Too much sugar /HFCS
and other refined carbs causes inflammation
Hyperglycemia/Glycation increases damaging AGEs
Why the hyperglycemia?
Excess dietary sugars and refined
carbohydrates increases blood glucose - usually
accompanied by prolonged high insulin levels.
Excess consumption of high fructose corn syrup (HFCS) - in
processed foods, sodas etc;
Insulin
resistance as in Type 2 diabetes - further increases blood sugar;
Advanced Gycation Endproducts (AGEs) do damage
GLYCATION of
sugar molecules lead to Advanced Glycation Endproducts (AGEs) -
some
of which are implicated in age-related chronic diseases including CVD
– Glycation is another
mechanism that causes significant damage and inflammation - this is the haphazard process (without the controlling action of an enzyme) of adding sugar
molecules (i.e. glucose, fructose, galactose) to lipid molecules or proteins, to
form a glycolipid or glycoprotein, and harmful by-products, aptly called AGEs (Advanced Glycation Endproducts).
AGEs can be formed outside or inside of the body:
– Exogenously - AGEs
are typically formed when sugars are cooked with proteins or fats. Also, food
manufacturers add AGEs to foods as flavor enhancers and colorants to improve
appearance;
– Endogenously -
glycations occur mainly in the bloodstream to some of the absorbed simple
sugars, i.e. glucose, fructose and galactose.
AGEs can directly damage biomolecules, such as
the endothelium, connective tissue collagen, elastin and fibrinogen(E.g. in blood vessel
walls)
– Glucose
and fructose glycate and
so inactivate the enzyme glutathione reductase, responsible for maintaining the
body's major cell-protecting antioxidant enzyme Glutathione(GSH) -
Glucose, glucose 6-phosphate
and
fructose all displayed a time-dependent inhibition of glutathione
reductase activity, suggesting that these sugars glycate this enzyme.
(Blakytny et al, 1992)
✔ Fructose and
galactose have about 10 TIMES
the glycation activity of
glucose. With the common practice of using
high fructose corn syrup (HFCS)
in many processed foods, fructose has become an excessive component in today's
Western diet; (Bunn & Higgins, 1991)
– Cholesterol and fat is
damaged by glycation - Increased amount and duration of
glucose in the blood
allows more glycation to occur, inflicting damage on tissues via lipid oxidation.
(Bucal, 1993)
– Hyperglycemia is positively correlated with
arterial disease in many diverse populations
✔ Hyperglycemia increases glyco-oxidation
- which
increases the formation of oxidized LDL, and its accumulation in the artery
wall;
✔ Circulating AGEs bind LDL cholesterol and
increase its accumulation in arterial wall – glycation of LDL cholesterol increases
the proportion of lipoproteins that are taken up via inflammatory cells and
decreases the proportion taken up by liver cells (hepatocytes) via classical LDL
receptors, thus contributing to atherosclerosis by increasing accumulation of
LDL cholesterol in the artery wall.
Organs and tissues NOT dependent on INSULIN for their absorption of
glucose
are more susceptible to damage from periods of hyperglycemia than other organs - i.e. kidneys, blood vessels, peripheral nerves and lenses of the eye.
Glycated sugar creates inflammation, which
activates defensive immune system macrophages:
– Scavenger cells with
special receptors for AGEs, called RAGEs - again how aptly named is
that!? – these RAGEs “get mad” and bind to the AGEs to remove them.
Bucal R et al. (1993) Lipid advanced glycosylation: pathway for lipid oxidation
in vivo.
Bunn and Higgins, (1991)
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