Gail Vines
From New Scientist magazine, vol 171 issue 2306, 01/09/2001, page 26
All the low-fat ready meals in the supermarket won't save you from heart disease. Gail Vines explains why sugar is the new fat
YOU try to look after yourself. You reduced your intake of saturated fat years ago, you're not overweight, you don't smoke. Basically, you don't consider yourself at risk of developing heart disease. Sorry to disappoint you, but there's something you've overlooked. Syndrome X.
The name, coined by Gerry Reaven of Stanford University in the late 1980s, sounds threatening, and with good reason. Syndrome X is a hidden but life-threatening perversion of bodily metabolism that is likely to hasten the end of anyone who has it. It's alarmingly common. What's more, evidence is growing that we can bring it on ourselves, by the way we eat. "We're suffering from chronic food intoxication," says Werner Waldhausl, editor of the journal Diabetologia.
In well-fed parts of the world, a third of the adult population may have succumbed already, and there will be plenty more in the pipeline. Most of them won't know that there's a problem yet -the early stages go unnoticed. All the same, the symptoms are all there: high blood pressure, raised levels of tell-tale fats called triglycerides found in the blood, and insulin resistance-an acquired resistance to the body's vital glucose-handling hormone.
Diabetes and heart disease are lying in wait for anyone with this group of symptoms collectively known as syndrome X. "The syndrome is a major cause of coronary heart disease," Reaven says, though nobody can yet be more precise than that. So what causes it? After decades of sometimes acrimonious debate, at last researchers may be nearing an answer.
The usual suspects are all there: fatness, sloth and a family history. But there's some good news from the latest studies of the biochemisty of syndrome X. What we eat and how we eat it can make a difference. One key insight is that the liver holds the secret to syndrome X. Manipulating the behaviour of this organ could keep at bay the twin perils of heart disease and diabetes. Another is that sugar could be as bad for your heart as saturated fat.
"We've long known that diets high in saturated fats are bad news," says Victor Zammit, head of cell biochemistry at the Hannah Research Institute in Ayr, Scotland. But we don't have to eat saturated fats to find our bodies awash with these dangerous molecules. As our liver deals with the products of digestion, it can flood the bloodstream with deadly saturated fats that are already within the body. Anything that encourages the liver to do this could be just as bad as ingesting saturated fat itself.
Evidence is emerging also that our "grazing" pattern of eating could partly explain why syndrome X is on the increase. Zammit believes that eating too frequently could be one of the triggers that turns your liver into a relentless fat-secreting machine.
This is how it works. Each time we eat, insulin is released into the bloodstream. This vital hormone, secreted by special cells in the pancreas, encourages our tissues-particularly our muscles-to gobble up the glucose surging through the bloodstream after a meal. That's all to the good, because glucose hanging about in the blood is dangerous stuff. It can stick to proteins and destroy their ability to do their job. Blindness, kidney damage and amputations may result.
But insulin has another vital role. After a meal, it stops the liver from releasing any fat, a potential metabolic fuel, into the blood. Why after a meal? It turns out that just like glucose, these fats are dangerous if they hang about in the blood too long. They are released as triglycerides, carried within molecular escorts known as very low density lipoproteins, or VLDLs. But in the blood they become altered biochemically in a way that makes them more likely to stick to artery walls. And of course once the arteries become narrowed by such fatty plaques, a heart attack may not be far away. These fats are particularly undesirable in the bloodstream just after a meal because the enzymes that can safely remove them from circulation are busy dealing with fat from the food you've just eaten.
Zammit and his colleagues have only recently discovered how this process can go wrong-in rats at least. He believes that the road to syndrome X begins with frequent high-energy snacks, exposing the liver to insulin for long periods without a decent break. In studies of laboratory rats, the researchers found that when insulin is present for long periods, it flicks a metabolic switch in the liver that prevents it from inhibiting triglyceride secretion. Instead, perversely, insulin stimulates the liver to release even more triglycerides, carried within heart disease promoting VLDLs (see Diagram). Zammit believes that the same process is likely to happen in people.
It's a vicious cycle. In turn, the excess triglycerides make muscle cells insulin-resistant, interfering with the signalling pathway that normally allows them to soak up glucose from the blood. As a result, more insulin needs to be secreted, and full-blown syndrome X is fast approaching.
