New research has weakened the perceived link between saturated fat and heart disease. Today, many experts agree that refined carbs pose a much greater danger.

Is it possible — even imaginable — that nearly everyone has been wrong about saturated fat and its connection to heart disease? Brace yourself. Based on a wave of new research, all the dietary admonitions about saturated fat could end up being little more than a huge mistake.

“The question is whether saturated fat is harmful or is just a bystander,” says Ronald M. Krauss, MD, a lipid specialist and the director of atherosclerosis research at the Children’s Hospital Oakland Research Institute. “Saturated fat may have an effect on cardiovascular disease (CVD) risk, but the effect is so small that we just can’t detect it. We shouldn’t be demonizing saturated fat.”

Krauss can back up his opinion with hard science. He and his colleagues recently analyzed 21 published studies involving almost 350,000 people who were tracked from five to 23 years. Their conclusion: People who consumed the most saturated fat did not have a higher risk of heart disease, stroke or any other form of CVD. They published their findings last year in the American Journal of Clinical Nutrition.

Krauss is by no means the first doctor to question the role of saturated fat in CVD. But, if he and other critics are right, it raises a couple of important questions: How could anti-saturated-fat advocates make such a huge miscalculation? And do we now have a license to eat saturated fat with abandon?

The answers aren’t as simple or straightforward as you might think.

There’s no denying that scores of studies over many years have shown a link between saturated fat and CVD risk. Krauss believes, however, that many of the saturated-fat-is-bad studies have not accounted for diets that included a lot of sugars, refined carbs and trans fats, along with saturated fats.

“It doesn’t make sense to focus on just one feature of the diet, such as saturated fat, while ignoring the health effects of the overall diet,” he says.

Origins of a Theory

The late Ancel Keys, PhD, a researcher at the University of Minnesota, first linked saturated fat and cholesterol with the risk of CVD in the 1950s.

Keys was hailed as a pioneer in the area of nutrition and health at the time; in January 1961, he made the cover of Time. Less than 20 years later, Congress was recommending that Americans ditch saturated fats in favor of more carbs, and soon food companies were hawking low-fat everything.

Keys’s research has come under increasing criticism in recent years. Gary Taubes, author of “Why We Get Fat and What to Do About It”, notes that Keys focused on the eating habits linking saturated fat to CVD in seven nations, “in which he could pretty much draw a straight line between saturated fat and CVD risk.”

According to Taubes, Keys ignored contradictory data from other nations, including France, where people ate a lot of fat but had a low incidence of CVD (the so-called French paradox), which would have led Keys to draw entirely different conclusions.

“More than 20 studies have shown that people who have heart attacks don’t eat more saturated fat than healthy people,” says Swedish researcher Uffe Ravnskov, MD, PhD.

Ravnskov, who has written several books on cholesterol, has been skeptical of the saturated fat–cholesterol theory of heart disease since the 1960s. “Eight studies have shown that people with stroke have eaten less saturated fat than healthy people,” he says. “And no dietary study has succeeded in lowering heart disease deaths by reducing intake of saturated fat.”

Enter Refined Carbs

Americans largely embraced the anti-saturated-fat gospel, substantially cutting their consumption from about 13.5 percent of total calories in the early 1970s to about 11 percent of calories by 2000. In 2006, the American Heart Association recommended that people cut their saturated fat even more — down to 7 percent of total calories, which is half of what people were eating 40 years ago. But there have been unforeseen consequences, Krauss notes. “If you cut down on saturated fat, what do you replace it with?”

Food manufacturers responded by creating thousands of products in which saturated fat and cholesterol were replaced with refined carbohydrates, sugars and trans fats. And therein lies the problem. Not only do trans fats drive bodywide inflammation, but foods rich in refined carbohydrates and sugars trigger sharp increases in blood-sugar and insulin levels, which then set the stage for weight and blood-sugar problems — the leading risk factors for type 2 diabetes and CVD. “Replacing saturated fat with refined carbohydrates and sugars does not decrease CVD risk,” says Krauss. “More and more, the evidence shows that eating more refined carbs and sugars increases CVD risk.”

