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.
Like you, I live north of the 49th. I was wondering if you have any pointers on how to convince my doctor to test my apoB and C Reactive Protein? NMR and VAP testing stateside just isn’t the card for me right now.
Thx for the time.
Dr Jay’s Reply:
If you are perceived to be at risk for CVD, a CRP is justified. Risk can be a family history of CVD events, if you have type 2 diabetes or if you have other markers of risk such as metabolic syndrome. Your age will also be a factor. If none of this applies to you, your doctor is going to resist ordering a CRP. Another more crude measure of inflammation is your white blood cell count. In Framingham, even within the normal range, elevations in WBC signalled increase CVD risk (mine is at the low end of normal, BTW). Lots of other things, like colds and minor infections, can elevate your WBC count so don’t panic if it high. If nothing else is going on and you have a nice low normal count, that is another reassuring indicator.
WRT to ApoB, I am not convinced yet that it adds a lot to what can already be deduced from the other lipid tests. It appears that it is currently being used mainly to track the progress of people on cholesterol lowering therapy. There is an argument that ApoA/ApoB ratio is a better predictor of risk than Cholesterol/HDL but the difference may not be all that great. Probably the most important markers are HDL and triglycerides. You want a high HDL and a low TAG. If you have that, and if your Chol/HDL ratio is good, you shouldn’t worry too much about the more esoteric tests.
Congratulations on the great metabolic control!
As you say, “tight” glucose control in the ACCORD trial was linked to higher cardiovascular deaths. I note that rosiglitazone was one of the drugs used in the effort for tight control.
Rosiglitazone within the last year was pulled from many markets and tightly restricted in the U.S., because of concern for heart toxicity.
-Steve
Dr Jay’s Reply:
That is correct. It raises the question of how much of the excess mortality in ACCORD could be attributable to rosiglitizone alone.
Thank you very, very much for the information Dr. Wortman!
I guess that’s the rub now. LCing has brought me from the brink of metabolic syndrome where these tests might be useful for my GP.
Right now my sugars, lipid panel are stellar by IGT or ‘normal’ definition (I’m also sporting a 3.1 with my WBC.) But if I let my LDL rise to levels like yours (I sit at 1.2,) my GP starts musing about simvastatin and ASA as per the CDA guidelines on the matter. I could just refuse his advice on the matter, but that wouldn’t be very respectful of his expertise. Making the argument about particle size though, might at least convey that it’s not just a flippant decision.
Dr Jay’s Reply:
At this point in time, there is little education directed at physicians to equip them to manage LCHF dieting, unfortunately. Even though the American Diabetes Association guidelines have endorsed LC diets as valid for weight loss for diabetics, nobody has developed a clinical practice guideline or other officially-sanctioned guide for physicians whose patients might want to try this option. I am working with some colleagues to try to correct this but it is a slow process. There is still a fairly large constituency out there that outright opposes this approach, too, which doesn’t help. At some point we will make a breakthrough. In the meantime, patients like you will know more than your doctors on the subject.
Your trigs/HDL ratio is Very Very Silly. I predict that you will actually get younger as you age!
Here in the UK I was originally told I was “not diabetic” because my GTT “only” hit 10.8 and not 11.1, despite my symptoms. However being that severely “prediabetic” my GP was originally treating me as if I actually was diabetic.
This has now been stopped, probably by accountants. I am no longer permitted an A1c. This doesn’t bother me overmuch as it’s always 5.6. Like you I don’t test as much as I did now I have largely got a working diet. I test when eating out, and every so often I will run a whole day to ensure nothing has changed.
What *does* bother me a lot is that I have now been told I cannot have any more lipid panels “we don’t test your cholesterol again after you’ve been put on a statin” said the nurse. Yes I admit I take 10 mg simvastatin, it drops my LDL from 4 where they panic even if I don’t, to about 2.6 and appears to have no side effects *for me*. I like to see what has and hasn’t changed as I believe the ratios particularly are indicators of metabolic function rather than directly related to CVD risk, which is why using meds to change the results doesn’t have the same effect as actually changing the metabolism through diet.
The latest crap science here is that diabetes must now only be diagnosed by A1c which must be over 6.5. “Prediabetes” needs an A1c over 6 and does not need to be notified to the patient. My late mother was assured she was “not diabetic” despite routinely running postprandials from 11 to 15, because her A1c was “only” 6.4. Now I “am not and never have been” prediabetic.
