The World Turned Upside Down: The Second Low-Carbohydrate Revolution (12 page)

Wide availability of vegetable oils
provided a potential
alternative to butter, lard and other sources of saturated fat.
Vegetable oils,
however, are liquid
s and, at least for baking, have to be converted
to a more useable form (like margarine or Crisco). You can do this with
the
process of hydrogenation; unsaturated oils are "unsaturated" with
respect to
how much hydrogen is attached to the carbon atoms. Hydrogenation turns
some of
the unsaturated fatty acids to saturated fatty acids, in
effect converting
the oil to a solid form. Unsaturated fatty acid molecules have more
rigid
structure (
Figure 5-5
)
and are harder to pack into
a solid which is why unsaturated fats tend to be liquid. Converting
some of the
unsaturated fatty acids into saturated ones made the material more
solid and
easier to work with. A side-reaction in the manufacture of hydrogenated
oil,
however, is the conversion of some of the oil to the trans-form. The
names
refer to structure. As shown in
Figure
5-5
, double
(unsaturated) bonds can be cis or trans; most naturally occurring fatty
acids
are cis so trans-fatty acids are not normally processed to a great
extent. (Note:
trans
-fats
are
unsaturated;
cis-
or
trans-
can
only refer to unsaturated bonds).

Figure
5-5.
Structure of fatty acids showing that
double bond have two
different possible geometric forms: cis (large parts of the molecule on
the
same side of the double bond, or trans (opposite sides of the double
bonds.
There is free rotation around single bonds so they have no such
geometrical
differences.

Some biochemists– notably
Mary
Enig
–tried to stop the introduction of products
containing
trans
-fatty
acids but
most chemists did not know much about
trans
-fatty
acids and with little support, the low-saturated-fat forces prevailed.
At least
for a while. When it turned out that
trans
-fat
was the form that correlated best with cardiovascular disease, this was
a
ready-made scapegoat and, presumably because it is an artificial
product, it
became the target of health agencies. These groups did not mention that
trans
-fat
in the food supply
arose from their own campaign against saturated fat. In the end,
trans
-fat
is a very small
part of the diet, its risk is probably greatly exaggerated and there is
universal acceptance of the need to remove it, but there is nothing
inherently
good about it and nobody wants to defend it.

In distinction to
trans
-fat,
saturated fat has always been part of the normal human diet and is a
normal
part of metabolism. Saturated fatty acids are synthesized in your body,
a
process that is stimulated by a
high
carbohydrate
diet. This has been known for
years. The process is
called
de
novo
lipogenesis and is in the biochemistry textbooks and while it is
acknowledged
that high dietary carbohydrates led to
de
novo
synthesis of saturated fatty acids, the
idea is immediately
forgotten when official dietary recommendations are being written. So
where did
we get the idea that fat and saturated fat, in particular, is
unhealthy? Again,
the story has been told many times, most succinctly in
The Rise and
Fall of Modern Medicine
,
most engagingly in
Good
Calories Bad Calories
but the death knell for
the low-fat idea was,
or should have been, the meta-analysis form 2010 (Thesis 9 in the
15 Theses). A collection of studies, some going
back 25 years was
not able to find any risk in dietary saturated fat.

The glucose-insulin
axis.

Carbohydrates are food. They are part
of
the human diet. They are
not poison but they can be a problem. We don't know the amount, if any,
that's
best for any particular person; there is no biological requirement for
any
carbohydrate as there is for protein or, to a lesser extent, for some
fat. Nor
do we know whether the type really matters. And glycemic index, or
"good carbs,
bad carbs" are still weak ideas. But we do know a lot. It's simple: "
high
in carbohydrates" is
bad advice for people who are overweight or especially for people who
have
diabetes or metabolic syndrome. For many of them, reducing carbohydrate
can
constitute a cure. And while we don't know for sure, it is likely that "
high
in carbohydrates"
plays a role in how we
get
fat and diabetic in the first place. And we know that insofar as it's
true,
it's because we have the underlying basic science: carbohydrates,
directly or
indirectly, through the hormone
insulin
,
control the response to other foods.
Anabolic hormones
stimulate building up of body protein and storage of body material
(anabolic
steroid hormones are most common in stories in the media because of
their
effect on muscle protein). Hormonal systems are very complex but
surprisingly,
in metabolism, insulin has an overpowering effect. Insulin is
predominant in
the storage of nutrients. It encourages storage of fat. It encourages
storage
of carbohydrate as
glycogen
and increases the synthesis of body proteins. Hormones communicate with
living
cells through the docking proteins known as receptors and they trigger
the
metabolic machinery within the cell.