The late Robert C. Atkins, MD, sounded the alarm about the increase in carb and sugar consumption in the 1980s, when he noticed a dramatic rise in obesity and type 2 diabetes. But his solution, a diet rich in saturated fats, was roundly criticized — mostly because people believed that Atkins advised avoiding all carbs, including vegetables, when, in reality, he meant refined carbs. It took years of research before his approach was eventually vindicated.

This may sound like heresy, but the science behind it is solid. Sabina Sieri, PhD, of Italy’s National Cancer Institute, for example, tracked almost 48,000 people over eight years and found that women who ate more refined carbs and sugars had a significantly greater risk of coronary heart disease than those with a lower refined-carb intake.

The Cholesterol Question

For several decades, medical and nutritional advice boiled down to this: Too much dietary saturated fat leads to higher levels of blood cholesterol and an increase in CVD risk. But several studies have shown that total blood cholesterol is not a reliable indicator of CVD risk, says Ron Hunninghake, MD, chief medical officer of the Riordan Clinic in Wichita, Kan., the largest nonprofit nutritional medical center in the United States. “That’s because half of the people who suffer a heart attack have normal cholesterol levels.”

To find a way to make sense of the relationship between blood cholesterol levels and CVD, researchers began looking at cholesterol fractions, such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL), to get a better handle on CVD risk. These LDL particles happen to be one of Krauss’s primary areas of expertise, and his findings have challenged conventional thinking about the role of saturated fat and cholesterol in CVD.

Although LDL is widely regarded as the “bad” cholesterol, Krauss argues that it has a good side: While “pattern B” LDL consists of small, dense particles that are more likely to infiltrate blood-vessel walls and set the stage for blockages, high blood levels of “pattern A” LDL, which consists of large, fluffy particles, are associated with a lower risk of CVD.

It’s true that saturated fat does increase LDL levels, Krauss explains — but not in the way most people would expect. “We’ve shown in our own research that in the great majority of individuals, this increase in LDL reflects an increase in pattern A LDL.” That’s the good form of LDL. Saturated fat also boosts levels of the “good” HDL form of cholesterol.

Diets high in refined carbs, on the other hand, boost pattern B LDL and lower HDL cholesterol — thereby increasing the risk of CVD. “Little will be gained if saturated fat is simply replaced by carbohydrates, especially if these are mainly refined starches and sugar,” says Walter Willett, MD, DrPH, who heads the nutrition department at the Harvard School of Public Health.

Research by Marianne U. Jakobsen, PhD, of Aarhus University Hospital in Denmark, supports this argument. In a study of more than 53,000 men and women over 12 years, Jakobsen found that people were more likely to suffer a heart attack if they cut back on saturated fat, but then replaced it with a couple hundred more calories a day from high-glycemic foods, such as white breads, muffins, potatoes and desserts. But, if the people in the study replaced saturated fat with low-glycemic foods like vegetables, fruits and whole grains, they were less likely to have a heart attack.

The key, it seems, is not limiting saturated-fat intake, but avoiding insulin-provoking foods such as refined carbs and sugars — basically what Atkins had argued. “Atkins wasn’t right about everything, but he was right about insulin,” says Taubes. “He was probably more right than anyone else at the time.”

Eat Like Your Ancestors

Krauss’s research and dietary recommendations are relatively consistent with what’s known as the Paleolithic diet — that is, ancient eating habits that some scientists consider the ideal diet.

Loren Cordain, PhD, a professor in the department of health and exercise science at Colorado State University in Fort Collins, says that ancient peoples typically ate a diet rich in lean protein, fish and vegetables, with carbohydrates coming largely from root vegetables. Even though the meats contained saturated fat and cholesterol, Paleolithic diets were devoid of any kind of processed carbohydrate and sugar, with the occasional exception of honey.

