Syndrome X

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How Fructose, Insulin and Syndrome X Can Change Your Life

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By Gail Vines

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.

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Syndrome X is Alarmingly Common

What´s more, evidence is growing that we can bring it on ourselves, by the

way we eat.

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 biochemistry 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 behavior 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. Zammit believes that the same process

is likely to happen in people.

What Happens To The Sugar In Our Diet

It´s a vicious cycle. In turn, the excess triglycerides make muscle cells

insulin-resistant, interfering with the signaling 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 that

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,

Koutsari and ne 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.

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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 metabolized 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 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 labeling 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

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.

How Much Fructose Is In Our Food

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 fiber 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 vegetable 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.

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New Scientist magazine, Volume 171 Issue 2306, January 9, 2001, page 26

The Journal of Nutrition, Vol. 131:2001 p 2074