Eventually our adipose cells-bombarded with extra calories to store in the form of triglycerides and glucose-succumb to insulin resistance too. In a final twist, the overloaded fat cells flood the blood with fatty acids which in turn start killing the insulin-secreting pancreatic cells. Insulin levels plummet, glucose accumulates in the blood even between meals-and a diagnosis of type 2 diabetes is made. If the patient fails to change their diet and lose weight, the destruction of insulin-secreting cells continues apace. Eventually, daily injections of insulin are needed just to keep the patient alive.
It's a frightening scenario, but we can do something about it. For a start, we can exercise to use as many of our muscles as possible, and to help them use up the extra fatty fuel. New research by physiologists at the University of Loughborough, Christina Koutsari and Adrianne Hardman, reveals that a moderate amount of daily exercise might even prevent the dramatic rise in blood triglyceride levels that happens when healthy volunteers are switched to a high-sugar diet.
But Zammit recommends that we also eat less often-leaving a good 4 or 5 hours between meals and cutting out snacks. He reckons our livers have evolved to cope with infrequent meals. Two meals a day could be better for you than continual snacking.
We have to watch what we eat as well as when. Eating or drinking certain things can increase fat secretion by the liver and have just as detrimental an effect as ingesting saturated fat itself. Drink too much alcohol, for instance-more than the equivalent of a glass or two of wine a day-and you stimulate your liver to churn out the very fats that promote heart disease.
The big surprise is that sugary foods could be just as damaging as fats and alcohol. "Foods high in fructose-and that includes ordinary sugar, sucrose, which is half fructose-may be just as bad as saturated fats," says Zammit. Both sorts of food are royal roads to syndrome X.
Over the past decade or so, various studies have suggested that the body treats fructose in a markedly different way from the simple sugar glucose. What's worrying is that fructose is selectively shunted towards the liver, and the formation of fats. For a start, it is metabolised in the liver to provide one of the building blocks of triglycerides. But a fructose-rich diet also directly stimulates the liver to secrete those dangerous triglycerides, just as bombarding the liver with insulin does. "Fructose could be mimicking what I think frequent insulin secretion does," Zammit explains. In the short term it could promote insulin resistance in muscle-the first step to syndrome X-and in the long term it could promote heart disease.
Not everyone agrees that fructose is dangerous. Some say there's not enough in our diet to have any noticeable effect. But a wealth of animal studies support the idea. Feed a lab rat fructose, at levels comparable to those in human diets, and it develops insulin resistance, even if it stays lean.
Last year, researchers at the University of Toronto in Canada fed a high-fructose diet to Syrian golden hamsters, which have a fat metabolism remarkably similar to humans'. In a matter of weeks, the hamsters developed syndrome X-including high triglyceride levels and insulin resistance.
And a powerful study of fructose's effects on humans was published last year. Clinical nutritionist John Bantle and his colleagues at the University of Minnesota at Minneapolis fed a diet containing 17 per cent of the total energy as fructose to two dozen healthy volunteers for six weeks. It sounds like a lot of fructose, but Bantle reckons that at least 27 million Americans eat this much in their diet.
They then fed the volunteers a diet sweetened with glucose and nearly devoid of fructose. The results were dramatic, particularly in the men, who proved to be more sensitive than women to fructose. Why this should be so is not yet clear. "The fructose diet produced significantly higher triglyceride concentrations in the blood, compared to the glucose diet," says Bantle. In men, levels were 32 per cent higher. More importantly, on the fructose diet, the triglyceride levels peaked just after meals-when these fats can do the most damage to our arteries. He'd like to see a marked reduction in the amount of fructose added to beverages and food in the Western diet.
"It's a wake-up call for the food industry," Zammit agrees. "Food manufacturers are good at labelling processed foods as '99 per cent fat free'. What they don't say is that they are 15 per cent sugars, which is probably worse than some fats." His concern is that "people may deliberately select low-fat processed foods, thinking they are making a healthy choice, and yet the product could be very high in fructose." And it's not just sweet tooths we must resist, it's our liking for sweet drinks. Zammit suspects that high-sugar soft drinks, now consumed in vast quantities, could be the most worrying component of the modern diet.
