Todd, i think this thread digs up interesting things.
I've some news on the EFA suppressing theme (see below).
You wrote:
>> If SFA was the right for cell membranes, why would the body try to pick
>> out the PUFAs? If very much SFAs are present?
>
>I suspect that a combination of both are used.
That is true. Membrans are made of PL's which has 2 places, for
fatty acids. One of it is saturated usually. The second "should" be
mono or ployunsaturated to keep the membrane permeable (e.g.to proteins).
There's no way to condemn SFAs as a whole. But it appears, that if
EFAs are *way* to few in relation to SFAs some deleterious effects
may arise.
For example, then membranes with two (instead of one) saturated FAs
are beeing made.
> I do not believe that cell membranes are
>supposed to consist entirely of SFAs.
Yes.
And EFAs which can't be made may also be necessary or better beneficial.
>Hardening of blood vessels (arteriosclerosis) is a result of
>calcification, not SFAs in cell membranes. Lack of EFAs may
>contribute to this, but an abundance of SFAs does not equal a
>lack of EFAs.
But abundance of SFAs and (!) MUFAs may imbalance the prostaglandin
hormones to an unvafourable direction and this certainly has the bad effect
on blood vessels (too much SFAs in membranes may add to this).
Amadeus:
>> I also find the paleo view important.
>> Saturated fat intake is obviously very unpaleo because never, anyplace
>> anytime in history man (or predecessors) has been exposed to amounts of
>> saturated fats.
>
Todd:
>But if you look at the fats in organ meats and marrow, which are
>predominantly saturated, and accept that these were the
>*preferred* edible portions, then it appears that significant
>amounts were eaten. ..
>Again, you are only counting muscle fat. Organ, structural and
>marrow fats are highly saturated.
What the experts said (remember Cordaine) was *overall* 4% fat in game..
(but still i don't suspect animals to have been a big part of the savannah
diet)
How can that be significant?
You mentioned organs. I couldn't find data on game liver so I tried lamb
liver. It has 2g SFA, 1g MUFA and 0.7g EFA per 100 g.
Thats low fat, low SFA (compared even to beef muscle) *and* is high in EFA.
I have looked at various game like caribou antelope and have found
a very low saturated and mono ratio to high EFAs.
It comes from the herbal food and slow rate of growth, i suppose.
I can't imagine a way to compute from game a fat composition so high in
saturated fat as beef is. Not nearly. They are fine EFA sources.
>And you are ignoring water
>fowl.
True i ignored it, because i can't imagine a big water fowl part in the
savannah (or anywhere in ice ages).
Though I looked at duck fat. It's 33:49:12 (SFA,MUFA,EFA). 12 % EFA.
Even this hard nature fat has a much higher EFA percentage than beef (3
fold).
>>..in ice shield times: wild game was high fat, but probably is very
>> unsaturated.
>
>Probably? Storage fats are highly saturated.
We can wait for a mammouth analysis or take the favourable caribou fat as an
example.
Erasmus:
>> "Test showed that....... above certain parts of OA compared to EFA
>> EFA activity is totally suppressed..."
>
Todd:
>What is OA? Is that oleic acid? What does he mean by "EFA
>activity"? Is that prostaglandin synthesis?
OA is oleic acid 18:1.
Insufficient or imbalanced prostaglandin synthesis is certainly the most
drastic effect of "suppressed EFA activity". As missing activity,
integration of non-EFAs in cell membranes seems possible but with a rather
long term effect. DHA in nerves is also a nice EFA activity.
> One important point,
>based on recent research is that lipoprotein(a) levels are an
>important risk factor for heart disease and *only* SFAs reduce
>Lp(a). This is probably post-Erasmus research.
Lp(a) beeing blamed intensely is mentioned by Erasmus and by Siminopulous.
And that their synthesis is governed by prostaglandin mechanisms.
SFAs reduce them?? Which?
About water fowl:
>> They can fly away.
>> Bows and arrows are a recent invention of only 40k years.
>> I don't expect them in glaciation nor in savannah.
>
>You're kidding, right? Spears can be thrown; rocks can be
>thrown. Dogs are pretty good at catching them too.
I think they *could* be hunted, but with limited success without arrows.
And i don't see big sweet-water environments in the ice ages.
Tropical fats:
>Well, there could be such a "local factor" or he could be just
>wrong about the alleged dangers of SFAs to begin with.
I've found the (or a) reference, that MUFA (and MUFA out of SFA)
supress EFAs:
"There is some evidence that an excess of oleic acid (..) may inhibit
prostaglandin production."
Reference 5 of http://www.westonaprice.org/tripping.htm .
This "Price" article otherwise *defends* saturated fats much
(mostly dairy and others).
And with it, i think i've found a key to the ambiguos reports on saturated
fats. It's the *type* of saturated fat.
Shorter chain seem ok, even beneficial (shorter chains from 4:0 to 12:0).
"Lauric acid, a 12-carbon saturated fatty acid found chiefly in mother’s
milk and coconut oil, and in smaller amounts in butter, seems to improve
the function of the omega-6 pathway."
That explains why shorter chain saturated coconut fat is not problematic
(and saturated milk fat which is even shorter chained).
Longer chain seems, problematic. Beef has predominately 16:0 and 18:0.
(btw 18:0 is stearic, which my candles are made of .. I wouldn't want
*that* in my venes).
16:0 and 18:0 are desaturated into 18:1 and 16:1 where they increase the
already high OA (18:1). OA is the culprit in the study above.
I know why: These oils make the omega-7 and -9 series of FAs.
They require *the same* enzymes which are necessary to put EFAs to work:
delta6desaturase, elongase (2*) delta5desaturase.
If the ratio of 18:1 and 16:1 to EFAs is exceptionally high then the EFAS
have too few enzymes left for processing
(69:15 mentioned as critical ratio in the study, beef reaches 80:15).
Results in... overall low prostaglandins (Series 1-3).
All series of prostaglandins have an impressive list problems emerging,
when they are missung. From hair falling out, over imune problems to CVD.
And to the bad: the prostaglandins which *are* made are more series 2
prostaglandins "bad guy" (because of w-3 to w-6 ratio and: In beef
additionally promoted arachidonic acid therein.
What you write about glucose intolerance and fats:
I agree in a general tendency, that fats (whichever) can help in
sugar problems because
1. they can burn *instead* if carbs and relieve this pathways
2. therefore they'll slow the glucose swings
2. they seem to slow digestion and carb uptake
Some certain fats may have quite different effects.
You mentioned some strange effect of myristic for example.
However this general fat-or-carb question doesn't exculpate beef fat
in any of its incriminations.
I doesn't betray wild game (eating in the wild).
Only beef, to a lesser degree all farmed animals, to a lesser degree fowl.
>Last year James Hays, an endocrinologist in Delaware, presented
>his results of a year-long study of a low-carb diet in which
>almost all the fat was animal fat. The results were improved
>glucose tolerance and improved lipids.
As i told with reasons: i'd expect that, especially for carbohydrate
diseased (diabetic, g.intolerant, and plain SADer).
Animal fat from dairy beeing shorter chain is probably better than
slaughter fat.
....
cheers
Amadeus Schmidt
"tender coconut taste greeeeat"
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