Sweet as! Four stories on sugars and sweetness feature in this issue of GI News.
Run Rodent, Run!
In September 2014, a study linking artificial sweeteners (aspartame, sucralose and saccharin) to the risk of diabetes hit the headlines. If you saw the headlines, you may have been tempted to bin your favourite alternative sweetener. What got lost in reporting was the fact that most of this research was in mice. They were overfed pure saccharin – the sweetener identified by the researchers as the most potent, and the focus of the majority of the research in the rodents. The result: it altered their glucose tolerance and gut bacteria (microbiome). The small observational study in humans tacked on the end of the report looked at all sweeteners, but it was in a very small number of people for this kind of research, and it only proves associations – not causality. Dr Alan Barclay has put some context around this.
- Saccharin has been around for over 100 years and the diabesity epidemic has only developed over the last few decades.
- The use of saccharin is decreasing. It is no longer a particularly popular alternative sweetener—aspartame (which was included in the study), stevia and cyclamate are much more widely used in Australia.
- The rats were fed around 17 times more saccharin than a typical (Australian) adult consumes according to the results of Australia’s most recent sweetener survey.
“Perhaps the simple conclusion” says Alan “should have been that it’s not a great idea to feed your pet mouse vast quantities of pure saccharin. The take-home? Ultimately, the dose makes the poison. Even too much water can kill you.”
Next time you see sensationalist headlines proclaiming “X” sweetener causes obesity / diabetes / heart disease, etc… ask: Was the research conducted in people; and would you consume the amount of sweetener the participants were fed on a regular basis over a long period of time? If you answer no, chances are the research finding does not mean much to you. If you choose to use an alternative sweetener to help cut calories or manage your blood glucose levels, do so in moderation (as in all things), and opt for using a variety of nonnutritive sweeteners to reduce the likelihood of excessive consumption of any single one.
We have a soft spot for things that taste sweet. Cats don’t. The mammalian sweet receptor is composed of two protein subunits, known as T1R2 and T1R3. Each is coded for by a separate gene. In place of a functional sweet taste receptor gene, researchers from the Monell Chemical Senses Center discovered that domestic cats (Felis silvestris catus) have a defect in the gene encoding the T1R2 protein that makes them unable to detect sweet tastes. They also detected the same gene defect in tiger and cheetah, suggesting that it is common to species throughout the cat family.
“This type of gene is known as a pseudogene and is somewhat like a molecular fossil,” comments Xia Li, PhD, a molecular geneticist at Monell. “It presumably once coded a functional protein, but no longer does so.” Li explains, “Genes contain signals that indicate the start and stop points for information about the amino acid sequence of a given protein. We found a deletion of 247 base pairs in the gene that codes for T1R2 in the cat. As a consequence of this deletion, the stop point is shifted. The T1R2 protein is not made and thus is unavailable to join with T1R3 to form a working sweet taste receptor.” This molecular change was very likely an important event in the evolution of the cat’s carnivorous behaviour according to the researchers.
But around 57.6 percent of the domestic cat population in the US is overweight or obese according to research carried out by the Association for Pet Obesity Prevention (APOP). Since it can’t be an excess of added sugars they are consuming, perhaps it’s a case of way too many calories and a super-sedentary lifestyle?
Our sweet tooth has a long history we reported in GI News in January 2013.The earliest visual evidence is in rock art dating back thousands of years that depicts honeycombs, swarms of bees, and honey collecting. But there is also much older evidence in the evolution of the mutually beneficial relationship between the honeyguide bird and the hunter-gatherer in Africa. Yale anthropologist Brian Wood and his co-researchers describe this in Evolution and Human Behaviour.