“Given our ancestral diet, meal plans fairly high in quality proteins and low in processed carbohydrates would seem to be what most people are best suited to,” says Cordain. “Our genes are virtually identical to those in people living 20,000 years ago, and we evolved eating lean proteins and vegetables. Eating a lot of processed grains and sugars is a total mismatch for our genetic heritage.”

That doesn’t mean you have to give up carbs altogether, or load up on saturated fats, to avoid a heart attack. As with most dietary issues, it’s a matter of finding a good balance. (See the sidebar, “A Bountiful Balance,” for some simple tips on healthful eating.)

Hunninghake generally concurs with this approach, but suggests that people tailor their carb intake to their weight, blood sugar and activity level. “If they’re good on all three counts, they can probably consume a little more in the way of carbs,” he says. “But if they’re overweight, have high blood sugar and are couch potatoes, they should be getting their carbs from high-fiber vegetables, not grains.”

Many people may find all this a bit disconcerting and confusing. And Krauss and Hunninghake’s advice does fly in the face of largely vegetarian diets recommended by some other physicians, including cardiovascular bigwigs like Dean Ornish, MD. In clinical trials, Ornish has had success reducing cardiovascular disease in subjects who adhere to a whole-foods, plant-based diet very low in saturated fat. But that doesn’t necessarily prove that avoiding saturated fat is a heart-healthy strategy.

“While these diets did reduce CVD, it’s not clear that reducing the saturated fat was what did it — most likely it was eating less junk food and more veggies,” says Hunninghake. “Nutrition isn’t religion. It should be based on science. And the evidence for scientific assumptions can and does change from time to time.”

This article was taken from Experience Life magazine, the best health magazine around!    www.elmag.com

In a report issued late last year by the Institute of Medicine, a committee of physicians and researchers cautioned against taking large amounts of supplemental vitamin D and calcium because they are unnecessary and potentially harmful. However, the committee did recommend slight increases in the Recommended Daily Allowances (RDAs) for calcium (1,000 to 1,300 mg/d) and vitamin D (600 IU/d).

If you follow the advice of the Institute of Medicine, you’ll increase your long-term risk of disease.

It’s always safer for researchers and physicians to take the more conservative approach when recommending supplements—except that it reveals a naiveté about clinical nutrition and can lead to chronic nutritional deficiencies and harm to patients. That is the case with this cautious increase in the RDA for vitamin D, combined with a warning about high-dose vitamin D supplementation. Maintaining the status quo by saying “no” to higher dose supplements carries relatively little risk, at least for doctors. It’s a very different story for the average person, though.

The truth is that three of every four Americans are deficient or marginally deficient in vitamin D, a number that most likely gets even worse during the winter months when people huddle indoors. (Ginde AA. Arch Intern Med, 2009;169:626-632.) By refusing to acknowledge the scale of vitamin D deficiency, and the easy and inexpensive means of treating it, the committee from the National Institute of Medicine is guilty of malpractice. The committee members have reversed the Hippocratic Oath, from “first do no harm” to “first do harm.” Their action, or lack of action, is simply unconscionable.

The situation was made even worse by incredibly sloppy reporting in newspapers, particularly by Gina Kolata of the New York Times. In her article in the NYT after the report came out, she simply related a summary of the Institute of Medicine’s report without critical comment by any expert on vitamin D, such as Michael Holick, M.D., Reinhold Veith, Ph.D., or Robert Heaney, M.D. No mainstream reporter would be so uncritical in echoing a self-serving news release from politicians or corporations. But then, the committee did not even include a recognized expert on vitamin D, so the cautious nature of report may have reflected the fact that the committee members were out of their depth.

The cost of ongoing vitamin D deficiencies will mount with susceptibility to infectious diseases and a greater risk of cancer, heart disease, and depression. But then, there is much more money to be made on treating these diseases than on preventing them.

With the fanfare of a holiday parade, drug companies a few years ago unveiled two new Cox-2 inhibitor drugs-Celebrex and Vioxx-to treat arthritis, inflammation, premenstrual syndrome, and potentially even cancer. All the hoopla paid off. Since then, doctors have written more than seven million prescriptions for these “super aspirin” drugs, earning hundreds of million dollars for their makers.

