[QUOTE=Paleobird;1058310]Real men drink tequila straight up. None of this frou frou stuff. Rum and Coke is for getting girls drunk in high school.:cool: Sheesh![/QUOTE]
:) I try to be a responsible "adult" now. My days of downing massive quantities of tequila are well behind me. I do have a bottle in the pantry at home though.
Some science to back up the people who experience "lack of satiety" (still being hungry) after having artificial sweeteners:
[url=http://www.ncbi.nlm.nih.gov/pubmed/22561130]Experience with the high-intensity sweetener... [Behav Brain Res. 2012] - PubMed - NCBI[/url] (GLP-1 is a hormone that increases insulin secretion & increases satiety)
"► Rats given dietary supplements sweetened with saccharin gained extra body weight. ► Saccharin-exposed animals were hyperglycemic during oral glucose tolerance tests. ► Hyperglycemia in saccharin-exposed animals was not due to changes in insulin release. ► Reduced release of GLP-1 was observed in saccharin-exposed animals. ► Decreased release of GLP-1 may explain both hyperglycemia and increased food intake.
rats given dietary supplements with the high-intensity sweetener saccharin, which provides a strong sweet taste, but does not deliver calories, exhibit poorer caloric compensation for novel sweet-tasting pre-meals in short-term intake tests  and . Further, over the long-term, consumption of a saccharin-sweetened yogurt supplements resulted in increased energy intake, increased body weight gain and increased adiposity relative to consumption of the same supplements sweetened with glucose"
Interesting paper. GLP-1 induces insulin secretion, but it also increases satiety (makes you feel full). The artificial sweetener conditions you to not produce as much GLP-1 as much if you had real sugar (weakens the normal response to sweet taste), which is why you would continue to feel hungry (while the real sugar induces GLP-1 properly and makes you feel full).
"The results... suggest that a primary deficit resulting from exposure to saccharin-sweetened diets may be a decreased secretion of GLP-1 in response to sweet tastes in the mouth...secretion of GLP-1 was significantly lower, and blood glucose levels were significantly higher, in animals previously exposed to saccharin [which then consumed] glucose. Based on principles of associative learning, experience with consuming a sweet taste that is not followed by the anticipated energetic consequence [actually intaking calories at the same time] could cause the sweet taste to become less effective at eliciting release of GLP-1 over time. Release of GLP-1 by sweet taste in the mouth would then become blunted even when caloric sweeteners are subsequently consumed. This diminished ability of sweet taste to release GLP-1 could underlie increased food intake, as both peripheral and central actions of GLP-1 during meals have been directly implicated in satiety.
A reduction in the release of GLP-1 could also lead to increased
blood glucose levels by a variety of mechanisms. For example, GLP-
1 can contribute to glucose homeostasis independent of effects
on insulin release, by enhancing glucose metabolism in skeletal
muscle, liver and adipose tissue, regulating of glucose transporter
expression, suppressing of glucagon release and slowing of gastric
emptying (e.g. [23,38–58]). Thus, for example, diminished release
GLP-1 in response to a sweet-tasting food or glucose solution could
promote more rapid gastric emptying which would then lead to
more rapid delivery of glucose to the intestines, and more rapid
elevations of blood glucose levels (e.g. [23,38–58]). Increased gastric
emptying would also lead to diminished gastric distension,
reducing another potential source of satiety signals that could
contribute to increased food intake. Further, decreased glucose
utilization in muscle, liver or adipose tissue related to decreased
levels of GLP-1 would lead to higher blood glucose levels (e.g.
[23,38,39,41,50,51,53]). Lower GLP-1 release could also result in
increased blood glucose levels due to diminished suppression of
glucagon release (e.g. [40,42,45,59]).
These data are consistent with the hypothesis that dysregulation
of energy balance and glucose homeostasis can occur following
exposure to high-intensity sweeteners.
Such results are consistent with the
hypothesis that rather than preventing or reversing overweight
and obesity, consumption of foods or beverages manufactured
with high-intensity sweeteners may contribute to dysregulation
of body weight by altering cephalic phase responses. This could
occur because high-intensity sweeteners interfere with conditioned
cephalic phase responses, because glucose-sweetened foods
enhance conditioned cephalic phase responses, or both. In any of
those cases, consuming diets prepared with high-intensity sweeteners
results in augmented food intake, body weight gain, altered
glucose homeostasis and diminished release of GLP-1 compared to
the same diets prepared with glucose."
We think we can outsmart nature, but it could be that humans have really screwed themselves over with all these "diet" products and fake sweeteners... In short, we are messing ourselves up quite good with all our unnatural foods.
anyway sorry for wall of text