The Sad Saga of Saturated Fat

14 May / 2013 / By Jeff Volek and Steve Phinney

Here s a fascinating paradox. Over the last 4 decades, nutrition policy makers ha
ve increasingly exhorted us to eat less saturated fat. As a result of this unre
mitting message, the general population believes this single nutrient, if not ov
ertly toxic, will at least cause wide-spread bodily damage. Additionally, foods
that naturally contain saturated fat (e.g., beef, pork, dairy, eggs, and tropic
al oils) have been branded unhealthy . The paradox here is that as the drum-beat
against saturated fats has increased, the actual science supporting this message
has fallen into shambles. So here s our question: should we all just be good ci
tizens and swallow this advice, even if the science behind it no longer pasts mu
ster?
Two generations of researchers have tried to prove that eating saturated fat cau
ses heart disease. Rather than growing stronger, as would be the case if this h
ypothesis were rock-solid, increasingly the scientific data is painting a pictur
e more akin to low fat Swiss cheese (i.e., not much there besides the holes). Take
, for example, multiple recent meta-analyses of large populations followed caref
ully for decades, examining what they eat and what they die of [1-4] All show
no consistent association between dietary saturated fat intake and risk for hear
t disease or death from all causes. In fact some of these studies show just the
opposite an inverse association of dietary saturated fat intakes and atheroscle
rosis or stroke. Interestingly, they also suggest that one s risk for a coronary
event increases when dietary saturated fat is reduced and replaced by carbohydra
te.
Here s the problem as we see it. By continuing to provoke fear about the harmful
effects of saturated fat, the likely response is that people will seek out foods
low in fat and higher in carbohydrate. And in reality, that s exactly what appear
s to be happening. According to a government-funded survey [5], Americans have
decreased their consumption of saturated fat and replaced those calories with an
even greater amount of carbohydrate. This dietary flip-flop of trading away sa
turated fat and replacing it with carbohydrate has occurred in the same time int
erval as rates of obesity and diabetes have rocketed skywards. This might be co
incidence, or more likely it s an extremely unfortunate unintended consequence.
Okay, so what we re essentially doing here is telling you that much of what we ve be
en taught about dietary fat is wrong. How could this be that all those wise pol
icy-makers backed up by legions of academic scientists have gotten this all wron
g? That s a long story, and a good place to start would be to read Good Calories,
Bad Calories by the investigative journalist Gary Taubes [6]. In short, 50 years
ago diseased coronary arteries were found to contain buildups of cholesterol an
d saturated fat. Professor Ancel Keyes of the University of Minnesota hypothesi
zed that too much of these two nutrients in the diet were the cause
i.e., his h
ypothesis was built on the flawed concept that you are what you eat . Then came we
ll-done studies showing that blood levels of saturated fats predict future cases
of heart disease [7-10] and diabetes [11-14], thus appearing to support Keyes hy
pothesis. But this works only if you believe this flawed sound-bite; a concept
that doesn t pass the red face test (as addressed in our prior blog post).
Obviously, the key question here is: what s the precise relationship between dietar
y saturated fat and blood levels of saturated fat?
For people who believe you ar
e what you eat , the answer is easy; and it follows from that easy answer that no
one wants to accumulate saturated fat on their hips or lining their arteries.
This is so instinctively logical that most people (including many prominent nutr
ition researchers) haven t bothered to question it. Simply put, the current natio
nal policy imperative don t eat saturated fat is based solely on a sound-bite. The
scientific evidence, however, clearly shows that dietary intake of saturated fa

