Date: Mon, 6 Apr 1998 21:00:07 -0700 (PDT)
From: Doug Skrecky
To: cran@listservice.net
Subject: folate, B6 and coronary heart disease risk
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"Folate and Vitamin B6 From Diet and Supplements in Relation to Risk of
Coronary Heart Disease Among Women"
JAMA 279(5): 359-364 February 4, 1998
Abstract:
Context: Hyperhomocysteinemia is caused by genetic and lifestyle
influences, including low intakes of folate and vitamin B6. However,
prospective data relating intake of these vitamins to risk of coronary
heart disease (CHD) are not available.
Objective: To examine intakes of folate and vitamin B6 in relation to the
incidence of nonfatal myocardial infarction (MI) and fatal CHD.
Design: Prospective cohort study
Setting and Patients: In 1980, a total of 80,082 women from the Nurse's
Health Study with no previous history of cardiovasular disease, cancer,
hypercholesterolemia, or diabetes completed a detailed food frequency
questionaire from which we derived usual intake of folate and vitamin B6.
Main Outcome Measure: Nonfatal MI and fatal CHD confirmed by World
Health Organization criteria.
Results: During 14 years of follow-up, we documented 658 incident cases
of nonfatal MI and 281 cases of fatal CHD. After controlling for
cardiovascular risk factors, including smoking and hypertension and intake
of alcohol, fiber, vitamin E, and saturated, polyunsaturated, and trans
fat, the relative risks (RRs) of CHD between extreme quintiles were 0.69
(95% confidence interval [CI], 0.55-0.87) for folate (median intake, 696
microgram/day vs 158 microgram/day) and 0.67 (95% CI, 0.53-0.85) for
vitamin B6 (median intake, 4.6 mg/d vs 1.1 mg/d). Controlling for the same
variables, the RR was 0.55 (95% CI, 0.41-0.74) among women in the highest
quintile of both folate and vitamin B6 intake compared with the opposite
extreme. Risk of CHD was reduced among women who regularly used multiple
vitamins (RR=0.76; 95% CI, 0.65-0.90), the major source of folate and
viatmin B6, and after excluding multiple vitamin users, among those with
higher dietary intakes of folate and vitamin B6. in A subgroup analysis,
compared with nondrinkers, the inverse association between a high-folate
diet and CHD was strongest among women who consumed up to 1 alcoholic
beverage per day (RR=0.69, 95% CI 0.49-0.97) or more than 1 drink per day
(RR=0.27; 95% CI, 0.13-0.58).
Conclusion: These results suggest that intake of folate and vitamin B6
above the current recommended dietary allowance may be important in the
primary prevention of CHD among women.
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Date: Wed, 8 Apr 1998 08:41:48 -0400 (EDT)
From: Ben Best
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Subject: Return from Arizona
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I have just returned from Arizona. In Tuscon, I attended a session
of the "Witch Trial" of the life-extensionist molecular biologist
Marguarite Kay. It looked like a "fishing expedition" -- the panelists
asked a variety of unrelated questions concerning her work and lab
management policies.
In Phoenix, I attended a cryonics conference. I was subjected the
usual harassment by a number of purported life-extensionists who seemed to
have a "fishing expedition" of their own to invalidate my practice of
CRAN. The assumption always seems to be that I am irrationally practicing
CRAN to a degree which is injurious to my health. The strongest criticisms
this time were that my immune system is vulnerable (on the basis of the
fact that CRAN mice are raised in sterile conditions -- and that the
claims of a strong immune response for CRAN animals as noted in Walford &
Weindruch's book are difficult to substantiate) and that CRAN has been
destructive of my mental function (on the basis of NO evidence -- I have
noticed no reduction in my mental capacities).
The other criticism is, as always, that I have sacrificed quality of
life. This might be true if I were a "live to eat" person, but eating is
far from the only pleasure in life -- and certainly not the most important
one for me. (Even survival itself is more important.) Not to say that I
don't get pleasure from eating -- since initiating CRAN my pleasure of
eating has become more acute than it ever was. As eating progresses,
however, there are diminishing returns of pleasure -- and I don't indulge
myself of those marginal values as much.
This list has been very quiet in my absense. I acknowledge that many
things that I have left unanswered from past exchanges -- hopefully I
can start to catch up on my backlog of replies in the next few days.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Wed Apr 8 18:26:36 1998
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Date: Wed, 8 Apr 1998 14:24:28 -0700 (PDT)
From: Doug Skrecky
To: cran@listservice.net
Subject: 20'th update on fly longevity experiments
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This is the 20'th update on my fly longevity experiments. I made two
mistakes with this run, one minor and one major. The minor one is that I
apparently forgot to include the non-toxic taurine larvicide in the onion
4X/chitosan 4X, and onion 4X/paprika combination bottles. The breeding
that occurred in these bottles, rendered any census impossible, and so
these bottles had to be discarded.
The major mistake was adding still boiling water (instead of boilED)
to all of the supplement bottles, without first testing to see if this
was beneficial. Fortunately I included a normal control using cool water,
in addition to a hot control using boiling water, for all of the three
breeding bottle fly sources. Thus I am able to learn from my mistake.
Using boiling water reduced fly longevity by two mechanisms. One was
purely physical. This involved the formation of tight cracks between the
fly food and the inside of the bottles. In some supplement bottles these
were narrow enough to trap and drown numerous flies in the moist fly
food. The onion 4X bottle was a great example of this, with all of its
flies being drowned by the day 34 census. Fortunately these cracks tended
to widen with time as the fly food slowly dried out, so that after the
day 34 census, few flies met their end in this way.
The other mechanism reducing longevity can be only speculated about.
After all the flies in the three hot control bottles had died, a few
still lived on in the corresponding cool water control bottles. This
appears to constitute a genuine aging acceleration phenomina. I presume
this is due to the boiling water destroying some of the vitamins in the
fly food and inducing subclinical nutrient deficiencies, which manifest
themselves late in life.
