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Sugar substitutes have now shown in a recent study a new danger not previously considered. Substitutes for sugar, long known to contribute to health concerns because of toxicity levels, have now shown to affect the function of good cholesterol (HDL). Most people think about the level of good cholesterol (HDL) present in their cholesterol test, but not about whether the HDL has the ability to do its job.

The above video by Dr. Jeff Bland, PhD in Biochemistry provides a great explanation to understand this new study even further.

Sugar substitutes such as aspartame, sucralose, acesulfame K and saccharin have long been a topic of controversy. Substitutes for sugar have been thought to be toxic because they are artificial and mostly affect neurological function. Sugar substitutes can also adversely affect other parts of the body and cause a myriad of symptoms.

A new study about sugar substitutes suggests a problem not previously considered. Sugar substitutes proved to affect the “function”…not the level of…HDL cholesterol. HDL cholesterol is the “good” type that need to be at certain levels to be cardioprotective (atheroprotective).

We are all focused on the levels of total cholesterol, HDL, LDL when we go to our doctor. Now we have new evidence that you could have proper levels of HDL, but they are not cardioprotective because of the ingestion of sugar substitutes. The only choice is to avoid at all costs.

The study also found that sugar substitutes cause premature cell death (senescence) and accelerate atherosclerosis (heart disease).

The following is the abstract of the study that was recently published:

Modified apolipoprotein (apo) A-I by artificial sweetener causes severe premature cellular senescence and atherosclerosis with impairment of functional and structural properties of apoA-I in lipid-free and lipid-bound state.

Abstract

Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular disease and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.

This abstract can be found here:

http://www.ncbi.nlm.nih.gov/pubmed/21533907

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