t compared to serum levels of saturated fat show little if any correlation. Thu
s our advice in our last post that we banish this flawed sound-bite and replace
it with: you are what you save from what you eat .
If dietary saturated fat intake has little to do with saturated levels in our bl
ood, then what does? There is, in fact, sound evidence that increasing the prop
ortion of carbohydrate in your diet is a major determinant of increased serum sa
turated fat levels. We know this because two respected research groups [15,16]
fed humans carefully measured diets either high in carbohydrate or moderate in c
arbohydrate. In both studies, blood levels of saturated fats went up dramatical
ly on the high carb diets (even though they were very low in fat).
On it s surface, this looks like a paradox. But with a little thought, it actuall
y makes sense. A high carbohydrate intake has two effects in the body that prom
ote higher levels of saturated fat. First, carbohydrates stimulate the body to
make more insulin, which inhibits the oxidation of saturated fat. Thus, when in
sulin levels are high, saturated fat tends to be stored rather than burned as fu
el. Second, a high carbohydrate intake promotes the synthesis of saturated fat
in the liver. This is particularly problematic for individuals with insulin resi
stance (characterized as carbohydrate intolerance in our recent book [17]).
Insulin resistance makes it harder for muscles to take up and use blood sugar. I
f it has a hard time getting into muscles to be burned, for the only alternative
for this excess blood sugar is to go to the liver for conversion into body fat.
This combination of decreased oxidation and increased synthesis of saturated f
at therefore results in accumulation of saturated fats in the blood and tissues.
The culprit then is clearly not dietary saturated fat per se, but rather consu
mption of more carbohydrate than an individual s body can efficiently manage. This
threshold of carbohydrate tolerance varies from person to person, and it can al
so change over a lifetime. Thus the skinny model promoting her particular versi
on of a low fat diet may actually thrive on it herself, but that doesn t mean that
it s right for you if you weren t born to be skinny. And of course, it also may no
t be right for her when she s 50 after her metabolism has changed.
So, you may be asking, if consumption of saturated fat is not associated with ha
rmful effects on the body, does this mean that this class of fats is completely
off the hook? Our response is that the science of nutrition is pretty complex,
so beware of black and white answers. Whereas dietary saturated fat intake is un
related to risk for chronic disease, higher saturated fat levels in the blood do
appear to pose a problem. As we noted, there is a lot of variation between indi
viduals in their responses to any one diet. Thus there is an unmet need for tes
ts that will guide individuals to the correct amounts of both carbohydrates and
saturated fat to match their personal metabolic tolerances.
In addition to the studies mentioned above in which high carbohydrate feeding in
creased blood levels of saturated fats, we have also conducted a pair of studies
[18, 19] comparing moderate carbohydrate to very low carbohydrate diets. Becaus
e these were not very low calorie diets, the low carb diets were naturally prett
y high in fat, containing 2-3 fold greater intakes of saturated fat than the mod
erate carbohydrate diets used as controls. The results were pretty striking
com
pared to low fat diets, blood levels of saturated fat were markedly decreased in
response to the low carbohydrate, high fat diets. Our data indicates that this
occurred because the low insulin levels accelerated the oxidation of all fats (
and particularly saturated fat); plus the relative paucity of dietary carbohydra
te meant there wasn t much of it to be converted into saturated fats. Thus, from t
he body s perspective, a low carbohydrate diet reduces blood saturated fat levels
irrespective of dietary saturated fat intake.
Now once we post this explanation of how saturated fats got such a bad rap, we k
now that we will get angry pushback from those advocates of low fat, high carb d

iets asking about all of the studies in rats and mice showing that high fat diet
s are bad for you (by which they mean those rodents
not you personally). To that
we offer two answers. First, rodents make lousy surrogates for human metabolism
. A myriad of drug and nutrient studies show dramatically different responses b
etween mice and men.
Second, most researchers who study high fat diets in mice
use 40-60% fat and 20-40% carbs (leaving about 20% for the protein). Even at 20
% carbs, this is still way too much to allow a mouse to adapt to fat burning lik
e humans do when they get their carbs at or below 10% of dietary energy. As a r
esult, at huge tax-payer expense, these many intermediate carb studies tell us not
hing useful about the human response to a well-formulated low carbohydrate diet.
And so we end this sad saga about poor, downtrodden saturated fats on a hopeful
note. Yes, dietary saturated fat continues to be scapegoated as the presumptive
cause of many health problems in developed countries. However we now know that
nutrition policy makers have indicted the wrong nutrient for the crime of raisi
ng blood saturated fat levels. If we can just banish the phrase you are what yo
u eat , however, perhaps the nutrition establishment would broaden their perspect
ive to consider how other offenders determine blood saturated fat levels and con
tribute to overall health and disease.
There is convincing evidence that dietary carbohydrate exerts an important influ
ence on how the body processes saturated fat. Thus, saturated fat, whether made
in the body or eaten in the diet, is more likely to accumulate when aided and a
betted by high levels of dietary carbohydrate, particularly in insulin resistant
individuals (as in type-2 diabetes or metabolic syndrome). Especially in these
substantial segments of our population, a one-size-fits-all recommendation to a
ggressively lower saturated intake with the expectation of lowering blood satura
ted fat levels is intellectually invalid and likely to backfire. Given our curr
ent epidemics of obesity and diabetes, we can t afford to continue diet policies b
ased on a tragically flawed, simplistic sound-bite.
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