Read an Excerpt
Chapter 1: Nutrition Issues
ANTIOXIDANTS ARE MAGICAL. At least when it comes to marketing. Just slap the word on the label of a food or beverage and watch sales zoom. That's because even people who have no idea what antioxidants are want more of these substances in their life than less. And they could be right. Or not. It seems the "free radical theory" of disease and aging may not be on as firm a ground as we have been led to believe. And if that is the case, antioxidants may not live up to their exalted status as the key to good health and longevity.
Back in the 1950s, Dr. Denham Harman proposed a theory that at the time seemed rather radical. Many ailments, including cancer and heart disease, as well as the aging process itself, he suggested, were the result of cumulative damage caused by reactive molecular species called free radicals. Since these were byproducts of metabolic reactions involved in energy production, their formation in the body was inevitable. Why? Because nutrients derived from food are slowly combusted in mitochondria—the small, membrane-enclosed regions of cells. And, as in any combustion process, oxygen is required. Unfortunately, as oxygen reacts with nutrients to produce energy, it also unleashes some "friendly fire" in the form of the notorious free radicals.
Different types of free radicals can appear, but they all descend from a highly reactive species of oxygen known as superoxide. Radicals are hungry for electrons and try to satisfy their appetites by feeding on innocent molecular bystanders. Since electrons are the glue that binds atoms in a molecule together, molecules that become the targets of free radical attack tend to fragment. Such damage in turn translates to disease, particularly when the victims of free radical onslaught are proteins, fats or molecules of DNA. Harman hypothesized that our bodies deal with free radicals by mounting "antioxidant defences." Vitamins E and C, along with enzymes such as superoxide dismutase, catalase and glutathione peroxidase, were quickly labelled as antioxidants, acknowledging their ability to neutralize free radicals in the test tube. Harman then buttressed his theory by feeding antioxidants to mice, claiming that the animals lived longer. The free radical theory was off and running.
Over the next couple of decades, researchers tested more and more substances in the laboratory for free radical–neutralizing effects, discovering a plethora of antioxidants. The likes of polyphenols, carotenoids and lipoic acid, all found in fruits and vegetables, obliterated free radicals in laboratory experiments. Since populations consuming more fruits and vegetables were known to be healthier, a seemingly obvious explanation now emerged: antioxidants in food prevent disease! A corollary was that dietary antioxidant supplements should also prevent illness, an idea that gave rise to a new market trend. Touting their antioxidant potential, vitamins, minerals, various seed and bark extracts, teas and exotic fruit juices began to vie for the public's attention. And they did so successfully. Sales of antioxidant supplements skyrocketed. Even skin creams joined in the game, hyping the efficacy of their antioxidant ingredients in the battle against the ravages of age.
But now the wheels on the antioxidant bandwagon are developing some squeaks. Since the 1990s, numerous randomized, placebo-controlled trials have investigated the effects of vitamin C, vitamin E, selenium and beta carotene, the classic antioxidants, on cancer and heart disease. While some studies offered hope, the majority failed to show any benefit associated with antioxidant supplements. Some, particularly those using beta carotene, actually suggested potential harm, for smokers at least. Recent studies have not brightened the outlook. The Selenium and Vitamin E Cancer Prevention Trial (SELECT) randomly assigned more than thirty-five thousand men to take either selenium, vitamin E, both or a placebo on a daily basis. The trial was stopped after five and a half years because no differences were observed between the groups in relation to prostate cancer risk. Similar results were noted in the Physicians' Health Study II. About fifteen thousand male physicians were enrolled and asked to take either vitamin C, vitamin E or a placebo for eight years. Neither vitamin had an effect on prostate cancer or total cancer. And now a major study on heart disease has thrown more cold water on the antioxidant theory. This time, the subjects were diabetics, who are, in general, predisposed to heart disease. In the Prevention of Progression of Arterial Disease and Diabetes Trial, more than a thousand adults aged forty or older were assigned, on a random basis, to take either a daily capsule containing a mix of antioxidants or a placebo for eight years. The antioxidants offered no protection against cardiovascular disease.
Could the free radical theory of disease and aging be totally wrong? Not likely. But neither is it the complete answer to the complexity of aging and disease. This is now underlined by a fascinating study on nematode worms at University College in London and Ghent University in Belgium. Granted, people aren't worms (in most cases anyways), but these tiny creatures do serve as an excellent model for the study of aging. Their normal life expectancy is only a few days, so any change is readily noted. The researchers managed to inactivate the worms' genes that code for superoxide dismutase, one of the prime antioxidant enzymes. They expected to see a reduction in life expectancy in response to increased oxidative stress; while there was evidence of increased free radical activity, the worms did not die any sooner. Aging apparently was unaffected by reducing antioxidant activity.