Carbohydrates are the major stimulus
for
secretion of insulin.
Persistent high insulin fluxes will bias the body towards storage, in
particular, storage of fat. So
dietary
fat is important but it plays a more passive role than is generally
said. The
rate at which fat gets stored depends on the hormones that are present.
A
"high-fat diet" with high carbohydrate is very different from a diet
with the
same amount of fat but lower carbohydrate: the carbohydrates may make
the
effect of the fat deleterious instead of beneficial. That's the bottom
line.

We teach first year medical students
that
the flow of fat from
the diet into stored fat or into the lipid markers used to characterize
cardiovascular risk is like the flow of water through a faucet.
Carbohydrates
control the faucet. If carbohydrates are low, flow stops and the fat is
oxidized. In the presence of high carbohydrate, insulin increases the
rate of
storage. This is overly simplified, of course, but it is not greatly
oversimplified. The main idea, that it is a control problem not a
too-much-stuff problem, is on target.

Fat metabolism is only part of the
picture. Insulin is a global
hormone and regulates carbohydrate and protein metabolism. Everybody
knows this
but not everybody wants to face it. If you confront nay-sayers, they
tell you
that the problem is very complex. So, how does it play out in the real
world?

It should be easy to get the answer.
Here's an experiment that is
pretty clear, or at least, should have been pretty clear. Brehm,
et al.
[45]
assigned 50 healthy, slightly obese women to an
ad libitum
low-carbohydrate diet or an
energy-restricted, low-fat diet for four months. The results (
Figure
5-6)
tells
you that the low-carb people lost significantly more weight.

Figure 5-6
.
Weight
loss on different diets. Redrawn from Reference
[45]

Diet Comparisons and
the Nutritional
Literature.

Reference
[45]
,
however, has good news
and bad news. Bad news first. The actual spread of individual values is
way
bigger than what is shown in the figure. It depends on statistical
details but,
put simply, there are different ways of showing variation in the data
and the
one in the figure – if you are already familiar with the terms, the
standard
error of the mean (SEM) – always makes your data look better than it
is. The
actual spread is about four times the size of the error bars. So the
bad news
is that outcome on the two diets are not highly predictable and from
the
presentation of the data you can't tell who did what. The good news is
that the
big winners must have been the people in the low-carb group. So, in
this kind
of experiment you don't know your odds but you do know which has the
possibility of the bigger payoff.

Really good news: read the Methods
section
and you find that this
experiment followed the protocol for
Foster's
paper
described above:

".. One group of dieters was
instructed to follow an
ad libitum diet ....The other group of dieters was instructed to follow
an
energy-restricted, moderately low-fat diet with a recommended
macronutrient
distribution of 55% carbohydrate, 15% protein, and 30% fat."

In other words, if you are in the
low-fat group you have to
count calories or at least follow the low-calorie meal plan that they
give you.
If you are in the low-carb group, you can do whatever you want as long
as you
keep carbs low. If the results are even the same, most of us are going
to be
happier doing the low-carb diet. This is how it was done in the
landmark Foster
paper and the pattern has been continued for numerous diet comparisons:
the
low-fat group must limit calories. The low carb group can eat
ad lib
as long as carbs
are low.

You don't always read the Methods
section of a paper unless
you are actually planning to repeat the experiment yourself or if there
is
something unusual that is specifically due to the details of how the
experiment
was carried. If there is something important in the methodology, it
should be
described in the body of the paper. I admit that when this was
published in
2005, I didn't realize that a low-calorie diet was pitted against an
ad lib
low-carb diet and,
in fact, that it was a pattern for diet comparisons of this type. The
rationale, of course, was that since the Atkins diet did not restrict
calories,
participants in the low-carb arm would only be instructed to reduce
carbohydrate
intake. This may be reasonable from a clinical point of view but it
does make
"the diet," rather than carbohydrate, that is, something easier to
control, the
independent variable.