On Tue, 1 Aug 2000 13:19:12 -0400, Todd Moody <[log in to unmask]>
wrote:
>
>Why do cell membranes need EFAs?
Cell membranes consist of phospholipids and can incorporate various
fatty acids. Which fatty acids are used, determines the properties of the
membranes. Trans fatty acids as the worst case are reported to hamper
the permeability of the membrane to some important substances.
More saturated fatty acids make the cell membranes more like saturated fats
are, in contrast to polyunsaturated fats. Harder, less flexible, less
permeable to nutrients. This can cause earlier death of cells. In arteries,
the walls like the membranes become harder and less able to fulfill their
function. This is a reason for the body to "strengthen" the artery walls by
deposits of cholesterol.
This information also explained in the "Fats that Heal, Fats that Kill".
>I agree that the muscle meat of wild game is very lean. My
>bowhunting friends tell me, however, that even deer have
>substantial kidney fat deposits, and these structural fats are
>highly saturated.
How much does this amount to? Which percentage gives a whole deer's
fat in saturated fat (including kidney fat, brain, marrow, subcutane)?
How much lean meat has such a deer?
If it was about 50kg of muscles, some kg of organs how substantial is the
kidney fat deposit? 1 lbs? 1kg? more?
>
>> Conclusion:
>> Beef which isn't grasfed only (nor fattened on grain) is unpaleo.
>> And its unpaleoness implies well documented health dangers.
>
>Overstated, I think.
Ok, how would you express it then? The facts are at hand.
> Even feedlot beef fat is also quite high in
>monounsaturated fats.
Not only saturated, but also monounsaturated fats compete with EFAs
on enzymes, but to a lesser degree. Then its a matter of EFA compared to
total fat.
In search of an arctic animal, i found at usda caribou, which is rather
northern, i think. And compared it to the best lean beef
(with only 9.7 % fat). And for fun to hamburgers and walnuts.
It has
Caribou Beef Hamburger Walnut
SFA 1.3 3.8 5.9 6.1
MUFA 1.0 4.1 6.9 8.9
PUFA 0.5 0.4 1.3 47.2
For hamburgers, you can see the added fat, but why are the PUFAs elevated?
(Probably from trans-fat containing frying fat, the composition was *not*
listed- because of toooo many derivates?)
Looks like mammouth (living in a climate comparable to caribou)
were much better than beef in composition.
If the usability of of PUFAs (EFA) is dependant on the relative percentage
of fat these numbers tell a interesting story.
> What they are clearly deficient in is EPA
>and DHA.
EPA and DHA are made of the precursor efa's. But this process is hampered
by a high part of more saturated fats.
>It is therefore important to find other sources for
>these, but the absolute amounts needed are still quite small.
>Note, for example, that fish oil studies show a ceiling effect
>at about three fish servings per week, resulting in w-3 intakes
>averaging less than a gram a day.
This w-3 amount is certainly measured for EPA (or DHA) as precursor to
prostaglandin making. Just by amount I'd expect that much more EFAs were
necessary for making cell membranes as for prostaglandins.
>.. the heart muscle works
>continuously, requiring a significant amount of fuel.
I recall about 9% of resting energy for the heart as opposed to 25% for the
brain.
> If its
>preferred fuel is *dietary* SFAs then that implies that, in a
>design sense, the heart "expects" a fair amount of SFA in the
>diet. The fact is that SFAs are, in general, good fuel, and not
>just for the heart.
The heart perfers to burn fat and as you tell, prefers SFA.
This is good fuel, but nothing else.
Why should it prefer SFA over, let say EFA with the same energy?
To spare EFA and to get rid of SFA, is my guess.
>This is undoubtedly why, when glucose is
>converted to fat, it is converted to saturated fat.
SFA is a simple carbon chain except for the end. This is the closest
to glucose which has a simple carbon chain with another end.
SFAs are simply the first step when generating fat out of (excess) glucose.
The next step is makin the fat unsaturated and longer chain.
The composition of body fat reflects the availability of fatty acids
at triglyceride making time.
Different humans have different percentages of FAs in body fat.
Farmed beef will be so saturated, because this is the quickest made
fat, when feeding up an animal, which is to grow fast.
>> This sounds not as when that saturated fats were especially helpful, but
>> worked when they *replaced* w-6 safflor oil.
>
>This certainly would count against your theory that SFAs compete
>for the same enzymes as the EFAs. If that were the case,
>replacing w-6 EFA with SFA wouldn't accomplish much.
It's not my theory, but what Erasmus describes as state of the art and
founded by study.
What you say counts against, that's right, but depending on the stage and
the kind of enzyme involved.
The study you mentioned is concerned on the (short term)
prostaglandin health effects.
From the stage of EFAs, LA and ALA compete for 3 enzymes
until AA or EPA is reached, including elongase.
(see picture at http://www.zonehome.com/images/efa.gif ).
LA competes ALA in all 3 enzymes.
SFA competes only for the elongase enzyme (given that the delta*desaturases
are more specialized).
In this way, excess LA w-6 fatty acid reduces this 3 steps in the
prostaglandin making pathway for ALA w-3.
SFA (and some MUFA too, according to Erasmus) reduces any EFA usage in any
pathway, may it be prostaglandins or cell membrans (e.g. by binding the
elongases).
My beef example above had 0.4 to 4.1+3.8 = 5% EFA as opposed to 17% for
caribou and 76% for a walnut.
EFA inclusion in cell membrane will involve such enzymes which make cell
membranes and not influence prostaglandins.
>> I don't consider it helpful
>> to totally stop w-6 intake.
>It would be just about impossible to do so.
If eating only beef fat (some 5% LA), which is suppressed in its effect
according to Erasmus' description, the case happens.
E.g. in Philip Thrifts description (so far).
Amadeus Schmidt
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