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Lets make sure I understand your argument and please correct me if I am wrong, which I often am.
“…thus, the fructose and glucose from hfcs can enter directly through the stomach lining without needing to be absorbed through the intestine, while the fructose and glucose in sucrose must first be separated by the sucrase enzyme in the intestine. while its true that stomach acid can dissolve the chemical bond in sucrose, this isn’t a very efficient process and most of the sucrose still needs to be broken down in the intestine by the sucrase enzyme. if it were an efficient process, the sucrase enzyme wouldn’t need to exist.”
the main importance of this fact, that sucrose digests more slowly, is that it allows for a slower, more controlled release of fructose and glucose into the bloodstream, rather than the instantaneous spike which occurs with the already unbound sucrose and glucose in hfcs.”
Now lets test this. If this were true then when individuals consume either sucrose or HFCS then we would see clear differences in leptin, insulin, satiation, etc.
As stated in my first response: ?Consumption of fructose-sweetened beverages resulted in glucose and insulin AUCs that were significantly lower than the AUCs induced by glucose consumption (P ?? 0.01, P ?? 0.001 glucose and insulin, respectively, Tukey’s posttest). As ex- expected, consumption of the HFCS- and sucrose-sweetened beverages resulted in glucose and insulin AUCs that tended to be intermediate between the higher AUCs induced by glucose consumption and the lower AUCs induced by fructose. – http://www.ncbi.nlm.nih.gov/pubmed/18469239
Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women.
” …when fructose is consumed in the form of HFCS, the measured metabolic responses do not differ from Suc in lean women. Further research is required to examine appetite responses and to determine if these findings hold true for obese individuals, males, or longer periods.” – http://www.ncbi.nlm.nih.gov/pubmed/17234503
” Compared with pure glucose, fructose is thought to be associated with insufficient secretion of insulin and leptin and suppression of ghrelin. However, when HFCS is compared with sucrose, the more commonly consumed sweetener, such differences are not apparent, and appetite and energy intake do not differ in the short-term.”
This is only the tip of the ice burg of data and I could posts data showing different results where Sucrose and HFCS do differ in responses but those studies tend to be on the other side of the spectrum and are poorly controlled. However there is some good research coming from San Diego State ( my alam mater) on the difference between honey and HFCS ( all by mark kern)
So Essentially I’m not promoting HFCS over sucrose or vic versa, I’m simply concerned with getting the science correct and the hypothesis that the bond in sucrose has a “meaningful” effect on leptin, insulin, and ghrelin as been shown to be erroneous. As James Rippe said: ?It’s like spitting into the ocean,?.
– Matt Stone
I think I have problem…I’m addicted to knowledge, please write a book to cure me of this awful and disgusting disease hahaScott Slifer-MosherParticipant
In Reference to your statement…”I’ve researched why HFCS might cause acne more readily than sucrose, and the most logical reasoning seems to be that HFCS is comprised of unbound fructose and glucose, whereas sucrose is comprised of bound fructose and glucose. Unbound, fructose and glucose need undergo no digestion and enter straight into the blood stream. The fructose is processed by the liver into triglycerides, whereas the glucose triggers insulin release….Now I’m sure all you health nerds have read this stuff before, but I just thought it was interesting that HFCS is entirely unbound and therefore rapidly assimilated, whereas sucrose needs to be digested, which equals slower assimilation.”
I have a difference of opinion based on my own research which I would Like to share:
First and foremost, let it be noted that HFCS is not just pure fructose and that it is basically the same as sucrose (50% Fructose:50% Glucose)
High fructose corn syrup is a misnomer… There is nothing high or large about high fructose corn syrup. Most HFCS mixtures fall between a range of 42% -55% fructose and the rest being glucose along with a very tiny percentage being from the by products of the chemical reaction. HFCS is even metabolized identically like sucrose in humans…
?By every metabolic process known to man, the body breaks down HFCS and sucrose identically,? Rippe adds.While the body does expend some metabolic energy to break sucrose into its two components, Rippe says it does not account for any notable energy expenditure. ?It’s like spitting into the ocean,? he notes. ?Sucrose is not healthier because you have to break that bond. – http://magissues.farmprogress.com/MDS/MS01Jan11/mds018.pdf
The only difference between Sucrose and HFCS is that glucose and fructose are bound in sucrose but with HFCS they are unbound and breaking that bond is pretty insignificant in the grand scope of digestion, metabolism, and cellular utilization.
