must acknowledge shortcomings of low-fat diet advocated by public health agencies

TC · medicine forum Guru Joined: 02 May 2005 Posts: 1814

http://www.ajcn.org/cgi/content/full/81/5/949

EDITORIAL

Optimizing the cardiovascular outcomes of weight loss1,2
Jennie Brand-Miller
1 From the Human Nutrition Unit, School of Molecular and Microbial
Biosciences, University of Sydney, Sydney, Australia

2 Address reprint requests to J Brand-Miller, School of Molecular and
Microbial Biosciences (G08), University of Sydney, Sydney, NSW 2006,
Australia. E-mail: j.brandmiller@mmb.usyd.edu.au.

See corresponding article on page 976.

The past 2 y have seen a steady stream of reports indicating that
restriction or modification of carbohydrate intakes can favorably
affect weight loss and cardiovascular disease (CVD) risk factors
(1-6). The article by Ebbeling et al (7) in this issue of the Journal
represents one more in favor of diets with a low glycemic index (GI) or
glycemic load (GL). Serum triacylglycerol concentrations in young
overweight adults with similar weight loss fell nearly twice as far
with the ad libitum low-GL diet as with the energy-restricted low-fat
diet, whereas concentrations of plasminogen activator inhibitor 1, an
important measure of thrombogenicity, significantly worsened (ie, rose)
in subjects who were following the energy-restricted low-fat diet. The
study was small (n = 23) and from a group at Harvard that had published
other studies on the same topic, but it was long-term (12 mo) and
carefully carried out.

That lowering daylong glycemia, with or without weight loss, might
improve CVD risk should not come as a surprise. Many intervention
studies have tested the hypothesis that low-GI diets will improve not
only glucose control but also lipid metabolism. Twenty years ago,
Jenkins et al ( Cool

showed in 3-way crossover studies that low-GI diets
improve triacylglycerol and total cholesterol concentrations in
hyperlipidemic subjects more than do conventional low-fat diets.
Recently, Patel et al (9) showed that women with advanced CVD who were
awaiting bypass surgery spent significantly fewer days in the hospital
than did their counterparts who were following a conventional low-fat
diet (7.1 and 9.5 d, respectively). Slowing the rate of carbohydrate
absorption per se by using the -glucosidase inhibitor acarbose was
found to reduce cardiovascular events by 50% over 3 y in a large
population with impaired glucose tolerance (IGT).

Long-term studies in animals have provided additional evidence that the
GI itself, and not fiber intake or any other confounding factor, is
important in relation to weight gain, body fat, and CVD risk. Animals
fed diets differing only in the type of starch (high- or low-GI) gained
body fat faster with the high-GI diet than with the low-GI diet (10).
Even when fed to similar body weight, high-GI diet-fed rats have more
body fat (71%), less lean body mass, and higher plasma triacylglycerol
concentrations than do low-GI diet-fed rats (11).

Large-scale observational studies show links-even in nondiabetic
persons-between the presence of postchallenge hyperglycemia and an
increased risk of chronic disease (12). In a meta-analysis of 39
prospective studies of nondiabetic cohorts, Levitan et al (13) found
that groups with the highest 120-min postload glucose concentration had
a 27% greater risk of CVD than did those with the lowest glucose
concentrations, and the relative risk was higher in women than in men
(1.56 and 1.23, respectively). Adjustment for traditional CVD risk
factors attenuated but did not abolish the relation. Moreover, Liu et
al (14) showed that average dietary GI and GL were also independent
predictors of 10-y prospective CVD risk in US women. The latter study
is particularly important, because it implies that postprandial
glycemia induced by carbohydrate foods in everyday settings (and not
glucose tolerance testing) is clinically relevant.

There has been fundamental progress in showing that glucose itself can
directly damage vascular cells, by a variety of mechanisms. All of
these mechanisms appear to reflect a single hyperglycemia-induced
process of overproduction of superoxide by the mitochondrial
electron-transport chain (15). Normal concentrations of glycemia such
as those encountered during a standard meal have been shown to acutely
decrease plasma antioxidant capacity, which reflects a significant
oxidative stress. Moreover, the vascular endothelium is a prime target
because endothelial cells, unlike many other cells in the body, are
unable to regulate glucose transport across the cell membrane.

