The World Turned Upside Down: The Second Low-Carbohydrate Revolution (20 page)

Figure
8-5
. Graphic from the article "Big Sugar's
Sweet Little Lies." in
by Gary Taubes and Cristin Kearns Couzens
[59]
.

The sugar graphic is huge and
over-powers
the figure. Since it
has different units, there was no particular reason to make the sugar
graphic
so large but
Mother Jones
is not
Annalen
der Physik
.
In fact, the increase in the past 30 years is quite small. Using the
numbers in
the figure:

% Increase in sugar = 120/132 = 9 %

Other data shows that the increase
was 15
% so we can even go
with that number. For comparison, in a comparable time period, the
increase in
the US for total carbohydrate was, for men, 23.4 % and, for women, 38.4
%

The idea, however, is that sugar has
a
very powerful, almost
catalytic effect. A little increase in sugar is supposed to be causal
in making
big changes. So, what happened in the thirty years that is presumed to
have
been a consequence of the 9 % increase in added sugars. Again, from the
figure:

% Increase in % diabetes = 4.3/6.8 =
63 %.

% Increase % US children obese =
11.4/16.9
= 67%

% Increase % US adults obese =
20.7/35.7 =
58%

Is fructose that powerful? If it is,
the recommended
reduction would certainly be a good thing. How likely is that? And, if
it is
that powerful, could it even be adequately reduced? A 9% increase, even
a 15%
increase in sugar consumption, caused a major increase in obesity and
diabetes;
the absolute changes are small but represent the entire population. To
show
that fructose is that powerful, the experiment would be easy to do –
compare
removal of fructose with removal of glucose and the results
should be
evident. Again, that experiment hasn't been done. Why not? We have good
experiments showing that if you take out carbohydrates and put in fat,
you get
significant benefit. Clear benefit, not a judgment call, not
statistics. And
it's carbohydrates across the board. If fructose is the most effective
of the
carbohydrates, it should not be hard to show that it was the player in
these
comparisons. That the experiment hasn't been done is suspicious. Or, at
least,
surprising.

High fructose corn syrups comprise
different mixtures of fructose
and glucose, but by far the most common is 55:45, more or less the same
ratio
as sucrose. Numerous papers have tried to show that they are different
in their
effects on humans or animals but it is clear that they are not.
Interestingly,
they do have different tastes and there are certain advantages to HFCS
in that
the fructose has a different effect than sucrose. While fructose,
glucose and
sucrose all taste sweet, they have different kinetic (time) effects.
Fructose
comes on strong and then disappears quickly, allowing the overtones of
other
tastes as in fruits to appear while the longer acting sucrose may mask
more
subtle flavors. However much you think that fructose has been misused
in
industry, it is part of cooking and should be understood for what it
can do.

Summary

Sugar, that is sucrose, and HFCS, or
their components,
glucose and fructose, are carbohydrates. They must have participated in
whatever effects the dramatic increase in carbohydrate had on the
epidemic of
obesity and diabetes. Whether and to what extent it is fructose as a
carbohydrate as opposed to fructose as a unique agent, even toxin, that
is
responsible for its deleterious effects is the question to be answered.
The
numerous studies on the dangers of fructose, however, are almost always
carried
out at high total carbohydrate making it hard to address the problem
accurately. While reduction in fructose is recommended, what happens
when you
actually do this is rarely studied and there is the suggestion of
another rush
to judgment analogous to lipophobia. A sober perspective on fructose
may be
difficult but a review of what we really know reinforces the close
relation
between fructose and glucose. Metabolism of the two sugars comes
together at
the level of the three carbon fragments, the triose-phosphates. Thus,
either
can give rise to the downstream products, triglycerides and
lipoproteins.
Fructose can be converted to glucose and to glycogen. The conclusion
still
seems to be that carbohydrate restriction is therapeutic while unique
effects
of removing sugar are still to be demonstrated. Both the media and a
major part
of the nutritional establishment appear to be unwilling to wait for
that proof
and the ascendancy of fructophobia seems to be real.

One of the threats of fructophobia is
that we have not
really given up on lipophobia. Saturated fat is still seen as a threat.
But is
it? And if it is, is it saturated fat in your blood or on your plate?
That's
next.

Answer to fructose
Puzzler

The major ingredient in Pop-tarts is
enriched flour. When I
posted this on my blog, one person said that although flour is the
first
ingredient, if you add up the high fructose corn syrup, dextrose and
other
things that contribute sugar, the sum of those will be larger. It is
suggested
that this is to hide the sugar content rather than the separate
physical and
food properties. An interesting idea but easily testable. The label
says that
there are 38 g of total carbohydrate but only 17 g of sugar.

Chapter
9

Saturated Fat. On your Plate or
in your Blood?

