Blocking sweet taste receptors can help body fight off sinus infections: Researchers identify amino acids that hold the key to the process -- ScienceDaily

 Bitter taste receptors in the upper airway are a first line of defense against sinus infections, but their ability to kill harmful toxins and pathogens is blocked when the sweet taste receptors are also stimulated. While glucose and other sugars are known to trigger these sweet taste receptors, researchers at the Perelman School of Medicine of the University of Pennsylvania have now shown amino acids can also have that effect. This new understanding could help pave the way toward new treatments for chronic sinus infections. The researchers published their findings in the journal Science Signaling this week."

Here's the paper:- Bacterial d-amino acids suppress sinonasal innate immunity through sweet taste receptors in solitary chemosensory cells

Aspartame may prevent, not promote, weight loss by blocking intestinal enzyme's activity: Study identifies possible mechanism behind sugar substitute's lack of effectiveness -- ScienceDaily

A team of Massachusetts General Hospital (MGH) investigators has found a possible mechanism explaining why use of the sugar substitute aspartame might not promote weight loss. In their report published online in Applied Physiology, Nutrition and Metabolism, the researchers show how the aspartame breakdown product phenylalanine interferes with the action of an enzyme previously shown to prevent metabolic syndrome -- a group of symptoms associated with type 2 diabetes and cardiovascular disease. They also showed that mice receiving aspartame in their drinking water gained more weight and developed other symptoms of metabolic syndrome than animals fed similar diets lacking aspartame.

Aspartame blocks a gut enzyme called intestinal alkaline phosphatase (IAP) that we previously showed can prevent obesity, diabetes and metabolic syndrome; so we think that aspartame might not work because, even as it is substituting for sugar, it blocks the beneficial aspects of IAP

Autism genes are selectively targeted by environmental pollutants including pesticides, heavy metals, bisphenol A, phthalates and many others in food, cosmetics or household products

The increasing incidence of autism suggests a major environmental influence. Epidemiology has implicated many candidates and genetics many susceptibility genes. Gene/environment interactions in autism were analysed using 206 autism susceptibility genes (ASG's) from the Autworks database to interrogate ∼1 million chemical/gene interactions in the comparative toxicogenomics database. Any bias towards ASG's was statistically determined for each chemical. Many suspect compounds identified in epidemiology, including tetrachlorodibenzodioxin, pesticides, particulate matter, benzo(a)pyrene, heavy metals, valproate, acetaminophen, SSRI's, cocaine, bisphenol A, phthalates, polyhalogenated biphenyls, flame retardants, diesel constituents, terbutaline and oxytocin, inter alia showed a significant degree of bias towards ASG's, as did relevant endogenous agents (retinoids, sex steroids, thyroxine, melatonin, folate, dopamine, serotonin). Numerous other suspected endocrine disruptors (over 100) selectively targeted ASG's including paraquat, atrazine and other pesticides not yet studied in autism and many compounds used in food, cosmetics or household products, including tretinoin, soy phytoestrogens, aspartame, titanium dioxide and sodium fluoride. Autism polymorphisms influence the sensitivity to some of these chemicals and these same genes play an important role in barrier function and control of respiratory cilia sweeping particulate matter from the airways. Pesticides, heavy metals and pollutants also disrupt barrier and/or ciliary function, which is regulated by sex steroids and by bitter/sweet taste receptors. Further epidemiological studies and neurodevelopmental and behavioural research is warranted to determine the relevance of a large number of suspect candidates whose addition to the environment, household, food and cosmetics might be fuelling the autism epidemic in a gene-dependent manner.

