Adrienne Smith wrote:

>He doesn't say anything about saturated fat causing insulin resistance.
>Type 2 diabetics can lose weight on a low carb/high saturated fat diet.
>Therefore, I do not believe that saturated fat causes insulin resistance.
>It may be true that certain individuals have problems with saturated fat --
>but the exception doesn't make the rule.  That would be like saying certain
>people stay slim and healthy on high carb, low fat diets and therefore
>everybody should eat high carb, low fat diets.  I believe lack of sunlight,
>cold weather, less physical activity and the accompanying lowering of
>thyroid hormones is a more plausible explanation for people gaining fat in
>the winter than saturated fat.
>
>

I don't have the book with me, but I'm pretty sure he does say that SFA
causes/worsens IR.  His claim, I believe, is that too much SFA alters
cell membranes, making them less receptive to insulin.  I know that he's
not alone in making this claim.  But I agree that some people (many
people, in fact) do lose weight on lowcarb diets that are high in SFA.
Furthermore, I have a suspicion that if there is an increase in IR
caused by SFA, it might be temporary.  As I recall Wolfgang Lutz did
repeated glucose tolerance tests over a period of a year and found an
initial worsening, followed by an improvement.  The "SFA question" may
be the single most confusing and controverted issue in nutrition these days.

When mammals (and other animals, for all I know) eat carbs, what they
can't quickly use or store as glycogen is converted to SFA, primarily
(98% or so) palmitic acid.  This is why Rosedale says to exercise after
dinner, especially if you happen to have more carbs than you should
have.  The idea is to try to burn as much glucose as possible *before*
the conversion to SFA.  That's reasonable advice, I think.  Anyway, what
he doesn't mention, but should have, is that mammals also have the
ability to convert SFA to MUFA--palmitoleic acid, I think.  This is why
beef fat, for example, is only about 45% SFA, rather than 98%.  I assume
this ratio is true of human stored body fat as well.  There is a
question as to whether the enzymes needed to convert SFA to MUFA
constitue a rate-limiting process, i.e., a bottleneck.

Some people who do a lowcarb high SFA diet experience a steep rise in
LDL cholesterol.  Setting aside the health implications of this, if
there are any, it's still worth asking what this means.  It could be
that the liver is making more LDL, which would indeed point to IR, or it
could be that the known tendency of SFA to downregulate the hepatic LDL
receptors, slowing reuptake of LDL from the blood, is the cause.  And
it's pretty mysterious that some people don't experience this at all,
but get a sharp reduction in LDL.

It may just be that in some people the metabolic machinery for handling
SFAs is just broken, but that doesn't really tell us much, does it?

Todd Moody
[log in to unmask]