What does all of this mean? That when it comes to health, disease and aging, nothing is as simple as it seems. And so it is with the free radical theory. Evidence is mounting against antioxidants being as important as we thought. But at the same time, we have more and more evidence for the benefits of increased fruit and vegetable intake. A conundrum? Not necessarily. Fruits and vegetables contain hundreds of compounds that may have positive effects that are not yet fully understood, and perhaps we have been overzealous in attributing magical effects to antioxidants.
The Cheez Whiz Effect
NEWS FLASH! The Food and Drug Administration in the U.S. has approved the addition of trans fats to dairy products, meal-replacement bars, soy milk and fruit juice. Now, I know what you're thinking: the agency has gone mad. Either that or it has capitulated to big business. After all, aren't trans fats a nutritional pariah? Are these not the nasty, artery-clogging substances that food producers and restaurants are being urged to purge from their repertoires? Well, the fact is that not all trans fats are fiends. The ones producers are considering adding to foods are not the same as the ones that are terrifying people with their artery-clogging potential. In fact, these trans fats may be good for us. It all comes down to some subtle differences in molecular structure.
Fats are composed of long chains of carbon atoms, joined to each other either by single or double bonds. It is the latter that give rise to the trans conundrum. Depending on the particular arrangement of atoms around the double bond, the chain of carbon atoms will be straight (trans arrangement) or bent (cis arrangement) at the position of the double bond. This may not seem to be very important, but the way a fat engages in biochemical reactions depends on its molecular shape. As a further subtlety, fat molecules can have more than one double bond, each with the cis or trans configuration. Furthermore, the double bonds may be located at different positions along the chain of carbon atoms. The trans double bonds that we worry about are the ones that are separated from each other by more than one single bond. These arise as a result of the hydrogenation process used to harden liquid vegetable oils to improve their keeping properties and to make them more suitable for frying. Unfortunately, these fats don't have excellent properties for keeping our health. They're the trans fats that have been linked with heart disease.
However, trans fats also occur in nature, particularly in meat and dairy products. But in these, the double bonds are separated from each other by just one single bond. Such fats are referred to as "conjugated" and have a completely different health profile from the ones that result from hydrogenation. Conjugated linoleic acid (CLA) contains two double bonds, either of which can assume the cis or trans configuration. The molecules of interest in terms of health benefits are those that have one cis and one trans double bond. Although technically these are trans fats, there is a world of difference between their biological activity and those of the trans fats that may lurk in your doughnut or order of french fries.
The story of the "good" trans fats started with an investigation of the "bad" properties of hamburgers. In the late 1970s, Dr. Michael Pariza at the University of Wisconsin became interested in the chemical reactions that take place when meat is cooked. Suspicion had been raised that carcinogens may form at high temperatures, and indeed these fears were realized. But much to Pariza's surprise, he also found that cooked hamburger contained some compounds with decided anti-cancer effects. These turned out to be the CLAs, which then understandably excited a number of researchers.
Before long, CLAs were also found to be present in dairy products, originating from chemical reactions in the stomachs of ruminating animals. That's where enzymes convert naturally occurring cis fats in the animals' diet to CLAs. When different dairy products were analyzed for CLA content, researchers were in for a surprise: that curious American concoction known as Cheez Whiz had a higher CLA content than any other food. This finding provided plenty of whimsical fodder for reporters who, with tongues planted firmly in cheeks, began to label Cheez Whiz as the new health food. Of course, the spread is no such thing— its CLA content is easily trumped by unhealthy doses of saturated fat and salt. The Cheez Whiz effect was actually not a boon for CLA research, as critics smirked at the prospect of an ingredient in this odd gustatory creation being touted as potentially "healthy." But they are not smirking at the mention of CLAs now.
A stunning amount of research has been carried out since the initial Cheez Whiz caper brought CLAs into the public spotlight. While no anti-cancer effect has yet been demonstrated in humans, animal models and cell cultures have repeatedly confirmed the initial finding. The greatest excitement, though, has been over CLAs' ability to reduce body fat while enhancing lean body mass. Although supplementing the diet with CLA does not result in a reduction of body weight, it is effective in reducing fat mass and increasing muscle mass. The most significant effects have been seen in people who have lost weight through a low-calorie diet and then put the weight back again, as commonly happens. But subjects who were supplemented with about three grams of CLA a day were more likely to regain the weight as muscle rather than fat. Other experiments have suggested that CLAs can enhance immune function and reduce atherosclerosis, high blood pressure and inflammation. Quite a grab bag of positive findings! Pretty alluring, especially given that no significant side effects have been noted.
As one might expect, producers have been itching to add these compounds to regular foods so that they can then be promoted as having health properties beyond simple nutrition. While dietary supplements of CLAs made by chemically treating sunflower or safflower oils have been available for a couple of decades, their status as food additives has been in a regulatory limbo. Until now. With the FDA giving the go-ahead, producers are set to crank out cookies, eggs, yogourt, milk— and who knows what else— enriched with these "good" trans fats. Whether the promise of CLA enrichment is fulfilled remains to be seen. While the right dose may offer certain benefits, the Holy Grail has not been found. And if you want some CLA enrichment before fortified foods come our way, well, yak cheese and kangaroo meat are the way to go. Or you can take a supplement. Michael Pariza does— three grams a day. As for me, I'd like more evidence. But I just might dip my broccoli in Cheez Whiz. Geez . . . I can't believe I said that.