Acceptance of carbohydrate
restriction is
still very slow. Even
as the nutritional establishment shifts its focus to fructose, it has
yet to
admit the failure of the war on saturated fat. This leaves us with two
barriers
to bringing carbohydrate-restriction into focus. There may be three or
four –
we can't forget meat as a presumed source danger, possibly as a source
of
saturated fat. When the experiments on the risk of sugar fail, the
careful
misleading writing and statistics will inevitably explain that it
hasn't failed
but it will have failed. And, there is always fiber waiting in the
wings but
when you look at the original data on fiber it is very weak. In the
end,
though, there is too much information out there. The trials in which
saturated fat
improves health when substituted for carbohydrate must come to the
fore. The
average consumer, however, will have trouble piecing it together and
will have
a tough time benefitting from the second low-carb revolution. Some
consumers do
recognize that whatever is wrong with fructose might need to be
generalized to
all carbohydrates.

An important principle, rarely tested
directly but surely
critical: "A high fat diet in the presence of carbohydrate is different
than a
high fat diet in the presence of low-carbohydrate." Failure to
understand this
principle and therefore failure to adequately test for the effect of
control
exerted by carbohydrate, accounts for numerous reports in the medical
and
popular literature describing the effect of a "high-fat diet" or even
"a single
high fat meal." The source of the high fat, however, may be a slice of
carrot
cake, a Big Mac
^®
or something else that is also
very high in
carbohydrate.

On saturated fat, the studies from
Jeff
Volek's laboratory at the
University of Connecticut provide the most telling evidence. There is a
tendency to look for truth in a multitude of studies especially in
nutrition
where it is hard to control all the variables. But the number of
experiments is
less important than the scientific design of the individual trials and
whether
it is easy to interpret the results. A study on 40 volunteers with
metabolic
syndrome from Volek's lab provides a classic case, carefully controlled
and
unambiguous.

A particularly striking result from
the study was the demonstration
that when the blood of volunteers was assayed for saturated fatty
acids, those
people who had been on a low-carbohydrate diet had lower levels than
those on
an isocaloric low-fat diet. This, despite the fact that the
low-carbohydrate
diet had three times the amount of saturated fat as the low-fat diet.
How is
this possible? Well, that's what metabolism does. What happened to the
saturated fat in the low-carbohydrate diet? The saturated fat was
oxidized
while (the real impact of the study) the low-fat arm was making new
saturated
fatty acid. Volek's former student Cassandra Forsythe extended the idea
by
showing how, even under eucaloric conditions (no weight loss) dietary
fat has
relatively small impact on plasma fat
[29]
.

A barrier to understanding the role
of saturated fat, is the
emphasis on "diets" where it is impossible to even get agreement on
definitions
and where an accidental or individual response may produce a strategy
that
works for somebody: the grapefruit diet is the generic ad hoc diet. We
will do
better speaking, instead, of basic principles. The key principle is
that
carbohydrate, directly or indirectly, through insulin and other
hormones,
controls what happens to ingested (or stored) fatty acids. Carbohydrate
is
catalytic, that is, exerts its effect on other nutrients. The fat in
the Big
Mac will not constitute any risk if you chuck the bun. You are what you
do with
what you eat.

The question is critical. The
scientific
evidence shows that
dietary saturated fat, in general, has
no effect on
cardiovascular disease
,
obesity or probably anything else, but
plasma
saturated fatty
acids
do. In particular, plasma saturated
fatty acids can be a
cellular
signal
. If your study dietary saturated fatty
acids under
conditions where carbohydrate is high or, more important, if your study
effects
in rodents where plasma fat better correlates with dietary fat, then
you will
confuse plasma fat with dietary fat.
An important
study
from
Spiegelman's group identified potential cellular elements that control
gene
transcription whose products bear on lipid metabolism
[60]
although, again, in rodents, where dietary fat correlates with plasma
fat (
Figure 9-1
).

It is important to know about
plasma
saturated
fatty acids. First, recall that, strictly speaking, there are only
saturated
fatty acids (SFAs).  What is called saturated fats simply mean
those fats
that have a high percentage of SFAs – things that we identify as
"saturated fats," like butter, are usually only 50 % saturated fatty
acids. Coconut oil is probably the only fat that is almost entirely
saturated
fatty acids but, because they are medium chain length, they are usually
considered a special case.

Figure
9-1
. The Role of Plasma Fatty Acids in Cell
Signaling. PGC-1
β
,
SREBP are intracellular signals that
control cell responses.