Artificial sweeteners are not the answer to childhood obesity. - PubMed - NCBI

While no single factor is responsible for the recent, dramatic increases
in overweight and obesity, a scientific consensus has emerged
suggesting that consumption of sugar-sweetened products, especially
beverages, is casually linked to increases in risk of chronic,
debilitating diseases including type 2 diabetes, cardiovascular disease,
hypertension and stroke. One approach that might be beneficial would be
to replace sugar-sweetened items with products manufactured with
artificial sweeteners that provide sweet tastes but with fewer calories.
Unfortunately, evidence now indicates that artificial sweeteners are
also associated with increased risk of the same chronic diseases linked
to sugar consumption. Several biologically plausible mechanisms may
explain these counterintuitive negative associations. For example,
artificial sweeteners can interfere with basic learning processes that
serve to anticipate the normal consequences of consuming sugars, leading
to overeating, diminished release of hormones such as GLP-1, and
impaired blood glucose regulation. In addition, artificial sweeteners
can alter gut microbiota in rodent models and humans, which can also
contribute to impaired glucose regulation. Use of artificial sweeteners
may also be particularly problematic in children since exposure to
hyper-sweetened foods and beverages at young ages may have effects on
sweet preferences that persist into adulthood. Taken as a whole, current
evidence suggests that a focus on reducing sweetener intake, whether
the sweeteners are caloric or non-caloric, remains a better strategy for
combating overweight and obesity than use of artificial sweeteners.

Artificial Sweeteners Induce Glucose Intolerance by Altering... : Obstetrical & Gynecological Survey

Noncaloric artificial sweeteners (NASs) are popular because of their low caloric intake and perceived health benefits for weight loss and normalization of blood sugar levels. Artificial sweeteners have been increasingly introduced as an additive into common foods as an alternative to high-caloric sugars. However, increased consumption has coincided with a dramatic increase worldwide in obesity and diabetes epidemics. Scientific data supporting the safety and benefits of NAS consumption are sparse and controversial.

Most NASs are not digested in the gastrointestinal tract and directly encounter the intestinal microbiota. The diet modulates microbiota composition and function in the healthy/lean state as well as in obesity and diabetes mellitus. Intestinal dysbiosis has been associated with propensity to metabolic syndrome.

The investigators studied NAS-mediated changes of microbiota composition and function of mice to determine whether chronic NAS consumption exacerbates glucose intolerance in mice. Formulations of saccharin, sucralose, or aspartame were added to the drinking water of mice. The data provide conclusive proof that NAS-mediated intestinal dysbiosis is directly responsible for the development of glucose intolerance in mice. Treating mice with antibiotics eradicated many intestinal bacteria and fully reversed artificial sweeteners' effects on glucose metabolism. Transfer of fecal microbiota from mice that consumed artificial sweeteners to “germ-free” mice resulted in a complete transmission of the glucose intolerance into the recipient mice. Incubating the microbiota anerobically with artificial sweeteners also induced glucose intolerance in the sterile mice. Profound changes in the population of intestinal bacteria have been linked to host susceptibility to obesity, diabetes, and other metabolic diseases in both mice and humans. Similar NAS-induced dysbiosis and glucose intolerance were demonstrated in healthy human subjects.

These findings show that NAS consumption in both mice and humans increases the risk of glucose intolerance through adverse metabolic effects mediated by intestinal dysbiosis. The data suggest that the widespread use of NAS should be reassessed.

Artificial sweeteners linked to abnormal glucose metabolism

Artificial sweeteners, promoted as aids to weight loss and diabetes
prevention, could actually hasten the development of glucose intolerance
and metabolic disease; and they do it in a surprising way: by changing
the composition and function of the gut microbiota – the substantial
population of bacteria residing in our intestines. These findings, the
results of experiments in mice and humans, were published today in Nature.
Among other things, says Dr. Eran Elinav of the Weizmann Institute's
Immunology Department, who led this research together with Prof. Eran
Segal of Computer Science and Applied Mathematics Department, the
widespread use of artificial sweeteners in drinks and food may be
contributing to the obesity and diabetes epidemic that is sweeping much
of the world.


