…..
In Lustig’s view, sugar should be thought
of, like cigarettes and alcohol, as something that’s killing us.
…...
let’s start by
clarifying a few issues, beginning with Lustig’s use
of the word “sugar” to mean both
·
sucrose (sugar refined for the most part from beets or sugar cane),
whether white or brown and
·
high-fructose corn syrup.
…...
Lustig’s argument,
however, is not about the consumption of empty calories.....It is that sugar
has unique characteristics, specifically in the way the human body metabolizes
the fructose in it, that may make it singularly harmful, at least if consumed
in sufficient quantities.
The phrase Lustig uses when he describes
this concept is “isocaloric
but not isometabolic.” This means we can eat
100 calories of glucose (from a potato or bread or other starch) or 100
calories of sugar (half glucose and half fructose), and they will be
metabolized differently and have a different effect on the body. The calories
are the same, but the metabolic consequences are quite different.
The fructose component of sugar and of H.F.C.S. is metabolized primarily by
the liver, while the glucose from sugar and starches is
metabolized by every cell in the body. Bruce Blumberg says that fructose itself is an obesogen. "Crystalline fructose doesn't exist in
nature, we're making that," he says.
"Fructose is not a food. People think fructose comes from fruit but
it doesn't. The fructose that we eat is synthesized. Yes, it's derived from food. But cyanide is
derived from food, too. Would you call it a food?"
|
Fructose |
Glucose |
|
liver |
every cell |
Consuming sugar (fructose and glucose) means more work for the
liver than if you consumed the same number of calories of starch (glucose).
And if you take that sugar in liquid form — soda or fruit juices — the fructose
and glucose will hit the liver more
quickly than if you consume them, say, in an apple (or several apples, to get
what researchers would call the equivalent dose of sugar). The speed with which
the liver has to do its work will also affect how it metabolizes the
fructose and glucose.
In animals, or at least in laboratory rats and mice, it’s clear
that if the fructose hits the liver in sufficient quantity and with
sufficient speed, the liver will convert much of it to fat. This
apparently induces a condition known as insulin resistance, which is now
considered the fundamental problem in obesity, and the underlying defect
in heart disease and in the type of diabetes, type
2, that is common to obese and overweight individuals. It might
also be the underlying defect in many cancers.
…....
…...
You secrete insulin in response to the foods
you eat — particularly the carbohydrates — to keep blood sugar in
control after a meal. When your cells are resistant to insulin, your
body (your pancreas, to be precise) responds to rising blood sugar by pumping
out more and more insulin. Eventually the pancreas can no longer keep up
with the demand or it gives in to what diabetologists
call “pancreatic exhaustion.” Now your blood sugar will rise out of
control, and you’ve got diabetes.
Not everyone with insulin resistance becomes diabetic; some
continue to secrete enough insulin to overcome their cells’ resistance to the
hormone. But having chronically elevated insulin levels has harmful effects of
its own — heart disease, for one. A result is higher triglyceride levels and
blood pressure, lower levels of HDL cholesterol (the “good cholesterol”),
further worsening the insulin resistance — this is metabolic
syndrome.
When physicians assess your risk of heart disease these days, they
will take into consideration your LDL cholesterol (the bad kind), but also
these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a
University of Texas Southwestern Medical Center nutritionist and the chairman
of the panel that produced the last edition of the National Cholesterol
Education Program guidelines, is that heart attacks 50 years ago might have
been caused by high cholesterol — particularly high LDL cholesterol — but since
then we’ve all gotten fatter and more diabetic, and now it’s metabolic
syndrome that’s the more conspicuous problem.
This raises two obvious questions. The first is what sets off
metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance? There are several
hypotheses, but researchers who study the mechanisms of insulin resistance now
think that a likely cause is the accumulation
of fat in the liver. …. What causes the liver to accumulate fat in
humans? ….. there’s also the very real possibility
that it is caused by sugar.
As it happens, metabolic syndrome and insulin resistance are
the reasons that many of the researchers today studying fructose became interested in the subject to begin with. If you
want to cause insulin resistance in laboratory rats, says Gerald Reaven, the Stanford University diabetologist
who did much of the pioneering work on the subject, feeding them
diets that are mostly fructose is an easy way to do it. It’s a “very obvious,
very dramatic” effect, Reaven says.
By the early 2000s, researchers studying fructose metabolism had
established certain findings unambiguously and had well-established biochemical
explanations for what was happening. Feed animals enough pure fructose or
enough sugar, and their livers convert the
fructose into fat — the saturated fatty acid, palmitate, to be
precise......The fat accumulates in the liver, and insulin resistance and
metabolic syndrome follow.
….... Stop feeding them the sugar, in either
case, and the fatty liver promptly goes away, and with it the insulin
resistance.
Similar effects can be shown in humans, although the researchers
doing this work typically did the studies with only fructose ….
Despite the steady accumulation of research, the evidence can
still be criticized …., because we never naturally consume pure
fructose. We always take it with glucose, in the nearly 50-50 combinations
of sugar or high-fructose corn syrup. And then the amount ….has typically been
enormous.
This is why the research reviews on the subject invariably
conclude that more research is necessary...... we’re
unlikely to learn anything conclusive in the near future. As Lustig points out, sugar and high-fructose corn syrup are
certainly not “acute toxins” of the kind the F.D.A. typically regulates and the
effects of which can be studied over the course of days or months. The question
is whether they’re “chronic toxins,” which means “not toxic after one meal, but
after 1,000 meals.” ….
So the answer to the question of whether sugar is as bad as Lustig claims is that it certainly could be. It very well may be true that sugar and high-fructose corn syrup, because of the unique way in which we metabolize fructose and at the levels we now consume it, cause fat to accumulate in our livers followed by insulin resistance and metabolic syndrome, and so trigger the process that leads to heart disease, diabetes and obesity. They could indeed be toxic, but they take years to do their damage. It doesn’t happen overnight. Until long-term studies are done, we won’t know for sure.
One more
question …. cancer. ….
... insulin
…... actually promotes tumor growth.
….................