Not sure if this is the place to post or not. When I saw this commercial, I instantly thought of the Cycle Diet Board . It goes something like this:
Girl is eating popsicle. Boy: "you shouldn't be eating that, it has high fructose corn syrup" Girl: "Why is that bad for me?". Boy: (silence) "I don't know". Girl: something about 'all things in moderation'. Naturally, sponsored by some corn council.
Anyway, I found it interesting. And also found myself thinking - could I actually say why corn syrups are bad? hmmm....
In case you're wondering why I suggest to avoid it and other refined sugars is that it's very hard on the liver. High fructose sugar is not the same as sugar cane or honey, it's not natural and the body isn't able to process it in the same way as sucrose. The body has a harder time recognizing the calories, which may actually increase appetite.
Here's a more scientific explanation from the
American Journal of Clinical Nutrition
This is just an exerpt from the research article. If you want to read the full article it's available inside the link.
Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity12
[/suP] George A Bray, Samara Joy Nielsen and Barry M Popkin
[size=-1]1 From the Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA (GAB), and the Department of Nutrition, University of North Carolina, Chapel Hill (SJN and BMP). [/size]
Absorption of fructose The digestive and absorptive processes for glucose and fructoseare different. When disaccharides such as sucrose or maltoseenter the intestine, they are cleaved by disaccharidases. Asodium-glucose cotransporter absorbs the glucose that is formedfrom cleavage of sucrose. Fructose, in contrast, is absorbedfurther down in the duodenum and jejunum by a non-sodium-dependentprocess. After absorption, glucose and fructose enter the portalcirculation and either are transported to the liver, where thefructose can be taken up and converted to glucose, or pass intothe general circulation. The addition of small, catalytic amountsof fructose to orally ingested glucose increases hepatic glycogensynthesis in human subjects and reduces glycemic responses insubjects with type 2 diabetes mellitus (12
), which suggeststhe importance of fructose in modulating metabolism in the liver.However, when large amounts of fructose are ingested, they providea relatively unregulated source of carbon precursors for hepaticlipogenesis.
Fructose and insulin release
Along with 2 peptides, glucose-dependent insulinotropic polypeptideand glucagon-like peptide-1 released from the gastrointestinaltract, circulating glucose increases insulin release from thepancreas (13
). Fructose does not stimulate insulin secretionin vitro, probably because the ß cells of the pancreaslack the fructose transporter Glut-5 (15
). Thus, when fructoseis given in vivo as part of a mixed meal, the increase in glucoseand insulin is much smaller than when a similar amount of glucoseis given. However, fructose produces a much larger increasein lactate and a small (1.7%) increase in diet-induced thermogenesis(17
), which again suggests that glucose and fructose have differentmetabolic effects. Insulin and leptin
Insulin release can modulate food intake by at least 2 mechanisms.First, Schwartz et al (18
) have argued that insulin concentrationsin the central nervous system have a direct inhibitory effecton food intake. In addition, insulin may modify food intakeby its effect on leptin secretion, which is mainly regulatedby insulin-induced changes in glucose metabolism in fat cells(19
). Insulin increases leptin release (21
) with a timedelay of several hours. Thus, a low insulin concentration afteringestion of fructose would be associated with lower averageleptin concentrations than would be seen after ingestion ofglucose. Because leptin inhibits food intake, the lower leptinconcentrations induced by fructose would tend to enhance foodintake. This is most dramatically illustrated in humans wholack leptin (22
). Persons lacking leptin (homozygotes) aremassively obese (22
), and heterozygotes with low but detectableserum leptin concentrations have increased adiposity (23
), whichindicates that low leptin concentrations are associated withincreased hunger and gains in body fat. Administration of leptinto persons who lack it produces a dramatic decrease in foodintake, as expected. Leptin also increases energy expenditure,and during reduced calorie intake, leptin attenuates the decreasesin thyroid hormones and 24-h energy expenditure (24
). To theextent that fructose increases in the diet, one might expectless insulin secretion and thus less leptin release and a reductionin the inhibitory effect of leptin on food intake, ie, an increasein food intake. This was found in the preliminary studies reportedby Teff et al (25
). Consumption of high-fructose meals reduced24-h plasma insulin and leptin concentrations and increasedpostprandial fasting triacylglycerol concentrations in womenbut did not suppress circulating ghrelin concentrations. Fructose and metabolism
The metabolism of fructose differs from that of glucose in severalother ways as well (3
). Glucose enters cells by a transportmechanism (Glut-4) that is insulin dependent in most tissues.Insulin activates the insulin receptor, which in turn increasesthe density of glucose transporters on the cell surface andthus facilitates the entry of glucose. Once inside the cell,glucose is phosphorylated by glucokinase to become glucose-6-phosphate,from which the intracellular metabolism of glucose begins. Intracellularenzymes can tightly control conversion of glucose-6-phosphateto the glycerol backbone of triacylglycerols through modulationby phosphofructokinase. In contrast with glucose, fructose enterscells via a Glut-5 transporter that does not depend on insulin.This transporter is absent from pancreatic ß cellsand the brain, which indicates limited entry of fructose intothese tissues. Glucose provides "satiety" signals to the brainthat fructose cannot provide because it is not transported intothe brain. Once inside the cell, fructose is phosphorylatedto form fructose-1-phosphate (26
). In this configuration, fructoseis readily cleaved by aldolase to form trioses that are thebackbone for phospholipid and triacyglycerol synthesis. Fructosealso provides carbon atoms for synthesis of long-chain fattyacids, although in humans, the quantity of these carbon atomsis small. Thus, fructose facilitates the biochemical formationof triacylglycerols more efficiently than does glucose (3
).For example, when a diet containing 17% fructose was providedto healthy men and women, the men, but not the women, showeda highly significant increase of 32% in plasma triacylglycerolconcentrations (27
). Overconsumption of sweetened beverages
One model for producing obesity in rodents is to provide sweetened(sucrose, maltose, etc) beverages for them to drink (28
). Inthis setting, the desire for the calorically sweetened solutionreduces the intake of solid food, but not by enough to preventa positive caloric balance and the slow development of obesity.Adding the same amount of sucrose or maltose as of a solid inthe diet does not produce the same response. Thus, in experimentalanimals, sweetened beverages appear to enhance caloric consumption.
Speaking of sweetners, is honey an ok food on the cycle diet? I hope you say yes b/c I've been using it in cooking instead of sugar. It tastes great in sweet potatoes or salmon and no one knew I didn't use sugar in my sweet potatoe dish.