tara said:jyb said:tara said:That would be very interesting to see, if it has been studied. :)jyb said:I have not seen hard numbers about this HBA1C for sugar versus PUFA. But it would be relevant to this discussion, certainly more relevant than exogenous dietary AGEs and stuff in my opinion.
There are certainly people out there who think high blood sugar is even worse than PUFA for HBA1C. But it seems difficult to know exactly because either one won't necessarily cause high HBA1C.
I had only heard about HBA1C being a measure of chronically too high blood sugar.
Hi Tara,
According to Perlmutter in " grain brain: ect...." ( ) :
« We now have evidence to show that elevated hemoglobin A1C is associated with changes in brain size. In one particularly profound study, published in the journal Neurology, researchers looking at MRIs to determine which lab test correlated best with brain atrophy found that the hemoglobin A1C demonstrated the most powerful relationship.When comparing the degree of brain tissue loss in those individuals with the lowest hemoglobin A1C (4.4 to 5.2) to those having the highest hemoglobin A1C (5.9 to 9.0), the brain loss in those individuals with the highest hemoglobin A1C was almost doubled during a six-year period. So hemoglobin A1C is far more than just a marker of blood sugar balance »
and also: ( from the same guy in the same book )
« You also should know that there’s now documented evidence proving a direct relationship between hemoglobin A1C and the future risk of depression. One study looked at more than four thousand men and women whose average age was sixty-three years and showed a direct correlation between hemoglobin A1C and “depressive symptoms.” Poor glucose metabolism was described as a risk factor for the development of depression in these adults. The bottom line: The glycation of proteins is bad news for the brain. »
But...... Chris Masterjohn ( and I found his explanations far more interesting and convincing than Perlmutter ) to the rescue [highlight=yellow]about glucose, glycation and hemoglobin A1C[/highlight] :
"..... The late 1960s hailed the first discovery that a similar reaction occurs in the blood of diabetics, producing HbA1c, a form of hemoglobin that's been damaged by glucose. Scientists then coined the term "glycation" to distinguish this aberrant and apparently pathological process from the normal and necessary "glycosylation" reactions that our enzymes deliberately carry out.
Although the division is somewhat artificial, we generally split the Mallaird reaction up into three stages: early, intermediate, and late (or "advanced"). HbA1c is an example of an "early glycation" product. It may seem strange, but because glucose flip-flops around a bit when it reacts with hemoglobin or other proteins during early glycation, it winds up producing messed up amino acids with names like "fructosyl-lysine" and "fructosyl-valine." Early glycation products derived from fructose have different names altogether. The "intermediate glycation" products are the dicarbonyls, [highlight=yellow]and it is the dicarbonyls that produce most of the AGEs.[/highlight] But here's the catch: [highlight=yellow]dicarbonyls can be formed in a number of ways, including some that have nothing to do with glucose[/highlight]."
Source: http://blog.cholesterol-and-health.com/ ... rom-o.html