|
| |
From turf@gelac.lasc.lockheed.comWed Nov 29 22:03:43 1995
Date: Wed, 29 Nov 95 11:29:07 EST
From: Brian McInturff <turf@gelac.lasc.lockheed.com>
To: zone@tgv.com
Subject: Fatty Acid Postings
Here are some postings on fatty acids and other subjects, mainly by Tim
Triche on sci.med.nutrition. I pulled them through dejanews.
-------------------------------------------------------------------------------
Re: Why is consuming fat bad? It is made in the body from AcetylCoA, anyway.
From: "Tim Triche, Jr." <tjt3@cornell.edu> ;
Date: 1995/11/11
MessageID: 480t8q$cnj@newsstand.cit.cornell.edu#1/1
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
>Is eating excess fat really that much worse than excess
>calories?
Well, in a sense they end up being one and the same. But among other
things, fat is not 100% efficiently metabolized, and the poorly
emulsified remnants can be converted to PEA's in the colon by bacteria.
This may lead to colon cancer.
Then there's the little issue of heart disease. Carbohydrates do not
need to be transported in lipoproteins; fats do. Certain situations
arising from a high-fat diet will lead to oxidized LP's (mostly LDL)
getting stuck on the walls of arteries. This starts a cascade of
reactions which usually ends up plugging the artery. If it's a coronary
artery, you have a heart attack. If it's in the brain, you have a
stroke. Glucose does not pose these problems.
> Glycolysis will break glucose to acetylCoA molecules, which
>will then be stacked up to highly reduced fatty acids, right?
Depends. The glucose in the blood can also be polymerized to glycogen,
the storage form of carbohydrates. When you're full on glycogen, THEN
you start converting CHO to fat.
> Hence,
>what is wrong with eating more fat as long as your calorie intake
>doesn't exceed the normal?
First off, most Americans and Europeans overeat anyways. Second,
there's the above mentioned problem with heart attacks. Of course,
Italians eat gobs of olive oil and have a ridiculously low CHD
incidence. Ditto for Cretans. Those MUFA's are are speci
al class of fats, though, and unless you're cooking everything in
olive oil, you're probably not consuming primarily MUFA's. (mono unsaturate
d fatty acids)
>Also, could someone technically survive well on a diet where all
>calories come from protein?
Until their kidneys failed. They would start having trouble seeing
before then, though; EFA deficiency would set in.
> Protein seems to me to be really the
>only esential nutrient, since it has necessary structural components
>(essential amino acids) that they body cannot synthesize.
It lacks essential fatty acids.
> Excess
>protein, once again, would be converted to various intermediates of
>the TCA cycle or some other pathway and could be used to make ATP.
>What is wrong with this logic?
Nothing on the surface. But the urea that is given off by the
deamination of proteins for energy goes somewhere. Guess where? Bingo,
your kidneys. Paul Anderson died of kidney failure at around 40, if
it's any help.
>Why all the anti-fat sentiment?
See above. MUFA's are the exception; they're darlings, but you still
wouldn't want to live solely on them. PUFAs are only necessary for
certain functions, and in small amounts, in adults. SFA's are great for
promoting heart attacks. (sarcasm.)
>Please answer if you know
Well, that's *what* I know. Ask around, and do some reading.
--
tim triche, jr - cornell chem/biochem '97 - real deal enterprises
the nutrition pages - http://deja-vu.oldiron.cornell.edu/~jabbo/
"any man who cannot explain his work to a 14 year old is a charlatan&q
uot; jb
-------------------------------------------------------------------------------
Re: To be flaxseed or Not to be??
From: "Tim Triche, Jr." <tjt3@cornell.edu>= ;
Date: 1995/11/05
MessageID: 47ivr3$5f3@newsstand.cit.cornell.edu#1/1
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
msnaik@ix.netcom.com (msnaik ) wrote:
>I been reading all this debate about saturated, mono-unsaturated and
>poly-unsaturated fat and I getting more confused.
