Researchers at Purdue University's Ingestive Behavior Research Center fed two groups of otherwise similar rats yogurt with Sweet 'N Low (an artificial sweetener containing saccharin) or yogurt sweetened with glucose ( "A Role for Sweet Taste: Calorie Predictive Relations in Energy Regulation by Rats," Susan E. Swithers, PhD and Terry L. Davidson, PhD, Purdue University; Behavioral Neuroscience, Vol. 122, No. 1):
Three different experiments explored whether saccharin changed lab animals' ability to regulate their intake, using different assessments --the most obvious being caloric intake, weight gain, and compensating by cutting back.
The experimenters also measured changes in core body temperature, a physiological assessment. Normally when we prepare to eat, the metabolic engine revs up. However, rats that had been trained to respond using saccharin (which broke the link between sweetness and calories), relative to rats trained on glucose, showed a smaller rise in core body temperate after eating a novel, sweet-tasting, high-calorie meal. The authors think this blunted response both led to overeating and made it harder to burn off sweet-tasting calories.
"The data clearly indicate that consuming a food sweetened with no-calorie saccharin can lead to greater body-weight gain and adiposity than would consuming the same food sweetened with a higher-calorie sugar," the authors wrote. (Science Daily)
Of course you can say this isn't relevant because these are rats, not people. But rats are very good predictors of human biology, which is why they are used as one of the two basic animal models in biomedical research (the other is mice). They are mammals and so are we, and have the same basic system architecture: lungs, kidneys, blood, etc. If they aren't of any use for biology, then much of basic molecular biology is also down the drain. That doesn't stop the industry from using this line to dismiss these studies (CNN video).
If the hypothesis that breaking the link between taste and caloric intake is responsible for over compensatory intake in other foods is correct, the same result would hold for all the other non-caloric sweeteners.
Eating behavior is complicated and not easy to study. Rats observed under controlled laboratory conditions are an important tool. The authors suggest that this might be a reason obesity has increased in parallel with consumption of diet foods and drinks. I think that's a pretty long stretch.
But when it comes to the contradictory information about diet we all ingest daily, who knows?
This is an interesting study, but from what I can gather it just means that those who do use artificial sweeteners need to pay closer attention to the numbers than to their stomachs. I do think the link between energy intake and perception is noteworthy, but I further think that humans being rational beings and having created calorieless ingestibles should summarily be able to rationalize how properly to deal with such a thing. Being overweight (and thus being motivated to drink diet soda and the like) is very rarely a glandular problem, but what with the hype surrounding obesity and its causes, I really wish people would take responsibility before pointing to all kinds of science to explain why they are fat and it's not their fault.
People have enough trouble in correctly estimating the true amount of food they consume. Most overweight people tend to underestimate the number of calories they ate [with recall] as a number of studies have shown. This may add to the problem of recalling or estimating the true caloric intake.
Dietcoupon, the study is relevant and important because of what it may say about sweet taste and dietary regulation, which is important as basic science and as an adjunct to studies of metabolic regulation. Moreover, metabolic regulation of appetite and of adipose deposition are relevant to many health problems, only some of which relate to general obesity.
Let's see it repeated first. But I have to note that the general news coverage I saw failed to mention that the reason they gained weight was that they overate when they were given foods sweetened with sugar. That pretty much ignores one possible human difference: people on diets will probably avoid foods sweetened with sugar. And the sweet foods, if I understand, are the key.
this is not new. i recall a couple of studies, maybe 20 years ago, of diet soda on severely obese people, hospitalized so their entire diet could be quantified. they werre switched from regular soda to diet and back, without their knowledge. when they were switched to diet soda, their intake of other food went up so as to keep their total caloric intake unchanged. when they were switched back to regular soda, however, their total food intake remained the same, so that their total caloric intake went up, compared to the start, all without their knowledge. this ratcheting effect reflected firstly, the fact that you can't just remove calories from the diet without the body knowing and protesting; secondly, the role of things like habit influencing daily caloric intake; and thirdly, the bias of bodily systems against reducing caloric intake. at the time, the specific effect was postulated to be learned reflex of insulin release when sweet taste is encountered, causing a drop in blood sugar which then had to be compensated.
just checking; is there any doubt in anyone's mind that the manufacturers of artificial sweeteners and diet sodas, etc. test their products looking for any link at all with actual weight loss, and that if they had seen any we would have heard about it, at length?
Weren't there studies in humans reported last year, where people who drank diet soda later ate more than those who drank sugared soda?
It makes sense. If our brains link sweet to energy, and we consume sweet which gives us none, the brain saying, "ok, must eat much more sweet to get energy" is perfectly logical. Not necessarily so, but not outlandish.
"But rats are very good predictors of human biology, which is why they are used as one of the two basic animal models in biomedical research (the other is mice)."
Sorry for the wandering but you are exactly right...and that is why rats and mice are the 'undiscovered' mammalian vector for H5N1...and that is why we will, without a shadow of doubt, have an H5N1 influenced pandemic in the future.
Nutrition medicine raised that subject a few times in the past and it could not be cleared up. As far as I remember last time I tried to make up my mind about the basic question behind that, insulin release studies after ingestion of sugar versus noncaloric sweeteners (in humans) were not conclusive but hinting more to the side of rather not using sweeteners (noncaloric) when trying to keep a healthy weight or aiming at weight reduction.
Guinea pigs are also quite good models I might add, for certain questions about human physiology.
Besides that: since most discoveries about what regulates food intake find abundance of signals to increase food intake and very little to depress intake, it is indeed pretty complicated.
From a more intuitive standpoint it makes a lot of sense: we are made for survival and abundance of food is a pretty recent phenomenon. The body is not easily tricked, nor easily starved (relative speaking).