Cox-2 is short for cyclooxygenase-2, one of the key enzymes that helps the body produce inflammatory hormone-like compounds called prostaglandins and cytokines. Cox-2 is essential-without it, we wouldn’t be able to fight infections or heal injuries. But when the body overproduces Cox-2, the result is chronic inflammation and pain.

The intensive marketing and advertising of Cox-2 inhibitors obscured why many people overproduce the enzyme. Too much Cox-2 appears to result from imbalances and deficiencies of certain nutrients. Rather than correct these underlying dietary problems, pharmaceutical Cox-2 inhibitors only mask the most visible symptoms. Relatively minor dietary changes, plus some vitamin and herbal supplements, correct the underlying problems.

Problems with Cox-2 Inhibitor Drugs

For years, people have used nonsteroidal antiinflammatory drugs (NSAIDS), such as ibuprofen, to treat the inflammation and pain associated with rheumatoid arthritis and osteoarthritis. NSAIDS ease inflammation by inhibiting the activity of both Cox-2 and Cox-1, the latter an enzyme that helps maintain homeostasis (biological equilibrium) protect the stomach lining. Because stomach ulcers occur in about 25 percent of NSAID users, pharmaceutical companies worked to develop NSAIDS that blocked only the activity of Cox-2. The idea was that a selective Cox-2 inhibitor would reduce inflammation but not irritate the stomach.

The motivation was profiting from a potentially huge market. An estimated 40 million Americans suffer from some form of arthritis. In a typical year, physicians write about 60 million prescriptions for NSAIDS-to say nothing of their over-the-counter sales. However, each year some half-million people develop complications from NSAIDS, with an estimated 80,000 people requiring hospitalization and 8,000 dying.

Though touted for their relative safety, Cox-2 inhibitors may be far more hazardous than originally believed. While gastrointestinal problems with Cox-2 inhibitors occur less frequently, they can be severe. Just four months after the FDA approved Celebrex, 10 deaths from the drug were reported. One study has even suggested that Cox-2 is important to the gut and healing ulcers, suggesting that pharmaceutical tampering with the enzyme may not be wise.

The Double-Edged Sword of Inflammation

Nutrients supply the most basic building blocks of the body’s powerful inflammatory compounds. The “parent” nutrient is linoleic acid, found in many foods but especially concentrated in vegetable oils (e.g., corn, soy, and safflower oils). The body converts linoleic acid to the omega-6 family of fatty acids, including arachidonic acid. Cox-2 plays a critical role in converting arachidonic acid to the hormone-like prostaglandin E2 (PGE2) and to the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFa), all of which promote inflammation.

According to Robert F. Grimble, Ph.D., of the University of Southampton, England, once an infection or injury stimulates production of IL-1 and TNFa, these two proinflammatory compounds can further stimulate each other, as well as IL-6. In addition, IL-1 and TNF a trigger the production of free radicals, which encourage the production of more proinflammatory cytokines. The proinflammatory reaction essentially feeds on itself, setting the stage for chronic inflammation.

Ideally, the body balances these compounds with a group of antiinflammatory compounds that originate with alpha-linolenic acid, found in cold-water fish, leafy green vegetables, and flaxseed. The body converts alpha-linolenic acid to the omega-3 family of fatty acids, which include eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Preformed EPA and DHA are also found in cold-water fish.

Much of the problem with inflammatory disorders actually stems from a lopsided imbalance in dietary intake of the omega-6 and omega-3 fatty acids-and the consequential cascade in proinflammatory activity. Artemis Simopolous, M.D., director of the Center for Genetics, Nutrition and Health in Washington, D.C., has shown that people historically consumed roughly equal amounts of the proinflammatory omega-6 fatty acids and the antiinflammatory omega-3 fatty acids.

However, over the past 30 years or so, Americans have replaced much of their dietary saturated fat (a bystander, so far as inflammation is concerned) with omega-6 fatty acids. Simopoulos estimates that people are now eating 20 times more omega-6s than omega-3s. From a biochemical standpoint, this sets the stage for powerful and chronic proinflammatory reactions.