IT'S A STRANGE WORLD. Health food stores promote dietary supplements of astaxanthin, claiming more powerful antioxidant benefits than with either vitamin E or beta carotene. It helps protect against the damaging effects of pollution, ultraviolet light and immune stress, they say. But in California, the state's supreme court ruled that private citizens can sue stores if they sell fish without declaring that astaxanthin has been added to their feed. What's going on?
Astaxanthin is a naturally occurring pigment found in a variety of algae that serve as food for krill, shrimp and crayfish, imparting an orange-yellow colour to these creatures. Algae produce astaxanthin for the same reason that many plant and animal species produce such antioxidants. They mop up the potentially harmful free radicals that are the by-products of metabolism and also offer protection from the damage that can be caused by ultraviolet light. This protection is transferred to the algae's predators, and then to the predators of those predators. Which explains why wild salmon develop their classic orange colour.
These days, however, most salmon are raised on fish farms. No, they're not genetically modified mutants that graze on the prairie, they are fish raised in penned-off areas of the ocean, where, instead of having to search for fresh krill, they can just lounge around waiting to be served a commercially concocted feast. But these pellets, made from fish too small and bony to be used for human consumption, lack the astaxanthin that gives wild salmon its colour. As a result, the flesh of farmed salmon turns out to be an unappetizing grey. And more grey means less green in the cash register. The answer to this little problem is to add astaxanthin to the feed.
The commercial production of astaxanthin is a huge industry, relying on three distinct processes. Sugar fermented by certain yeasts can produce the compound. It can also be extracted from specially grown algae. But the most economical, and therefore the most common, process relies on a fourteen-step chemical synthesis from raw materials sourced from petroleum. Actually, the name astaxanthin refers to any one of three very closely related compounds with very subtle differences in molecular structure. The ratio of the three produced by any of the commercial processes is the same, but differs from the ratio found in wild salmon. A technique known as high-performance liquid chromatography (HPLC) can be used to separate and quantify the three stereoisomers of astaxanthin, and hence determine whether the sample came from wild or farmed salmon.
Why should anyone care about this? Because wild salmon is prized more by consumers than farmed salmon! Some claim that they prefer the taste, but most who care about the origin of their salmon are concerned about their health. They've heard of studies showing that farmed salmon are higher in toxins such as PCBs than the wild variety. This may well be the case, since the meal fed to farmed salmon is made from fish often caught in more polluted parts of the ocean than where wild salmon feed. Whether these trace amounts of PCBs are of any health significance is debatable. My guess is that they are not. But what is beyond debate is that wild salmon fetch a higher price. So selling farmed salmon as wild is a lucrative, but obviously unethical, proposition. When it comes to a contest between ethics and profits, however, profits often triumph. So we shouldn't be too surprised that an investigation by The New York Times revealed that a number of stores were selling farmed salmon masquerading as wild. Samples were purchased from eight popular establishments and sent to a laboratory specializing in HPLC analysis. Six of the stores were found to be selling "fake" wild salmon.
Nobody likes to be duped in this fashion, especially not Californians, who tend to react to any type of perceived artificial meddling in their food supply with religious fervour. In many cases, the "meddling" was misunderstood, and consumers declared their outrage about their salmon being recklessly coloured with some artificial "chemical." I wouldn't be surprised if some of the anti-colourant demonstrators were popping astaxanthin antioxidant pills purchased in their local houses of worship, the health food stores. There is, of course, no health issue with the astaxanthin colourant in salmon, no matter what its origin. But people do have a right to know what they are buying. However, suing over whether a fish gets its astaxanthin colouring from dining on krill or from eating fish meal seems to be an overzealous and inappropriate use of the legal system.
If going to court over a colourant is deemed justified, just imagine the scenario when the litigious American consumer discovers that the farmed-fish industry is contemplating replacing some of the fish meal with a product made from grains and plant oils. As the population of the small fish used to make salmon feed declines, this is becoming a financially attractive proposition. And this substitution really could have a health consequence.
Norwegian researchers enlisted sixty coronary heart disease patients to study the health effects of eating salmon raised either on fish oil or on canola oil. For six weeks the subjects consumed three salmon meals a week and had their blood sampled for inflammatory substances as well as for various markers of cardiovascular disease. As was to be expected, the subjects who ate the fish reared on fish oils had higher levels of the heart-healthy omega-3 fats in their blood, but they were also found to have lower levels of two key markers of inflammation, vascular cell adhesion molecule-1 and interleukin-6.