Taken together, intervention, observational, and experimental studies
suggest that postprandial glycemia plays a greater role in CVD than is
generally acknowledged, perhaps more so in women than in men. Because
decreasing the intakes of total and saturated fat has been the goal of
efforts to reduce the incidence of obesity and CVD, high-carbohydrate
foods have been recommended, not so much because of their intrinsic
nutritional merit, but because they fill the calorie space formerly
occupied by fat. But one of the more subtle changes in the food supply
over the past few decades has been the replacement of traditionally
processed grains by more highly processed, high-GI cereal products.
Less-processed foods are more likely to contain slowly digested
carbohydrates because the starches and sugars remain closely embedded
in the plant's original botanical structure, surrounded by bran and
other barriers that inhibit starch gelatinization. In contrast, modern
methods of food production using finer flours, extrusion technology,
and high temperatures and pressures increase starch gelatinization and
thus the rate of digestion in vivo. Compared with sugars, high-GI
starchy foods receive little attention, and yet they have a greater
capacity than do sugars to increase the glycemic and insulinotropic
potency of the whole diet.

Because the overweight are now the majority in most industrialized
nations, we can no longer afford to direct dietary guidelines to just
the "healthy" population. Moreover, we need efficacious guidelines that
work in practice, not just in theory. During the past 2 decades, when
low-fat diets and plenty of cereal foods were actively promoted, health
trends were the opposite of those we would wish. Along with obesity,
the diagnoses of type 2 diabetes and IGT have soared, "maturity-onset"
diabetes is being diagnosed in children, and the metabolic or insulin
resistance syndrome affects 1 in 4 adults. Even normal-weight
individuals can have the metabolic syndrome and thus a higher risk of
CVD. Diseases such as polycystic ovarian syndrome, nonalcoholic
steatohepatitis, and fatty liver, which have their roots in insulin
resistance, have also reached alarming proportions.

It must now be clear that the conventional low-fat diet (with no
consideration of the nature of the starch) is not the ideal diet for
most of the population. Dietary Guidelines for Americans 2005 (16)
sensibly gives greater emphasis to increased consumption of whole
grains rather than to refined grains. However, this is unlikely to
improve daylong glycemia, because many so-called whole-grain breads and
breakfast cereals produce as much postprandial glycemia as do their
white-flour counterparts (17). Moreover, recommending whole-grain and
high-fiber cereals is nothing new-nutritionists have been doing that
for at least 50 y. A high proportion of the population will dismiss
outright any suggestion of eating whole grains or whole meal. We
urgently need nutrition messages that fire the imagination and
encourage even unmotivated people to adopt effective dietary strategies
that reduce the risk of chronic disease. In Australia and the United
Kingdom, the GI has become a popular concept in its own right. The
message that slowly digested carbohydrates can "keep you fuller for
longer" is one that the general public, young and old, intuitively
understands. Indeed, many people warm to a plan that helps keep blood
sugar concentrations "under control." Furthermore, as Ebbeling et al
(7) point out, their ad libitum low-GL diet is less extreme and
restrictive than is either a low-energy, low-fat diet or a
low-carbohydrate diet, and it still produces better outcomes.

It may be argued that the evidence for a role of GI or GL in weight
management and CVD prevention is still insufficient to justify the
place of either in nutrition advice to the general public. We need to
clarify whether reducing the GL of the diet by changing the type of
carbohydrate (substituting low-GI sources of carbohydrate for high-GI
sources) or by substituting protein or fat for carbohydrate [or a
combination of all 3 alternatives as Ebbeling et al (7) did] will have
different metabolic consequences. Nevertheless, we must also
acknowledge the shortcomings of the conventional low-fat (ipso facto
high-GI) diet currently advocated by public health agencies and must be
prepared to entertain the idea that the GI might be a useful and
appealing concept after all.

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TC

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