For reference and for others:
PUFA =3D Poly Unsaturated Fatty Acid
MUFA =3D Mono Unsaturated Fatty Acid
SFA =3D Saturated Fatty Acid
EFA =3D Essential Fatty Acid
FFA =3D Free Fatty Acid
TG =3D Triglyceride
HDL =3D High Density Lipoprotein
LDL =3D Low Density Lipoprotein
CHD =3D Congestive Heart Disease
>1) Saturated fats such as animal fats and Crisco are deemed bad but we
> do need some of it.
No. You can do quite well without any saturated fats in your diet. In
fact, you'll probably do best this way.
>2) Mono-unsaturated fats are darling of nutritionists. I have not read
> any adverse article about them.
They're still 9 kcal/g, but yes, they do seem to be the healthiest. On
the island of Crete, where 40% of kcals are from fat, and almost all of
that is oleic acid (MUFA from olive oil), the incidence of CHD is
ridiculously low. The people of Crete get only 8% of their FA's from
saturated fats on average. Also, MUFA's seem to lower LDL levels
without touching HDL levels.
>3) I read in one of those Muscle magazines that poly-unsaturated fat
> was an essential source of Linolenic acid and only flaxseed oil was
> a good source of it. It also reportedly contains Omega-3 fats.
> Still some others claim that ingestion of poly-unsaturated fats can
> be downright detrimental to your health, poisonous etc. Who is
> right?
First off, quit reading "those muscle magazines". I am an ACSM chapter
member, a former ACE trainer, an Olympic-style lifter working towards
competitive weights, and have been a three sport athlete for years.
Nothing in the muscle magazines ever contributed to my performance
positively. If you're going to read a muscle mag, read MILO.
Next topic. Linoleic acid and linolenic acids *are* both PUFA's; they
are the common names for cis-9,12-octadecadienoic acid and
cis-9,12,15-octadecatrienoic acid. If you hadn't already guessed,
there's a reason people use common names for fatty acids! =3D) Anyways,
PUFA's are indeed where these acids fall, but plants in general are good
sources of both, not just flaxseed oil. Flaxseed oil is incidentally
prone to rancidity (autoxidation reactions) and in my opinion is a poor
idea. The reason you need a minimum of 5% or so PUFA's in your diet is
that they lead to the synthesis of eicosanoids (PG's and the rest) which
are 20-carbon signal molecules formed by cyclooxygenase and prostacyclin
(two enzymes) from dietary fats. The way that EFA deficiency, i.e. not
enough fats to make PG's from, was discovered was by tube feeding of
people without any fat in the diet. Something to be avoided, but then
again, I've never heard of a EFA deficiency which wasn't a result of
tube feeding.
Both sides are right - PUFA's are easily turned into polyepoxides or
attacked by radicals, especially conjugated PUFA's. But some are
necessary for your health. The best way to approach this is to get your
PUFA's from fish and from plants, and never to cook foods in PUFA's.
(the heat speeds up radical attacks and oxidation reactions in the
PUFA's and you end up with semi-"rancid" food.)
--
tim triche, jr - cornell chem/biochem '97 - real deal enterprises
the nutrition pages - http://deja-vu.oldiron.cornell.edu/~jabbo/
"any man who cannot explain his work to a 14 year old is a charlatan" jb
-------------------------------------------------------------------------------
Re: Flaxseed Oil
From: "Tim Triche, Jr." <tjt3@cornell.edu>= ;
Date: 1995/11/09
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
dduchaine@aol.com (DDuchaine) wrote:
>And yes, free radical damage _might_ be increased in
>consuming PUFAs. But you could say the same thing
>to endurance athletes: too much oxygen from running,
>bicycling, etc, may speed up the aging process.
Not anymore, at least, not unequivocally. Some of the studies done for
the 1992 symposium on physical activity, fitness, and health in the
general population looked at levels of exhaled pentanes, a good
indicator of whether radical damage occurs. What they all seem to
conclude is that, indeed, athletes may be increasing the amount of
radicals evolved - any biophysicist would be able to justify this based
on the principles underlying aerobic metabolism, but I am not a
biophysicist - but at the same time certain classes of enzymes and
metalloproteins seem to increase in transcription rate as well. So, in
trained athletes, you have more radicals being spun off, but there are
also more acceptors for the radicals. And think for a moment about what
that translates into for resting athletes who recover fully in training.