If Californians think that the lack of labelling indicating the source of astaxanthin in salmon flesh is worth pursuing in court, they will certainly be most upset when they find out that their farmed salmon is being fed more like a cow than like a fish. But there is nothing illegal about this, so they may just have to drown their sorrows in a glass of carrot juice. Organic, of course. Perhaps fortified with a shot of astaxanthin.
IT'S ANNOYING when facts get in the way of a good story. Like the one about Vincent Van Gogh mutilating his ear in a thujone-induced fit. Thujone is a naturally occurring compound found in wormwood, one of the plants used to flavour absinthe, the legendary liquor that enthralled artists and writers during the latter years of the nineteenth century and the early part of the twentieth. The "green fairy," as it was called, contained up to 75 per cent alcohol by volume, but its real kick was supposedly the "special" sensations induced by thujone. I have often told the story, pieced together from accounts in the scientific and popular literature, of Van Gogh being driven round the bend by thujone, with the compound possibly even contributing to his suicide. As a finale, I would recount how Dr. Paul Gachet, Van Gogh's personal physician, looked after his funeral and unknowingly adorned the grave with a wormwood bush that grew roots, eventually enveloping the casket. Van Gogh, I would say, was in the clutches of thujone in death, as he had been in life. Alas, recently uncovered facts suggest that we have to look elsewhere in an attempt to rationalize the artist's irrational behaviour. Thujone was not the culprit.
As it turns out, absinthe's naughty reputation isn't scientifically justified. Its status as a wicked, mischief-causing beverage can be traced not to carefully controlled experiments, but to a guinea pig, a murderer, some puritan prohibitionists and the French wine industry. Here's that story. Factual, at least as far as I can make out.
Absinthe was first formulated in Switzerland around 1790 by distilling an alcoholic brew infused with botanicals and herbs that included anise, hyssop, lemon balm, Florence fennel and Artemisia absinthium, or wormwood. The classic green colour is the result of adding chlorophyll extracted from herbs to the distillate. While it isn't clear who first came up with this concoction, we do know that the recipe ended up in the hands of Major Daniel-Henri Dubied, who claimed that it enormously enhanced his sexual performance. The major then sold the recipe to his son-in-law, Louis Pernod, who seconded the bedroom effect, added a claim of "indigestion remedy," and began mass production in 1797.
Whether because of these purported special properties or its high alcohol content, absinthe became very popular, especially among artists, who took to indulging daily, and excessively, during l'heure verte. There was talk of enhanced creativity, but there were also murmurings about psychotic episodes, hallucinations and, according to some, permanent brain damage. Tracking down the origin of these accusations is difficult, but absinthe likely served as a convenient scapegoat for the inebriated antics associated with the bohemian community.
The flames of innuendo were fanned in 1864, when Dr. Valentin Magnan carried out the first-ever investigation into wormwood oil. Magnan placed a guinea pig in a glass cage with a sample of wormwood oil, and another one in a cage with a supply of alcohol. As might be expected, the latter animal lapped at the alcohol until he became drunk, but unexpectedly, the guinea pig exposed to just the vapours of wormwood oil went into convulsions. This primitive experiment drove the first nail into the coffin that would bury absinthe fifty years later. Magnan went on to isolate thujone from wormwood and confirmed its toxic potential by showing it caused convulsions followed by death in a dog. When the good doctor claimed to have evidence (never confirmed) that alcoholics who consumed absinthe were more likely to exhibit delusional behaviour and convulsions, the writing for the demise of absinthe was on the wall. The French wine industry, noting the increasing popularity of a competitor, was happy to jump on the anti-absinthe bandwagon alongside prohibitionists. And then came a catalytic moment.
A horrendous crime shook Europe in 1905. Jean Lanfray, a Swiss labourer, murdered his pregnant wife and two children in a drunken rage after she refused to polish his shoes. He had consumed seven glasses of wine, six of cognac, two crème de menthes, coffee with brandy and two shots of absinthe. Ignoring the stunning alcohol consumption, prosecutors claimed a clear case of "absinthe madness," a condition never scientifically demonstrated. Lanfray escaped the death penalty because "absinthe made him do it," but couldn't escape his own conscience— he eventually hung himself in his prison cell. The case set off an epidemic of moral indignation and triggered petitions to ban absinthe. By 1915 most countries, with the notable exceptions of the U.K., Spain, Portugal and Sweden, had made the sale of the drink illegal. The stated reason was that thujone in absinthe incited peculiar behaviour.
The myth that the original version of absinthe contained dangerous amounts of thujone persisted for almost a century—despite the fact that nobody had actually measured the thujone content of absinthe before blaming the drink for misdeeds. The amount thought to be present was actually estimated from what was known to be present in wormwood— and poorly estimated, as it turns out. In 2009 vintage bottles of absinthe were chemically analyzed for the first time and found to contain about 25 milligrams of thujone per litre, the same as in the currently available "low-thujone" versions, and far less than the 250–350 mg/L that had been previously claimed. We now know that even these levels are way below those that cause convulsions or hallucinations. Why, then, did so many absinthe imbibers experience such dreadful effects? Simple: they were plain drunk. So it seems that while thujone did not drive Van Gogh into the grave, the facts about this compound have buried my story about the artist being in its clutches. And if anyone wants to try some "pre-ban" absinthe, it is available. A bottle will set you back about three hundred dollars. But don't worry. It will not trigger any ear-mangling.