On a positive note two observations stand out in this run. First
hawthorn appears to increase life span. Secondly the factors responsible
for the longer life span associated with cinnamon or sage
supplementation, appear to be lipid soluable, since addition of the fat
binding fiber chitosan eliminates this effect.
I am trying something different for my eighth run. All flies used here
have been "pre-aged" in holding bottles containing taurine larvicide for
29 days prior to use. About 75% of the flies in these bottles had already
died before the eighth run had even been begun. I had anticipated some
mortality, and so had used 5 holding bottles. However even with the
increased number of fly sources, I found that I did not have enough flies
to commence a full sized run. I did the best I could here, with the flies
available. Since these aged flies were virtually unable to fly I upended
each holding bottle, and dumped the flies into one bottle prior to use.
The advantage here is that the flies from all five holding bottles are
homogenized so that five control bottles are not needed to account for
variations in average fly age from different bottles.
The main advantage of using pre-aged flies is that the eighth run
will be completed quick enough, that I doubt that rotting of the fly food
would be much of a factor limiting life spans. It is possible that larger
differences in longevity might manifest themselves with this change in
procedures.
I would like to thank Robert Ettinger and Andy Zawacki for donating
the acetyl-carnosine for the eighth run. I am told that this is from
Russian sources.
Seventh Run PERCENTAGE SURVIVAL ON DAY
BB# Supplement 10 17 27 34 41 46 55 64 71 74 77 83 85 88
_____________________________________________________________________
1 cntl 1 89 69 63 46 37 29 23 11 6 6 3 0 - -
1 hot cntl 1 94 90 70 62 50 28 16 2 0 - - - - -
1 creatine 97 85 68 62 41 32 15 3 0 - - - - -
1 creatine 4X 89 67 48 26 15 11 7 0 - - - - - -
1 fennel 96 91 74 57 39 30 13 4 0 - - - - -
1 fennel 4X 79 79 63 42 33 17 0 - - - - - - -
1 gaba 88 75 75 44 31 13 0 - - - - - - -
1 gaba 4X 95 90 65 40 30 20 0 - - - - - - -
1 garam masala 93 79 57 36 36 29 21 7 0 - - - - -
1 garam masala 4X 100 87 67 27 13 13 13 0 - - - - - -
1 guggulipid 90 80 35 15 5 5 0 - - - - - - -
1 guggulipid 4X 100 81 63 44 31 19 19 0 - - - - - -
1 hawthorn 95 89 68 68 58 47 26 16 5 0 - - - -
1 hawthorn 4X 100100 88 88 75 50 38 25 6 6 0 - - -
1 lemon peel 100 82 59 47 41 29 18 0 - - - - - -
1 lemon peel 4X 83 67 42 33 21 17 4 0 - - - - - -
1 l-lysine 89 67 61 33 22 17 11 6 0 - - - - -
1 l-lysine 4X 60 50 30 15 15 5 5 5 5 5 0 - - -
1 l-ornithine 64 71 64 36 21 14 14 14 7 0 - - - -
1 l-ornithine 4X 56 56 19 19 13 13 13 0 - - - - - -
2 cntl 2 94 84 77 45 32 16 10 10 6 6 0 - - -
2 hot cntl 2 69 59 48 38 34 7 3 3 3 0 - - - -
2 onion 4X 87 60 20 0 - - - - - - - - - -
2 on 4X/chitosan 4X 96 85 48 44 41 33 19 15 4 4 4 0 - -
2 on 4X/chitosan 8X (breeding! - discarded)
2 on 4X/cr picolinate 4X 84 68 24 16 8 4 0 - - - - - - -
2 on 4X/cr picolinate 8X 77 41 14 9 5 5 5 0 - - - - - -
2 on 4X/cinnamon 96 85 73 62 46 31 23 15 15 12 12 4 4 4
2 on 4X/cinnamon/chit 4X 100 38 23 8 8 11 11 0 - - - - - -
2 on 4X/paprika (breeding! - discarded)
2 on 4X/paprika/chit 4X 79 42 37 26 21 16 11 5 5 5 5 5 5 5
2 on 4X/sage 4X 95 77 59 45 41 45 23 18 14 9 9 0 - -
2 on 4X/sage 4X/chit 4X 41 29 18 12 12 6 6 0 - - - - - -
3 cntl 3 96 92 80 64 60 40 20 4 4 4 4 4 4 4
3 hot cntl 3 83 58 48 40 25 18 8 8 0 - - - - -
3 shark cartilage 95 63 43 30 18 10 8 5 3 0 - - - -
3 shark cartilage 4X 85 60 18 5 0 - - - - - - - - -
3 silymarin 83 51 20 11 6 0 - - - - - - - -
3 silymarin 4X 86 52 29 24 14 14 0 - - - - - - -
3 thiodiproprionic acid 96 78 48 39 22 17 17 9 4 0 - - - -
3 thiodiproprionic 4X 83 61 44 33 17 17 6 6 0 - - - - -
3 trimethylglycine 77 55 27 18 14 9 5 0 - - - - - -
3 trimethylglycine 4X 82 59 27 5 0 - - - - - - - - -
3 l-tyrosine 77 46 23 15 15 8 0 - - - - - - -
3 l-tyrosine 4X 65 59 47 41 24 24 24 6 0 - - - - -
Eighth Run
cntl 1
cntl 2
acetyl-carnosine: 1/32 tsp
acetyl-carnosine 4X: 1/8 tsp
aged garlic: 75 mg (Kyolic formula 100)
aged garlic: 300 mg
almond: 1/4 tsp
cardamon: 1/16 tsp
cardamon 4X: 1/4 tsp
chili: 1/16 tsp
chili 4X: 1/4 tsp
coriander: 1/16 tsp
coriander 4X: 1/4 tsp
echinacea: 31 mg augustifolia & 31 mg purpurea
echinacea 4X: 125 mg augustifolia & 125 mg purpurea
tomato: 1/16 tsp
tomato 4X: 1/4 tsp
water reduced: used 3 instead of 6 tablespoons of water,
with 20 mg Carolina Biological 4-24 fly food
Note: 1 gm taurine added to all bottles to eliminate breeding
Glass milk bottles are used to contain flies.