Tom-Any comment on the amplification in mice and rat gut? Is that the right term. They tested the mice and found the infected little bastard had ten times the virus of other animals in there in the endemic ones. Is that from the cannibalism of the dead?
What bothers me in these tests/discussions is that diet soda/ regular soda are considered the only two options. People do not seem to consider water to be a reasonable alternative.
I think if you never drink water when thirsty, you only consider "sweet" drinks and therefore substitute regular soda, fruit juice or chocolate milk if diet is not available. That creates a lot of extra calories.
Am I wrong or is there a lot of salt in soda? Also not good if you are just thirsty.
Drink tap water! Diet soda is just overpriced dyed and flavoured tap water.
Randolph. No I don't think so...but history has proven there is no better vector than mice and rats...and the laboratory has proven that they are very efficient processors of H5N1.
Also if you go back to environmental inteface at shorelines...there are a number of rat-like relatives (muskrat etc) and there are also ferret-like relatives as well (mink etc) so the three primary laboratory species used to model human disease behaviour also happen to be at the primary infection points including shorelines and farm-houses.
I am going to be writing a summary for PFI soon but also...a pertinent recent pivotal question in my mind is why H5N1 likes to preferably snuggle up to cities...if you think about it...if humans are not the vector for this...then it has to be rats and mice.
...and if they would do the minimum of testing, I think they would prove it.
Revere. Sorry for the thread drift. I just wanted to answer Randolph's question.
tom: I don't know what history you are talking about. Mice and rats are usually not vectors for disease (although for some they are reservoirs) and there are few epidemic diseases for which they are even important in that regard (plauge being one, although the vector there is a flea). There is no evidence that they are an existing reservoir for flu although it is possible. Handwaving is not sufficient here.
Revere. I think that is exactly the point.
I believe that as time goes on, it will become more evident that H5N1 is unlike any other influenza virus in history...and after I wrote the note to Randolph I realized that rats and mice have never been the reservoir vectors for any adapted virus in the past...and in addition, there were no reported die-offs of wild birds or poultry in and before 1918 either...and maybe more importantly, there were no reports that the virus had the ability to kill birds or their eggs.
Also I would cite the unique way that H5N1 has been circulating in wild birds and predominately waterfowl.
There really is only one way for H5N1 to want to 'snuggle' up to cities when common sense would be that this could not happen if farm animals-wild birds were the predominant reservoir and vector of infection.
Rats and mice do there rather indescrimate food behaviors connect all of the interfaces and secondly you get their droppings in both animal feed and human food and in kitchens etc...They are a far more effective vector than bats would be because bats are not so closely associated and adapted to both humans and farm animals.
There has never been an influenza virus that has ever pulled-off what H5N1 has...it has not gone away like it should have...it is continuing do advance inexplicably...
...There can only be two real explanations: rats and mice are the hidden reservoir and vector and it is highly unlikely that somehow a precursor of this bug inadvertently got out of a lab somewhere.
As far as the illusion of Biosecurity on farms or in these vaccine plants that have to keep birds and eggs alive in a pandemic...never going to happen.
...and you said...this is conjecture...a hypothesis at this point.
Sorry...I meant to say that this virus seems to have a human fingerprint on it...as in it is not natural but a precursor of this virus must have escaped from a lab somewhere...or in other words...it is too good to be natural.
Secondly, the last line should have read...and you are quite right in pointing out that I am hand waving...this is most definitely conjecture at the moment.
Thanks as always.
Sena: There are a number of diseases for which rodents are reservoirs, although it is usually not Mus musculus and Rattus norvegicus which is what Tom DVM was referring to. But even for hanta (deer mouse?) this isn't a significant contagious disease like influenza which I gather was his point. So there is nothing particularly logical about the fact that mice and rats can be infected making them a significant reservoir. They can be infected by an awful lot of agents but they are reservoirs for human disease in few and those are not major epidemic diseases (although they can cause outbreaks).
You are quite right...I stand corrected.
Does anyone know how many other vaccines (mumps-rubella-measles etc) are produced with chickens and eggs?
I think a lot of the vaccines that were produced in fertilized hen's eggs are now produced in chick embryo cell lines, aren't they?
Me, I'd nominate class Insecta as the best vectors for human disease (other than humans.) They beat anybody in Mammalia or Aves all hollow for ubiquity, population numbers, species diversity, and brevity of life cycle.
I've always said,
"NOW FAT PEOPLE ARE NOT ONLY EATING FOOD, THEIR PUTTIN' SHIT INTO THEIR BODIES THAT ISN'T EVEN FOOD"
Non caloric substance has no ability to produce work...which must be done.
Um...exactly how old is this particular study? I don't know of a single diet drink that currently is made with saccharin.
The soft drink companies used this sweetener in the 70's and early 80's, after that aspartame. The recent articles I have seen concerning these effects have always mentioned Equal (aspartame) as the one to be worried about. So which is it?
d: This is a new animal study. It is a study of rats fed yogurt with and without saccharin as a sweetener. Its results may be saccharin specific or related to the more general feature of saccharin that it is a non-caloric sweetener and hence more general.
R E G: No, most of the diet soft drinks contain 15-35 mg sodium per 8 oz. Not a problem, and IIRC Diet-Rite and a few others claim to have no sodium.
The thirst comes from two things: the sugar & whatever in regular soft drinks may make them hypertonic, so body water will be lost to the gut before it is reabsorbed, so blood becomes slightly hypertonic which triggers more thirst. The other factor in some soft drinks is the diuretic effect of caffeine [most colas, mtn. dew and a few others]. This diuretic effect is lessened in habituated caffeine consumers.
And most studies show that consumers of large amounts of regular sodas do not have a compensatory decrease in other calories. If anything, they consume even more calories than can be attributed to the calories in soda.