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High
fructose processed foods linked to obesity,
gout, hypertension, diabetes, cholesterol
and fatty liver
There has been a "cloud"
over the health benefits of fructose added
to processed foods over the last few decades.
Food manufacturers have been adding pure
fructose to foods in the quest to lower
the glycaemic index (GI) of the food because
fructose does not affect insulin production
therefore is considered to be a low GI sugar
(this is contrast to glucose which does
raise insulin levels). The food industry
have also been adding fructose in the form
of corn syrup (popular in the United States)
or sucrose (this is half fructose) to foods,
especially low fat/diet foods to improve
flavour. There is emerging evidence that
this may be making the obesity epidemic
even worse, starting with damage to our
liver cells, the hepatocytes.
The only organ in your body that can take
up fructose is your liver and this is where
the problem begins. In contrast, glucose
can be taken up by every organ in the body,
only 20% of glucose load ends up at your
liver - the rest is metabolised by muscles,
brain, kidneys, heart etc. .
Fructose increases uric acid which in turn
increases blood pressure and causes gout
(where uric acid crystals are deposited
in joints)
Fructose increases phosphate depletion of
the hepatocyte which ultimately causes an
increase in uric acid. Uric acid is an inhibitor
of nitric oxide - nitric oxide is your naturally
occurring blood pressure lowerer.
Fructose increases fat production in the
liver (also known as denovo lipogenesis)
which in turn increases blood fats like
cholesterol and triglycerides (glucose does
not do this) and liver fat (which could
result in non-alcoholic fatty liver disease).
In fact fructose is being metabolised via
the same pathway as alcohol and is actually
damaging your liver in the the same way
as alcohol. Fructose causes deposition of
fat within the liver so it is actually like
alcohol and alcohol is like a fat. So in
contrast to glucose, it can be said that
fructose behaves like a fat.
Fructose increases inflammation which in
turn increases insuln levels in the long
term: fructose initiates an enzyme called
Junk one in the liver which stimulates the
inflammation pathway. This in turn stops
the insulin receptor in your liver from
working resulting in higher insulin levels
in the body (pancreas responds to this situation
by pumping out more insulin in the hope
to get the insulin working) . Eventually
insulin resistance sets in where your insulin
receptors are no longer responding to the
excessive amounts of insulin and thus less
glucose gets into the cells and more remains
in the blood (this is when diabetes is diagnosed).
High insulin levels stimulate the conversion
of sugar to fat which means you will be
storing more fat in the liver (which could
result in non-alcoholic fatty liver disease)
and more fat in fat cells, especially around
the abdomen and internal organs (resulting
in abdominal/visceral obesity).
Fructose doesn't raise your insulin in the
short term because there's no fructose receptor
on your beta cell in your pancreas which
produces insulin but there is a receptor
for glucose (fat also does not increase
insulin production). However, in the long
term fructose will raise insulin due to
the effects on inflammation in the liver
which in turn can make you insulin resistant
(mentioned above).
Bottom
line: A low fat diet containing fructose
(as sugar or pure fructose) is really a
high fat diet because fructose behaves like
a fat. We were not designed to eat a lot
of refined sugars, we're supposed to be
eating our carbohydrate, particularly our
fructose, with high fibre in unprocessed
foods like fruit and vegetables. If you
are trying to lose weight, lower your blood
pressure, blood fats or fatty liver reduce
your intake of sugars/fructose in processed
foods that do not contain fibre (like soft
drinks, fruit juices, sweet yoghurts, cakes,
biscuits, fructose sweetened protein drinks
etc) even if the label says low GI.
Source:
ABC Health Report - Dr Norman Swan interviews
Obesity expert Dr Robert Lustig Professor
of Pediatric Endocrinology, University of
California http://www.abc.net.au/rn/healthreport/stories/2007/1969924.htm
Last
Updated: July 2008
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