Entire experiment is located on a card table near a window.
Fly life spans tend to be longer in runs during the winter,
due to the lower temperatures.
Also note: (to my knowledge)
Every major university in North America has a fly lab.
None are currently doing fly longevity experiments.
>From owner-cran@ListService.net Sat Apr 11 14:46:42 1998
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Date: Sat, 11 Apr 1998 13:46:39 -0700 (PDT)
From: Doug Skrecky
To: cran@listservice.net
Subject: (fwd) Comments On Satiety Index
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From: fanman51@aol.com (FANMAN51)
Newsgroups: misc.health.diabetes
I think we all are aware of Rick Mendosa's great Diabetes web site. He
has a page on the value of various foods to satisfy hunger. As I look over his
reporting of the results of this study, a number of thoughts occure to me:
1) Potato is rated highest of all foods in ability to satisfy hunger. I don't
dispute the potato's sustaining power but wonder how this fits with the
Glycemic Index of the potato being far from favorable. ( that is, it breaks
down rather quickly.) One would think that a food that sustains well would be
one that broke down very slowly.
2) One problem I see with this Satiety index is that it considers only the
results during the first two hours after consumption of the food being studied.
So, we are supposed to believe that popcorn and eggs have nearly identicle
ability to stave off hunger. Sorry, I just can't buy this. The full value of
eggs in delaying hunger , to me, is evident only if you were to study the time
period beyond two hours. By this time the benifits of popcorn would be a dim
memory, while eggs would be carrying you comfortably towards lunch. Another
problem I have here is that there seems to be no consideration of how the eggs
might be prepared. In my own experience, scrambled eggs are much more
sustaining than fried eggs. Perhaps, because scrambled eggs, at least the way
I eat them, are cooked more throughly. Or perhaps scrambled eggs break down
slower because the yolk fat is interspersed with the protein of the "white".
We know that fat is slow to digest.
3) Apples and Grapes: These two foods have a satiety index of 197 and 162
respectivly. This puts them in the top rank of sustaining foods. Yet my own
experience is that these two foods have absolutely zero ability to sustain.
Perhaps, this is just me?
4) I see no ranking for "refried beans". Though beans in general are ranked
rather highly, my own experience has been that the fat in refried beans makes
them particularly slow to break down. When dieting and being plagued with
hunger pangs I will eat a small amount of this food every 2-3 hours. One
serving (four oz) of Taco Belle beans has 190 calories. Even if you ate
nothing but this every 2.5 hours you would consume only 1300-1500 calories per
day. And at least in my case, I am totaly free of hunger. Incidently, eating
twice the amount does not sustain for twice as long, at least in my experience.
Regarding the amount of fat you might be ingesting here, there are nine grams
of fat per serving. So seven servings in the course of a day would amount to
only 63 grms, just about what the dietician has me limited at on a 1800 calorie
diet. Incidently, I'm not recommending anyone restrict their diet so severly
as this. I only mention it as a temporary measure to control hunger that has
become extreme.
Mike
>From owner-cran@ListService.net Sat Apr 18 09:09:47 1998
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Date: Sat, 18 Apr 1998 11:09:40 -0400 (EDT)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Technical problems with the CRAN list
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The ISP (Internet Service Provider, Esosoft) supporting the CRAN list
has some peculiar policies which have recently caused me a few headaches.
They offer a limited amount of disk space on which accumulate monthly
files of postings along with topical and chronological indexes of those
postings. I have been copying the monthly files and the indexes to my
website on a monthly basis.
In early April, when I went to copy the March files, I discovered that
almost everything was gone from my ISP's disk. I then learned that the ISP
(1) does not provide means for clients to delete files and (2) wipes the
disk clean as soon as the disk space limit is reached.
I found this particularly disturbing both because I had not known about
the policies (it is reportedly described in the lengthy user's manual) and
because I thought that March had been a particularly good month for the
CRAN list with the discussions of the role of fat in diet.
I finally agreed to buy a bit more disk space and to pay my ISP to
restore all of the lost files from back-up. My ISP agreed that I could
e-mail requests to delete unnecessary files from the disk space they
provide. Even with this, their re-constructed version of the messages file
for March was missing postings after March 26th. I did my best to append a
number of messages I had saved from my own e-mail.
On Friday, I posted cran.9803 to my website collection of CRAN postings
at http://www.benbest.com/CRAN/ The indexes are there too, but they are
missing a couple of references to postings at the end of March.
Hopefully, now I can get caught-up on answering many of the loose
threads from our discussions on fats in March.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sat Apr 18 16:12:56 1998
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Date: Sat, 18 Apr 1998 18:11:42 -0400 (EDT)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Dietary fat composition and arrhythmia
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A year ago I reported that when I dropped my weight to 112 pounds I
experienced cardiac arrhythmias (bigeminal ventricular extrasystoles). My
speculation about why this occurred focused on excessive cortisol or
catecholamines. Now I am considering the possibility that my extreme
low-fat diet (less than 10% calories from fat) may have been a factor.
Two studies indicate that the relative proportion of kinds of fats can
have a marked effect on vulnerability to cardiac arrhythmias. (Sudden
ventricular fibrillations are responsible for 50% of cardiovascular deaths
in developed nations.) One study used rats [AMERICAN JOURNAL OF CLINICAL
NUTRITION 57:207-212 (1993)] and the other study used marmoset monkeys
[MOLECULAR AND CELLULAR BIOCHEMISTRY 116:19-25 (1992)].
