that for men ApoB should be somewhere between 0.55-1.25 g/L. In a Framingham Offspring study, it was found that 1.00 g/L was at the 50th percentile and that men whose ApoB was greater than 1.20 had elevated CVD risk. With these data in mind, I am happy with my ApoB of 0.95 g/L.
As you can see, my thyroid appears to be functioning normally.
And, last but certainly not least, my CRP is very low. This may, arguably, be the most important test of the whole lot. We know that this whole range of chronic diseases, from obesity to metabolic syndrome to type 2 diabetes and cardiovascular disease, is underpinned by inflammatory processes. Jeff Volek et al, has been showing that if you follow a range of inflammatory markers, a low-carb diet delivers a powerful anti-inflammatory effect. We also know that these chronic conditions belie a state of high oxidative stress, as well. Oxidative stress and inflammation go hand in hand. We know that it is in that high inflammatory/high oxidative stress milieu that oxidization of cholesterol, damage to cell membranes, injury to blood vessels and interference with metabolic functions occur and that these drive chronic disease. If oxidative stress and inflammatory levels are low, the potential damage of higher LDL or elevated glucose is much less an issue. As I said earlier, it is perhaps the inflammation reducing effect of statins that delivers a benefit. Evidence in support of this idea can be found in the JUPITER study where a cohort of men with normal LDL but elevated CRP clearly benefitted from statin therapy.
I am not advocating statins, however, I am advocating carb-restriction. No drug, or combination of drugs, can deliver the range of therapeutic benefits that these blood tests demonstrate. I have a slide I use in my lectures which lists the 20 classes of drugs used to treat metabolic syndrome and type 2 diabetes. Meanwhile, one simple dietary change delivers a better result. If you subscribe at all to Occam’s Razor, you will know which is the right therapy.
These test results are consistent with my previous tests since I have been following a very low carb diet. Now, can you see why it is perhaps not irresponsible for me to test infrequently? Can you also see that, if more type 2 diabetics were to follow a low-carb diet as I do, there would be tremendous savings to the health care system, not just in testing but in reductions in complications as a result of improved management? At some point, the evidence will become so overwhelming that this will have to become the first line treatment. Or, the cost of the failure of the conventional approach will grow to the point that the current system of care will collapse under its weight.
I’ll report back again in a year or two … or three.