Indeed, inflammation plays a role in many diseases, including arthritis, gingivitis and most of “-itis” diseases. Recent research has pointed to the role of inflammation in heart disease, stroke, and even Alzheimer’s disease. In addition, Bruce N. Ames, Ph.D., of the University of California, Berkeley, has estimated that chronic inflammation and infection cause about one-third of all cancers.

This relationship between diet, inflammation, and cancer was recently demonstrated by researchers at the American Health Foundation, Valhalla, New York. In animal experiments, they noted that corn oil (rich in omega-6) increased Cox-2 activity, whereas fish oil (rich in omega-3) blunted Cox-2 activity. The researchers also showed that the omega-6 fatty acids could promote the growth of colon cancer, whereas the omega-3 fatty acids prevented cancer.

In addition to a diet containing too many omega-6 fatty acids, a shortage of nutritional antioxidants, such as vitamin E, also contributes to chronic inflammation. The proinflammatory cytokines, IL-1 and TNFa, trigger the release of free radicals. A diet rich in antioxidants-found chiefly in vegetables and fruit-can help neutralize these free radicals. But relatively few people-9 to 34 percent, according to different researchers-eat the recommended five daily servings of vegetables and fruit. Between an excess omega-6 fatty acids and a lack of omega-3 fatty acids, and inadequate intake of antioxidants, the body’s proinflammatory reaction goes out of control, leading to chronic inflammation and pain.

Quenching the Fires of Inflammation

The simplest and most biochemically sound way of turning down the body’s proinflammatory prostaglandins and cytokines is by restoring a balance between pro- and antiinflammatory foods. From a dietary standpoint, this means switching from vegetable oils to extra-virgin olive oil (high in antiinflammatory omega-9 fatty acids). It also means avoiding most processed (boxed, canned, or frozen) foods, because their makers frequently add omega-6 fatty acids. By eating simple unprocessed foods-such as baked chicken, a salad, and steamed vegetables-it becomes easier to consume a more balanced ratio of omega-6 and omega-3 fatty acids.

However, if you’re like most people, you’ve been eating a diet high in omega-6 fatty acids and low in antioxidants for years. Simply restoring a balance is not enough to quickly offset accumulated damage, because the fatty acid composition of the body’s cells reflects their dietary ratios. It’s imperative to increase consumption of antiinflammatory fatty acids and antioxidants.

These are the supplements to emphasize:

• Omega-3 essential fatty acids

Found in fish oils, EPA and DHA are essential building blocks for the body’s antiinflammatory prostaglandins (e.g., prostaglandin E1) and for turning off Cox-2 and the body’s proinflammatory cytokines (IL-1, IL-6, and TNFa). In addition, omega-3 fatty acids block the activity of an enzyme that breaks down joint cartilage. Daily dosage: 3 or more grams.


• Vitamin E

Although Cox-2 and prostaglandin E2 levels rise with age, animal studies have shown that vitamin E supplements reverse the increase in Cox-2 and prostaglandin E2. Vitamin E also turns off nuclear factor-kB (NF-kB) and activator protein-1 (AP-1), compounds that turn on inflammatory genes. One recent study found that arthritics taking supplements of natural vitamin E (600 mg twice daily) for 12 weeks had their pain reduced by about half. Daily dosage: 400-800 IU.


• Polyphenols and Flavonoids

Researchers at Case Western Reserve University, Cleveland, recently reported that the antioxidant polyphenols in green tea had antiinflammatory properties by inhibiting Cox-2 and TNFa. Genistein inhibits prostaglandin E2 and Cox-2, and quercetin inhibits the activity of inflammation-promoting “adhesion” molecules. It’s likely that Pycnogenol, grape seed extract, and other flavonoids work through similar mechanisms. Daily dosage: 25-500 mg.