Both studies used sheep fat (saturated), sunflower seed oil (w-6
unsaturated) and fish oil (w-3 unsaturated), but the rat study also used
olive oil (mono-unsaturated). The monkey study used 94% primate meal
supplement with 6% selected fat (by weight). The rat study used 75%
replacement of saturated fat by sunflower seed oil & olive oil, and 25%
replacement by fish oil. The animals were at least middle-aged at the
beginning of the study, and feeding was prolonged prior to attempted
induction of arrhythmia (12 weeks for rats, 24-30 months for monkeys).
The rat study induced arrythmias by ischemia (blood vessel
occlusion), whereas the monkey study used electrical stimulation.
Incidence of ventricular fibrillation is summarized:
rat monkey
--- ------
sheep fat (saturated) 42 % 45 %
olive oil (mono-unsaturated) 36 % N/A
sunflower seed oil ( w-6 ) 8 % 13 %
fish oil ( w-3 ) 0 % 0 %
Both studies observed that the diets had a marked effect on the
membrane composition of cardiac muscle. The minimal reduction arrythmia by
olive oil indicates that the effect on muscle composition rather than
blood cholesterol or free radical oxidation was the most important factor.
Monkeys on a saturated fat diet had higher heart rate & blood pressure as
well as lower end diastolic volume & left ventricular ejection fraction.
Unfortunately, these studies say nothing about the effects fo a low fat
diet. I had been attempting to lower dietary fat by any means possible --
and I paid little attention to fat composition. However, since the w-3 and
w-6 fatty acids cannot be synthesized by the body (and are therefore
essential in the diet), it is very possible that I was adversely affecting
the composition of my heart muscle -- and that this was contributory to my
arrhythmias. (Arrhythmia is the leading cause of death for anorexics --
although electrolyte deficiency is often an important factor in these
cases.)
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sun Apr 19 02:30:30 1998
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From: "Phil Harris"
To:
Subject: Re: Dietary fat composition and arrhythmia
Date: Sun, 19 Apr 1998 09:28:01 +0100
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> From: Ben Best
> A year ago I reported that when I dropped my weight to 112 pounds I
> experienced cardiac arrhythmias (bigeminal ventricular extrasystoles). My
> speculation about why this occurred focused on excessive cortisol or
> catecholamines. Now I am considering the possibility that my extreme
> low-fat diet (less than 10% calories from fat) may have been a factor.
SNIP
Ben, as low-fat-diet person for many years, I am interested. Ornish
recommends 25g fat per day (with sat fat below 6g). For a 2400 kc per day
intake this is below 10%. What was your estimated fat intake in grams? Had
to be below 15g ? 15g is supposed to be the threshold of deficiency.
Presumably deficiency gets especially important if your fat reserves get
exceptionally low.
Occasional arythmia is not usually the same as fibrillation and is quite
common and harmless in otherwise healthy people. However young fit guys can
be at risk of sudden death from fibrillation. Asian immigrant labourers in
Singapore (?) had an epidemic while living on polished rice and this was
traced to Vit B6 deficiency. Guess that might apply also to anorexics but
not you.
Normally people doing lowish to moderate aerobic activity burn fat in
preference to glycogen during this activity. Presumably mobilised fat
rather than in-situ fat. Quote "even skinny marathon runners have enough
reserves to run theoretical 3 marathons without refuelling" They say that
during athletics endurance training, by doing moderate excercise while
hungry, you can train your liver to facilitate the fat burning . Were you
running your heart on exceptionally low available fuel?
There is a whole world of investigation into heart rythyms used for
prognosis of a variety of conditions. The balance between the sympathetic
and parasympathetic system which alter rythyms, is associated with stress
control and various hormone levels, ie cortisol and DHEA.
best wishes
Phil Harris
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Date: Sun, 19 Apr 1998 13:10:38 -0400 (EDT)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: TRANS fatty acids -- conclusive proof of a health hazard?
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On Sun, 22 Mar 1998, Paul Wakfer wrote:
> Ben Best wrote:
> >
> > On Sun, 22 Mar 1998, Paul Wakfer wrote:
> >
> > > Ben Best wrote:
> > > > There is some concern about the effects when
> > > > *trans* fatty acids are incorporated into membranes where *cis* fatty
> > > > acids would normally be.
> > >
> > > There isn't just some *concern*. Trans fats have been quite conclusively
> > > been proven to be more harmful than any kind of cis fats.
> >
> > I have heard this -- which is why I mentioned it -- but I have not
> > seen substantiation. My MODERN NUTRITION text denies that the harmfulness
> > of trans fats has been established. If you know that it has been proven
> > conclusively, can you state explicitly what the demonstated harm is and
> > supply a reference to studies in reputable journal? I would like to
> > learn more about this. So far I have only seen unsubstantiated claims,
> > and when I look for evidence I haven't found any.
>
> The following is the paper that I was thinking of. There are others.
>
>
> Am J Clin Nutr 1997 Oct;66(4 Suppl):1006S-1010S
> Health effects of trans fatty acids.
> Ascherio A, Willett WC
> Department of Nutrition, Harvard School of Public Health, Boston, MA
> 02115, USA.
>
> trans Fatty acids are formed during the process of partial hydrogenation
> in which liquid vegetable oils are converted to margarine and vegetable
> shortening. Concern has existed that this process may have adverse
> consequences because natural essential fatty acids are destroyed and the
> new artificial isomers are structurally similar to saturated fats, lack
> the essential metabolic activity of the parent compounds, and inhibit
> the enzymatic desaturation of linoleic and linolenic acid. In the past 5
> y a series of metabolic studies has provided unequivocal evidence that
> trans fatty acids increase plasma concentrations of
> low-density-lipoprotein cholesterol and reduce concentrations of
> high-density-lipoprotein (HDL) cholesterol relative to the parent
> natural fat. In these same studies, trans fatty acids increased the
> plasma ratio of total to HDL cholesterol nearly twofold compared with
> saturated fats. On the basis of these metabolic effects and the known
> relation of blood lipid concentrations to risk of coronary artery
> disease, we estimate conservatively that 30,000 premature deaths/y in
> the United States are attributable to consumption of trans fatty acids.
