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#sweeteners — Public Fediverse posts

Live and recent posts from across the Fediverse tagged #sweeteners, aggregated by home.social.

  1. Between agave, sugar, and honey 🍯 which is your favorite sweetener?

    Let’s hear your choice 👇

    #Food #Sweeteners #Honey #Agave #Sugar #Poll

  2. Do we believe a paper written by two authors funded by the sweetener industry and which, perhaps too conveniently, report no harm? They could have cherry-picked among the abundant and divergent reported evidence to fit a preconceived point of view given their obvious conflict of interest with their funders and employers. I would like to see an entirely independent original study, rather than a mere review (no new data included) of published literature.

    What we know so far is that most edible substances in tiny fractions can hardly cause any harm. Harms arise from excessive consumption (high quantity) and lack of variety (low quality). A diet coke once a month won't have any long lasting deleterious effects, but once a day is very likely to hurt you.

    If you want a general rule of thumb: don't eat anything that your great grandma – the last generation in your family past that lived entirely off the land they cultivated with their own hands, and who lived to 94 years old in good mental and physical health – wouldn't have eaten.

    Hope you found this interesting.

    6/6

    #sweeteners #nutrition #sugars

  3. Then there is this review (no original work, merely a commentary on multiple studies):

    "Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release"
    Renwick and Molinary, 2010
    cambridge.org/core/journals/br

    CAVEAT: both authors funded or employed by the artificial sweetener industry. They have a conflict of interest and thankfully they have declared it.

    "Thus, the extensive in vivo human database ... shows that low-energy sweeteners do not have any unwanted effects on appetite or subsequent food intake, insulin or blood glucose levels, glucose homeostasis or blood pressure."

    "It seems that the authors of papers who reported elegant research on the molecular biology or glucose signalling in the intestine and who speculated about a possible loss of equilibrium between taste receptor activation, nutrient assimilation and appetite were unaware of the extensive database demonstrating the safety and efficacy of low-energy sweeteners."

    Turns out studies in animals used a dose of sweeteners far higher than what is allowed as a daily intake in humans:

    "Any physiological perturbations, such as changes in glucose homeostasis, produced at the levels of intake by human subjects would have resulted in serious adverse sequelae at the 100-fold higher dose levels used in animal safety studies. Regulatory safety studies include numerous pre-defined endpoints including blood biochemistry measurements, which would have revealed any significant effect on glucose homeostasis. It should not be forgotten that the Acceptable Daily Intake (ADI) for low-energy sweeteners are 100-fold lower than the daily intakes that did not produce any adverse effects in animals."

    5/6

    #sweeteners #nutrition #sugars

  4. Then in 2014, a study in mice found another possible mechanism, coexisting with the one above:

    "Artificial sweeteners induce glucose intolerance by altering the gut microbiota"
    Suez et al. 2014
    nature.com/articles/nature1379

    "Here we demonstrate that consumption of commonly used NAS [non-caloric artificial sweeteners] formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota."

    The above means that eating sweeteners impacts bacteria in the gut in a way that causes glucose intolerance. These effects can be cancelled by killing the gut bacteria with antibiotics:

    "These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment,"

    And conversely, the effect can also be transferred to another mouse that didn't consume sweeteners simply by giving it the gut bacteria of a mouse that did, or by giving it bacteria cultivated in the lab that was exposed to sweeteners:

    "and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS."

    There are many studies in humans on the impact of sweetener consumption as a replacement for sugar, but the evidence seems inconclusive either way: it is not found to be beneficial for obese patients or patients with diabetes, but it is not found to be deleterious either.

    4/6

    #sweeteners #nutrition #sugars

  5. A consequence of a type of gut cells tasting sugars is that they then stimulate other types of gut cells (enterocytes: the enteric system is the gut) to absorb more sugar:

    "Glucose and galactose enter enterocytes through the Na+, glucose cotransporter 1 (SGLT1) ... The amount of expression of SGLT1 in enterocytes is regulated by diet: high carbohydrate diets or supplementation with sugar- or sucralose-sweetened drinking water elevate SGLT1 expression and glucose-uptake capacity"

    Above, sucralose is a strong sweetener.

    And note that the effect disappears if the sugar taste receptors gustducin or T1R3 are removed from the genome of a mouse:

    "Mice genetically modified to lack gustducin or T1R3 fail to increase SGLT1 expression or glucose uptake on a high sugar diet or when fed artificial sweeteners like sucralose, implicating these taste signaling elements in regulation of SGLT1."

    3/6

    #sweeteners #nutrition #sugars

  6. Also in 2009, a study showing how taste receptors are not just in the mouth but also in the gut, and what implication this has for sweeteners:

    "Taste Cells of the Gut and Gastrointestinal Chemosensation"
    Egan and Margolskee, 2009
    pmc.ncbi.nlm.nih.gov/articles/

    "A number of researchers had speculated that chemosensory detection of glucose and other macronutrients in the lumen of the gut might utilize cells and receptors like those of the tongue ... The gut “tastes” sugars and sweeteners in much the same way as does the tongue and by using many of the same signaling elements."

    When we eat sugar, the gut absorbs it into the blood, and insulin is released into the blood to keep the concentration of sugar within a desirable window (not too high and not too low; a process generically called homeostasis) by making fatty cells, muscle cells and the liver absorb sugars from the blood and store it. But it turns out that it's the tasting of sugars in the gut that stimulates insulin release, more than the presence of sugar itself in the blood:

    "It has long been known that orally ingested glucose is much more effective than [delivery of] intravenous glucose in raising plasma insulin concentrations (this is called the incretin effect) ... Glucose in the gut lumen leads to secretion, in a concentration-dependent manner, of incretins ... which in turn augment insulin release from the pancreas. Yet, how glucose in the gut lumen stimulates release of incretins was not known until 2007: glucose in the gut activates sweet taste receptors and gustducin present in the intestine’s enteroendocrine L cells, leading to release of GLP-1 from these cells."

    2/6

    #sweeteners #nutrition #sugars

  7. My son asked me about artificial sweeteners and their effect on us. This is what I sent him.

    There are hundreds of studies. Here I will comment on a handful.

    Note that sweeteners go by many names. Sometimes by the actual name of one of the substances, like sucralose (see the wikipedia: en.wikipedia.org/wiki/Sucralos ) or saccharin (en.wikipedia.org/wiki/Sacchari), and sometimes by generic names like nonnutritive sweetener (NNS) or artificial sweetener (AS), or similar. They are called nonnutritive because the body cannot extract any nutritional value from them, only sweet taste. And they are called artificial because most often they are a product of a laboratory-induced chemical modification of an otherwise natural substance. For example, sucralose is formed by the chlorination of sucrose: adding chloride to sugar (and then testing on animals that such a modification is not poisonous).

    In 2009:

    "Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms"
    Mattes and Popkin, 2009
    pmc.ncbi.nlm.nih.gov/articles/
    sciencedirect.com/science/arti

    "The addition of NNS [nonnutritive sweeteners] to diets poses no benefit for weight loss or reduced weight gain without energy restriction. There are long-standing and recent concerns that inclusion of NNS in the diet promotes energy intake and contributes to obesity."

    1/6

    #sweeteners #nutrition #sugars