Recent Study on Postprandial BG & Cardiovascular Risk

[finsit]

This has just come out last year and sounds very interesting. As it seems, regardless of one being diabetic or non-diabetic the safest BG range seems to be between 70-110 mg/dl. This reminds me again of Dr. Richard K. Bernstein, who survived type-1 diabetes now for over 75 years and still very much active and healthy and has always said that a healthy person's BG should not rise above 90 mg/dl even after a meal (on low-carb) thus avoid oxidative stress that can lead to CVD. All makes sense to me, even though if i am unable to achieve it...



Link to full study: https://www.frontiersin.org/articles/10.3389/fcvm.2020.570553/full

Thoughts?

 

[Pura Vida]

This has just come out last year and sounds very interesting. As it seems, regardless of one being diabetic or non-diabetic the safest BG range seems to be between 70-110 mg/dl. This reminds me again of Dr. Richard K. Bernstein, who survived type-1 diabetes now for over 75 years and still very much active and healthy and has always said that a healthy person's BG should not rise above 90 mg/dl even after a meal (on low-carb) thus avoid oxidative stress that can lead to CVD. All makes sense to me, even though if i am unable to achieve it...

same for me. even on low Carb and A1C6.4 will have to go even lower carb

Link to full study: https://www.frontiersin.org/articles/10.3389/fcvm.2020.570553/full

Thoughts?

 

[Lamont D]

This has just come out last year and sounds very interesting. As it seems, regardless of one being diabetic or non-diabetic the safest BG range seems to be between 70-110 mg/dl. This reminds me again of Dr. Richard K. Bernstein, who survived type-1 diabetes now for over 75 years and still very much active and healthy and has always said that a healthy person's BG should not rise above 90 mg/dl even after a meal (on low-carb) thus avoid oxidative stress that can lead to CVD. All makes sense to me, even though if i am unable to achieve it...

View attachment 52353

Link to full study: https://www.frontiersin.org/articles/10.3389/fcvm.2020.570553/full

Thoughts?

Having been (mostly) in normal blood levels for the last eight years, my physical health is really great for an OAP.
I had a full cat scan a few months back and other than wear and tear, I was given a clean bill of physical health.

It does work (for me!)

 

[Oldvatr]

This has just come out last year and sounds very interesting. As it seems, regardless of one being diabetic or non-diabetic the safest BG range seems to be between 70-110 mg/dl. This reminds me again of Dr. Richard K. Bernstein, who survived type-1 diabetes now for over 75 years and still very much active and healthy and has always said that a healthy person's BG should not rise above 90 mg/dl even after a meal (on low-carb) thus avoid oxidative stress that can lead to CVD. All makes sense to me, even though if i am unable to achieve it...

View attachment 52353

Link to full study: https://www.frontiersin.org/articles/10.3389/fcvm.2020.570553/full

Thoughts?

The use of the words "this hypothesis" may be a clue that this is a prospective study not an actual experiment to prove the relationship. It may be a venture to raise funding to do this type of study, but the snippet you posted does not contain any clue as to how it might be constructed.

The paper title ends in a question mark.? so is indeed a hypothesis

 

[Bubbleblower]

how it might be constructed.

Transient Intermittent Hyperglycemia Accelerates Atherosclerosis by Promoting Myelopoiesis

This is the graphical abstract:

 

[Oldvatr]

As I said, it is a hypothesis and has no evidence backing it up that is referenced. Neutrophils are the crash team that go out to repair damage in the blood system. They are generated from the marrow by our immune system. Once in the blood, they need glucose to maintain their respiratory activity (i.e. to live) and use the GLUT-1 enzyme as the main glucose transfer portal into the neutrophil. It does not use insulin so is a basal function. Other basal functions are the nervouus system, and the blood brain barrier all of which seem to use GLUT-1. High glucose levels are known to reduce the production of GLUT-1, and to increase it when glucose levels are low, so the effect is generally self regulating. So this mechanism is more susceptible to high basal glucose levels than TIH, so I disagree wth one of their main statements, that the process is unregulated, and also with their assumption that TIH is more harmful than the basal levels.

Is a glycated neutrophil bad for us? Certainly neutrophils are associated with atheroschlerosis since it is already established that it is the repair of damaged blood vessels that leads to the build up of plaque in the arteries. What it does not answer is why the damage occurs on the arteries, not the veins, and again mainly in the aortic arteries leading to CVD attacks (MI). Neutrophils are in our plumbing in plentiful supply. If their hypothesis is valid, then it would lead to plaque all over our body, and cause more strokes than heart attacks. So I find this paper to be weak

We as diabetics already know we have a higher risk of CVD, but I am not sure this theory explains why, Certainly keeping glucose levels within the normal range is a good target, but as the authors point out, actually reducing this effect does not lead to better morbidity outcome. I reckon that once the plaque cement has stuck nothing will shift it. I see outside my window they are digging up the road again, and apparently lining the sewer pipes, which is an interesting serendipity moment considering this discussion. A parallel universe, perhaps?

 

[Ronancastled]

Loads of older studies linking lower FBG to a reduction in CVD risk.
We know the markers of many pre-diabetics meet the classic overweight/sedentary profile.
I'm wondering if it's a bit cause & effect, chicken & egg so to speak.

 

[Oldvatr]

Loads of older studies linking lower FBG to a reduction in CVD risk.
We know the markers of many pre-diabetics meet the classic overweight/sedentary profile.
I'm wondering if it's a bit cause & effect, chicken & egg so to speak.