> Epidemiologic studies, although not conclusive on their own, are
> consistent with adverse effects of this magnitude or even larger.
> Because there are no known nutritional benefits of trans fatty acids and
> clear adverse metabolic consequences exist, prudent public policy would
> dictate that their consumption be minimized and that information on the
> trans fatty acid content of foods be available to consumers.
Immediately following the review you cited is a review that challenges
the conclusions of the preceeding article [JOURNAL OF CLINICAL NUTRITION
66(suppl.):1011S-1117S (1997)]. Moreover, the authors of the study you
cited (Ascherio & Willett) have been criticized for their strong claims &
strident language [AMERICAN JOURNAL OF PUBLIC HEALTH 85(3):410-411 (1995)]
(although this debate seems to focus on a "duke-it-out" between Shapiro &
the stident duo). Controversy over this issue is likely to linger at least
until there are randomized clinical trials (none have yet been done).
A report by the FDA in 1985 (HEALTH ASPECTS OF DIETARY TRANS FATTY
ACIDS, F.R. Senti) concluded that there is no evidence of a harmful effect
in humans at the existing dietary levels. Animal studies in that report
showed no evidence of toxic effect. A more recent Expert Panel [AMERICAN
JOURNAL OF CLINICAL NUTRITION 62:655S-708S (1995)] supported this
conclusion, based on an estimate that *trans* fatty acids constitute 4-12%
of American fat intake (2-4% of calories).
The Expert Panel noted the increased popularity of tub margarines
(11-28% *trans* fat) over stick margarines (19-49% *trans* fat) since the
1960s. Vegetable shortenings have decreased from 26% to 17% and fast food
chains have decreased *trans* fat content of frying oil from 30% to 15%.
(But *trans* fat from cheese corn chips increased from 33% in 1978 to 54%
in 1988. The 3 foods which were most highly associated with an increase in
*trans* fat in human body adipose tissue were brownies, pastry and
margarine [AMERICAN JOURNAL OF CLINICAL NUTRITION 67:25-30 (1998)]. I
believe that the claim that the effects of *trans* fats on HDL or LDL
are not much different than those of saturated fat -- and the high levels
of saturated fat still consumed -- are the basis for the claim that the
effects of *trans* fats are (*relatively*) negligible. Trans fats also
reduce rancidity, which could also be a consideration.
The Expert Panel report noted that *trans* fatty acids are less
susceptible than *cis* fatty acids to free radical initiated autoxidation:
"Trans bonds have lower pi electron density than do cis double bonds,
which causes metal ions to form weaker complexes with trans fatty acids
than with cis fatty acids."
Approximately 3-8% of the fatty acids in butter, cheese, milk, beef
and mutton are *trans* fats (grass-fed cattle have higher trans-fat than
grain-fed cattle). Trans fats from animal sources, but not those from
hydrogenated oils have been linked to coronary heart disease [AMERICAN
JOURNAL OF CLINICAL NUTRITION 62:522-523 (1995)]. Another study found
that, despite the adverse effect on blood cholesterol levels, *trans*
fatty acids were no more likely to cause atherosclerosis than their *cis*
counterparts [PROSTAGLANDINS, LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
57(4&5):399-402 (1997)].
Despite all this controversy, I am inclined to avoid *trans* fatty
acids. Currently, salad oils are 8-17% trans, shortenings (cookies,
pastry, donuts) are 14-60% trans and margarines are 16-70% trans (84% of
margarine fat is hydrogenated soybean oil). I don't eat any of these
foods. Although I have now softened my stance on eliminating fat from
my diet as much as possible, I will continue to avoid saturated fat &
*trans* fat as much as possible. Even if *trans* fat is no worse than
saturated fat for LDL cholesterol, there is evidence that the effect
on reducing HDL cholesterol is worse [CANADIAN JOURNAL OF PHYSIOLOGY AND
PHARMACOLOGY 75:211-216 (1997)] (although this does not mean that
atherosclerosis or heart disease is necessarily worse).
Trans linoleates are devoid of essential fatty acid activity and they
retard rat growth more than diets deficient in essential fatty acids.
Trans, trans 18:2-w6 decreases the conversion of linoleic to
gamma-linolenic acid in rat liver microsomes [HANDBOOK OF LIPIDS IN HUMAN
NUTRITION Gene Spiller, Ed. (1996) page 92]. I am also suspicious of the
effect of *trans* fatty acids on the membranes of cardiac muscle and
neurons. It seems to me that the *trans* fatty acids could more easily
substitute for their *cis* counterparts than could saturated fatty acids
-- while lacking biological activity (my speculations).
The margarine industry obtained much of its business by virture of the
presumed health benefits of margarine over butter (although lower cost is
obviously important). Concern that hydrogenated soybean oil is creating
"medically deleterious" *trans* fatty acids has driven DuPont, Calgene and
other companies to seek manipulation of plant DNA as a means of altering
the composition of plant oil [SCIENCE 279:2019 (1998)].
So although the evidence against *trans* fatty acids is still
controversial, there are good grounds to suspect harmful effects.
Most important is the fact that *trans* fatty acids are an unnecessary
source of calories with no known health benefits.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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Date: Sun, 19 Apr 1998 16:11:16 -0400 (EDT)
From: Ben Best
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cc: Ben Best
Subject: Is Aspartame useful in the practice of CRAN?
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In 1987 the Calorie Control Council (Atlanta) reported that
approximately 40 million Americans used artificial sweeteners for
weight-control. It seems reasonable to ask if a sugar substitute might be
of value for reducing calorie consumption.