• Silymarin

A cell-culture study found that silymarin, the antioxidant extract of milk thistle, inhibited Cox-2 formation. This role of silymarin may partly explain why earlier cell-culture studies found it to inhibit the growth of prostate, breast, and skin cancers. Daily dosage: 100-200 mg.


• Rosemary

This common kitchen herb is rich in ursolic acid and many of its derivatives. In laboratory experiments, Swedish researchers found that the ursolic acid extract of rosemary was a potent inhibitor of Cox-2 activity. Daily dosage: 100 mg.


• Cat’s Claw

Known as una de gato and Uncaria tomentosa, this Peruvian herb has a long history as a remedy for inflammatory arthritis. Recent cell-culture and animal experiments at the Albany Medical College, New York, found that cat’s claw inhibited inflammation by blocking the activity of NF-kB. Daily dosage: Because products vary, follow label directions.

The take home message in all this is relatively simple: pharmaceutical drugs, while providing rapid relief of symptoms, do not correct the underlying cause of chronic inflammation. The cause is frequently a diet that’s either unbalanced or lacking in key nutrients. No drug can correct a nutritional deficiency or imbalance. Only nutrients can do that.

The never-ending arguments about evolution and creationism (or intelligent design) mystify me. I can’t understand why one of the most beautiful and fascinating aspects of biology is so controversial.

Evolution is all about change, adaptation, and dumb luck. It’s nature’s version of the Las Vegas crapshoot. It’s exciting, and sometimes scary.

From a biological standpoint, evolutionary changes result from a genetic roll of the dice (every time an egg is conceived) or from mutations (random changes to our genes). Most of these changes don’t mean a thing, a few alter our appearance or increase our risk of disease, and once in a while they give us nature’s version of seven-eleven.

Cancer is a good example of evolution in action. Cancers evolve, and they are a microcosm of the entire evolutionary process. I doubt that anyone would ever argue that cancer is just a theory.

Cancers develop from mutations that change the programming of our genes and the behavior of cells. When doctors treat cancer with chemo or radiation, they destroy the weakest cells, but cells with treatment-resistant genetic mutations survive. That’s natural selection—part of the evolutionary process—and that’s why most cancers eventually return.

The randomness of evolutionary process can be unforgiving or serendipitous. You never know how the dice will roll. A moth born bright yellow becomes easy pickings for a bird. But a moth of a different color may blend in to its surroundings, survive, and pass its lucky genes onto another generation.

A century and a half ago, Charles Darwin noticed how different beaks among Galapagos finches were adapted to different types of food. Birds born with maladapted beaks couldn’t feed themselves and so they died off, whereas birds with beaks suited to a particular island’s food sources flourished.

Segues from one species to another take a long time. Monkeys did not turn into human beings overnight—their evolution occurred through a lot of minor changes over millions of years. That’s a difficult time scale for most people to imagine. After all, many of us have trouble imagining what life was like 100 years ago.

It takes my breath away when I think about how life changes through the evolutionary process. I wish I could see a time-lapse film depicting all the little biological changes in the transition from primates to humans, or how mammals returned to the sea and became whales and dolphins. But the millions of years these changes take make that kind of film impossible.

Don’t ask me why all this happens or how it got started. I’m pretty humble about things like that, and rather than ascribe them to one thing or another, I’ll admit that I just don’t know. I can live with not knowing.

I do believe that the irony in all this is that creationists have also evolved. They’ve evolved from a literal Biblical explanation of life on Earth to the more clever argument of intelligent design. I believe that’s a good example of change and adaptation. Too bad they don’t see their own evolution or appreciate the wonder of how life evolves. I think it’s the greatest show on Earth—maybe not in the heavens, but definitely here on Earth.

Excess use of sodium:

Campbell’s is like the Microsoft of the soup world. The company dominates the soup business, but it’s products…well…taste like crap.

Their soups are at best bland and mushy. Some contain so much salt that they’re the human equivalent of a salt lick. For example, Campbell’s Chicken Noodle Soup provides a whopping 890 mg of sodium per serving, and 2,225 grams of sodium for a standard 10.75-ounce can.

