Heart disease and blood sugar numbers

[LucySW]

I've just seen this blog post by Dr Michael Eades, who I respect more and more and more as I read through his blog backlist. (I like to squander time I should be spending working reading up on nutritional science blogs. Poor me, alas - money'll be tight soon.) This one was written in 2006, but it presents a mind-boggling study I had never heard of, the Whitehall Study. (Government-funded in the UK, NB, not privately funded.) It was an association study, but as he says, it's a pretty good association study. It shows pretty clearly how heart disease, and ultimately death from same, accompany high blood sugar.

"18,403 nonindustrial London-based male civil servants aged 40-64 years were examined between September 1967 and January 1970. In brief, measurements included height, weight, blood pressure, six-lead electrocardiogram, lung function (forced expiratory volume in 1 s and forced vital capacity), plasma cholesterol concentration, and a glucose tolerance test. A self-administered questionnaire was completed regarding employment grade, smoking habits, health status, and physical activity."​

All these nice professional skilled über-white-collar types were given a GTT and classified into three groups according to their results: normal, glucose-intolerant, and outright diabetic. That was in 1967-70.

Then 33 years later, they looked at the same group of guys and quantified death rates from all-cause mortality and from heart disease. More of the diabetics had died, but as Eades says, the really interesting divergence was between 'normal' levels of 95 mg/dl (5.3 mmol/L) and 85 mg/dl (4.7 mmol/L). After ten years, heart disease mortality started to go up at levels over 95 mg/dl. But after 33 years, it started to rise at levels over 85mg/dl.

He flags the original article, here. It was published in January 2006. Eades is an American MD with a blog who is a low-carb advocate. He wrote Protein Power.

But I urge people to read the Eades post.

And I note that these numbers match Bernstein's target numbers. 4.6 fasting, 5.2 post-meal.

 

[Diamattic]

I have read some things on the Whitehall study. This post below sheds some light on some flaws in his study.

In summary - the original study you refer to did not study women, and did not take into account job type, or stress level.

http://scienceblogs.com/thepumphandle/2012/10/03/inequality-stress-and-health-the-whitehall-studies/

EDIT - Also, the whitehall study excluded men with known diabetes, they only used men with 'glucose intolerance (6.2-11.1)'. To me this means these men may or may not have been on some type of medication to control this.

When you think about the timeline here 33 years. At the end of the study, the youngest man would have been 73, and the oldest being 97.

 

[Clivethedrive]

I've just seen this blog post by Dr Michael Eades, who I respect more and more and more as I read through his blog backlist. (I like to squander time I should be spending working reading up on nutritional science blogs. Poor me, alas - money'll be tight soon.) This one was written in 2006, but it presents a mind-boggling study I had never heard of, the Whitehall Study. (Government-funded in the UK, NB, not privately funded.) It was an association study, but as he says, it's a pretty good association study. It shows pretty clearly how heart disease, and ultimately death from same, accompany high blood sugar.

"18,403 nonindustrial London-based male civil servants aged 40-64 years were examined between September 1967 and January 1970. In brief, measurements included height, weight, blood pressure, six-lead electrocardiogram, lung function (forced expiratory volume in 1 s and forced vital capacity), plasma cholesterol concentration, and a glucose tolerance test. A self-administered questionnaire was completed regarding employment grade, smoking habits, health status, and physical activity."​

All these nice professional skilled über-white-collar types were given a GTT and classified into three groups according to their results: normal, glucose-intolerant, and outright diabetic. That was in 1967-70.

Then 33 years later, they looked at the same group of guys and quantified death rates from all-cause mortality and from heart disease. More of the diabetics had died, but as Eades says, the really interesting divergence was between 'normal' levels of 95 mg/dl (5.3 mmol/L) and 85 mg/dl (4.7 mmol/L). After ten years, heart disease mortality started to go up at levels over 95 mg/dl. But after 33 years, it started to rise at levels over 85mg/dl.

He flags the original article, here. It was published in January 2006. Eades is an American MD with a blog who is a low-carb advocate. He wrote Protein Power.

But I urge people to read the Eades post.

And I note that these numbers match Bernstein's target numbers. 4.6 fasting, 5.2 post-meal.