>It would be interesting to look at mortality rates in
>populations consuming high (or even moderate)
>amounts of PUFAs.
It would be an interesting study. I'm not sure if any have been done;
there are quite a few on MUFA intake and mortality (negative
correlation) but I haven't seen any on PUFAs in general. A while back
there was a rash of studies in _Metabolism_ on certain PUFAs and
mortality rates (mostly w-3 FA's, not very original studies), but I
haven't been following any journals with interest this year.
--
tim triche, jr - cornell chem/biochem '97 - real deal enterprises
the nutrition pages - http://deja-vu.oldiron.cornell.edu/~jabbo/
"any man who cannot explain his work to a 14 year old is a charlatan" jb
-------------------------------------------------------------------------------
Re: Flaxseed Oil
From: "Tim Triche, Jr." <tjt3@cornell.edu>= ;
Date: 1995/11/07
MessageID: 47odc3$ha1@newsstand.cit.cornell.edu#1/1
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
>you have only one reference and its 15 years old!
Absolutely, positively false. Any good biophysics or structural biology
text should cover lipid peroxidation, singlet oxygen attacks on double
bounds, and polyunsaturate autoxidation.
Where exactly do you think the research on free radicals started?
Unbeknownst to many of the hucksters selling antioxidants these days,
the mechanisms are well documented. The problem with PUFA autoxidation
and radical attacks (i.e. hydroperoxyl) is that the products are
extremely difficult to predict with certainty, and the attacked lipids
may themselves become active as radicals under certain attacks.
Ever wondered what paint was? Put some variety of PUFA in a skillet and
heat the hell out of it. Rapid polymerization catalyzed by the high
heat leads to a multiply branched alkane polymer...PAINT...and that's
what USED to be the PUFA. These reactions happen more slowly and less
often in the comparatively cooler tissues, but they still happen.
Why would you challenge a chemist on chemistry? I'm beginning to wonder
whether you can evaluate claims objectively. Most of my examples are
from a presentation by one of my professors, JT Brenna. Reading
material might consist of (for example) an orgo text, a biochem text,
Helmut Sies' _Oxidative Stress_, Guido Marinetti's _Disorders of Lipid
Metabolism_, and more specialized books from the likes of VCH, Academic
Press, or Springer-Verlag. Don't criticize something just because it's
"out of date"; many of the reaction mechanisms have been known for so
long that 15 years ago is RECENT. Chemistry is now focused more on NMR
specs of proteins and the like than determining how oxidation reactions
propagate in fats. A reflection of this is the literature, which for
all I know may no longer contain many current studies of reactions like
these. That doesn't mean older refs are invalid; it means the field has
not changed a lot since the mechanisms were first discovered. The
biochemical results of such peroxidations, on the other hand, are a hot
biochemical topic; there you will find much evaluation of quenching
enzymes, compounds, and complexes. But the mechanisms of formation are
still the same.
--
tim triche, jr - cornell chem/biochem '97 - real deal enterprises
the nutrition pages - http://deja-vu.oldiron.cornell.edu/~jabbo/
"any man who cannot explain his work to a 14 year old is a charlatan" jb
-------------------------------------------------------------------------------
Re: Flaxseed Oil
From: "Tim Triche, Jr." <tjt3@cornell.edu>= ;
Date: 1995/11/07
MessageID: 47odsq$ha1@newsstand.cit.cornell.edu#1/1
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
Ascorbyl palmitate would be a poor choice for preventing autoxidation of
polyunsaturates. BHT might help, but I think Angelo's point was that
cooking with polyunsaturates is a stupid idea.
Also, have you ever heard of pericyclization or light-induced radical
attacks? I have heard that most refrigerators, even some over 15 years
old, have these ingenious devices in them called LIGHT BULBS. If you
open your door to your fridge to get your flaxseed oil out, you may have
already started an autoxidation reaction in the stuff. Bad idea if you
ask me.
Why not get your PUFA's from vegetable sources, or better yet, fish?
Once inside the body there is still opportunity for PUFA's to be
oxidized other than inside the mitochondria (which contains radicals
from this process and harnesses them to generate usable energy, rather
than chain reactions). MUFAs are more resistant to peroxidation and do
not seem to downregulate the levels of LRP or LDLr found in the liver,
hence they provide a good energy source while not contributing
needlessly to radical propagation.