O.J. Versus Red Bull
"PYRIDOXINE!" "GLUCURONOLACTONE!" The words spew out with something close to contempt from the speaker's mouth as he ambles through a lab filled with brightly coloured liquids where technicians are seen to be using these ingredients to formulate some sort of beverage. Not the sort of chemicals we want to be defiling our body with, he implies, as he walks over and picks up a glass of orange juice. "Ingredients: fresh air, rain and sunshine," he declares. "Healthy, pure and simple." And with these words of wisdom the television ad for Florida orange juice comes to an end.
Before going any further, let me state that I think orange juice is a great beverage, and just the thing to start the day with. But that "pure and simple" beverage is composed of hundreds of different compounds, including some with tongue-twisting names like beta-cryptoxanthin, hesperitin-7-rhamnoglucoside and L-3-ketothreohexuronic acid lactone. Would it be comforting to learn that the last one is just the chemical term for vitamin C? And that the first one is a carotenoid, and the second a polyphenol, both of which are antioxidants linked to good health? The point, of course, is that the benefits or risks of a food or beverage are determined by the specific properties of its components, not by the number of syllables in their names. True, orange juice does not contain glucuronolactone, but that is not why it is a healthier beverage than Red Bull.
Why bring up Red Bull? Because that's the drink that features glucuronolactone as an ingredient and that apparently has cut into sales of orange juice. Glucuronolactone is an ominous-sounding synthetic compound, so it was a natural target for the orange juice TV campaign, especially given the ridiculous email that circulates about it. This much-forwarded diatribe maintains that glucuronolactone was an artificial stimulant developed in the 1960s by the American government. Nonsense. Glucuronolactone can be found in the body as a natural product of glucose metabolism, and the amount found in a can of Red Bull is unlikely to have any negative effect. It is added to the drink with the insinuation that it increases energy, but that claim is unproven.
Red Bull is a curious beverage introduced to the Western world by Dietrich Mateschitz, an Austrian entrepreneur who encountered an "energy" tonic in Thailand called Red Water Buffalo. He thought that "bull" would sell better in the West and changed the name appropriately. Right on! Red Bull, inexplicably, now sells about two billion cans a year. The major ingredients were then, and are now, glucuronolactone, taurine (an amino acid), vitamins, sugar and caffeine. There is little evidence that Red Bull, which to me tastes like carbonated cough medicine, has any stimulant effect other than what can be ascribed to the caffeine it contains. How much caffeine? Roughly equal to that found in a cup of coffee and twice the amount in a cola beverage. Compared with orange juice, "energy drinks" like Red Bull are nutritional paupers.
Sure, orange juice is high in sugar, which is why low-carbohydrate diets like Atkins (happily on the wane) urge limited consumption. But if you cut out orange juice, you are also cutting out an excellent source of folate, potassium, flavonoids and carotenoids, all of which have been linked with health benefits. High blood pressure is more likely in people who consume less potassium. Indeed, a study at the famed Cleveland Clinic showed that drinking two glasses of orange juice a day resulted in a modest reduction in blood pressure. Researchers at the University of Western Ontario found that three glasses a day may help keep the doctor away. When they studied twenty-five patients with high levels of LDL, or "bad" cholesterol, they found that drinking orange juice increased HDL, the "good" cholesterol, by some 20 per cent, and that the ratio of LDL to HDL, a good measure of cardiovascular risk, decreased by 16 per cent.
And now we have a study that suggests that orange juice, in doses as little as one glass a day, may even stave off arthritis. In this case, the beneficial compounds appear to be carotenoids, the orange-coloured pigments found in a variety of fruits and vegetables which may reduce inflammation through their antioxidant effect. Researchers at the University of Manchester analyzed data from some twenty-five thousand subjects who had filled out dietary questionnaires. They compared people who eventually developed arthritis with those who did not and found that the average daily intakes of two specific carotenoids— namely beta-cryptoxanthin and zeaxanthine— were lower in subjects who came down with arthritis.
Of course, excess of anything is not good, either. Just ask the lady who ended up in hospital with an extremely high potassium level in her blood. Doctors could not figure out what was going on until she sheepishly admitted that she had been drinking about five litres of orange juice a day. Why? Because she had read about the silly Orange Juice Diet, which claimed that large doses can cleanse and rejuvenate the body. Well, instead of rejuvenating her, the huge dose of potassium almost killed her.
One last thing. A study at the University of Reading examined the effects of different kinds of breakfast on the IQ of children. Guess what: drinking orange juice in the morning improved their IQ. So maybe if people drank their OJ in the morning, they would be less likely to fall into the trap of a ridiculous diet craze and more likely to realize that there are better reasons to limit drinks like Red Bull than the fact that they contain glucuronolactone and pyridoxine.