Oh and Type 2s are no longer permitted meters or strips.
I will take two pictures to the grave with me. One is of a GP inspecting my mother’s feet for gangrene, presumably considering amputation (she’d already been put forward for dialysis) while telling her to eat “lots of brown bread, and fruit, that’s really good”. The other is of a different GP the size of a bungalow assuring me that “everyone has to eat carbs or you have no energy”. How I stopped myself from retorting “works for you, does it?” I’ll never know
http://www.trackyourplaque.com/blog/2008/12/flat-tummy-or-why-your-dietitian-is-fat.html
Current NHS statistics show an increase in amputations for Type 2s. This can only increase with the New Diagnostics. Can you say saving pennies in order to save pounds?
DISCLAIMER: these are GPs, not a few hospital doctors and consultants etc. are much more clueful. One such suggested that what we are currently seeing is accelerated ageing even in young people. I pointed him to Peter
http://high-fat-nutrition.blogspot.com/2008/07/age-rage-and-ale-oxldl.html
and a bunch of following posts
Hi Jay.
I had read from several reports that CVD risk poorly correlates with LDL. (That is, LDL is not a univariate indicator of CVD risk.) The reason, it is thought, is that small dense LDL are the LDLs that oxidize and lodge in arteries, whereas large buoyant LDL are not a CVD risk.
Research has found an important univariate indicator, namely, the ratio of triglycerides to HDL, which appears to be a good proxy for direct measurement of the amount of sdLDL (a lower TRG:HDL ratio indicating less sdLDL). [ See Small dense LDL particles – a predictor of coronary artery disease evaluated by invasive and CT-based techniques: a case-control study, Lipids in Health and Disease 2011, 10:21] Blood tests in the US indicate the degree to which the LDL profile is pattern A (large, bouyant) or pattern B (small dense), but not here in Canada yet.
I resume that the reason TRG:HDL is a good proxy is that sdLDLs are LDLs that were packed with triglycerides instead of mostly cholesterol. Cholesterol is an anti-oxidant, so LDLs without cholesterol are more prone to oxidation. High HDLs presumably gather sdLDLs and take them to the liver. So high HDL is very good and low triglycerides is very good.
Without a direct measurement of sdLDL in Canada, it seems to me the apo B to LDL cholesterol ratio should be an important marker. The reports I have read say Apo B indicates the number of LDL particles. It follows that the higher the average cholesterol per LDL particle and the lower the average triglycerides per LDL particle, the lower the CVD risk. What I have been doing for the past couple of years is calculating ratios of LDL/Apo B and TRG/Apo B from my results.
The interesting implication is that more LDL while lowering triglycerides increases the LDL/Apo B ratio and lowers the TRG/Apo B, which shows higher average LDL size, lower sdLDL probability and therefore lower CVD risk. (The raw Apo B score is not univariate because the LDL particle can either be full of cholesterol or triglycerides.) Lacking Canadian testing for pattern A or pattern B, I compared my LDL/Apo B average to Gary Taubes’s, who has posted his numbers on his blog. He is well into pattern A (large buoyant) and my LDL/Apo B is higher than his and my TRG/Apo B less than his, so I deduce that I must also be well within pattern A.
A high-fat, low-carb diet, from my observations, decreases TRG (good), increases HDL (good) and to the extent it increases LDL and APO B, the average LDL per Apo B is increased, which should not increase CVD risk. My physician is puzzled that my LDL is high side but every other indicator is exemplary. Indeed, a normal TRG:HDL ratio (Canadian measurement) is between 1.0 and 2.0. Since going high-fat, low-carb, mine has dropped to around 0.25, well into the “ideal” range for minimal CVD risk.
As you have noted, high-fat, low-carb is a metabolic game changer and the interpretation of tests needs to be reconsidered.
Murray
Hi Dr Wortman,
Congrats on the metabolic control..
I was wondering if you could recommend a good Naturopathic Doctor in or around Vancouver, i want to start the low carb diet but due to previous surgeries(ileoanal reservoir procedure), i feel more secure if i follow the diet it with the guidance of a naturopathic doctor, so that i can get enough electrolytes which are very important as i don’t have most of my colon..