Indeed. This paper talks about ROS.
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC4310837/
In the OP post the paper starts with high glucose triggering ROS from the neutrophils. The paper above does not seem to implicate bad glucose control, but rather blames ROS for causing diabetes. Personally I would have thought that glucose embedding itself in the blood corpuscle (HbA1c) would be suspect rather than tiny neutrofils which is what it is designed to do to keep them going with basal glucose. Glycated haemoglobin seems to be a stress marker since it does not seem to have function associated with it.

 

[Bubbleblower]

why the damage occurs on the arteries, not the veins

Supposively glucose spikes cause hardening of the arteries, because they produce large quantities of reactive oxygen that kill cells in the anterior wall. And then

the repair of damaged blood vessels leads to the build up of plaque in the arteries

I have seen video footage from Prof. Hirotaka Watada of this happening in mice.

If their hypothesis is valid, then it would lead to plaque all over our body

That’s exactly what I have, occlusions, stenoses, aneurysms, trombi, you name it, everywhere.
I like it the authors think outside the box even if their hypotheses are flawed.

 

[Bubbleblower]

According to the author of this article burning sugar forms methylglyoxal, which causes inflammation of the arteries. He also says pyridoxamine may prevent this.

 

[Mbaker]

I hope this is widely read. Some of the advice on the forum makes me shudder regarding exceptable upper limits, come to think of all diabetic / non diabetic numbers; numbers I know to be way out of bounds are waved through. I recall someone hitting an 11 mmol/L after a meal and being told this was alright.

It seems that the sugar demon can perform a Jedi mind bending trick , at times. Bernstein may be strict, but he is absolutely correct, what a living legend.

 

[Oldvatr]

According to the author of this article burning sugar forms methylglyoxal, which causes inflammation of the arteries. He also says pyridoxamine may prevent this.

methylglyoxal is a natural product produced during the oxidization of any carbohydrate, and not just sugar. It will also occur when metabolising proteins or fats.. It is a natural by product found in nature, and Manuka Honey is one of the highest sources of this compound in its natural form.

It is one of the low order metabolites on the pathway to producing or synthesising ALA and pyruvic acid prior to full oxydisation when we 'burn' carbs. It probably does occur during conflagration of sugar as in 'burn sugar'. Not sure if the theory expressed by the author has any proof .

 

[Bubbleblower]

Not sure if the theory expressed by the author has any proof .

Labexperiments have shown peaks in methylglyoxal do indeed cause inflammation of the arteries and there is an association found between methyglyoxal levels and CVD:

Higher Plasma Methylglyoxal Levels Are Associated With Incident Cardiovascular Disease and Mortality in Individuals With Type 2 Diabetes

 

[Oldvatr]

Labexperiments have shown peaks in methylglyoxal do indeed cause inflammation of the arteries and there is an association found between methyglyoxal levels and CVD:

Higher Plasma Methylglyoxal Levels Are Associated With Incident Cardiovascular Disease and Mortality in Individuals With Type 2 Diabetes

This study starts with a cohort of people who have already suffered at least one CVD prior to entry into this study. Like buses, these events have a natural tendency to group together. and repeat events are expected, and therefore not random. Thus the cohort already has damage caused by unknown factors, and the assumption that the MG levels have a causal effect is not proven, It may be that the MG levels are an underlying marker to some other mechanism at play.

MG is known as the ubiquitous carbonyl, since it forms part of the normal pathway of metabolism to form ATP from hydrocarbons (carbs, protein , fat) so is not in itself unexpected. It could be due to an increase in ketosis for example. Reducing MG may be difficult to achieve since we would not functtion without producing it. LDL has a similar problem in that elimination of it would be fatal.

 

[Bubbleblower]

This study starts with a cohort of people who have already suffered at least one CVD prior to entry into this study.

61% had prior CVD and the data were adjusted for that. They found:

"Higher MGO levels were associated with total (hazard ratio 1.26 [95% CI 1.11–1.42]) and fatal (1.49 [1.30–1.71]) CVD and with all-cause mortality (1.25 [1.11–1.40]), myocardial infarction (1.22 [1.02–1.45]), and amputations (1.36 [1.05–1.76])"

 

[Oldvatr]

61% had prior CVD and the data were adjusted for that. They found:

"Higher MGO levels were associated with total (hazard ratio 1.26 [95% CI 1.11–1.42]) and fatal (1.49 [1.30–1.71]) CVD and with all-cause mortality (1.25 [1.11–1.40]), myocardial infarction (1.22 [1.02–1.45]), and amputations (1.36 [1.05–1.76])"

The use of Hazard Ratios is worrisome. Depending on which ststistics package they are using then these can be very misleading indeed. The original (PETO) method of analysis was banned a few years ago because it was found to be easily manipulated to give false associations. The more recent Pareto method overcomes this. The figures quoted here do not use the 'p' value so seem to be the older Peto method results.

There may be many causes of an elevated MGO marker, and post prandial glucose levels may well be related to the increase since that is the peak of the metabolic activity. The term sugar being burnt is meaningless since much of the plasma glucose will be stored and not burnt.

 

[Bubbleblower]

The researchers did not use the PETO method as you can read in the “research design and methods” section, right on top. The word “significantly” implies p-values, which you can find in table 7.

Anyway, more and more research shows the importance of avoiding glucose spikes and doctors are with it.