THECOUCH at aol.com
THECOUCH at aol.com
Mon Mar 29 21:29:45 PST 2004
Here is an article from Pub Med, it may have more references for you. I
routinely ask clients to avoid HCFS, and at least here in the US it is extremely
challenging to do. It is in everything.
At one time recently I also found a document on the Internet regarding a
lawsuit in international court--I believe the US wanted Mexico to be forced to
import more HCFS and use it in its soft drinks instead of their own domestically
produced sugars. I also recall the move was being sponsored by a senator from
a state that produced a lot of corn--Iowa maybe?
I find it interesting that the only dietitian who was quoted in the article
you share represents Coca Cola and Sara Lee and no peer-reviewed research was
Monika M. Woolsey, MS, RD
Polycystic Ovary Syndrome: The Perfect Endocrine Storm
Tucson, Arizona, April 24-25, 2004
<A HREF="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14522742">Am J Clin Nutr. 2003 Oct;78(4):804-5; author reply 805-6.</A><IMG SRC="http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-notfree-ajcn-entrez.gif" WIDTH="150" HEIGHT="35" BORDER="0" DATASIZE="943">
Fructose, weight gain, and the insulin resistance syndrome.
Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ.
Department of Nutrition, University of California, Davis 95616, USA.
This review explores whether fructose consumption might be a contributing
factor to the development of obesity and the accompanying metabolic abnormalities
observed in the insulin resistance syndrome. The per capita disappearance
data for fructose from the combined consumption of sucrose and high-fructose corn
syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both
plasma insulin and leptin act in the central nervous system in the long-term
regulation of energy homeostasis. Because fructose does not stimulate insulin
secretion from pancreatic beta cells, the consumption of foods and beverages
containing fructose produces smaller postprandial insulin excursions than does
consumption of glucose-containing carbohydrate. Because leptin production is
regulated by insulin responses to meals, fructose consumption also reduces
circulating leptin concentrations. The combined effects of lowered circulating leptin
and insulin in individuals who consume diets that are high in dietary fructose
could therefore increase the likelihood of weight gain and its associated
metabolic sequelae. In addition, fructose, compared with glucose, is
preferentially metabolized to lipid in the liver. Fructose consumption induces insulin
resistance, impaired glucose tolerance, hyperinsulinemia,
hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear.
Although there are existing data on the metabolic and endocrine effects of dietary
fructose that suggest that increased consumption of fructose may be detrimental
in terms of body weight and adiposity and the metabolic indexes associated
with the insulin resistance syndrome, much more research is needed to fully
understand the metabolic effect of dietary fructose in humans.
-------------- next part --------------
An HTML attachment was scrubbed...
More information about the PHNUTR-L