Here is a good read: Follow this
link. I found it to be educating.
Here is a reference for more on this (full text is free - and a very good read):
<div></div><div id="QUOTEHEAD">QUOTE</div><div id="QUOTE"> Am J Clin Nutr. 2002 Nov;76(5):911-22. Links
Comment in:
Am J Clin Nutr. 2003 Oct;78(4):804-5; author reply 805-6.
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.
PMID: 12399260 [PubMed - indexed for MEDLINE]
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This is not to say we become instantly fatter when eating fructose, but I think that when we are fully carb-loaded additional fructose will only lead to more fat. As my simulation software (and from researchers discussions) the amount of fat in diet directly affect the long term fat mass level. DNL becomes an issue at very high carb intake. Fructose is a good sugar when we are braking a fast, for example as part of a breakfast, when liver glycogen is low. For me, I think that 70-80 grams of fructose at this point is max (liver capacity to store glycogen). At any other point, when we have feasted on other carbs...
Post workout is not the time for slow carbs like fructose - it stays in the liver - we need monosaccarides at that time. At all other times stick to starchy, low glycemic carbs.
I have not visited BR.com for a while... I guess there are more data available today on the effects of fructose but I do not think any new data would alter the metabolic pathway, or anything.
For anyone who cares, here's some stats...
2008-11-18:
Weight: 70,4 kg (154,9 lbs) (+0,8 kg [1,8 lbs] from yesterday) (+0,9 kg [2,0 lbs] from start, 90 days ago)
Routine: Recovery
Energy expenditure: 2684 kcal (BMR: 1636 kcal; Activities: 610 kcal; TEM: 439 kcal)
Energy intake: 2948 kcal (+264 kcal)
Macros: 46% (288g) P; 35% (248g) C; 19% (59g) F
