On Mon, 7 Aug 2000 09:45:58 -0400, Todd Moody <[log in to unmask]>
wrote:
>Well if you eat 100g of walnuts you get about 5.6g of SFAs,
>almost all of which are long-chain (16:0 and 18:0). If you eat
>100g of beef (composite) you get 8.5g of SFAs, almost all of
>which are long-chain. If you choose leaner cuts (see bottom
>round, trimmed to 1/8 inch fat, for example) then 100g gets you
>4.4g of SFAs (mostly long-chain), less than walnuts. It also
>gets you more protein, but a lot less MUFA and PUFA.
Such a nut has very much more fat that any animal.
(65g for walnut or hazelnut 60g and now 8.2% for the kangaroo instead of the
previous 4% overall as stated by Cordain)
Protein isn't that much difference (15g for the nuts 22g for the game).
But the *ratio* of EFAs to other fats is very high on the efa side
with the nuts, exceptionally low with beef (0.24:4.9 = 0.05)
and game (antelope now) has .44:1.26 = 0.34.
(I always compute EFA : MUFA+SFA ) as ratio of EFAs to
competing fats.
>
>But as you know, not all PUFAs are equal. You have chosen
>walnuts for an example. They are unusual (among nuts) in that
>they are relatively high in w-3 fat.
Yes, walnut is exceptionally good.
Walnut (47:15 = 3.13!). Hazelnuts are a shure mesolithic mass food
and not so EFA or w-3 rich. But still compute with
Hazel (8:45+4) = 0.16 (threefold of beef).
>Since you claim that both SFAs and MUFAs are competing with EFAs
>for enzymes, then perhaps what matters is the ratio (SFA +
>MUFA)/PUFA, in which case nuts certainly do better than meats.
>But most nuts have an extremely high w-6:w-3 ratio (with the
>exception of walnuts), whereas meats do not.
That's the reasoning given by the reference of Price and of Erasmus.
Shorter chain SFAs as 16:0 are not or only slower converted to 18:1 and 16:1
MUFAs with are reported to "suppress EFA activity" at a ratio of
15:69 (= 0.21 in my examples).
Not *all* nuts or plants are therefore acceptable as (sole) fat source.
Hazel for example cannot be a sole healthy fat source. To reach
the critical value of 0.21 3 g EFAs had to be added for 100g food.
You can also consider various other fat sources.
Almost all natural sources have superior or reasonable
EFA percentages in fats. Including game, nuts and also lowfat
food as green plants.
Even cereals (whole, fresh of course) i take oats as example
oats = (2.5:1.2+2.2) = 0.73 .
Only farmed beef is exceptionally low in EFAs. And in a protein+fat diet
you need horrible high amounts of fat.
>I doubt it. Cordain's kangaroo study suggests that even in arid
>Australia there is still a good deal of fat to be harvested from
>the carcass of even a lean animal like a kangaroo.
Do you doubt my statement aboute fat availability in arid climates,
or the low genetic influence of arctic-like environments?
Now that Cordain computes 8.2% overall fat for that kangaroo
(instead of 4% with the wild unugulates before) the numbers are changed
bit (while fat will still vary from season to season).
Now we have 46:54 calories from fat to from protein.
While (always according to cordaine) from 35% cal from protein
begins to be toxic (this is "rabbit starvation" i suppose).
This means that even if you go to the upper limit of tolerable
protein intake (35%) you'd still have to discard some meat of the animal
(from 54 to 35, quite a lot). This is of course possible and even more
in cold climates which fattier animals (15%).
But does it make sense to live that close at the upper limit of protein
toxicity? If you have nothing else of course.
But most plants provide their energy without burdening much protein "stress"
on the kindneys and liver. While still provinding abundant of protein
for structural purposes (>> RDA).
(we are not endangered by cookies and cakes here)
> My guess is
>that such foods were exploited as completely as possible, for a
>very long time.
Sure maybe. My guess is, that plants would have been the preferred
caloric source, as long as available. For the notes reasons.
But besides nuts i only come to tubers as a denser plant food.
>Then nuts are going to be problematic, since most of them are
>overwhelmingly composed of MUFAs.
Where do you see a problem with too much EFAs? They can be nurnt as well.
> And the EFA ratios would cause
>further problems. This may be why many people get acne, an
>inflammatory response, from heavy consumption of nuts.
I agree.
Thats the case for some nuts. Notably hazels, which are cheap too.
And also cereal grain foods. This is what i think why the early neolithic
people, who had with grains lentils and flax were so successful.
Inflammation could be quite a problem i suppose.
>> Foods containing arachidonic acid (AA) like beef work independent of
>> D6D and above mentioned enzymes but are producing Series 2 ("bad guy")
>> prostaglandins only.
>
>This is incorrect. More recent work indicates that dietary AA
>has little or no effect on prostaglandins.
Can you give some reference for this? And also what did "persuade you"
that dietary AA wouldn't be a problem?
AA release from cell storage is modulated by some substances.
E.g. EPA.
>Dairy fats do have some short-chain SFAs, but the long-chain ones
>are overwhelmingly predominant. In coconut oil, medium-chain
>fats (10:0, 12:0, and 14:0) predominate, with long-chain fats
>next, and short-chain last.
Butter has about 50% of its *saturated* fat as long chain (16 or 18) which
could interfere with the EFAs. That's a good reduction.
Coconut oils 10 to 14:0 i assume too short to enter the
d6d... pathway.
>Then the populations mentioned above should be very sick. Why
>aren't they?
Because membranes prefer 18-chain long FA.
And more important, the have probably enough of EFA sources.
Zebu cattle are very low fat and also high in EFA if i recall right.
>But if your theory is right, animal fats should interfere with
>glucose tolerance, by making membranes less permeable to glucose.
>Why isn't that so?
Maybe your studies have included eather enough EFAs in the diet
or sources other than 18:0 and 16:0 e.g. by supplying fish as animal
or dariry as fat or added supplements.
Permeable membranes pass more glucose and insulin.
But any burnable fat was certainly compensated by reduced carbohydrate
= less need for it all.
>Glucagon is also stimulated by protein (and, incidentally, by
>stearic acid).
This stimulation by 18:0 is strange to me.
And also why 18:0 should *decrease* cholesterol.
Except that 18:0 stiffer membranes use less cholesterol.
>>... kangaroo .... I'd like to see a whole animal analysis, with sums.
>
>Well, that will be in the published version, no doubt. I'm
>betting that the whole-carcass fat breakdown will be about 45%
>SFA, 50% MUFA, and 5% PUFA.
Ok, lets see. 5% PUFA would be well below the critical limit.
And also well below antelope or other games muscle fat.
What shall we bet? (about the 5%)
ok, heading to hunt a salad now.
Boy, what do we have for monster postings........
cheers
Amadeus
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