2014 Study: Normal Sugar Consumption Not Associated With Health Problems

Wilfrid

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tara said:
jyb said:
tara said:
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.
That would be very interesting to see, if it has been studied. :)

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...." ( :wavingyellow ) :

« 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
 

LucH

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tara said:
I am curious about whether there are other interpretations, for instance it would be interesting if there were a strong correlation with PUFA consumption or PUFA blood levels and Hb1Ac. I took this to be Jyb's meaning.
I've made some searches for "science". Here is the result ;)

There is a correlation between PUFA consumption and HbA1c blood levels. But the problem is much more complex.
Let me tell you to be clear:
There are many sorts metabolites derived from AGEs (Advanced Glycated End-Products). The most dangerous in vivo is methylglyoxal (MG).
But our body can manage very well AGE if you don’t shoot the plug too far, with antioxidants, if you don’t suffer from inflammation or diabetes…
Up to 90 % of AGE come from endogenous sources, not from food (exogenous).

So, in this view, we can say fats are much more deleterious / dangerous than sugars. But it must be toned:
PUFA are 10 x easier oxidized than sugars. But again we have to tone (bring nuance).
Fatty acids are fragile when not saturated. The more double bonds, the more fragile, as you already know.
Olive oil is an exception because it contains many antioxidants (polyphenols), and not many omega-6. But this oil must be labelled; otherwise, it could be cut with other oils. 8 – 10 $ for one liter oil is usual here.

PUFA is 10 x more fragile than sugars. But we are talking about glucose. When you take fructose, the problem is nearly the same. Fructose is nearly 10 x more fragile than table sugar.
The term 'advanced glycation end-product' is somewhat misleading in the sense that they are not formed only by glycation. Glycation refers to glucose molecules binding to protein or lipid molecules, but it can also happen by fructation, which is essentially the same thing but this time with fructose.
To neutralize those MG we need selenium. But when people are in-toxified, they are deprived of. Use NAC to preserve it (N-acetyl cysteine). Don't forget there is interaction between vitamins C E and Selenium (spare effect).

Trace Minerals
Your body’s internal antioxidant defences, including superoxide dismutase, catalase, and glutathione peroxidase all depend on trace minerals as cofactors for their function. Zinc and manganese are of particular importance for sustaining whole-body resistance to ionizing radiation.
When you are 55 years old, you’d better assist the metabolism.
Exerpt:
"The accumulation of adduct formation such as lipofuscin is implicated in normal aging and age-related diseases. The contribution of carbonyl compounds and then protein adduct formations by advanced interaction of sugars/lipids with amino acids/peptides contributes to the abnormal cellular redox metabolism."
:yellohello
LucH

*) Interesting Links:
Glyoxalase against AGEs.
Methylglyoxal (MG) is an important precursor for AGEs. Normally, MG is detoxified by the glyoxalase (GLO) enzyme system (including component enzymes GLO1 and GLO2). Enhanced glycolytic metabolism in many cells during diabetes may overpower detoxification capacity and lead to AGE-related pathology.
Detoxification of MG reduces AGE adduct accumulation, which, in turn, can prevent formation of key retinal neuroglial and vascular lesions as diabetes progresses. MG-derived AGEs play an important role in diabetic retinopathy.
http://www.pubfacts.com/detail/22143324 ... al-neurogl
Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology. Diabetologia 2012. A K Berner et al.

Protein carboxylation
Carbonyl Stress in Aging Process: Role of Vitamins and Phytochemicals as Redox Regulators.
By Volkan Ergin et al. October 2013

AGE from sugar and fat
http://inhumanexperiment.blogspot.be/20 ... -than.html
Fats and AGEs: PUFAs Are Even Worse than Fructose!

References:
- Tessier FJ, Birlouez-Aragon I. Health effects of dietary Maillard reaction products: the results of ICARE and other studies. Amino Acids. 2012 Apr;42(4):1119-31. Review. PubMed PMID: 20949364. Pas citée
- Uribarri J, Woodruff S, Goodman S, Cai W, Chen X, Pyzik R, Yong A, Striker GE, Vlassara H. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010 Jun;110(6):911-16.e12. PubMed PMID: 20497781.
- Luevano-Contreras C, Chapman-Novakofski K. Dietary advanced glycation end products and aging. Nutrients. 2010 Dec;2(12):1247-65. Epub 2010 Dec 13. Review. PubMed PMID: 22254007; PubMed Central PMCID: PMC3257625. (texte complet accessible gratuitement)
- Steenvoorden MM, Huizinga TW, Verzijl N, Bank RA, Ronday HK, Luning HA, Lafeber FP, Toes RE, DeGroot J. Activation of receptor for advanced glycation end products in osteoarthritis leads to increased stimulation of chondrocytes and synoviocytes. Arthritis Rheum. 2006 Jan;54(1):253-63. PubMed PMID: 16385542.
- Loeser RF, Yammani RR, Carlson CS, Chen H, Cole A, Im HJ, Bursch LS, Yan SD. Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis. Arthritis Rheum. 2005
 

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