Photo courtesy Brian Wood
“When searching their woodlands for nests of honey bees, Hadza hunter-gatherers (an ethnic group that has traditionally subsisted from hunting and gathering who live in northern Tanzania near Lake Eyasi) are often helped by the Greater Honeyguide (Indicator indicator), a bird that flies ahead of them, leading them to nests of the honey bee, Apis mellifera …. During a typical guiding sequence, a honey-hunter follows the bird as it swoops, widely fanning its feathers, from one perch to another, and the two engage in an ongoing exchange of whistles and chatter. The honeyguide eventually perches near the nest of an A. mellifera colony, which is usually inside a tree. The honey-hunter then conducts a final search for the exact tree and nest location. After finding the nest, the honey-hunter lights a torch, climbs up to the nest entrance, blows in smoke to subdue the bees, chops open the tree with an axe, and reaches in for the honeycomb. While this happens, the honeyguide usually perches quietly nearby. The special nature of the Hadza-honeyguide relationship is attested to by the fact that honeyguides often perch comfortably within arrow-shot distance of Hadza, even though men hunt other bird species of similar size.”
What is the origin of this behaviour? … We propose that in a first, commensal phase, honeyguides preyed upon the bee nests and discarded honeycomb that hominins made available through their honey hunting. In a second, mutualistic phase, honeyguides evolved the habit of actively leading hominins to bee nests. Finally, in a third phase of manipulative mutualism, hominins began to actively change the payoffs received by honeyguides – either by actively “rewarding” them or by reducing their immediate payoff. The Hadza we observed did not actively reward honeyguides, but such may occur in other contexts … Based on within-species mtDNA variation scientists conservatively estimate that I. indicator is at least 3 million years old. We think it is reasonable to assume that an initial commensal association between hominins (Ardipithecus ramidus or an Australopithicine) and honeyguides arose in the Pliocene.”
Who can resist a story about jet-lagged mice? We can’t, and neither could Ted Kyle of ConscienHealth. Those headlines about jet-lagged mice and jet-lag causing obesity all come from a new publication in Cell that’s really about the effect of a disrupted sleep cycle on gut microbes. You can read all about it HERE.
Coca-Cola is about to launch the lower-kilojoule Coca-Cola Life in Australia. Like Pepsi Next, it’s a blend of stevia and sugar that provides the sweetness. So what is stevia? This edited extract from The Ultimate Guide to Sugars and Sweeteners reproduced courtesy The Experiment Publishing (New York) explains.
Stevia’s leaves contain steviol glycosides – some of the sweetest plant compounds that have been successfully commercialized as high-intensity sweeteners. Stevioside and rebaudioside A are the two you will find in foods and beverages and in tabletop and pourable products. They have zero calories and no impact on blood glucose levels, because the body does not metabolize them and they are excreted.
The favorite marketing word to describe steviol glycosides is “natural” because they come from a plant and are not entirely created in a laboratory beaker. Manufacturers tend to describe the extraction process as similar to making tea: steeping the leaves in water, then purifying the sweet extract. In fact, the journey through the laboratory to get to the sweetener in the packet or box is a little more complicated. Here’s how it was described in the JEFCA Compendium of Food Additive Specifications: ‘The leaves are extracted with hot water and the aqueous extract is passed through an adsorption resin to trap and concentrate the component steviol glycosides. The resin is washed with a solvent alcohol to release the glycosides and the product is recrystallized from methanol or aqueous ethanol. Ion exchange resins may be used in the purification process. The final product may be spray-dried.’
Stevia consumer products come in sachets, tablets, liquids, and spoon-for-spoon granules. As with other high-intensity sweeteners, the ingredients list for stevia will include bulking and anticaking agents so you can pour it into a cup of coffee or measure it into your cooking and baking. In fact, when you buy stevia, you are often buying a lot of erythritol; in some brands over 99 percent of the product is erythritol. For this reason, some products are low calorie, not zero calorie, so it is important to check the ingredients list.
So, is it better for you? “It does have benefits over sugars,” says dietitian Dr Alan Barclay. “It is a good option for people who want to cut back on calories (kilojoules) and for those who need to avoid blood glucose spikes. But adding stevia to soft drinks to replace all or some of the sugars does not provide a licence to anyone to drink large quantities of these beverages. It’s no panacea. It is a better option, but water is the best choice if you want a cool drink. And claims that stevia is a key ingredient in the fight against obesity are overblown.”