I’ve been a longtime advocate of staying away from processed and canned foods, but I have a confession to make. For years one of my favorite snacks has been canned baked beans. They’re part of my passion for beans in any shape or form. Beans contain protein, healthy fatty acids, lots of fiber and the building blocks of carnitine—a vital nutrient for proper brain, muscle and cardiac function.
But as I opened a can of beans the other day, I happened to glance at the label. Out leapt one of my biggest nutritional don’ts: high fructose corn syrup (HFCS).
Needless to say, I immediately canned the can, contents and all. The lesson for me was to more strictly practice what I preach, and to always read labels—no exceptions.
10 Percent of All Calories
I’m more alarmed than ever about the dangers of high fructose corn syrup. This cheap sugar alternative, which is made from cornstarch, is seriously bad news. It’s another man-made toxic burden for the body, and probably worse for our health than we ever thought.
HFCS serves not only as a sugar alternative, but also as a means to enhance a product’s shelf-life. As such, food manufacturers use it in practically everything. Soft drinks and processed foods are especially notorious for it, as are canned foods (even, as it turns out, my precious canned beans). On average, Americans consume about 12 teaspoons of HFCS per day, or approximately 1 in every 10 calories.
The list of potential dangers of high fructose corn syrup is long. The more you consume, the more you put your liver, kidneys and arteries at risk; the more likely you are to put on weight; and the more prone you become to metabolic syndrome, a forerunner to diabetes, hypertension and heart disease.
When I discovered HFCS was in canned beans, I’d just come back from the environmental medicine conference in Dallas that I wrote about last month. One of the speakers there was Jean Monro, M.D., a British physician who had spoken about HFCS. She reported that about 25 percent of her patients with metabolic syndrome lack enough of the enzymes needed to process HFCS, either because of a genetic defect, or because they’d consumed so much of the substance that their enzymes had become exhausted and ineffective.
The inability to properly process HFCS often leads to an increase in the level of uric acid in the body. Uric acid is a normal product of cellular breakdown, but too much of it can lead to health problems. Most significantly, it can inhibit the ability of endothelial cells to produce nitric oxide—a substance that’s crucial for keeping arteries properly dilated. In fact, the connection between fructose and uric acid is regarded as a potential cause of high blood pressure and kidney disease (a common side effect of chronic hypertension). The link has also been reported in medical literature in relation to fructose-induced metabolic syndrome.
Additionally, Dr. Monro revealed that many of her patients with chronic fatigue syndrome also have difficulty with fructose metabolism. The fatigue may stem in part from fructose interfering with cellular energy production.
As I listened to Dr. Monro’s talk, it became even more obvious to me—and it was pretty clear before—that our overconsumption of sugar alternatives is killing us in many ways. There are a lot of differing views on how to reform health care, but I say let’s cut down on the high fructose corn syrups and sugar alternatives for starters. That might put a lot of junk-food companies out of business, but summum bonum (“for the highest good”). In this case, the higher good is the collective health of America.
A Source of Mercury Contamination
At the end of her talk, Dr. Monro dropped a real bombshell. She cited a new report that HFCS may be contaminated with mercury, a potent neurotoxin. The mercury comes from an agent used in the processing of HFCS called caustic soda (lye). Some of the industrial plants that make caustic soda use outdated technology that requires mercury.
After the conference, I quickly looked up the report, which was published in a 2009 issue of the journal Environmental Health. Researchers had concluded that “mercury contamination of food products, as a result of the use of mercury-contaminated HFCS, seems like a very real possibility.” They found mercury in 9 out of 20 samples of HFCS from several manufacturers. Then, using the estimated amount of HFCS consumed per person each day in the U.S., they determined that people may be ingesting up to 28 mcg of mercury per day, a level possibly exceeding “other major sources of mercury.”
Why am I suggesting you read these reports? Because they provide more evidence of the danger lurking in our food supply and how sloppy our government oversight is. The second report was initiated by David Wallinga, M.D., one of the research participants in the first study. He is director of the food and health program at the Institute for Agriculture and Trade Policy in Minneapolis, a nonprofit organization that works locally and globally to promote fair and sustainable practices pertaining to food, farming and trade. Along with several colleagues, Dr. Wallinga set out to learn if mercury was really present in popular foods and drinks sold at supermarkets. They purchased 55 name-brand food items that included HFCS as the first or second ingredient on the label and then sent them for testing at a commercial laboratory.
Sure enough, when the results came in, one in three products had detectable levels of mercury. The lab found mercury at levels several times higher than detectable limits in some snack bars, barbecue sauces, sloppy joe mixes, yogurt and chocolate syrup. Though measured “only” in parts per trillion—a seemingly infinitesimal level—the highest concentrations are nonetheless troubling, because you want a level of zero. Even the minutest amounts of mercury accumulate in the body over time, slowly poisoning enzyme systems and eroding health. In unborn and young children, it takes very little time for mercury to seriously damage the nervous system.
Curiously, no mercury was detected in the majority of beverages tested, though it was found close to the detection limit in some sodas. That’s a bit of a relief, since sweetened beverages are a major source of HFCS in the typical diet.