Some early studies indicated that weight gain among users of
artificial sweeteners was actually greater than among non-users [APPETITE
11(supplement):85-91 (1988)]. Claims were made that artificial sweeteners
actually stimulates appetite. But a thorough review of the many studies on
this question has debunked these claims [PHYSIOLOGY & BEHAVIOR 55:139-143
(1994)]. The fact that people with weight problems show a greater use of
artificial sweeteners should not be surprising -- and this fact does not
prove that sweeteners produce weight problems or are of no value for
restricting calorie intake. What is needed for proof is controlled studies
-- and such studies have been done with aspartame.
One study gave subjects a large bowl of pudding or jello sweetened
with sucrose or aspartame. The subjects were encouraged to eat as much of
the pudding or jello as they wished. Despite the fact that the sucrose
added at least an additional 170 calories, there was no difference in the
amount of pudding or jello consumed. And there was no statistically
significant difference in total calories eaten 2 hours later in a
self-selected meal. It didn't even matter much whether subjects were aware
or unaware (unblinded or blinded) of whether they were eating
sucrose-sweetened or aspartame-sweetened pudding or jello [APPETITE
13:115-127 (1989)]. This would seem to indicate that aspartame can reduce
calorie intake on a short-term basis. But what about long-term?
A long-term randomized controlled clinical trial was conducted with
163 obese women who lost an average of 10 kg (22 pounds, 10% of body
weight) during a 19-week weight-loss program. The women were randomly
divided into aspartame and non-aspartame groups. The women were users or
non-users of aspartame both during and after the weight-loss program.
Three years after the weight-loss period, the non-aspartame group had
gained an average of 9.4 kg (20.7 pounds), whereas the aspartame group had
gained an average of 4.6 kg (10.1 pounds). [AMERICAN JOURNAL OF CLINICAL
NUTRITION 65:409-418 (1997)]. This result would seem to indicate that
aspartame could be of benefit for the practice of CRAN.
An article in the JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
[55(11):1115-1123 (1996)] raised claims that aspartame causes brain
cancer. Circumstantial evidence given referred to a correlation between
the introduction of aspartame into the US market and increased brain
cancer in the American population. Rat studies reputedly indicated
increased brain tumors with aspartame -- and claims were made that
nitrosylation of aspartame in the gut results in a potent mutagen.
All of these claims were countered by a study/review in the JOURNAL OF
THE NATIONAL CANCER INSTITUTE [89(14):1072-1074 (1997)]. Analysis of
cancer patients showed no relationship between aspartame consumption and
cancer -- "no suggestion of a dose-response relation based on age at first
consumption, number of years of consumption, or frequency of consumption."
There had been questions concerning the interpretation of a number of rat
experiments, but the FDA finally decided that the evidence did not support
an association between aspartame and cancer. Mouse studies had been
uniformly negative, and a subsequent rat study also found no association.
Analysis of kinetics indicated that nitrosation of aspartame is primarily
of the terminal amino group, rather than of the amide (which would be
mutagenic). The mutagenic activity of aspartame after nitration was shown
to be very weak "at concentrations considerably higher than normal human
intake levels".
These results are re-assuring, but for a person who wants/expects to
live a very long time, even a very weak mutagenic effect is a matter of
concern. Nonetheless, my use of aspartame is limited to Designer Protein,
Herbal Mix, Metamucil and non-fat yogurt. I don't drink coffee or soda pop
and the only other "sweets" in my diet are fruits & vegetables.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sun Apr 19 15:17:04 1998
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Date: Sun, 19 Apr 1998 17:14:28 -0400
From: Paul Wakfer
Organization: The Institute for Neural Cryobiology
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Ben Best wrote:
> A long-term randomized controlled clinical trial was conducted with
> 163 obese women who lost an average of 10 kg (22 pounds, 10% of body
> weight) during a 19-week weight-loss program. The women were randomly
> divided into aspartame and non-aspartame groups. The women were users or
> non-users of aspartame both during and after the weight-loss program.
> Three years after the weight-loss period, the non-aspartame group had
> gained an average of 9.4 kg (20.7 pounds), whereas the aspartame group had
> gained an average of 4.6 kg (10.1 pounds). [AMERICAN JOURNAL OF CLINICAL
> NUTRITION 65:409-418 (1997)]. This result would seem to indicate that
> aspartame could be of benefit for the practice of CRAN.
Ben, I don't see that your conclusion follows. The eating psychology and
possibly even the physiological of CRAN practitioners is vastly
different (at least, near the low weight goal) than obese dieters.
> my use of aspartame is limited to Designer Protein,
> Herbal Mix, Metamucil and non-fat yogurt.
Neither the Designer Protein, Herbal Mix nor any other products now
available for the Life Extension Foundation (where I understand yours
are from) contain aspartame. I think they are in essential agreement
with your conclusions about aspartame. If they need to use a sweetener
for palatability they now use stevia.
-- Paul --
PS. For anyone interested the URL below is now open for perusal.
wakfer@gte.net Voice/Fax: 416-968-6291 Page: 800-805-2870
The Institute for Neural Cryobiology - http://neurocryo.org
Perfected cryopreservation of Central Nervous System tissue
for neuroscience research and medical repair of brain diseases
>From owner-cran@ListService.net Tue Apr 21 12:46:03 1998
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Date: Tue, 21 Apr 1998 14:46:00 -0400 (EDT)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Dietary fat composition and arrhythmia
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On Sun, 19 Apr 1998, Phil Harris wrote:
> > From: Ben Best
>
> > A year ago I reported that when I dropped my weight to 112 pounds I
> > experienced cardiac arrhythmias (bigeminal ventricular extrasystoles). My
> > speculation about why this occurred focused on excessive cortisol or
> > catecholamines. Now I am considering the possibility that my extreme
> > low-fat diet (less than 10% calories from fat) may have been a factor.
> SNIP
>
> Ben, as low-fat-diet person for many years, I am interested. Ornish
> recommends 25g fat per day (with sat fat below 6g). For a 2400 kc per day
> intake this is below 10%. What was your estimated fat intake in grams? Had
> to be below 15g ? 15g is supposed to be the threshold of deficiency.
