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The Truth about Sucralose

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Sucralose, synthetic, organochlorine, gut, bacteria, IBD, metabolic syndrome, damaging cytochrome p-450, a plant sugar, hydrogen-oxygen, sweetness, glucose, fructose, cancer cells, E. coli, Splenda, Type-2 diabetes, Metabolic Syndrome, weight loss, Crohn’s, Proteobacteria, Dr. Xiaofa Qin, New Jersey Medical School, synthetic, organochlorine
The Truth about Sucralose

Sucralose is a synthetic, organochlorine sweetener; far from being inert, it damages good gut bacteria levels, the gut lining and is linked to IBD and Crohn’s, while damaging insulin, increasing Type-2 diabetes and metabolic syndrome and damaging cytochrome p-450.

What is Sucralose?

Sucralose is sucrose, a plant sugar, modified with 3 chlorine atoms replacing three hydrogen-oxygen groups. This chlorination heightens the sweetness.

Sucrose itself is a sugar made by plants – a disaccharide, containing a molecule of glucose and a molecule of fructose. White refined sugar is made from it and this is loved by yeasts, cancer cells and E. coli.

Sucralose was accidentally discovered when researching and developing an insecticide.

It is now a general purpose sweetener – commonly found in small packets, drinks and food products. It is both water- and fat soluble and so its use is widespread. It is zero calories.

Splenda

The major brand using sucralose is Splenda.

Splenda also contains maltodextrin (bulking agent) and dextrose (from corn). In fact, only 5% of Splenda is sucralose.

The problems with sucralose:

1. Sucralose and Type-2 diabetes – rather than cutting the risk of Diabetes by switching away from sugar, a study (1) showed a daily diet soft drink was associated with a 67% greater risk of Type-2 diabetes and a 36% greater risk of metabolic syndrome. After taking sucralose, the test subjects plasma glucose levels WENT UP! Apparently, this is because sucralose can lower insulin levels.

Go to: Metabolic Syndrome

2. Sucralose and weight loss – a 2013 study (2) of teenagers showed that switching them to diet soda using sucralose made no difference to their weight.

A second study (3) across an 18 month period, resulted in children who consumed a Diet drink a day only being 1 kilogram lighter that those consuming a normal can of fizzy soft drink. This was despite the fact that the Diet soda group consumed 46,627 less calories – equivalent to a 23-30 day fast!!! 641 children in two matched samples were involved.

3. Sucralose promotes IBD and Crohn’s – in a 2018 Study (4) Splenda promoted dysbiosis, and an expansion of Proteobacteria and E coli in mice. Researchers concluded it could increase bloating, inflammation and IBS. This was backed up in real life in Canada. Canada was the first country to approve sucralose, in 1991. Despite previously having a lower incidence of gut problems and IBS, in the years following approval of sucralose, the incidence of Inflammatory Bowel Disease jumped. In a study (5) by Dr. Xiaofa Qin of New Jersey Medical School, it was concluded that sucralose is actually worse than saccharin through potent inhibition of gut bacteria (6), inhibition of digestive proteases and increases in cytochrome p450 and gut wall damage. 65-95% of sucralose just passes straight through the gut. Qin concluded that. While saccharin was bad, sucralose was much, much worse. Over a 20 year period, IBD cases in Canada rose almost 650%.

4. Sucralose reduces levels of ‘good’ bacteria – in a controlled 12-week study (7) with rats, the group taking Splenda had reduced levels of ‘commensal’ bacteria at the end of the study. A contributory factory was that Splenda actually changed the pH of the gut, making it more alkaline. Good bacteria like an acid gut!

Go to: Why you need an acid gut and alkaline cells

5. Sucralose is not an ‘inert’ compound – it is not Biologically inert; it appears to alter glucose, insulin and glucagon-like peptide 1 (GLP-1). Since it also affects cytochrome p-450 it may even interfere with some drugs (8). Sucralose is, after all, a synthetic, organochlorine, sweetener. Yummy.

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References

  1. https://pubmed.ncbi.nlm.nih.gov/19151203/
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856475/
  3. https://pubmed.ncbi.nlm.nih.gov/22998340/
  4. https://pubmed.ncbi.nlm.nih.gov/29554272/
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3202359/
  6. https://pubmed.ncbi.nlm.nih.gov/18800291/
  7. https://pubmed.ncbi.nlm.nih.gov/24219506/