In Volek's experiment, 40 overweight
subjects were randomly
assigned to one of two diets
[30, 31,
61]
. A very low-carbohydrate
ketogenic diet, (VLCKD)
provided a macronutrient distribution of about 12% carbohydrate and 59%
fat
(28% protein). The low-fat diet (LFD) composition was %CHO:fat:protein
=
56:24:20. The group was unusual in that they were all overweight and
would be
characterized as having metabolic syndrome: all demonstrated the
features of
atherogenic dyslipidemia, a subset of metabolic syndrome markers that
describes
a poor lipid profile (high triacylglycerol (TAG), low HDL-C, high
small-dense
LDL (so-called pattern B)).

Volek's work is striking for the
differences in weight loss
between two diet regimens. Participants in the study were not
specifically
counseled to reduce calories but both groups spontaneously reduced
caloric
intake. People in diet studies tend to automatically reduce calories.
The
response in weight loss between the two groups, due to the
macronutrient
composition of the plans, was dramatically different. People on the
very
low-carbohydrate ketogenic diet (VLCKD) lost twice as much weight on
average as
the low-fat controls despite the similar caloric intake. And, although
there
was substantial individual variation (
Figure 9-2
.),
9 of 20 subjects in the
VLCKD group lost 10% of their starting body weight, more weight than
that lost
by any of the subjects in the LFD group. In fact, nobody following the
LFD lost
as much weight as the
average
for the low-carbohydrate group. The major difference is between the
VLCKD and LF
appeared in the changes in whole body fat mass (5.7 kg vs 3.7 kg).

Figure
9-2
. Weight Loss in the study of 40
overweight subjects with
metabolic syndrome. Data from Volek, et al.
[30,
31,
61]
.

I
t
is generally considered
that deposition of fat in the abdominal region is more undesirable than
subcutaneous fat. This fraction was found to be reduced more in
subjects on the
VLCKD than in subjects following the LFD (-828 g vs -506 g). Volek's
study thus
provides one of the more dramatic effects of carbohydrate restriction
on weight
loss. Similar results had preceded it, though, and these have been
frequently
criticized for increasing the amount of saturated fat (whether or not
any
particular study actually increased saturated fat). Although the
original
"concern" was that this would lead to increased plasma cholesterol,
eventually
saturated fat became a generalized villain and, insofar as any science
was
involved, the effects of plasma saturated fat were assumed to be due to
dietary
saturated fat. The surprising outcome of Volek's study was that there
was, in
fact, inverse correlation between dietary and plasma SFA. Surprising
because
the effect was so clear cut (no statistics needed) and because an
underlying
mechanism could explain the results.

On your plate or in
your blood?

The dietary intake of saturated fat
for
the people on the VLCKD
was 36 g/day, threefold higher than that of the people on the LFD (12
g/day).
When the relative proportions of circulating SFAs in the triglyceride
and cholesterol
ester fractions were determined, however, they were actually lower in
the
low-carb group. Seventeen of 20 subjects on the VLCKD showed a decrease
in
total saturates (the others had low values at baseline). In
distinction, only
half of the subjects consuming the LFD showed a decrease in SFA. When
the
absolute fasting TAG levels are taken into account (low-carbohydrate
diets
reliably reduce TAG), the absolute concentration of total saturates in
plasma
TAG was reduced by 57% in the low-carbohydrate arm compared to 24%
reduction in
the low-fat arm, again, despite the fact that LFD group had reduced
their
dietary saturated fat intake. One of the saturated fatty acids of
greatest
interest was palmitic acid or, in chemical short-hand, 16:0 (16 means
that
there are 16 carbons and 0 means there are no double bonds, that is, no
unsaturation).

Figure
9-3
. Total saturated fatty acids in the
plasma triglyceride
fraction in the study of 40 overweight subjects with metabolic
syndrome. Data
from Volek, et al.
[30, 31,
61]

How could this happen? The low-fat
group
reduced their SFA intake
by one-third, yet had more SFA in their blood than the low-carbohydrate
group
who had actually increased intake. Metabolism is about change.
Chemistry is
about transformation.

De Novo Lipogenesis

We made the generalization that there
were
roughly two kinds of
fuel, glucose and acetyl-CoA (the two carbon derivative of acetic acid
that
went into aerobic metabolism). The big principle was that you could
make
acetyl-CoA from glucose, but (with some exceptions) you couldn't make
glucose
from acetyl-CoA, or more generally, you can make fat from glucose but
you can't
make glucose from fat. How
do
you make fat from glucose? Part of the picture is making new fatty
acids, the
process known as
De novo
Lipogenesis (DNL) or more accurately
de
novo
fatty acid synthesis. The mechanism for
making new fatty acids
is, in a rough sort of way, the reverse of breaking them down. You
successively
patch together two carbon acetyl-CoA units until you reach the chain
length of
16 carbons, palmitic acid. This fatty acid can be further processed.
Palmitic
acid can be elongated to stearic acid (18:0) or de-saturated to the
unsaturated
fatty acid, palmitoleic acid (16:1-n7, 16 carbons, one unsaturation at
carbon
7).