By the way, pyridoxine is just vitamin B6. Where can one get it besides Red Bull? Well, it's a natural component of orange juice!
Does Organic Mean Better?
THE BATTLE HAS BEEN RAGING back and forth ever since synthetic pesticides and fertilizers were introduced into agriculture: is organic produce safer and more nutritious than the conventional variety?
Organic, of course, was once the norm. Until the twentieth century, all farming was "organic." If you wanted to fertilize your fields, you used manure or decomposing plant material. If you wanted to control insects, you used toxic, but of course "natural," compounds of arsenic, mercury or lead. Nicotine sulphate extracted from tobacco leaves killed insects effectively, and by the nineteenth century, pyrethrum from chrysanthemums was also available for insect control. Dusting crops with elemental sulphur was an age-old practice for reducing infestation by pests and fungi. And then, in the twentieth century, synthetic pesticides and fertilizers entered the picture. Why? Necessity, as has often been said, is the mother of invention. Crop losses were too great to feed the growing population, soils were being depleted of nutrients, and the toxic effects of arsenic, mercury and lead-based insecticides had become apparent.
Chemists rose to the challenge and developed fertilizers to replenish the soil and an array of pesticides to ward off insects and fungi. Yields increased, and the hungry were fed. At least in the Western world. With produce abundant and tummies full, we now had the luxury of turning towards other food-related concerns. Like the risks of the newfangled agrochemicals. After all, insecticides were designed to kill insects, so they obviously had toxic potential. Their effect on non-target species, such as interference with the egg-laying abilities of birds, began to raise questions about their effect on human health. Consumers began to hark back to the good old days when produce had been "chemical-free." They wanted uncontaminated, pesticide-free food grown without synthetic fertilizers. They wanted to go organic.
Some farmers complied. If that's what people wanted, they would go back to growing food the old-fashioned way. No pesticides, no synthetic fertilizers and none of those novel bogeymen, genetically modified crops. Sure, yields would be reduced, and the produce might look less appealing, but as long as consumers were willing to pay a premium, farmers would meet their needs. Indeed, consumers fearful of pesticide exposure were willing to pay more for organic produce, which they surmised would also be more nutritious. After all, doesn't Mother Nature know best?
A number of field trials were organized to compare the nutrient composition of organically and conventionally grown crops and produce. These focused mainly on antioxidant content, based on the general belief that it is these substances that account for the benefits of a diet high in fruits and vegetables. This is actually not as well established as most people think. While there is overwhelming evidence that a diet high in fruits and vegetables is healthy, there is no hard evidence that this is due specifically to antioxidant content. In theory, the assumption is reasonable, because antioxidants, at least in the laboratory, can neutralize free radicals, which have been linked with a variety of health problems. But fruits and vegetables contain hundreds of different compounds, and it isn't clear which ones are responsible for the health benefits. Studies with isolated antioxidants have proven to be disappointing.
Some, but certainly not all, studies have shown that organically grown foods are higher in antioxidants. This isn't surprising, because crops left to fend for themselves without outside chemical help will produce a variety of natural pesticides, some of which just happen to have antioxidant properties. And how much of a difference in antioxidant content is there between organically and conventionally grown foods? According to a four-year study carried out at the University of Newcastle, organic food is some 40 per cent richer in antioxidants. The researchers even suggest that this means we can eat fewer fruits and vegetables in our quest for good health, as long as they are organic. This is not a very compelling argument. Foods are extremely complex chemically, and measuring the amounts of a few antioxidants may not be a proper reflection of nutritional value. For that, we need feeding studies. Do rodents thrive on organic diets? Nobody knows. And are humans who eat organically healthier? Nobody knows.
There are some other questions that come to mind as well. What about disease-causing organisms that may be present in manure used as organic fertilizer? Or fungal metabolites, which are more likely to be found in organic foods because they are not protected by insecticides? Fumonisins, for example, produced by Fusarium moulds, are carcinogenic and have also been linked with birth defects in humans. Moulds take root where insects have damaged the crop. Such damage is less likely if the crops are protected through genetic modification. Inserting a bacterial gene that codes for the production of a toxin that has no effect on humans can protect these crops from insects. But, of course, genetic modification is not allowed in organic agriculture. Too bad, because if we look to increase nutrient content, this is the way to go. A line of genetically modified tomatoes, with almost eighty times more antioxidants than the conventional variety, has already been developed at the University of Exeter. Now, that is a far greater nutritional difference than between organic and conventional produce. Imagine the benefits we could have if organic farmers embraced genetic modification!
What, then, is the bottom line here? If cost is not an issue, organic may indeed be an appropriate choice. There is no doubt that it is a more environmentally sound practice. But for most people, cost matters, and if they commit to going organic all the way, expense and lack of availability may find them consuming fewer fruits and vegetables. Emphasis really should be on consuming at least seven servings of fruits and vegetables a day, not on whether these are organic or not. There is one more point to be made: pretty soon, there will be ten billion people coming to dinner. And there is no way they are going to be fed organically.
