by Craig Weatherby
Sugar has plenty to answer for from a public health perspective. And dental caries are far from the worst or even the most likely consequence of overindulging one’s sweet tooth (Crackers and other sticky carb-rich snacks generate cavities more reliably).
Modern food manufacturers add sugar to almost every packaged product, and their motivation derives from the effects of human evolution. Our primeval craving for simple carbohydrates, especially sugars, causes us to respond to sweet tastes by sending a signal from palate to brain proclaiming “dude, this is high-value food.”
But what once served as a critical capacity—one that helped early humans choose the most energy-rich forage—now causes us to over-consume sugary sodas, coffee drinks, pastries, candies, and gratuitously sweetened processed foods of every description.
|Corn syrup: innocent bystander or insidious obesity-inducer?|
The sharp rise in Americans’ consumption of high-fructose corn syrup, largely due to its displacement of costlier cane sugar in soft drinks, has been blamed for this nation’s obesity epidemic.
The rationales for this widely touted hypothesis are 1) that fructose is more fattening than cane sugar (sucrose) and 2) that the rise in HFCS consumption tracks the rise in obesity quite closely.
However, when you look more closely, the evidence for this link appears weak .
First, there is no metabolic reason why fructose should be substantially more fattening than cane sugar, which acually contains more fructose than HFCS. In fact, obesity rates have risen at comparably rapid rates in countries where cane sugar remains the dominant sweetener.
And correlation does not prove causation. If it did, we could blame the sharp rise in obesity on consumption of soybean oil, which tracks the rise in obesity rates just as closely as the rise in HFCS intake.
In fact, soybean oil is high in omega-6 fatty acids, whose pro-inflammatory properties may promote abdominal weight gain in particular (See “Omega-3s Seen to Fight Metabolic Syndrome”).
It’s probably the quantity of calories we ingest (sugar-derived or not), rather than the kind of sugar consumed that counts most when it comes to weight control.
And sugar now comes in many forms, from the traditional cane sugar (sucrose) and honey to the manmade high-fructose corn syrup found in everything from tomato sauce to mayonnaise.
The direst dangers of excess sugar are increased risks of diabetes and cardiovascular disease, with many studies showing that excess blood sugar leads to “glycation” of LDL cholesterol and thereby to build up of arterial plaque.
Not coincidentally, elevated levels of an inflammation marker called C-reactive protein enhance uptake of glycated LDL cholesterol by immune system cells: an effect that promotes formation of arterial plaque (Zhong Y et al 2006).
This recently discovered effect may turn out to explain why elevated blood levels of C-reactive protein—and the pro-inflammatory diets that cause them—are associated with increased risk of developing cardiovascular disease.
Sugary drinks and snacks seen to raise risk of killer cancer
Thanks to revealing new research from Sweden, we can now add increased risk of pancreatic cancer to the list of sugar’s evil effects (Larsson S et al November 2006).
Scientists at Stockholm’s respected Karolinska Institute have been publishing a series of cancer studies based on large population surveys, designed to reveal any dietary risk factors (See “Fatty Fish Seen Curbing Women’s Kidney Cancer Risks” and “New Cancer-Risk Findings Rank Seafood and Poultry Far Safer than Processed Meats”).
The new study involved almost 80,000 healthy women and men, and the results points an accusatory finger at sugar with regard to pancreatic cancer.
Pancreatic cancer is an uncommon but frequently fatal form of cancer, and it is promoted by the chronically elevated levels of insulin associated with poor glucose control: a dysfunction induced by sugar-heavy diets.
The new Karolinska study began in 1997 when scientists asked the participants about their diets, and ended in June 2005, when they used the Swedish cancer registry to identify 131 people from the group who’d developed cancer of the pancreas.
As lead author Susanna Larsson said, “It is perhaps the most serious form of cancer, with very poor prognoses for its victims. Since it’s difficult to treat and is often discovered too late, it’s particularly important that we learn to prevent it.”
The Swedish findings indicate that the risk of developing pancreatic cancer correlates closely with the average amount of sugar in a person’s daily diet.
Compared with people who rarely drank sweetened beverages or creamed fruit (a popular Swedish treat), those who did so habitually ran sharply increased risks:
- People who consumed sweetened soda or fruit-based drinks twice a day or more were 90 percent more likely to develop pancreatic cancer.
- People who added sugar to food or drinks (e.g. coffee) five times a day or more were 70 percent more likely to get pancreatic cancer.
- People who ate creamed fruit at least once a day were 50 percent more likely to develop pancreatic cancer.
In addition to cutting back on sugar consumption, recent research suggests that higher intake of vitamin D may help prevent pancreatic cancer (Sockeye salmon is the richest food source by far; see “Vitamin D Seen Slashing Risk of Pancreatic Cancer”).
While a prior Karolinska study failed to find any protective effect from diets high in fruits and vegetables, diets rich cruciferous veggies (e.g., cabbage, broccoli, kale, Brussels sprouts) seemed to provide some anti-cancer protection to the pancreas (Larsson S et al Feburary 2006).
- Larsson SC, Bergkvist L, Wolk A. Consumption of sugar and sugar-sweetened foods and the risk of pancreatic cancer in a prospective study. Am J Clin Nutr. 2006 Nov;84(5):1171-6.
- Larsson SC, Hakansson N, Naslund I, Bergkvist L, Wolk A. Fruit and vegetable consumption in relation to pancreatic cancer risk: a prospective study. Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):301-5.
- Colaco CA, Roser BJ. Atherosclerosis and glycation. Bioessays. 1994 Feb;16(2):145-7. Review.
- Lyons TJ. Glycation and oxidation: a role in the pathogenesis of atherosclerosis. Am J Cardiol. 1993 Feb 25;71(6):26B-31B. Review.
- Zhong Y, Li SH, Liu SM, Szmitko PE, He XQ, Fedak PW, Verma S. C-Reactive protein upregulates receptor for advanced glycation end products expression in human endothelial cells. Hypertension. 2006 Sep;48(3):504-11. Epub 2006 Jul 17.