The World Turned Upside Down: The Second Low-Carbohydrate Revolution (10 page)

Figure 4-3
. Comparison of low
(blue) and high (red) carbohydrate
diets at 6 and 12 months. Results
from a multi-center trial in which 63 obese men and women were randomly
assigned to either diet. Data from Foster ,
et al
.
[37]
. Figure from Volek
& Feinman
[38]
,
used with permission. DBP, diastolic blood pressure; HDL, high-density
lipoprotein-cholesterol, so-called "good cholesterol;" TAG,
triglycerides.

Ad lib vs. calorie
restriction

Beyond the obvious bias, Foster's
study was compromised in
its experimental design. People in the low-fat group were directed to
consume
an explicitly low calorie diet. They were required to eat what they
were told.
In the low-carb group, in distinction, participants were allowed to eat
anything that they wanted as long as they kept carbs low. (Even if you
believe
that the diets were actually equal, which diet would you go for?) This
protocol
was used because Foster,
et
al.
was not testing the principle of reducing
insulin fluctuations
as a means of controlling metabolism. The study was not testing, as in
the
title, "a low-carbohydrate diet for obesity," but rather "The Atkins
Diet,"
and, perhaps in the authors' mind, what was tested was Atkins himself.
The
Atkins diet said that you didn't have to count calories. The experiment
was
testing two principles: that carbohydrate restriction meant greater
satiety
allowing you to regulate calories implicitly and that the Atkins diet,
calorie-for-calorie will be more effective for weight loss. Testing
both at
once was more demanding than isolating the variables. That the
low-carbohydrate
diet produced the better effect may have been due to either or both the
greater
satiety or the reduced energy efficiency (from the standpoint of
storing fat).

The dietary protocol was not the only
problem. Data were
analyzed according to the bizarre method known as intention-to-treat
(ITT). In
this method, data from the people who had dropped out of the study were
included in the study by "imputing" values based on previous
measurements. The
difference between "imputing" and making stuff up is hard to figure
out. ITT
doesn't make any more sense than you think (discussed in
Chapter 23
)
but that's how things are. Beyond the lack of reasonableness,
intention-to-treat always makes the better diet look worse than it
actually is.
In the event, though, workers in carbohydrate restriction were
sufficiently
happy to see the positive outcome that they were disinclined to be too
critical
of the methods. At face value, the lipophobes had had their shot and
they lost.
They tried to maintain a a façade of impartiality while still putting the
burden
of proof on low-carb, but basically it was a loss. So, what happened to
the
first low-carb revolution? Why didn't it move forward? How did low-fat
loyalists prevail in the face of such strong scientific evidence?

What stopped it?

It was an opportunity. The public had
a chance to see if the
low-carbohydrate idea would work. Many did try it and many had good
success.
Popular articles were written about it. What happened? If it wasn't the
thing
for everybody, it seemed to work for most who tried it. Frequently, it
seemed
miraculous. People described it as "pounds melted away." Why didn't it
move
forward? First, there was poor understanding of what was involved and
there was
a proliferation of products designed to make it easier because it was
perceived, incorrectly for most people, as a difficult strategy. This
allowed
the company Atkins Nutritionals® and many others to sell a lot of
products many
of which were not clearly helpful. They are still doing that. There was
little
disappointment in the low-carb community when the company declared
bankruptcy.
Since resurrected its approach to low-carb principles is tied to
offering
substitutes for what you are giving up. There was a proliferation of
companies
and products containing sugar alcohols – carbohydrates that are
digested slowly
if at all and therefore were presumed to not contribute to blood
glucose.
Untested and poorly understood, sugar alcohols gave some people
intestinal
problems but, more important, they cast what should have been a
straight-forward diet in a slightly bizarre light. But, in the end, the
nutritionists and the Professors of Medicine stopped it.

Second, let's kill all
the dietitians.

''The first thing we do, let's kill
all the lawyers'' –
William Shakespeare,
Henry
VI, Part II

What was remarkable about the whole
state
of affairs was that the
low-fat strategy had failed in competition with a real alternative.
Low-fat had
failed in numerous large scale trials starting with the Framingham
study but
here it could not compete with a low-carb diet even with the experiment
set up
in their favor and with the authors' putting a positive spin on it. It
was a
direct challenge to nutritional orthodoxy but they did not go gentle
into that
good night. What torpedoed the first low-carbohydrate revolution, was
the
nutritionists. They had the chance to tell the public "if you do want
to try a
low-carbohydrate diet, this is what we recommend." Instead, they acted
as if
Foster's paper had never existed and they ignored those studies that
followed
it which further supported carbohydrate restriction.