Just This Once
I SUSPECT IT WASN'T TOO DIFFICULT to get ethics committee approval for the study. Neither was it hard to find volunteers willing to wash down a slice of carrot cake with a milkshake. And basically, that's all the fourteen subjects had to do. Twice. The first time, the cake and milkshake were prepared with a saturated fat, and a month later the same meal was prepared with a polyunsaturated fat. Well, in truth, there was a little more to the task. The subjects had to donate blood samples before and after the experiment and also had to undergo a simple test to measure blood flow in their arms. This involved using a pressure cuff to stop flow and then measuring how quickly the blood vessels dilated to restore circulation once the pressure was released. The more readily a blood vessel dilates, the better shape it is in, and the common assumption is that blood vessels in the arm reflect the condition of vessels elsewhere in the body, including the heart.
Why the interest in carrot cake and milkshakes? Because these two delights can be prepared either with a saturated fat such as coconut oil, or a polyunsaturated fat like safflower oil. And it was the post-meal effect of these different types of fat that interested researchers at the Heart Research Institute in Sydney, Australia. Dr. David Celermajer, one of the principal investigators, had carried out previous work on HDL cholesterol, the substance that the lay press has justifiably labelled as "good" cholesterol. He found that there was more to the activity of HDL than just the commonly accepted mechanism of acting like a garbage truck that picks up excess cholesterol and prevents it from depositing in coronary arteries. HDL, Celermajer had found, was also capable of interfering with the production of "adhesion molecules" by cells in the inner lining (endothelium) of arteries. These molecules enable cholesterol to form deposits called plaque, which in turn cause arteries to be narrowed, restricting blood flow. A plaque that bursts can trigger the formation of a blood clot, which can then completely choke off blood flow and cause a heart attack.
Celermajer had a theory that the anti-adhesion activity of HDL was diet dependent and wondered if the composition of a single meal could have an effect. He chose to study this possibility by isolating HDL from the subjects' blood before the experimental meal as well as three and six hours after. He incubated endothelial cells in the lab in the presence of this HDL, then added a chemical (tumour necrosis factor alpha) known to stimulate the production of adhesion molecules and measured the ability of the various HDL samples to interfere with the process.
The results were surprising. While there was no significant difference in the amount of HDL present, samples taken from the volunteers after the unsaturated-fat meal had a much greater ability to prevent the formation of the nasty adhesion molecules than samples taken after the saturated-fat meal. Clearly, it wasn't the amount, but the quality of HDL that mattered! The tacit assumption has been that the higher the level of HDL in our blood, the greater protection it affords against heart disease. Now, thanks to this study, we are learning that there is more subtlety here, and the same level of HDL may be more protective or less protective, depending on its specific chemistry, which in turn may be determined by something as simple as our most recent meal.
The blood-flow experiments that were part of this study also yielded interesting results. After the saturated-fat meal, arteries in the arm took significantly longer to dilate after applied pressure had been released. This suggests that a meal high in saturated fat can impair the ability of arteries to dilate in response to a need for increased blood flow. And that is not a good thing.
The notion that a single meal can have such negative effects is certainly not welcome, as it seems to undermine the "just this once" argument. How often have we used that one before digging into a piece of cake? "I don't really feel like oatmeal with flax this morning. I'll have some sausages, eggs and hash browns. Maybe with a Danish. Just once can't hurt, can it?" Well, maybe it can. The saturated-fat content of the meal used in this study was roughly equivalent to that found in a cheeseburger, a large order of fries and a shake. Not an unusual combo for many. On the other hand, let's remember that the anti-adhesion effect of HDL was measured in cells in the lab, not in the volunteers' bodies. And as some critics have pointed out, the safflower-oil meal had far more vitamin E than the coconut-oil meal, and this, rather than the type of fat, may be responsible for the observed effects. But I would bet on the fat effect.
So, I think, would researchers at the University of Calgary, who had thirty healthy university students eat either a typical McDonald's high-fat breakfast or a low-fat, high-carbohydrate cereal breakfast, both with the same calorie content. After the meals, the students were subjected to various stressful tasks such as keeping their arms in ice water or doing math problems. Blood pressure, heart rate and the ability of blood vessels to dilate were all more favourable after the low-fat breakfast. And remember, these were healthy people!
But let me leave you with a bit of good news. It seems the bad effect of a high-fat meal usually peaks about four hours after the meal. And a study at Indiana University has shown that a forty-five-minute walk on a treadmill two hours after eating can prevent the effect. So if you're going to have that smoked meat sandwich with fries, take a good, long walk afterward to contemplate your sin.
