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The Results Are In!!

@Jasperville

I subscribe to a non-scientific personal theory that the more haemoglobin we carry in our red blood cells, the higher our HbA1c will be. The HbA1c measure the glucose in the haemoglobin. The more haemoglobin we have, the more glucose will be able to bind to it. And vice versa.

When we have a full blood count the amounts of red blood cells, and the amounts of haemoglobin are counted. RBC is the number of red blood cells. MCH is the amount of haemoglobin. (MCH = mean corpuscular haemoglobin). My MCH has always teetered on the edge of the higher range, most often just over it. I blame this for my much higher than expected HbA1c results compared with rigorous finger prick testing and wearing a Libre sensor. My current HbA1c is 42, equated to an average of 7mmol/l. As I hardly ever see 7s - maybe once a week I may see up to 7.5 for half an hour after my Sunday roast - I cannot comprehend how this can create an average of 7. This is why I blame my MCH values and the large amount of haemoglobin I carry in my red blood cells. By the way, all other blood counts are bang on normal, and my meter is plasma blood calibrated, so the readings are equivalent to any plasma tests.

Your theory also holds true. If you have spikes to 10 sometimes, but spend much of the rest of the time in the 5s, those spikes will cause a lot of glucose to stick to your haemoglobin and it stays there. It doesn't fall off simply because there are mostly 5s. The lower readings don't negate the few high ones.
 

I think we're in agreement. The current TG, while well under the threshold of clinically bad, is out of step with other indicators, because they're all between OK and great (what experts currently consider OK to great). Eg, the systolic blood pressure is close to the median value for the population, and HDL value is in the top quartile. Yet another surprise is the contrast between the percentile positions of two lipid components, HDL and TG.

I affrm my previous post. If I were dissatisfied with the value of a marker for a disease (cardiovascular disease in this case), a good next step would be to test directly for the disease. This is a reasonable step for old people. Past 60, age is the strongest risk factor for CVD.

Thank you for making me aware of Sikaris. Professor Gerald Reaven, who developed the theory of the "metabolic syndrome" (cardiometabolic syndrome, insulin resistance syndrome) is a pioneer of the belief that TG are a key villain in atherosclerosis and a powerful risk factor for diabetes. Does Sikaris say 1.5 is actual near optimal for TG?

Having TG near 1.4 might be partially due to genetics. Moreover, it's imaginable that a TG that high would be dangerous to some individuals and safe for others, due to individual genomic differences. For comparison, there's a gene mutation that causes people to have fasting glucose between 5.5 and 7.0, but the condition on its own is benign and nonprogressive. When tested for fasting glucose, these people would qualify as having IFG, they'd be instructed on the danger of progression to diabetes, when in fact they are in no danger. This condition is called MODY 2.
 

It's actually the reverse. Look up interferences HbA1c.

But you're on to something: the A1c will only be accurate at a narrow range of haematologic values, because it's a measure of the progress of a slow chemical reaction, namely the joining of a molecule of haemoglobin to a molecule of glucose. The A1c measures (in principle at least, leaving aside certain interferences) the percent glycation (joining to glucose) that has occurred after 12 weeks. Its old unit of measurement (with values like 5.0, 6.5) was the actual percentage. If you distribute 10 pie slices among 20 people, one slice per person, then 50% will be served. 10 slices to 15 people, and now 67% will be served. So if your red blood cell count or your total haemoglobin are on the low side -- like mine -- A1c will be falsely high.

The topic we are touching on is chemical reaction kinetics, which is reaction speed. Between two people with identical glucose concentration but difference in available haemoglobin, the person with less haemoglobin will have the higher A1c, all other things being equal.
 

I agree, with reference to the second article. I only read the abstract. But it's certainly true that this idea of CVD risk increment with A1c increments was never meant to be taken as valid for all values of glucose, rather just for excessive values of glucose. This can be seen from the famous DCCT graph of the risk of microvascular complications -- CVD is the macrovascular complication -- and similar graphs. (Google on dcct microvascular complications > Images.) The DCCT graph has been criticised for being the product of a study of Type 1 patients, when the vast majority of diabetics are Type 2. On the other hand, whenever I read tutorials on diabetes, it'll say that research has found the same trend lines for Type 2 patients too.

