[PHNUTR-L] Fructose

[THECOUCH at aol.com]

Chris,

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 
quoted.  Hmmm...

Regards,


Monika M. Woolsey, MS, RD
<A HREF="http://www.afterthediet.com/">http://www.afterthediet.com</A>
Polycystic Ovary Syndrome:  The Perfect Endocrine Storm
Tucson, Arizona, April 24-25, 2004



Am J Clin Nutr. 2002 Nov;76(5):911-22.  <A HREF="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Display&dopt=pubmed_pubmed&from_uid=12399260">Related Articles,</A><A HREF="javascript:PopUpMenu2_Set(Menu12399260,'','','','','');">Links</A>  

Comment in: 
<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...
URL: http://mailman2.u.washington.edu/pipermail/phnutr-l/attachments/20040329/645dfceb/attachment-0001.html