> Presumably deficiency gets especially important if your fat reserves get
> exceptionally low.
I have gone for months weighing my food, but I have only occasionally
done monthly statistics. My calculations for October 1996 showed my
average daily fat intake to be 14.3 grams on an average 1428 calories per
day.
There is no generalized fat-deficiency, as such. The body can
synthesize as much fat as it needs, except it cannot synthesize the
w-3 and w-6 fats -- so these are essential in the diet. The major point I
was making in my posting is that deficiency of essential fatty acids in
the diet can be hazardous by reducing the w-3 & w-6 content of membranes
-- membranes of heart muscle in the examples I gave. Since I was trying to
minimize ALL fat indescriminately, I was also minimizing the essential
fatty acids. Therefore, if my body wasn't getting enough fat to repair or
make new membranes, it would manufacture saturated or monosaturated fats
and these would predominate in the membrane composition (to the detriment
of heart function).
> Occasional arythmia is not usually the same as fibrillation and is quite
> common and harmless in otherwise healthy people.
Extrasystole's are common -- actually athletes in peak condition have a
higher incidence of them at peak training than when they are training. But
they are not always harmless -- they CAN be a warning sign. Regular
bigeminal extrasystole's like I was having are more serious than an
occasional irregular beat.
> Normally people doing lowish to moderate aerobic activity burn fat in
> preference to glycogen during this activity. Presumably mobilised fat
> rather than in-situ fat. Quote "even skinny marathon runners have enough
> reserves to run theoretical 3 marathons without refuelling" They say that
> during athletics endurance training, by doing moderate excercise while
> hungry, you can train your liver to facilitate the fat burning . Were you
> running your heart on exceptionally low available fuel?
Fatty acids for exercise "fuel" can be saturated (and are probably
best to be saturated to reduce free-radical activity) -- and can be
manufactured by the body. Exercise begins with muscles using liver &
muscle glycogen for "fuel" -- but after half-an-hour of moderate aerobic
exercise the body will be using mostly fat as "fuel". I understand that
the liver typically has enough glycogen for 2 days of exertion (I'm not
sure at what level), but I doubt that it would be enough for 3 marathons.
I am talking off of the top of my head, and can look this up if anyone is
interested.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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From: "Phil Harris"
To:
Subject: Re: Dietary fat composition and arrhythmia
Date: Tue, 21 Apr 1998 23:46:55 +0100
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Ben
I found your info on different kinds of arythmias interesting. I
checked up the Ornish book; he is an MD and he was trying to get it right.
He actually talks about 14g fat per day as the minimum safe limit for the
average person but recommends a range of 15-35g per day. Following your
thought, I presume that 14g allows for a variety of distributions of the
essential fatty acids in different fat intakes. I feel the need for more
info than I have. My guess is that if there was any effect from your low
fat intake, your low weight (or maybe your still dropping weight) and low
fat reserves also were contributory. It is hard to imagine you creating
much fat from your 1400Kcal per day even for essentials. We are talking
competitive resource distribution?
I put in that bit about common and harmless arythmias (also from Ornish)
because people might be uneccessarily alarmed. Yours was an unusual case
by the sound of it. I take your point though that it could be worth
checking.
Like you, I would like to get a better handle on this sports medicine
stuff. They seem very sure of it. The story seems to be you do not use much
glycogen as a first resource and that steady aerobic activity draws mostly
on fat. In trained athletes, fat is reported as the main source of energy
upto 70% of maximum activity rates. You certainly do not run marathons on
glycogen, which is a relatively small store. But I need to know more.
best wishes
Phil Harris
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Date: Wed, 22 Apr 1998 18:44:21 -0400 (EDT)
From: Ben Best
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Subject: Re: Dietary fat composition and arrhythmia
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On Tue, 21 Apr 1998, Phil Harris wrote:
> I found your info on different kinds of arythmias interesting. I
> checked up the Ornish book; he is an MD and he was trying to get it right.
> He actually talks about 14g fat per day as the minimum safe limit for the
> average person but recommends a range of 15-35g per day. Following your
> thought, I presume that 14g allows for a variety of distributions of the
> essential fatty acids in different fat intakes.
Phil,
I think by attention to the kinds of fat taht are eaten, a very low
level of fat can be consumed. Fats are more likely to contain pesticides
and other organic toxins, so it is safer to get calories from
carbohydrates or proteins -- as long as there are enough essential fats
and not so much protein as to damage the kidney. My new strategy is to
minimize *saturated* and *trans* fats as much as possible.
> My guess is that if there was any effect from your low
> fat intake, your low weight (or maybe your still dropping weight) and low
> fat reserves also were contributory. It is hard to imagine you creating
> much fat from your 1400Kcal per day even for essentials. We are talking
> competitive resource distribution?
I'm not completely clear what you are saying here. I am not now on as
rigorous a regimen as I was last year. But if fat is needed for energy,
and calories are adequate, fat can be manufactured. A skinny person (and
a short person) needs fewer calories -- so don't get too hung-up on the
numbers.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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From: Ben Best
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On Sun, 19 Apr 1998, Paul Wakfer wrote:
>
> Ben Best wrote:
>
> > A long-term randomized controlled clinical trial was conducted with
> > 163 obese women who lost an average of 10 kg (22 pounds, 10% of body
> > weight) during a 19-week weight-loss program. The women were randomly
> > divided into aspartame and non-aspartame groups. The women were users or
> > non-users of aspartame both during and after the weight-loss program.
> > Three years after the weight-loss period, the non-aspartame group had
> > gained an average of 9.4 kg (20.7 pounds), whereas the aspartame group had
> > gained an average of 4.6 kg (10.1 pounds). [AMERICAN JOURNAL OF CLINICAL
> > NUTRITION 65:409-418 (1997)]. This result would seem to indicate that
> > aspartame could be of benefit for the practice of CRAN.
