Posted on 10/01/2009 5:16:58 PM PDT by neverdem
Used to happen to me a lot. I would ask a smoker to please go somewhere else with a cigarette and they thought it would be funny to blow smoke at me. Since the ban that didn't happen.
If that happened, you deserved it.
If it did not happen, then I will invoke a Joe Wilson quote: "You lie!"
I deserved it? For asking someone not to smoke around me. What kind of asinine statement is that?
A proper one.
It is a legal substance.
There are plenty of other things going on upon which you could more properly focus your outrage.
It's 55 parts fructose to 45 parts glucose. That's 22% more fructose, but only 10% more than occurs in sucrose(std/ sugar).
A sigificant part of those higher sugars is maltose. That's a glucose dimer. I suspect the rest of the higher sugar component is significanly glucose n-mers. Nevertheless, fructose is ~1.2 times as sweet as sucrose and glucose is ~0.8 times as sweet. That means there should be no significant difference in the development of NASH between groups consuming either sugar exclusively, other than possibly the 10% difference.
Outrage? I think you are projecting. Regardless if it is legal it still affects people around you. Simply asking someone not to smoke around me while I am working should not be too much to ask. That you think it's okay, in fact preferable that someone should be able to blow smoke in my face, says you are a selfish, self absorbed inconsiderate person. You have the chip on your shoulder not me. All I wanted was some consideration. Since I, at times, couldn't get it then the ban was to my advantage hence the support.
Your comments reveal you to be a shallow person.
What’s the significance? This is quibling. Whether it is almost a 5/4 ratio of fructose to glucose, or almost a 4/3 ratio, overall excess fructose tends to hepatic de novo lipogenesis.
6/5.
"... overall excess fructose tends to hepatic de novo lipogenesis."
There's no evidence that supports this conclusion. The excess is only 10% and there's no mechanisms, or pathways that would prevent the fructose in sucrose from producing the same effects.
Oh, holy crap!
Your nation is collapsing around you and you are concerned about some fictitious crowd blowing tobacco smoke in your general direction.
Pitiful beyond description.
Fictitious my ass! Which is about the same as you.
You fascists have won this one for the time being.
The advocates of freedom will ultimately kick your ass when the time comes and the opportunity arises.
There's no evidence that supports this conclusion. The excess is only 10% and there's no mechanisms, or pathways that would prevent the fructose in sucrose from producing the same effects.
Seek and you shall find. Check the 1st link in comment# 1. There are related citations linked at PubMed. Check at this link. Get the entire article by clicking where it says FREE near the upper right.
Fructose consumption as a risk factor for non-alcoholic fatty liver disease.
BACKGROUND/AIMS: While the rise in non-alcoholic fatty liver disease (NAFLD) parallels the increase in obesity and diabetes, a significant increase in dietary fructose consumption in industrialized countries has also occurred. The increased consumption of high fructose corn syrup, primarily in the form of soft drinks, is linked with complications of the insulin resistance syndrome. Furthermore, the hepatic metabolism of fructose favors de novo lipogenesis and ATP depletion. We hypothesize that increased fructose consumption contributes to the development of NAFLD. METHODS: A dietary history and paired serum and liver tissue were obtained from patients with evidence of biopsy-proven NAFLD (n=49) without cirrhosis and controls (n=24) matched for gender, age (+/-5 years), and body mass index (+/-3 points). RESULTS: Consumption of fructose in patients with NAFLD was nearly 2- to 3-fold higher than controls [365kcal vs 170kcal (p<0.05)]. In patients with NAFLD (n=6), hepatic mRNA expression of fructokinase (KHK), an important enzyme for fructose metabolism, and fatty acid synthase, an important enzyme for lipogenesis were increased (p=0.04 and p=0.02, respectively). In an AML hepatocyte cell line, fructose resulted in dose-dependent increase in KHK protein and activity. CONCLUSIONS: The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption.
Yes.
Significant figures... 1.2 is closer to 1.22 than 1.25.
Thanks for the link. Note that the authors consider the 50% fructose component of sucrose as having the equivalent effect as an equal amount of fructose from HFCS. ...which is what I thought and still think. The study applies only to overweight folks. It does not apply to folks that burn fructose in muscle. If the fructose consumption occurs before exercise and insulin's been released as a consequence of glucose introduction. I note that fructose absorption lags glucose absorption from the intestine and the presence of glucose enhances muscle absorbsion of fructose.
I think the bottom line is that regardless of where the calories come from, if the glycogen stores in the muscle and liver are full, additional sugar consumption, that won’t end up driving muscle, or in substrate cycling is going to fat.
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