Look at this graph from a different study, Figure 1 at http://www.who.int/diabetes/publications/report-hba1c_2011.pdf. Its purpose is to compare the three diagnostic tests. In science and engineering these curves with this shape are sometimes called "knee curves". Figure 1 is depicts the rise in the risk of diabetic retinopathy (specifically in its nonproliferative stage, which is the earlier stage). This and similar graphs are where the diagnostic cut points of A1c 48, fasting plasma glucose 7.0 came from.

The point is that the risk below A1c 6.0% (42) is essentially a flat 0%. I'm sure the graphs of risk for CVD look the same.
 
KevinPotts said:
Eating for a week before the test.


Sent from my iPhone using DCUK Forum
Click to expand...

That's interesting, as I remember you had at least a steak then, and possibly other sources of saturated fats?
So its possible the week of food immediately prior to the review was the heavy influence on your trigs, and LDL after your fast?

Even Hendrik seems to be back tracking on high LDL and trigs now.

https://drmalcolmkendrick.org/2016/04/25/what-causes-heart-disease-part-xii/
https://drmalcolmkendrick.org/2016/07/12/what-causes-heart-disease-past-xviii/
 


Not true, read
http://journals.aace.com/doi/pdf/10.4158/EP161209.CO

It varies depending on what causes the anemia.
Many will give a low Hba1c.
 

Just touching on your question on optimal, I don't believe I have ever heard an optimal level, aside "less than", then the amount varying, depending on who is making the statement it almost seems. Professor Sikaris talks about "under 1.5". Of course, ignoring any potential for the genetic influence, Kevin may find his trigs continue to improve over time. Purely out of curiosity, I just looked back over my own trig history, and I can state that whilst my TC has varied a bit, the trigs have, without exception, with each iteration of testing. Having got to 0.76, I doubt that can continue, much longer, if at all.
 
SunnyExpat said:
Not true, read
http://journals.aace.com/doi/pdf/10.4158/EP161209.CO

It varies depending on what causes the anemia.
Many will give a low Hba1c.
Click to expand...

You're wrong, because the article you cite is off topic. @Bluetit1802 was speaking of only one kind of blood disorder, and it's not the kind your article addressed.

Low red blood cell count (not high) will cause falsely high A1c values. Your reply cites an article that addressed red blood cell survival time -- which is a different matter from red blood cell count or concentration. On top of this, your source mentioned that a list of interferences (interferences to the A1c test) is provided the NGSP Website. The NGSP declares -- low red blood cell count.
 
No, anemia is low red blood cell count.
Depending on what has caused the low red blood cell count, (anemia), as the reference will explain, it can be artificially high or low.
 
SunnyExpat said:
No, anemia is low red blood cell count.
Depending on what has caused the low red blood cell count, (anemia), as the reference will explain, it can be artificially high or low.
Click to expand...
Not according to the World Health Organisation and NGSP.

The reference does not say what you say it says.

The article is not about the notion of "varieties of low red blood cell count". The article is about varieties of red blood cell disorder, actually, it's about one particular particular RBC disorder, and that is not low count.

NGSP is the analytical chemistry agency charged with the nitty-gritty details of standardising HbA1c tests by different manufacturers and assessing their quality.
 
Last edited by a moderator:
'But not all anemias will lower HbA1c levels. Both iron deficiency anemia and pernicious
anemias, for example, are associated with a longer RBC survival, which is associated with an
increase in HbA1c levels'

I can only read that one way.
I guess you read it differently.
 

Yeah, you keep mixing up RBC count with RBC lifespan, which I've already pointed out. You keep applying the term 'anemia' variably between posts, more loosely or more strictly, which impedes accountability for one's statements.

Iron deficiency anemia is not RBC. Pernicious anemia -- that's a type of deficiency in vitamin B12, nothing to do with blood cells -- is not RBC count. RBC survival is not RBC count.
 
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