?The only practical difference between sucrose and HFCS is in the bonding. The glucose & fructose in HFCS is mainly free and unbonded, while it is bonded in sucrose. However, this makes no *meaningful* difference in regards to metabolism in the body. The bonds in sucrose are quickly broken when sucrose hits the acid environment of the stomach. This means that once sucrose hits the stomach, it’s no different from HFCS. Once you get to the small intestine, metabolism is *exactly* the same. This *little bit of difference* does not lead to the problems Dr. Lustig talks about. The fact is, HFCS and sucrose are identical as far as your body is concerned. The difference in bonding wouldn’t make a shred of difference in regards to your health. – http://www.alanaragonblog.com/2010/02/19/a-retrospective-of-the-fructose-alarmism-debate/
Further Evidence from Haval at the Department of Molecular Biosciences, School of Veterinary Medicine, Davis CA:
“Consumption of fructose-sweetened beverages resulted in glucose and insulin AUCs that were significantly lower than the AUCs induced by glucose consumption (P ?? 0.01, P ?? 0.001 glucose and insulin, respectively, Tukey’s posttest). As ex- pected, consumption of the HFCS- and sucrose-sweetened bev- erages resulted in glucose and insulin AUCs that tended to be intermediate between the higher AUCs induced by glucose consumption and the lower AUCs induced by fructose.” – http://www.ncbi.nlm.nih.gov/pubmed/18469239
We also need to take into account the vehicle of transportation…I.e Liquids v.s Solids that are delivering the calories as this plays a huge role as well:
“There are several mechanisms that may account for this phenomenon. The act of masticating the solid may provide an internal satiety signal not triggered by simply swallowing the liquid. Haber et al 24 reported higher satiety ratings from individuals consuming apple slices that had to be chewed when compared to ratings after eating apple puree or drinking juice that required less mastication. Both early pancreatic exocrine and endocrine responses to oral stimulation with viscous or solid stimuli are greater than those to ?uids.25 ? 27” — http://www.nature.com/ijo/journal/v24/n6/pdf/0801229a.pdf
Essentially liquid calories are inferior to solid calories in terms of compensating food intake, but also it doesn’t matter which sweetener is used but rather the vehicle in which that sweetener is added to (i.e. solid or liquid).
Also I think you may be confused about fructose metabolism as Fructose is metabolized into more than just triglycerides… and sometimes depending on the state of the person little to no fatty acids are produced during fructose metabolism:
The Fate of Fructose Summarized:
50% Turned into Glucose
25% Turned into lactate
17% Turned into Glygoen
8% left for DNL or being directly oxidized to C02 via the TCA cycle
Last but not Least, keep in my mind that percentage’s in process like DNL can be misleading. When looking at the increases in DNL we see that after a fructose load DNL increased by a whopping 30% from baseline but the actual amount being converted to FA is not 30%. Meaning that the process increased by 30%, not the end products…the end products only increased slightly. For instance lets say you have 10 marbles and the process by which you acquire marbles increased by 30% but the rate in which you acquire marbles is 1 marble per 2 weeks or month… the increase in actual marbles is only maybe 10.3 or 11 but the 30% makes you thinks it is a lot more then it actually is. Just remember that there is difference between a percentage increase in Fatty synthesis and the actual end products.
“… fructose caused a qualitative induction of DNL, that is, the fraction of circulating palmitate derived from DNL rose to ca. 30%, but ` 5% of the fructose load was converted to VLDL-FA.” – http://www.ncbi.nlm.nih.gov/pubmed/10365981