Nevertheless, as Dr. Wallinga told me, the findings have uncovered another potential and troubling source of mercury exposure. “Our point wasn’t to focus on the levels, but just to say, ‘Here is an avoidable practice that seems to be introducing a new source of mercury into the food supply,’ ” he said. “The question is, why are we using an outdated technology—particularly for a food ingredient that accounts for 1 out of 10 calories the average person ingests?”
Still Legal in the United States
The reason some food products have traces of mercury while others do not is likely tied to which plant made the caustic soda that was used to process the HFCS. Most facilities in the U.S. supposedly don’t use mercury-based technology anymore, but four still do. More to the point, Dr. Wallinga said, is that in our global economy, the caustic soda could very well have come from factories overseas.
Where is the FDA in all this? Interestingly, the initial discovery of mercury-contaminated HFCS, in 2005, was made by a longtime environmental investigator for the FDA. Unfortunately, though, the agency does not have a mercury surveillance program for food ingredients such as added sugars or preservatives made with caustic soda. Mercury is routinely detected by FDA testing in fish, liver and poultry; seafood is a primary source of mercury in the diet. In addition, the farming industry often uses fishmeal as feed for certain livestock, including chickens, swine, dairy cattle and farmed fish, which increases the level of mercury in those animals.
Some countries have banned the use of mercury in the manufacture of caustic soda and other food ingredients. Others, including the U.S., have not. In 2007, then-Sen. Barack Obama sponsored a bill (S. 1818) to phase out such use in by 2012. Nothing has happened since.
For consumers, the safest solution is to avoid any foods in which HFCS is high on the ingredient list. I’ve been saying that for a long time, and now I’m shouting it from the rooftops.
Sucralose Takes a Hit, Too
Before wrapping up, I’d like to mention another popular sugar alternative that was the subject of some sour notes at the Dallas conference. It was Splenda (sucralose), a noncaloric artificial sugar alternative made from sucrose. Splenda is made using a chlorine process that renders sucralose 600 times sweeter than sugar and unabsorbable in the body—that way it doesn’t have to be identified as a carbohydrate. In short, Splenda provides the sweet taste without the calories. Consumers put it in drinks, cereals, and baked goods. It is also used as an ingredient in more than 4,000 products, including soft drinks, medicines, and even vitamins.
Supposedly Splenda is safe, but there have been hundreds of complaints about its GI side effects. At the conference, Mohamed Abou-Donia, Ph.D., a professor of pharmacology and cancer biology at Duke University, reported on a 12-week study in which he fed laboratory rodents store-bought Splenda at levels equivalent to those approved by the FDA for humans.
Sugar and HFCS—What’s the Difference?
Common natural cane sugar is pure sucrose, a compound containing one molecule each of glucose and fructose. HFCS is 45–55 percent fructose, and the rest glucose. The sucrose is a natural sweetener. The different forms of HFCS are synthetic amalgamations appearing nowhere in nature.
He found several troubling results:
The animals showed increased body weight.
There was a significant disruption, and reduction, of the beneficial intestinal bacteria—especially Lactobacillus acidophilus and Bifidabacteria, which are important to bowel function, the body’s ability to fight pathogens and overall health. (These same bacteria are heavily marketed in many yogurts. However, most nonorganic yogurts contain HFCS, which may negate the health benefits of the probiotic bacteria.)
There was an elevation of certain intestinal proteins that could interfere with the absorption of nutrients and medication.
Dr. Abou-Donia disclosed that his study was supported in part by a grant from the Sugar Association. I asked him about that, because the purpose of the association is to promote sugar consumption. He said that the association never told him what to do. His research goal was to determine whether there were any GI problems related to Splenda. He found that there were.
Interestingly, a report by an “expert panel” of independent consultants that criticized Dr. Abou-Donia’s research was recently published online by a toxicology journal. His study was declared “deficient in several critical areas” by critics who argued that his results could not be interpreted as evidence that Splenda produced adverse effects in rats. Dr. Abou-Donia laughed. “Hired guns,” he said. “They didn’t conduct a study, they only criticized mine.”
After the talk, I consulted with Tom Sult, M.D., a physician in Sartell, Minn., who is a clinical expert on beneficial bacteria.
“There are a number of things that can cause dysbiosis, an unhealthy imbalance between the beneficial and harmful bacteria in the gut,” he explained. “Antibiotics, stress, and intestinal infections cause dysbiosis. Splenda and other sugar alternatives may do so as well. The early evidence suggests that disruption of the bacterial flora may result in a higher extraction and absorption of calories from food, with weight gain as a result.”
Abou-Donia MB, et al. Splenda alters gut microflora and increases intestinal P-glycoprotein and cytrochrome P-450 in male rats. J Toxicol Environ Health. 2008;71(21):1415–1429.
Brusick D, et al. Expert panel report on a study of Splenda in male rats. Regul Toxicol Pharmacol. 2009;55(1):6–12. [Epub 2009 Jun 28].
Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men. BMJ. 2008;336(7639):309–312.
Dufault R, et al. Mercury from chlor-alkali plants: measured concentrations in food product sugar. Environ Health. 2009;8:2.
Nakagawa T, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol. 2006;290(3):F625–F631.