Really interesting analysis. Thanks for this great considered response. Thinking about it and please excuse me if I've got things back to front, but……when blood donors donate blood, it’s thought that they lose approximately one tenth of their blood volume. Consequently, they lose one tenth of preformed HbA1c. In this scenario, the bone marrow compensates for the blood loss by an increase in erythropoiesis, resulting in an increased flow of newly formed erythrocytes devoid of HbA1c. As glycation of hemoglobin is a relatively slow chemical process, the increased synthesis of erythrocytes would therefore, theoretically, result in a drop in HbA1c for a significant amount of time thereafter - weeks rather than days. So regardless of iron levels, wouldn’t bloodletting affect the correct interpretation of glycemic control?
Ooh that’s a great point. It’s worth mentioning that other studies which measure glucose and insulin instead of HbA1c see improvements in glucose as well (eg F S Facchini. Diabetes Care. 1998 Dec). However I just had a look at a Dutch study on blood donation and A1c and they see reductions in A1c up to 9 weeks after. In the “High-Ferritin Type 2 Diabetes” study they say the reason they took the first outcome measure at 4 months was to account for the loss of Ht which they expected to return to baseline at 4 weeks. So it’s interesting to find reductions in A1c are seen up to 9 weeks - and perhaps some of the reduction in A1c in that study was in fact due to the removal of “pre-formed” HbA1c.
In any case I would re-iterate my comments in the piece. I don’t think the data are a slam-dunk but I think there’s definitely something about iron metabolism which negatively influences glucose control.
Great article Nicola on a topic which is so controversial......there is certainly no simple answer but I thought you gave a really sensible and reasonable overview. The Fe hypothesis is particularly interesting and this was a new one for me so thanks for that.
Thanks Dr Max! Yes I think it’s very complex and interesting. I hope people continue researching it so we can understand a bit more, and speculate less!
Looks to me that you have a fixed view and you are trying very hard to make the data support your view. Not surprised by this as you are a dietician. It’s very simple. T2D is caused by eating too many carbs. Why is there any need to find another cause?
Not sure that T2D is caused by eating carbs. Insulin resistance, weight, lack of activity and genetics seem to be main causes. And the symptom is an intolerance to carbs.
No, no, no. T2D is defined as having high average blood glucose (measured by HBA1C). High blood glucose is caused by eating carbohydrates, pure and simple. Stope eating carbs, and you *cure* T2D. It is so simple. Why do people want to make this more complicated???
That’s the symptom. The cause is a combination of insulin resistance and beta cell dysfunction, probably caused by being overweight. The symptom can be controlled by low carb diet. You can’t cure it. I got mine into remission with low carb diet and weight loss.
Wrong. Type 2 diabetes is *defined* as having an A1C above a certain limit. If you reduce your A1C below that limit by not eating carbs (ie glucose) then you are no longer a T2 diabetic *by definition*. The A1C level is not a symptom, it is the way the disease is defined.
I appreciate it’s easy to take what one wants from someone observation studies but I have deliberately tried(!?) to avoid leaning too much on epi studies and instead draw from experimental studies which ae designed to determine causation.
And you succeeded in that by looking at the components in red meat.
What I was questioning was the dramatic claim made by the paper, and hence the media, which might show a correlation but in no way shows a causation.
The almost unlimited factors that influence our health are surely too many to ‘adjust’ for, for example how the meat was cooked, what the exercise routine was of the subjects, what the socioeconomic status was of the subjects, what was eaten with the meat, what was their refined carbohydrate intake.
I would say at this stage it is impossible to say that red meat is causative of T2d based on this study, but maybe it’s part of the web, and maybe as you highlight iron is a contributing factor.
Trouble is the public will now interpret this as black and white and reduce or stop eating red meat. It seems to me a shame that we live in a society where the media shouts about something in its infancy of our understanding which then affects so many people’s behaviours.
We need bods like you who do understand the science better to help us see the greyness, and help us properly calibrate where this sits on our current understanding maturity overall, so we don’t take these studies as black and white, unless they are.