The only thing you need PUFA's for is eicosanoid formation, and most
Americans seem to get enough that EFA deficiencies are practically
nonexistent outside of clinical settings.
In light of all this (pun intended, GROAN), it seems like a "Bottle O'
Potential Rancidity" is a poor purchase, whereas a cold-water fish or
perhaps some sushi from one is a good purchase.
"The microbe is nothing; the terrain is everything." - Louis Pasteur
Pay attention to the matrix in which a molecule is held.
--
tim triche, jr - cornell chem/biochem '97 - real deal enterprises
the nutrition pages - http://deja-vu.oldiron.cornell.edu/~jabbo/
"any man who cannot explain his work to a 14 year old is a charlatan" jb
-------------------------------------------------------------------------------
Re: Ephederine, Caffeine, Aspirin, Cranberry J= uice
From: "Tim Triche, Jr." <tjt3@cornell.edu>= ;
Date: 1995/08/31
MessageID: 425g0u$juo@newsstand.cit.cornell.edu#1/1
-------------------------------------------------------------------------------
sender: tjt3@cornell.edu (Verified)
Ephedrine is a CNS stimulant, a sympathomimetic amphetamine analog,
which makes you feel "wired" or "speedy". It will indeed increase your
thermogenesis, on the order of 1% to 1.5% varying individually.
However, it tends to diurese you (make you pee a lot) and will
consequently lead to decreased blood viscosity. This, along with the
vasoconstriction of certain areas due to a sympathetic reflex from the
brain, will lead to increased blood pressure and may end up causing
TIA's (transient ischaemic attacks, or micro-strokes) in those who
forget to rehydrate, who are already stressed-out Type A people, or who
are hypertensive. For fit athletes, your combination may be helpful,
but it's banned in international and national level competitions.
Believe me, I know - I have competed at a national or state level in
lacrosse, soccer, judo, wrestling, cross-country mountain biking, and
mid-length foot races. I feel that the potential for tolerance and the
"crutch" aspect of amping up on a CNS stack negates the potential
benefits.
Anyways, caffiene is a methylxanthine, a member of a family of compounds
which most people are unwittingly familiar with. Its relatives include
theophylline from teas, theobromine from mate and teas, and several
other aromatic hydrocarbons with varying degrees of stimulatory effect.
What caffiene does to you is essentially the same as ephedrine, but on a
different set of receptors. Its thermogenic potential seems to be
around 1% to 2%, but it's only going to add a little to the effects of
ephedrine, maybe 0.5% or so. Again, it is a diuretic and will raise
systolic blood pressure.
Aspirin does not stimulate anything, but rather it inhibits the enzyme
cyclooxygenase, preventing the body from manufacturing the normal
quantity of thromboxanes (blood clotting factors) from the 20-carbon
PUFA's. In so doing, it increases blood viscosity and all=
ows lowered
systolic and diastolic blood pressures, as there is less incentive for
platelet aggregation factors (blood clot "director" proteins) toact.
It may allow fit athletes to safely use the aforementioned stack, but
because of the competitive advantage and training edge that such drug
use gives the athlete, it's still not legal to use them.
Finally, cranberry juice acidifies the gut and urine, causing the
normally weakly acidic methylxanthine and amphetamine knockoffs we
discussed earlier to precipitate out into the urine somewhat. This
doesn't mean they aren't absorbed, but they will act more slowly and
eliminate faster, so if you're doing this stack before a workout, this
is good advice. As you may have guessed, nobody's planning on outlawing
cranberry juice, so even if you avoid the drugs, the juice is a good
idea to keep your cells hydrated and your bodily transport systems
active.
Dan Duchaine will likely have different opinions, as he markets a great
product of this nature in terms of efficacy, but overall I feel that
athletes will not gain a long-term benefit from such drug abuse. None of
the above is medical advice, and neither will Dan's be, but that hardly
means you should skip reading the background material given above. I am
a licensed and certified athletic trainer, and a biochemistry/chemistry
major, so I have at least some experience in the lab with this stuff. I
also happen to have used it myself during activity, and ended up junking
it.
