On Sat, 5 Aug 2000 07:55:22 -0400, Todd Moody <[log in to unmask]>
wrote:

>Yes, but I also think we are reaching the limit of what we have
>to say.  Let me try to summarize my view.

I hope there isn't a predetermined limit what we have to say.
Thanks god we are able to learn.
But it's good to find a stop point sometime.

I've seen, that you discussed exactely the SFA topic in detail before.
I'll try to summarize my view too.

1.I think there's rather good evidence, that the fats of any natural
(paleo-) fat sources are very different from most fat sources
available today.
-Most important and most deleterious of all (this seems an agree point of
 many) beeing "synthetical" trans fatty acids, found in margarine ,
 "shortenings", convenienve foods and heat processed vegetable oils.
 The deleterious effects seem to arise even in small quantities as with
 other toxins.
-Slaughter fats of farmed animals (first of all beef) are different to wild
 game:
 The most striking difference i find is the rather low *ratio* of EFAs
 compared to all the other fats (SFA and MUFA).
 (SFA may be computed without short chain saturated fats, which are pure
 fuel and don't  interfere with EFAs)

Nature fat sources from vegetables (the richest source beeing nuts)
generally have very high EFA and low SFA parts. (e.g. walnut 6:9:47)
Nature fat sources from animals (out of the arctis a rarer source) are
higher in SFA and MUFA  and have a relative high EFA percentage
(e.g. caribou 1.3:1:0.5, beef 2.3:2.6:0.24).

2.High percentages of animal (and other) fat in the food are probable only
for rather short timeframes in human history. If you accept the CroMagnon
anchestorship this are only 30ky of 200ky. And this also betrays only
the CroMagnon groups which invaded ice age Europe. Regarding the lower
bioproductivity in glaciated climates this was probably a limited
percentage.

4.Long chain saturated fats and monounsaturated fats decrease the
availability of essential fatty acids, which have a fundamental
overall health effect by determining prostaglandins.
This by crowding out EFAs from the enzymes which ought to put them to work.
delta-6-desaturase (D6D), elongase, and delta 5 desaturase.
The working of D6D is further diminished by some more factors as are
-trans fatty acids
-insulin (source for me only Sears)
-alcohol
-cholesterol (source for this only Erasmus)
Foods containing arachidonic acid (AA) like beef work independent of
D6D and above mentioned enzymes but are producing Series 2 ("bad guy")
prostaglandins only.

Foods containing EPA like fish oil or brain work independent of
D6D and above mentioned enzymes and can produce Series 3
prostaglandins which can downregulate AA usage again.

Foods containing gamma-linolenic acid (GLA) like evening primrose oil ,
borage, blackcurrant, and hemp can help producing series 1 prostaglandins
("good guy") by surpassing the D6D conversion step needing only
elongase of the above.

5.Examples of real-world people which are thriving in presence of
much saturated fat (Masai, Samburu, Jamaicans) are likely to rely mostly
on short chain SFAs as are found in the dairy and coconut they consume.
And in the probable presence of enough EFAs by slow growing cattle or fish.

6.Unavailability of EFAs in presence of long chain EFAs possibly leads
to usage of sticky SFAs in cell membranes, makem them less elastic and less
permeable. Further they reduce the usability of cholesterol, which is
otherwise used in cell membranes.

7.Replacing carbohydrate by fats helps prople diseased by
diabetes or glucose intolerance. Probably obesity too.

So far.
Now just a few notes to your text:

> And the most potent
>stimulator of desaturase enzymes is glucagon.  The best way to
>keep insulin low and to produce glucagon is to eat a low-carb,
>high-protein diet.

Glucagon is produced shortly after insulin levels after a meal goes down,
to ensure a constand blood sugar as necessary for our brain.
This should be the case the whole night and 2-3 hours after a meal.
Right?
A high protein meal as well as a carb meal produces a insulin surge.

>  I believe that in the context of such a diet,
>and perhaps *only* in that context, the body handles SFAs well.

Maybe. Jamaicans are certainly not low carb nor very high in protein.

>If you simply add animal fat to a diet that is already high in
>carbs, as many studies do, you have problems, because the
>carb+fat combination is a very potent stimulator of insulin
>release.

Possible and seems obvious when looking at the standard diet people.

>3. Between 1910 and 1970 (in the U.S.) consumption of animal fats
>went down somewhat, while overall fat intake went up.  In 1910,
>84% of fat eaten was animal fat,...
>  But the main point is that ...
> the animal fats were apparently not causing trouble.

Ok, how much was dairy and how much overall calories were from fat 1910?

>I think we'll agree that this has a lot to do with the trans fats
>in hydrogenated oils (which also, incidentally, raise Lp(a)
>levels).
strong agree.

>..  Note also that Drs. Eades, in
>conjuntion with Dr. Cordain, are in the process of re-studying
>whole-carcass fat composition of wild game and, according to
>their book, preliminary results suggest that the numbers will be
>much higher than previously estimated.  This research is supposed
>to be published later this year.

We'll see. Of course they can change their minds.
In the complicated computation in your (Cordaine's) kangaroo posting
suddenly the bodyfat of kangaroo rose from almost  nothing to 50%
of food energy. I'd like to see a whole animal analysis, with sums.

I think the aborigines  know what they do.. if they leave a dead
kangoroo if it's not fat enough. Keyword protein toxicity.

> This supports the dietary
>principle that fat and carbohydrate intake should be inversely
>proportional to each other.  If this principle is adhered to, I
>doubt that SFAs present a problem.

I think the type of fat (which SFAs? are EFAs onboard?) can't be ignored
in this case.

have a good time

Amadeus