I have diabetes 2 and high cholesterol
thanks so much for the previous reply too..
Kind Regards,
Sandy
As for your elevated FBG level, I have the same thing, have been LCHF since 3/21/10 after finishing GCBC.
HYPERLIPID on HIGH FASTING BG LEVELS ON LCHF
http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html
I think he explains this (he has same issue but his HbA1c is very very good; mine is not great at 5.8).
(1) Had you heard about Hyperlipid’s explanation?
(2) Also, how important IS exercise? Lost my weight without it, “a la Taubes”… Could it help my HbA1c ?
Dr Jay’s Reply:
I had not seen Hyperlipid’s explanation but it is consistent with my understanding of the relationship between fatty acids and glucose as fuels for skeletal muscle. It makes sense that, if the body is resorting to gluconeogenesis for its glucose needs, that it wouldn’t want the muscle cells to burn it up when it is needed elsewhere (CNS, lens, sperm, renal cortex), especially when the muscle is happy burning fatty acids. So, the idea that the muscle cells would withdraw insulin receptors when fatty acids are abundant is perfectly logical. On the other hand, why would gluconeogenesis continue when blood sugars were starting to get high? Insulin should rise and shut off gluconeogenesis in that event. I think insulin resistance in the liver is part of the answer but I don’t know why it wouldn’t correct with LCHF. In either case, a FBG under 6 for a type 2 diabetic on no meds is not such a bad result, especially when the HbA1c is also under 6. Compare those values to what most people are able to achieve on meds and the “diabetic diet”.
As to exercise, yes, I think it would get your HbA1c down a little more. Resistance exercise seems to be the best for improving insulin resistance in the muscle. It appears that burning up the stored glycogen causes the muscle to want to let some glucose in to restore glycogen supplies. I have been doing high-intensity interval training lately and will see if that improves my HbA1c next time I get it checked.
Two things I’ve observed: in not a few diabetics their A1c does not bear a direct relationship to their spot BG values. Some have an A1c that they can accurately predict but in others it is reproducibly high, or low compared to what it “should” be. In some cases fructosamine appears more “accurate”.
Not a few nondiabetics eating low carb/Paleo etc.also show a higher A1c than “expected”.
This may be down to blood cells living longer (or shorter) than average, or may be down to some other factor relating to a body not being flooded with excess glucose and insulin.
Growing more muscle produces more GLUT-4 receptors. Using the muscle translocates them near to the cell surface ready to gobble up glucose. My A1c hasn’t shifted much, it’s still higher than it “should” be, but the glucose variation has reduced significantly and on occasion when eating out I can stuff my face with more carbs than I expect (not always though).
I’m with Mark Sisson
move slowly a lot
run very fast occasionally
lift heavy things
much more functional than doing excess amounts of cardio then going face down in the carbs
Dr Jay’s Reply:
I discussed cardio vs resistance exercise with Fred Hahn at the Nutrition and Metabolism meeting in Baltimore earlier this year. He says the same thing, that it is the density of mitochondria that is the most important factor. After reading “Sugar Nation” by Jeff O’Connell, I decided to try high intensity interval training instead of my usual cardio workout. So far so good, – my waist shrunk by about an inch but the real test will come when ski season starts a couple of weeks from now. I will keep you posted.
Peter at Hyperlipid has dug out some interesting material on mitochondria, and I have J Stanton at gnolls.org on my reading list.
Soon as I finish this coffee I’m off out for a prolonged walk in the winter sunshine, followed by some heavy gardening or box lifting.
When (hypothetically) my mitochondria were looking only to glucose for fuel, my BG and energy levels were all over the place. Now they have (re)learned to burn fat and ketones everything has evened out.
It took not only high carbs but also low fat (mostly Omega 6) to actually make me gain weight, predominantly belly fat.
The interesting bit is that during my high carb days I could double my strength without any apparent change in my muscles (I could halve it again even more easily). Now my muscles not only get stronger, they get appropriately bigger.
Also I no longer “bonk” and need to carb up every few hours. A Type 1 friend maintains his A1c mostly below 5 with a low carb diet, about 20 units of insulin and endurance level cycling, and likewise finds he no longer “bonks” unlike his carb-fuelled nondiabetic companions.
http://www.nutritionandmetabolism.com/content/1/1/2
Stephen Phinney’s take on the subject.