The dangers of fructose are not yet widely known, and the amounts consumed in the average Western diet have shot up since the 1970s. The sucrose molecule is half fructose and half glucose, so eating anything with ordinary sugar in it gives you a dose of the stuff. Worse still, food manufacturers in the late 1960s started to use a cheap sweetener, corn (maize) syrup, which is virtually pure fructose. It's now added to all sorts of food, including most breakfast cereals and a vast range of processed foods.
From 1975 to 1990, fructose consumption from corn sweeteners increased tenfold in the US. Surveys dating from the late 1980s put the average US consumption of fructose at about 9 per cent of dietary energy intake, which means that many people will be consuming far more. "Metabolic effects on the population from this rapid change may not be apparent for some time," reckons Judith Hallfrisch of the National Institute of Aging in Baltimore. But give fructose a few decades to wreak its metabolic havoc, and the next generation of epidemiologists may be picking up the pieces.
Of course, it's tempting to think you might be one of the lucky ones who will never develop insulin resistance. People differ in their susceptibility to syndrome X, no doubt partly as a result of their genetic makeup-though the key susceptibility genes have yet to be tracked down. Fetal nutrition and diet in early infancy may be equally important, as David Barker of the University of Southampton argues. Babies who are undernourished in the womb and shortly after birth seem to be particularly susceptible to syndrome X, especially if they are well fed in later life and become overweight.
Even if the genetic cards are stacked against you, there's intriguing evidence that diet can still make a difference. Consider the Pima, Native Americans of southern Arizona, nearly all of whom are cursed with a "thrifty genotype". Their metabolism is especially geared to laying down fat in preparation for times of famine. By old age, nearly all have developed type 2 diabetes. Even by age eight, most are already insulin resistant. But this plague only struck after the Pima people were introduced to Western foods. Pima Indians who ate a typical Western diet were found to be two and a half times as likely to develop diabetes as those who ate a somewhat more traditional diet over the 10 years of the study. Genes are not necessarily destiny.
But scientists acknowledge that to change our ways, we need help-if only to resist all those tempting convenience foods now filling our supermarket shelves. If the food industry is reluctant to take the new health messages on board, it could be "strongly regulated" to produce a tasty but healthy diet, argues editor Waldhausl. Such a change might even be in food producers' own interests. Perhaps, says Waldhausl, the industry will one day be forced to pay damages "similar in scale to those awarded against the tobacco industry today" to consumers made fatally ill by eating their products.
THE take-home message from the latest nutritional research is that if you feel like something sweet, reach for a piece of fruit. Fructose is found in fruit and vegetables, but unlike processed foods it's present in vanishingly small amounts and is bound up with complex plant fibre and other nutrients that offer many health benefits. In 1999, researchers at Harvard even went so far as to suggest that every extra fruit or serving of veg consumed each day reduced the risk of a stroke by a whopping 6 per cent.
But it's not just sugars we need to watch. The kinds of fats we eat also have an enormous impact on our long-term health, says Len Storlien, director of metabolic research at the pharmaceuticals company AstraZeneca. Instead of struggling to eat far less fat overall, he argues that people should reduce their consumption of saturated fat by switching to olive oil and polyunsaturated fats, especially marine fish oils. These can suppress the liver's release of harmful triglycerides. A diet high in these polyunsaturated fatty acids combats syndrome X.
Gerry Reaven of Stanford University, who coined the term syndrome X, couldn't agree more. But he's also convinced that the "low-fat" message has encouraged people to eat more insulin-stimulating carbohydrate instead, fuelling the epidemic of insulin resistance.
There's a third, albeit controversial strategy to avoid syndrome X: eating "slow-release" carbohydrates that arguably don't provoke the same rush of insulin. These are complex carbohydrates with lots of plant fibre-such as barley, millet and brown rice-and those that the body can digest only slowly, such as pasta, beans and lentils. Storlien would like to see the food industry create foods that take longer to digest. While at the University of Wollongong in Australia he collaborated with a company marketing a novel bread. Made with corn starch high in the polysaccharide amylose, the white bread is digested much more slowly than ordinary bread. This month two such breads will be launched in Britain.
Further reading:
* : "Insulin stimulation of hepatic triacylglycerol secretion and the etiology of insulin resistance," by Victor A. Zammit and others, in The Journal of Nutrition, vol 131, p 2074 (2001)
Gail Vines
From New Scientist magazine, vol 171 issue 2306, 01/09/2001, page 26
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