You Are What Mommy Eats
WE'RE GETTING FATTER. No doubt about it. The World Health Organization estimates that a seventh of the world's population is overweight, and about 300 million people can now be classified as obese. What's going on? The answer would appear to be pretty simple: we are eating more and exercising less. But that answer may be a tad too simple. Some researchers maintain that our increased calorie intake and decreased calorie expenditure are not enough to account for the "epidemic" of obesity we are witnessing. We had better have a look, they say, not only at the gluttonous amounts of processed foods we consume, but also at the packaging it comes in.
Until recently, such a notion would have seemed absurd. But now some intriguing research suggests that exposure in the womb to environmental chemicals, such as some of the fluorinated compounds used in grease-proof packaging, can be a predisposing factor for obesity. Of course, developing babies don't order pizzas, but their carriers have been known to make the odd call. And what mommy eats, the embryo eats. And if mommy eats hormone-like chemicals, baby may pay the price.
The usual suspects here include chemicals in detergents (nonylphenol ethoxylates), pesticides (atrazine, DDT, lindane), flame retardants (polybrominated diphenyl ethers) anti-fouling paints (tributyltin) and compounds leaching from plastics (bisphenol A, phthalates). Connecting these to weight gain seems off the wall, but it may not be. After all, hormones are commonly used to make cattle gain weight more quickly. While there is scant evidence that humans are being affected by tiny amounts of these endocrine disruptors, some animal studies do point to the possibility.
Retha Newbold's work at the U.S. National Institutes of Health is a case in point. Her interest was in diethylstilbestrol (DES), the classic estrogen-like compound that was once used to prevent miscarriage in women, unfortunately with tragic consequences. Their "DES daughters," as they came to be called, had an increased risk of clear-cell adenocarcinoma, a rare cancer. Newbold was investigating how DES might interfere with hormone systems when she made a surprising discovery. Injecting pregnant mice with tiny amounts of DES resulted in their offspring exhibiting unusual weight gain. Although food consumption and activity levels in the exposed mice were no different than in controls, by sixteen weeks of age, they had 25 per cent more body fat!
Diethylstilbestrol is not the only compound that has shown such an effect. Other researchers have connected in utero exposure to bisphenol A, phthalates and perfluorooctanoic acid (PFOA) with weight gain in rodents. Bruce Blumberg of the University of California actually coined a new term for such substances, calling them obesogens. His original interest was in the hormone-like effects of tributyltin, a fungicide used in paints, especially those used to protect ships' hulls from barnacles. Blumberg was taken aback when female molluscs exposed to the chemical grew male sex organs. Better see what it does to mice, he thought. Well, when pregnant mice were treated with tributyltin, their offspring showed unusual weight gain.
But, as the common saying goes, humans are not giant rodents. And, obviously, we can't expose pregnant women to suspected endocrine disruptors. So human evidence for the obesogen theory is hard to come by. Surprisingly, some support comes from, of all people, smokers. Smoking generally is associated with weight loss, but when women puff away during pregnancy (as unbelievable as that is), their offspring are twice as likely to be obese by the time they reach school age. In animal models, prenatal exposure to nicotine produces a similar effect.
What about post-natal exposure? Richard Stahlhut and colleagues at the University of Rochester have linked higher levels of phthalates in men's urine with more belly fat. Previously, low levels of testosterone have been associated with abdominal obesity, and phthalates, at least in animal studies, depress testosterone. So a connection between phthalates and jiggling bellies is plausible. And the connection may not be limited to men. Recently, researchers at Mount Sinai School of Medicine in New York investigated exposure to phthalates by looking for the metabolites of these compounds in the urine of some four hundred girls in East Harlem. The heaviest girls had the highest level of phthalate metabolites in the urine. Of course, such an association does not prove that phthalates are responsible for weight gain. Maybe the heavier girls ate more high-calorie processed foods, which would expose them to more phthalates used in packaging.
Obesity is a complex phenomenon, with multiple potential contributing factors. For example, studies have shown that sleep deprivation can lead to weight gain, and data show that the average daily sleep has decreased over the past few decades from nine hours to seven. Smoking reduces weight, and there are fewer people smoking. Some drugs, especially antidepressants and antipsychotics, produce weight gain, as do antidiabetics and beta-blockers. The age at which women have babies is also a factor. Having an older mother is a risk factor for obesity, and since 1970 the average age of first pregnancy has increased by about two years.
Believe it or not, even air conditioning and heating may be connected to obesity. Maintenance of body temperature requires energy expenditure, meaning that more calories are burned when we have to cope with high or low temperatures. Interestingly, in the southern U.S., which has an extremely high obesity rate, the percentage of homes with central air conditioning has increased from about 30 to 75 per cent since 1980. When people are comfortable, they eat more.
Taking all this into account, jumping on the endocrine-disruptor/weight-gain bandwagon is premature. It is more important to worry about the quantity of food in the package we put into our mouth than about the quantity of chemicals the package puts into the food. And until the laws of thermodynamics are repealed, the way to lose weight is still the old-fashioned way: eat less and exercise more.