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Sweet Sodas May Promote Alzheimer’s
12/31/2007
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Findings add another reason to avoid sodas; fruit juice antioxidants may cancel out their sugars' effects

by Craig Weatherby


What about fruit juices?

Clearly, sugar in liquid form is not great for weight control.


Fruit juices contain just as much sugar as sodas do, so they may also be guilty on that score, though likely somewhat less so, thanks to the known metabolic effects of their antioxidants.


The question is, do fruit juices also contain enough beneficial antioxidants to cancel out the negative effects of their high amounts of sugar?


The answer, based on preliminary evidence, is “probably”. As we reported, the participants in a large American study who drank juices at least three times per week enjoyed 76 percent less risk of Alzheimer’s disease, compared with those who drank juice less than once a week.


Participants who drank juices one to two times a week experienced only a 12 percent risk reduction, compared with those who drank juice less than once per week.


The risk reduction was strongest among the study participants who possessed the gene linked to the most common (late-onset) form of Alzheimer’s disease, and in the most sedentary subjects.

See “Alzheimer’s Risk Curbed by Antioxidants in Fruit and Vegetable Juice.”

We wonder whether enough of the antioxidants in the herbs and roots with which real, natural root beer is made remain would render it less harmful than other sodas. If you know, drop us a line!

Surprisingly, before researchers at the University of Alabama decided to examine the possibility, no one had ever tested the brain effects of adding sugary liquid to the diet of mice.


As the scientists said, there is compelling evidence that drinking lots of sugar-sweetened drinks promotes obesity, which is a major risk factor for adult diabetes, which in turn is associated with greater risk of Alzheimer’s disease. In addition, high-fat diets promote underlying signs of Alzheimer’s in mice.


The Alabama team divided mice bred to develop an Alzheimer's-like condition in to two groups.


One group got sugar-sweetened watercontaining 10 percent sucrose (cane sugar)and the sugar-swilling rodents suffered greater losses in learning skills and memory compared with mice that drank plain water.


The “soda” group also underwent a two- to three-fold increase in the amount of beta-amyloid protein in their brains, which forms the “plaque” associated with Alzheimer’s.


The Alabamans also found a 2.5-fold increase in brain levels of apoE: a compound associated with higher levels of amyloid protein and plaque, which suggests that sugar promotes Alzheimer's-related plaque by increasing production of this undesirable chemical.


The authors came to an obvious conclusion: “These data underscore the potential role of dietary sugar in the pathogenesis of Alzheimer's disease, and suggest that controlling the consumption of sugar-sweetened beverages may be an effective way to curtail the risk of developing Alzheimer's disease.”


And as lead author Dongfeng Cao told Reuters Health, “Our findings are of tremendous importance given that the consumption of sugar-sweetened beverages has increased dramatically over the past decades and will most likely remain high in modern societies.”


Sugary water also made mice fat and diabetic, despite eating less food

After four months, the animals given sugar water weighed 17 percent more than the mice that drank plain water, despite being given the same amount of food to eat.


The sugar-drinking mice ate less food than those given plain water, they consumed 15 percent more daily calorie, and they got 43 percent of their total calories from the sugar water.


The sugar-swilling mice also developed early signs of diabetes and had very high levels of fat in their blood.


Source

  • Cao D, Lu H, Lewis TL, and Li L. Intake of Sucrose-sweetened Water Induces Insulin Resistance and Exacerbates Memory Deficits and Amyloidosis in a Transgenic Mouse Model of Alzheimer Disease. J Biol Chem. 2007 282: 36275-36282. First published on October 17, 2007; doi:10.1074/jbc.M703561200

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