Hope this helps.
"A moment of silence is a Zen shout!"
Tim Triche, Jr.
Ithaca
-------------------------------------------------------------------------------
Re: Essential Fatty Acids (article)
From: Guess.Who@Leiden (Angelo Schouten)
Date: 1995/06/29
MessageID: 3suff6$n11@highway.LeidenUniv.nl#1/1
-------------------------------------------------------------------------------
In article <DAwIFn.HJu@midway.uchicago.edu>, bmdelane@ellis.uchicago.edu
says...
>The issue was: ocean fish oftn contain high levels of synthetic
>organic toxins, as well as heavy metal toxins. Farm-raised fish seem
>likely not to have this prob (tho' that would depend on the
>farm). Then someone said that farm-raised fish don't have the same
>PUFAs (PUFAs are here assumed to be good), perhaps b/c the temp. of
>the water is higher.
>Me: where's the evidence?
>--
>Brian M. Delaney
Brian,
Moreover what is the point. Food -including fish- has been deliberately
contaminated for years without further notice. One tends to classify
fish a s
non-consumable, while one is eating methylbromide treated and heavy
metal r ich
lettuce, and what about cows (and their meat) grazing the green
pastures.
Silly isn't it.
Anyway this is for Steven Fowkes and his fishy hypothesis:
In view of the discussion on PUFA, deep/shallow water fish
and
free radicals, I have this on *mammals*. May this correlate to
the interest in the fishy discussion. Mammals are more fun.
The idea is the deeper the water, the colder the fish, the higher
the [PUFA]. The warmer the fish the more PUFA breakdown
(conversion into bioactive _radical intermediates_ metabolites -
prostaglandins??)?
[Body temp-PUFA-prostaglandin]
Body temperature in mammals is regulated by a balanced release of
5HT and norepinephrine NE in the preoptic anterior hypothalamus
PO/AH. However , the E prostaglandins are consistently
hyperthermic when injected intrahyothalamically or
intraventricularly in all placental mammalian species so far
examined and for this reason have been desribed as "ideal general
mediator for raising temperature"
There is convincing evidence supporting a role for the E
prostaglandins in fever (1) but it is not known whether they are
also involved in normal thermoregulation (2).
Previous observations (3) have shown that both heat and cold
stress can alter the release from the PO/AH of factors affecting
body temperature.
It has already been emphasized (4) that the PO/AH is unlikely to
be the only source of PGE in cisternal cerebrospinal fluid CSF
and that intraventricular injections of exogenous pyrogen may
stimulate prostaglandin biosynthesis in several subcortical
structures adjoining the walls of the ventricles.
[Endoperoxides and free radicals]
About two prostaglandin endoperoxides PGG2 (15-hydroperoxy-PGE2)
and PGH2, intermediates in the conversion of arachidonic acid
into PGE2 and PGF(2alpha)(5):
Vascular smooth muscle (rabbit aorta strip) was strongly
stimulated (triphasic change blood pressure: transient fall ->
short-lasting rise -> sustained reduction) by the endoperoxides
(5)
Intravenous infusions of PGE1 to healthy man caused flushing and
became more intensive with increasing doses (6). This lead to an
increase in heart rate and stroke and decrease in peripheral
resistance by an simultaneously a less pronounced increase in O2
uptake. The effect of PGE1 on free fatty acid FFA metabolism
showed that in general the FFA concentration increased.
Literature:
(1) Feldberg, W and Milton A. S., The pharmacology of
Thermoregulation, ed P.Lomax pp 302-310, Karger Basel
(2) Dey, P.K., et al J. Physiol. (London) 241:629-649
(3) Myers, R.D. et al Science 161:572-573
(4) Feldberg, W., et al J Physiol. (London) 234:279-303
(5) Hamberg, M., Proc. Natl. Acad Sci USA 70:899; ibid. 71:345
(6) Carlson L.A. et al Acta Med Scand 183:423; ibid. 75:161
I hope this will do nicely,
Best regards,
Angelo Schouten (I will have a new E-mail address early next week)
Correspondence to:
PO Box 6229
2702 AE Zoetermeer
The Netherlands
-------------------------------------------------------------------------------
|