Nutrition has never been highly
thought
of. The field derives
from the practical job of making menus. The advances of physiology and
biochemistry meant that nutrition had increasing overlap with more
solid
science, but the field was, and is, very slow to change. In the real
world,
nutritionists have attempted to put on the mantle of professionalism
and are
currently trying to establish the newly re-named Academy of Nutrition
and
Dietetics (AND) with the legal right to be the sole voice on nutrition
and to
legally repress anybody else. They recently exercised this power by
trying to
stop low-carb blogger Steve Cooksey from "offering counseling" on his
blog
despite appropriate disclaimers (
Figure
4-4). Currently challenged in court on second
amendment grounds, the case highlights the adversarial state of
nutritional
science. And for those familiar with computer logic, my witticism is to
refer
to our own group as OR (Objective Research) and the Cooksey affair as
NAND-gate.

Underlying all of the resistance,
however,
is the idea that only
long term large scale studies are important and so we are able to
ignore
smaller studies which, because they are better controlled, actually
give you
more information. And again, there was also the assumption, never said
out
loud, that there were long-term studies supporting a low-fat diet, a
"prudent"
diet, a diet of moderation that had good success and that could be the
one for
all of us and, even better, would fix things if you did get fat. There
is no
such diet and there never was. Again, vaporware. There
were
long-term studies
but they had consistently failed. Not just one. Almost all failed. The
Framingham Study, the Oslo Heart Study
[39,
40]
,
Western Electric Study
[41]
and probably two dozen
others, tabulated and explained in the irreverent style that they
deserve by
Anthony Colpo
[24]
including the Women's Health
Initiative
[42-44]
. They
showed no value in reducing
dietary fat or saturated fat for prevention of heart disease or
anything else.
And, in the biggest trial of all, the population trial, the diet of the
whole
American people during the obesity epidemic, it was increased
carbohydrate, not
fat, that was actually harmful.

Figure
4-4
. Excerpt from Steve Cooksey's blog post
and red-line by AND
(Academy of Nutrition and Dietetics).

To be fair to the nutritionists, the
doctors did their part.
Undeterred by their lack of training or experience in biochemistry or
nutrition, it was
de rigeur
for junior faculty in a department of medicine to write a review
trashing the
Atkins diet, now taken as the generic name for all low-carbohydrate
diets. Some
of these critiques cited, as the major flaw, that the diets failed to
conform
to the USDA or other dietary guidelines. In other words, they faulted a
diet
that thought the USDA recommendations were bad for not conforming to
those
recommendations. Using the question as part of the answer is what was
called
"begging the question" when it meant something specific. (It was
probably a
dumb phrase anyway).

Failure to accept
failure.

Stepping back and looking at the big
picture, the most striking
thing was the inability of low-fat diets even those low-fat diets that
did
lower cholesterol, to provide a significant impact on cardiovascular
outcome
or, really, anything else. Very large, very expensive clinical trials
of
low-fat dietary strategies fail. Most failed big. And they keep doing
them and
our tax dollars keep paying for them. Second, in those cases where we
didn't
have outcome data (how many people had a heart-attack and how many
died) and,
instead, had to look at the risk factors, the different cholesterol
forms, HDL,
LDL and their sub-fractions, it turned out that reducing fat was at
best
ambiguous and it was frequently dietary carbohydrate that had the major
effect.
As carbohydrates were increased, most of the risk markers got worse.
The
markers and their association with outcome were not sufficient to
attribute
cause but that had not stopped interpretation when it was low-fat that
reduced
risk factors.

As we go beyond the original idea of
total
blood cholesterol as a
major risk factor – less than half of the people who have a first heart
attack
have high cholesterol – as we look at the different forms of the
lipoprotein
particles (this is what is really measured in the clinical tests of
blood
cholesterol), carbohydrate restriction becomes the "default diet," the
remaining alternative, the one to try first for general health. At same
time,
though, while low-carbohydrate diets look better for CVD risk factors,
we have
the same problem that we have with fat: there is little in the way of
evidence
that lowering carbohydrate could actually prevent CVD. Given its
success in
treatment of the collection of health markers referred to as metabolic
syndrome
(again, our main arguing point), it would be surprising if reducing
carbohydrate did not help in prevention but at this point, what we know
is very
little. We are left with the real possibility that, not only is there
nothing
at all to the diet heart hypothesis, that is, not only is dietary fat
not
involved, but there is the possibility that, outside of well-defined
genetic
conditions like familial hypercholesterolemia, diet is just not a major
player
in cardiovascular disease. Very surprising given our current view of
things and
likely to change as we learn more but you have to go with the data.

Summary

The first low-carbohydrate
revolution,
around 2002, was
precipitated by Gary Taubes's deconstruction of the diet-heart
paradigm,
probably more accurately described as calling attention to the
self-deconstruction by continued failure of experimental tests. In
combination
with the multi-center study headed by Gary Foster, the door was open
for
examination of just what scientific support there was for low-fat ideas
and
whether the iconoclastic diets based on carbohydrate restriction might
not be
better. The nutritional establishment, however, refused to accept the
results
and more or less continues to stone-wall carbohydrate restriction. It
will
require a second revolution. To understand what the issues really are
requires
some familiarity with nutritional biochemistry. The macronutrients are
the main
focus. That's next.