Yes very interesting ,dr Bernstein is absolutely right,most dr's are way behind in diabetes understanding, my doc actually said " your too low now ,we'll have to get your bs up to around 6.5 mmols, at that , i laughed and left. I now am averaging 3.8 am fasting , 4.8 post breakfast and 5.5 2 hrs post dinner on average.

 

[Celsus]

Hi Lucy,
The Whitehall studies (yep, you had two) are actually very famous and well known. But they were not at all centred around diabetes, so its quite a selective (and for them a convenient) view your sources are pulling out of from them here. I can only recommend you to read the full study text instead of such narrow extract taking things out of context.

The Whitehall studies were conducted to investigate the social determinants of health. And it was not just "nice professional skilled über-white-collar types" as you refer to that were in this. (not sure even why you try to make such story out of that?). The whole point of the Whitehall studies were exactly not that. As the goal was to examine the long-term health difference between different social classes, specifically with regards to cardiovascular prevalence and mortality rates.

Conclusion of the studies were a strong association between grade levels of civil servant employment and mortality rates from a range of causes. Men in the lowest grade (doorkeepers, mail runners, etc.) had a mortality rate three times higher than that of men in the highest grade (administrators). So do not worry so much about your bg level, as that have much less influence on your health than many other parameters. The best you can do for your health is to become an administrator and not be the doorkeeper!

 

[LucySW]

I think we knew that, Celsus. And whatever the original aims of this study were, this paper is about one particular finding. That's quite legitimate.

Now - did you vote DF?

 

[Celsus]

I think we knew that, Celsus. And whatever the original aims of this study were, this paper is about one particular finding. That's quite legitimate.

Now - did you vote DF?

OK Lucy, I thought you just wrote yourself that you had never heard about these studies before?

If you read the full study, you will see that those with the higher bg response result also had higher lipid levels. Reason why the small bg level variance and impact on cardiovascular disease is taken out of context. Hyperlipidemia is a major risk factor for cardiovascular disease which therefore overshadows the potential effect of smaller variation in bg in same individuals in study sample. Socially less well off tend to also eat more sugary and fatty foods, and as result typically often end up with higher morbidity/mortality rates at lower ages than better well off. Next to this, many more life styles differences between upper class and lower class public servants that also plays in. And that as you say, is probably well understood by most today.
But bg may not be the cause but the effect. Cause and effect is one of the most commonly misunderstood concepts in science and is often misused by lawyers, the media, politicians and even scientists themselves, in an attempt to add legitimacy to research. The basic principle of causality is determining whether the results and trends seen in an experiment are actually caused by the manipulation or whether some other factor may underlie the process. Some examples of this are especially rife in alternative therapy, when a group of scientists announces that they have found the next healthy superfood or that a certain treatment cured swine flu. Many of these claims deviate from the scientific process and pay little heed to cause and effect, diluting the claims of genuine research in the field. Like e.g. the researchers Balnaves and Caputi, looked at the academic performance of university students and attempted to find a correlation with age. They found that older, more mature students performed significantly better. However, as they pointed out, you cannot simply say that age causes the effect of making people into better students. Such a simplistic assumption is called a spurious relationship, the process of 'leaping to conclusions.' (our case here with the minimal bg level variation). In fact, there is a whole host of reasons why a mature student performs better: they have more life experience and confidence, and its maybe their last chance to succeed. Mature students may well have made a great financial sacrifice, so they are more determined to succeed. Establishing proper cause and effect criteria is extremely difficult.

Why do you ask me if I voted for a right-wing populist party?
I left Denmark for more than 25 years ago, politics do not have my interest, and I have been a foreign immigrant living in many different countries around the world. Next to this, you actually loose any voting right after been outside Denmark for 2+ years. Which probably is all good in my case, as I do not know the names of the politicians, what they stand for and even some new party names I have no clue about.

 

[phoenix]

You are comparing apples with pears. Your 4.6 mmol/l is not the same as 4.6mmol/l in this study. All we can say is that there was a linear relationship which started below that of those diagnosed with diabetes and there was a lower threshold. (they actually didn't measure fasting glucose either; and even had they done so, the cut off for a diabetes diagnosis would have been higher than today)

What they don't say in this paper but do in a later paper . http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2440932/?report=reader (similar analysis but a few years later on stroke and glucose levels)

However, to interpret our findings, it is necessary to point out that the blood glucose test was non-standard in several respects: (1) it was post-challenge; (2) the challenge itself (50 g) was lower than has been used elsewhere (75 g); (3) capillary rather than venous was drawn; and (4) whole blood rather than plasma was assayed.