Really interesting analysis. Thanks for this great considered response. Thinking about it and please excuse me if I've got things back to front, but……when blood donors donate blood, it’s thought that they lose approximately one tenth of their blood volume. Consequently, they lose one tenth of preformed HbA1c. In this scenario, the bone marrow compensates for the blood loss by an increase in erythropoiesis, resulting in an increased flow of newly formed erythrocytes devoid of HbA1c. As glycation of hemoglobin is a relatively slow chemical process, the increased synthesis of erythrocytes would therefore, theoretically, result in a drop in HbA1c for a significant amount of time thereafter - weeks rather than days. So regardless of iron levels, wouldn’t bloodletting affect the correct interpretation of glycemic control?
Oh, that’s interesting! I hadn’t thought of that. Now I wonder, too!
Ooh that’s a great point. It’s worth mentioning that other studies which measure glucose and insulin instead of HbA1c see improvements in glucose as well (eg F S Facchini. Diabetes Care. 1998 Dec). However I just had a look at a Dutch study on blood donation and A1c and they see reductions in A1c up to 9 weeks after. In the “High-Ferritin Type 2 Diabetes” study they say the reason they took the first outcome measure at 4 months was to account for the loss of Ht which they expected to return to baseline at 4 weeks. So it’s interesting to find reductions in A1c are seen up to 9 weeks - and perhaps some of the reduction in A1c in that study was in fact due to the removal of “pre-formed” HbA1c.
In any case I would re-iterate my comments in the piece. I don’t think the data are a slam-dunk but I think there’s definitely something about iron metabolism which negatively influences glucose control.
Thanks for your comment!
Great article Nicola on a topic which is so controversial......there is certainly no simple answer but I thought you gave a really sensible and reasonable overview. The Fe hypothesis is particularly interesting and this was a new one for me so thanks for that.
Thanks Dr Max! Yes I think it’s very complex and interesting. I hope people continue researching it so we can understand a bit more, and speculate less!
You're the best, Doc! Love everything you do!
TY!
Looks to me that you have a fixed view and you are trying very hard to make the data support your view. Not surprised by this as you are a dietician. It’s very simple. T2D is caused by eating too many carbs. Why is there any need to find another cause?
Not sure that T2D is caused by eating carbs. Insulin resistance, weight, lack of activity and genetics seem to be main causes. And the symptom is an intolerance to carbs.
No, no, no. T2D is defined as having high average blood glucose (measured by HBA1C). High blood glucose is caused by eating carbohydrates, pure and simple. Stope eating carbs, and you *cure* T2D. It is so simple. Why do people want to make this more complicated???
That’s the symptom. The cause is a combination of insulin resistance and beta cell dysfunction, probably caused by being overweight. The symptom can be controlled by low carb diet. You can’t cure it. I got mine into remission with low carb diet and weight loss.
Wrong. Type 2 diabetes is *defined* as having an A1C above a certain limit. If you reduce your A1C below that limit by not eating carbs (ie glucose) then you are no longer a T2 diabetic *by definition*. The A1C level is not a symptom, it is the way the disease is defined.
Doc, have you researched anything on the association between dairy & prostate cancer?
Lots of work put into that analysis, thank you.
I’m just wondering whether there’s a trap here of seeing correlation rather than causation.
I appreciate it’s easy to take what one wants from someone observation studies but I have deliberately tried(!?) to avoid leaning too much on epi studies and instead draw from experimental studies which ae designed to determine causation.
And you succeeded in that by looking at the components in red meat.
What I was questioning was the dramatic claim made by the paper, and hence the media, which might show a correlation but in no way shows a causation.
The almost unlimited factors that influence our health are surely too many to ‘adjust’ for, for example how the meat was cooked, what the exercise routine was of the subjects, what the socioeconomic status was of the subjects, what was eaten with the meat, what was their refined carbohydrate intake.
I would say at this stage it is impossible to say that red meat is causative of T2d based on this study, but maybe it’s part of the web, and maybe as you highlight iron is a contributing factor.
Trouble is the public will now interpret this as black and white and reduce or stop eating red meat. It seems to me a shame that we live in a society where the media shouts about something in its infancy of our understanding which then affects so many people’s behaviours.
We need bods like you who do understand the science better to help us see the greyness, and help us properly calibrate where this sits on our current understanding maturity overall, so we don’t take these studies as black and white, unless they are.
A voice like that in all this noise is gold.