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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.
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, 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 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 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 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 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.
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.
New Scientist
magazine, Volume 171 Issue 2306, January 9, 2001, page 26
The Journal
of Nutrition, Vol. 131:2001 p 2074
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