Artificial sweeteners induce glucose intolerance by altering the gut microbiota

Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements

The negative impact of consuming sugar-sweetened beverages on weight and other health outcomes has been increasingly recognized; therefore, many people have turned to high-intensity sweeteners like aspartame, sucralose, and saccharin as a way to reduce the risk of these consequences. However, accumulating evidence suggests that frequent consumers of these sugar substitutes may also be at increased risk of excessive weight gain, metabolic syndrome, type 2 diabetes, and cardiovascular disease. This paper discusses these findings and considers the hypothesis that consuming sweet-tasting but noncaloric or reduced-calorie food and beverages interferes with learned responses that normally contribute to glucose and energy homeostasis. Because of this interference, frequent consumption of high-intensity sweeteners may have the counterintuitive effect of inducing metabolic derangements.

'Light' sodas may hike diabetes risk: study (Update)

The paper noted previous research which had showed that aspartame—for long the most used artificial sweetener—has a similar effect on blood glucose and insulin levels as the sucrose used in regular sweeteners.

Read more at: http://medicalxpress.com/news/2013-02-sodas-hike-diabetes.html#jCp

Fructose and sugar substitutes alter gut microbiota

High consumption of fructose, artificial sweeteners, and sugar alcohols affect host-gastrointestinal microbe interactions and may contribute to the development of metabolic disorders and obesity, according to research published in the September issue of Obesity Reviews.

Read more at: http://medicalxpress.com/news/2012-09-fructose-sugar-substitutes-gut-microbiota.html#jCp

saccharin and other sweeteners may paradoxically foster overeating.

At some level, the brain can sense a difference between sugar and no-calorie sweeteners, several studies have demonstrated. Using brain imaging, San Diego researchers now show that the brain processes sweet flavors differently depending on whether a person regularly consumes diet soft drinks.The new findings may help explain an oft-observed association between diet soda consumption and weight gain, the researchers say. Once fooled, the brain’s sweet sensors can no longer provide a reliable gauge of energy consumption.

Long-term consumption of aspartame and brain antioxidant defense status.

The present study investigated the effect of long-term intake of aspartame, a widely used artificial sweetener, on antioxidant defense status in the rat brain. Male Wistar rats weighing 150-175 g were randomly divided into three groups as follows: The first group was given at a dose of 500 mg/kg body weight (b.w.); the second group was given aspartame at dose of 1,000 mg/kg b.w., respectively, in a total volume of 3 mL of water; and the control rats received 3 mL of distilled water. Oral intubations were done in the morning, daily for 180 days. The concentration of reduced glutathione (GSH) and the activity of glutathione reductase (GR) were significantly reduced in the brain of rats that had received the dose of 1,000 mg/kg b.w. of aspartame> whereas only a significant reduction in GSH concentration was observed in the 500-mg/kg b.w. aspartame-treated group. Histopathological examination revealed mild vascular congestion in the 1,000 mg/kg b.w. group of aspartame-treated rats. The results of this experiment indicate that long-term consumption of aspartame leads to an imbalance in the antioxidant/pro-oxidant status in the brain, mainly through the mechanism involving the glutathione-dependent system.

Splenda Causes Cancer Concern

Following the discovery in a new study that mice have a higher risk of developing cancer after eating the popular British-made low-calorie artificial sweetener sucralose (Splenda), a leading cancer scientist calls for urgent research

Effects of artificial sweeteners on body weight, food and drink intake.

Far from benefiting body weight, long term treatment with  saccharin, cyclamate or  acesulfame-K based sweeteners, and aspartame increased body weight in mice.

Waistlines in people, glucose levels in mice hint at sweeteners' effects: Related studies point to the illusion of the artificial

"Diet" soft drink consumption is associated with increased waist circumference in humans, and aspartame raised fasting glucose (blood sugar) in diabetes-prone mice.

The toxic effects of aspartame have been known for decades following John Olney's pioneering work with excitotoxins in 1969:
In 1981, this paper , by Takasaki et al showed that feeding aspartame to thirsty young  mice produced ledions in the arcuate nucleus, the hypothalamic region that controls appetite.

Other work has also linked aspartame to weight gain Yang 2010 and others