They also point out

It should also be noted that men in this cohort were surveyed in the 1960s when, due to the lower prevalence of obesity, diabetes and raised blood glucose were much less common than they are today. Following on from this, it is possible that the threshold we identified for an increased risk of total and stroke mortality is higher in more recently established cohorts that have used contemporary test procedures

1) whole blood v plasma
using an autoanalyser in the 1960s but using venous rather than capillary blood (so not directly comparable either)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915443/pdf/pubhealthreporig00066-0061.pdf



2) capillary whole blood/plasma
. This still gives a significant difference .
Meters used to give results from whole blood. Now they use an algorithm to convert whole blood readings to plasma readings . Conversion chart here: http://www.diabetes.co.uk/whole-blood-readings-to-plasma-converter.html 4.6mmol/l on a modern meter would have read 4.1mmol/l on many meters from 2008 and before.
Again not comparable because of different methodology


I need to give credit, since it wasn't me who found the first chart
http://carbsanity.blogspot.fr/2011/10/keep-leptinade-flowing-im-going-to-die.html. She also emphasises that a raised glucose level in a 2 hour OGTT points to an underlying problem in glucose dispersal ie effect; not cause. Have a look also at the comments. I think one from Dr Kurt Harris that makes some very valid points )

 

[Celsus]

You are comparing apples with pears. Your 4.6 mmol/l is not the same as 4.6mmol/l in this study. All we can say is that there was a linear relationship which started below that of those diagnosed with diabetes and there was a lower threshold. (they actually didn't measure fasting glucose either; and even had they done so, the cut off for a diabetes diagnosis would have been higher than today)

What they don't say in this paper but do in a later paper . http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2440932/?report=reader (similar analysis but a few years later on stroke and glucose levels)


They also point out

1) whole blood v plasma
using an autoanalyser in the 1960s but using venous rather than capillary blood (so not directly comparable either)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1915443/pdf/pubhealthreporig00066-0061.pdf
View attachment 13781


2) capillary whole blood/plasma
. This still gives a significant difference .
Meters used to give results from whole blood. Now they use an algorithm to convert whole blood readings to plasma readings . Conversion chart here: http://www.diabetes.co.uk/whole-blood-readings-to-plasma-converter.html 4.6mmol/l on a modern meter would have read 4.1mmol/l on many meters from 2008 and before.
Again not comparable because of different methodology


I need to give credit, since it wasn't me who found the first chart
http://carbsanity.blogspot.fr/2011/10/keep-leptinade-flowing-im-going-to-die.html. She also emphasises that a raised glucose level in a 2 hour OGTT points to an underlying problem in glucose dispersal ie effect; not cause. Have a look also at the comments. I think one from Dr Kurt Harris that makes some very valid points )

Thank you Phoenix,
Excellent post and retrieval of relevant study reviews - And on top, a fun and joyful read around the subject of trial data interpretation!

Especially the last link with comments from Evelyn and Dr. Kurt Harris hits it home.
Quote: "Bottom line, this study does nothing to point to some "clear" evidence that postprandial glucose levels of 140 mg/dL are in any way, shape or form harmful. This study looked at the postprandial glucose levels after two hours from a standardized 50g challenge. If we're going to use PHD recommendations, spread out over three meals, this would be the starch dose per meal. Even if your BG doesn't fall back below whatever the values are from this study, does that mean the glucose excursion is harmful? No. It only means that you may be insulin resistant to a degree that puts you at risk and you can assess that risk with such a test. It does not mean the glucose levels themselves are harmful, indeed if they were not benign the human race would likely have been wiped off the planet by now. "

And Dr Harris' point is probably not understood well by many low carbers, but an established fact:
"It's actually the VLC eaters that have higher physiologic IR and higher fasting BG to compensate for less reliable dietary glucose delivery. The body's compensation for VLC that is attempting to make BG more stable in a glucose-scarce dietary regime means higher fasting BG and lower BG rises with the typical VLC meal.

When going back to moderate carbs, the post meal BG may rise more, but the fasting and inter-meal BG falls due to reduced physiologic IR."