New Research Shows There’s No Free Lunch When it Comes to Artificial Sweeteners
When summer rolls around it’s tempting to use food and drink with artificial sweeteners in an attempt to cut down on calories, but no research has ever convincingly shown that using these products contributes to weight loss. In fact, recent research suggests that they may actually confuse the body’s response to sweet tastes and contribute to weight gain.
The artificial sweetener sucralose (brand name Splenda®) is increasingly found in processed foods. Sucralose is sugar with its chemical structure changed to create a chlorocarbon, or a sugar with chlorine added. This causes it to pass through the body largely unabsorbed, which means that it doesn’t add calories. Splenda® is FDA-approved for use in food, and is widely found in processed foods and drinks, from yogurt and iced tea, to cookies and chewing gum.
Splenda® can be Gut Wrenching
Research suggests that Splenda® may be doing damage as it passes through the intestines. According to an article in Dr. David William’s newsletter Alternatives, research with rats has shown that “…Splenda® can reduce the amount of beneficial bacteria in the intestines by as much as 50 percent, increase the pH level in the intestines, increase body weight, and cause the re-routing or inactivation of certain drugs through the alteration of glycoprotein levels.”
Splenda® has Something in Common with Organochlorine Pesticides
There doesn’t seem to be any free lunch when it comes to artificial sweeteners. The sucralose molecular structure resembles the organochlorine pesticides such as DDT, lindane and endosulfan. Although 85 percent or so of sucralose passes through the digestive system without being absorbed, the 15 percent that does get absorbed may be problematic.
According to James Bowen M.D., in an article titled The Lethal Science of Splenda, a Poisonous Chlorocarbon, “Any chlorocarbons not directly excreted from the body intact can cause immense damage to the processes of human metabolism and, eventually, our internal organs. The liver is a detoxification organ which deals with ingested poisons. Chlorocarbons damage the hepatocytes, the liver's metabolic cells, and destroy them.
“In test animals Splenda® produced swollen livers, as do all chlorocarbon poisons, and also calcified the kidneys of test animals in toxicity studies. The brain and nervous system are highly subject to metabolic toxicities and solvency damages by these chemicals. Their high solvency attacks the human nervous system and many other body systems including genetics and the immune function. Thus, chlorocarbon poisoning can cause cancer, birth defects, and immune system destruction. These are well known effects of Dioxin and PCBs which are known deadly chlorocarbons. Just like aspartame, which achieved marketplace approval by the Food and Drug Administration when animal studies clearly demonstrated its toxicity, sucralose also failed in clinical trials with animals. Aspartame created brain tumors in rats. Sucralose has been found to shrink thymus glands (the biological seat of immunity) and produce liver inflammation in rats and mice.”
Why Not Have Some Real Sugar!
Americans have become habituated to the intensely sweet taste of artificial sweeteners and it’s long past time to kick that habit. If you have a yearning for something sweet, why not just have some real sugar! It’s natural, it doesn’t take much to sweeten up food and drink, and it hits the pleasure centers of the brain, which the artificial sweeteners do not. Even better, have some fresh fruit, which comes packaged with nutrition and fiber.
Nakagawa Y, Nagasawa M, Yamada S, “Sweet taste receptor expressed in pancreatic beta-cells activates the calcium and cyclic AMP signaling systems and stimulates insulin secretion,” PLoS ONE. 2009;4(4):e5106. Epub 2009 Apr 8.
Abou-Donia MB, El-Masry EM, Abdel-Rahman AA et al, “Splenda® Alters Gut Microflora and Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Male Rats,”
Journal of Toxicology and Environmental Health, Part A, Vol 71, Issue 21 January 2008, pp 1415-1429.