Spiking products with monosodium glutamate (MSG):

Campbell’s now owns Swanson, the maker of various chicken broths and stocks. Until recently, Swanson spiked its tasteless products with monosodium glutamate (MSG), a flavor enhancer. But MSG is well documented as a cause of Chinese Restaurant Syndrome.
I’m not joking. Every Chinese restaurant used to boost the flavor of its meals by adding MSG. But a fair number of customers complained of neck and muscle aches afterwards, the result of MSG. So now, a lot of Chinese restaurants don’t use MSG anymore.

But I digress.

All ingredients not listed:

Swanson recently introduced organic chicken, beef, and vegetable broths. Sounds like a great idea, right?

Well, on the company’s web site, the Swanson folks fess up to the fact that their broths contain 550 mg of sodium for each one-cup serving. A typical bowl of soup would contain about two cups, so that would add up to 1,100 mg of sodium. And maybe one blood-pressure cuff.

But no where on the Swanson website is a full listing of the products’ other ingredients. Ditto for the Campbell website. This is more than just peculiar, because even such junk-food hustlers as McDonalds, Pizza Hut, and Starbucks list all of the ingredients in all of their products on their websites. (For example, a venti-size Starbucks banana coconut frappuccino with whipped cream provides 730 calories, including a quarter-pound of sugars.)

So that left me wondering what Swanson and Campbell might be hiding.

So I clicked to contact customer service and wrote a brief email asking for a complete list of ingredients for the Swanson Organic Chicken Broth. Sounds simple enough, right?

A few days later, campbellsoup@casupport.com responded:

“All of our products have nutritional labels that include the calorie, sodium, fat, cholesterol and carbohydrate content for a single serving. However, it is important to note that product recipes change frequently and ingredients are periodically added or replaced. Therefore, we suggest that you check each package for the most current nutritional information…

“I hope I’ve been able to answer your question. Please contact the Consumer Response Center or visit Campbell’s website if you have additional questions.”

So I wrote back and said that they had NOT answered my question. And I also wondered, adding a list of full ingredients to the website can’t be all that difficult, could it? After all, it’s got to be easier to update a web page compared with…say, reformulating the ingredients in an industrial-size soup manufacturing facility.

Finally I went to both my local supermarket and Whole Foods, but did not find Swanson’s organic broths on the shelf. So their ingredients remain a mystery to me.

And after all this, I’m left wondering: Why couldn’t Campbell’s just be more up front about their ingredients and list them on the company’s website. Unless they really want to hide what’s in them.

Despite the worldwide economic recession, one type of business seems to be profiting: candy shops.Most of us have our comfort foods. It may be chicken soup, a slice of pizza, or a chunk of chocolate. A recent article in the New York Times reported that business in candy shops is booming. Business is especially good for inexpensive sweets, such as Hershey Kisses, compared with more expensive indulgences.

Interestingly, this sweet-tooth trend coincides with another trend, a shift from high-fructose corn syrup (HFCS) back to old-fashion sugar (sucrose). Beginning in the 1980s, HFCS became the sweetener of choice in processed foods, soft drinks, and candies. It was sweeter than sucrose, had a longer shelf life, and less expensive. Consumption of HFCS skyrocketed, while sucrose consumption plummeted – though the average American’s consumption of all added sugars has continued to climb to about 160 pounds per year.

Sucrose is a chemical compound, whereas HFCS is a blend of fructose and glucose, which leads to different metabolic effects. HFCS does a better job of raising triglycerides (a marker of diabetes and heart disease risk), and is more likely to lead to weight gain (in comparison to sucrose).

A lot of people (including me) complained about HFCS, and the giant junk food companies apparently listened. They’ve started returning to sucrose as a sweetener in frozen dinners, tomato sauces, salad dressings, and other products. With incredible audacity, companies are now describing sucrose as natural and healthy.

Natural and healthy? While HFCS does appear worse than sucrose, that doesn’t make sucrose a healthy alternative. The ideal dietary solution is to emphasis fresh foods and to avoid packaged foods, especially those with any type of added sugar.