>
> Ben, I don't see that your conclusion follows. The eating psychology and
> possibly even the physiological of CRAN practitioners is vastly
> different (at least, near the low weight goal) than obese dieters.
Paul, I presented the results of two experiments. One was a short-term
study using an equal number of male & female between the ages of 18-35 who
"were within the normal range of weight for height. This experiment
indicated that eating satisfaction can be achieved with a reduced amount
of calories when aspartame is used rather than sucrose for sweetening. The
second experiment involved obese women users and non-users of aspartame
over a 3 year period following a weight-loss program. This experiment also
indicated that aspartame could reduce calorie consumption when substituted
for sugar.
I acknowledge that it is an extrapolation to say that this constitutes
evidence that CRAN practitioners could substitute aspartame for sugar and
reduce calorie intake with equivalent eating satisfaction (or
dissatisfaction) over a long-term period. But the extrapolation seems
reasonable to me. Even though I don't know why aspartame works, I don't
know why it would work for normals & the obese, but not for CRAN
practitioners. You gave me no clue to your thinking. What feature of
CRAN would make this phenomenon unlikely to apply?
You only cited the long-term obese study and not the short-term normal
study. Reading over what I wrote, I can see that I did not mention that
the subjects were of normal weight. You might have assumed that those
subjects were obese also. Sorry for omitting that factor.
I'm a little bit surprised by your response however, because it seems
to me that you have had arguments with one or more CRAN practitioners who
claim that supplements cannot possibly be of additional benefit to CRAN.
You, by contrast, seem to support the view that supplements can be of
benefit to anyone. Is this a double-standard? What are the relevant
physiological parameters?
> > my use of aspartame is limited to Designer Protein,
> > Herbal Mix, Metamucil and non-fat yogurt.
>
> Neither the Designer Protein, Herbal Mix nor any other products now
> available for the Life Extension Foundation (where I understand yours
> are from) contain aspartame. I think they are in essential agreement
> with your conclusions about aspartame. If they need to use a sweetener
> for palatability they now use stevia.
Actually, Designer Protein is sold by LEF, but it is not manufactured
by them and it does not contain stevia. I had forgotten, however, that
the "Natural Flavor" Designer Protein that I take has no sweetener
whatsoever. You are right about Herbal Mix -- LEF switched from aspartame
to stevia.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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Date: Thu, 23 Apr 1998 02:48:17 -0400 (EDT)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Fat versus carbohydrate for energy
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On Sun, 19 Apr 1998, Phil Harris wrote:
> Normally people doing lowish to moderate aerobic activity burn fat in
> preference to glycogen during this activity. Presumably mobilised fat
> rather than in-situ fat. Quote "even skinny marathon runners have enough
> reserves to run theoretical 3 marathons without refuelling" They say that
> during athletics endurance training, by doing moderate excercise while
> hungry, you can train your liver to facilitate the fat burning . Were you
> running your heart on exceptionally low available fuel?
My copy of MODERN NUTRITION IN HEALTH AND DISEASE (M.Shils, et.al.,
1994, page 673) states:
"Theoretically, fat is capable of sustaining light work for long
periods without supplementation. In contrast, the body's glycogen store
would be exhausted within half a day if used exclusively. In practice,
light occupational work relies mainly on fat use delaying considerably the
exhaustion of carbohydrate stores. At exceptionally high work loads, the
capacity to oxidize fats is insufficient to meet the energy needs. At
these work rates, carbohydrate therefore plays the central role in energy
provision...
"Omitting carbohydrate from the diet for more than 1 day will result
in increased ketone-body production, degredation of body protein, and loss
of cations and water. These effects are counteracted by a minimum intake
of about 100 g of carbohydrate (600 mmole glucose units) per day."
100 grams of carbohydrate is only about 400 calories, not very much.
This statement was not qualified in reference to the weight of the
individual, so presumably it would apply to someone weighing 250 pounds.
In that case, someone weighing 120 or less (I was under 120 during
October 1996, I believe) would probably require much less -- because the
energy demands are much less. I believe this is an important reason why
CRAN works -- less glucose is required, therefore lower blood glucose
results in less glycation (protein cross-linking). My "fuel" was adequate
for my reduced needs.
An interesting excerpt from REVIEW OF MEDICAL PHYSIOLOGY by William F.
Ganong (1993):
"In a 70-kg man, carbohydrate reserves total about 2500 kcal,
stored in 400 g of muscle glycogen, 100 g of liver glycogen, and 20 g of
glucose in extracellular fluid. In contrast, 112,000 kcal (about 80% of
body fuel supplies) are stored in fat and the remainder in protein.
Resting muscle utilizes fatty acids for its metabolism, and so does muscle
after exercise. In the fasting human at rest, the brain accounts for
70-80% of the glucose utilized, and red blood cells account for most of
the rest."
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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Date: Thu, 23 Apr 1998 03:03:53 -0400
From: Paul Wakfer
Organization: The Institute for Neural Cryobiology
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Subject: Re: Is Aspartame useful in the practice of CRAN?
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Ben Best wrote:
> You only cited the long-term obese study and not the short-term normal
> study. Reading over what I wrote, I can see that I did not mention that
> the subjects were of normal weight. You might have assumed that those
> subjects were obese also. Sorry for omitting that factor.
Yes, this was a logical assumption and a major part of the reason why I
replied as I did.
> I'm a little bit surprised by your response however, because it seems
> to me that you have had arguments with one or more CRAN practitioners who
> claim that supplements cannot possibly be of additional benefit to CRAN.
> You, by contrast, seem to support the view that supplements can be of
> benefit to anyone. Is this a double-standard? What are the relevant
> physiological parameters?
This does not follow at all. The two things are not the same at all. In
fact, I don't classify Aspartame in the same category as vitamin/mineral
supplements since it has no *nutritional* value whatever. It is not even
"empty calories". Maybe it is simply "empty non-calories", but as a
general rule I think that it is unwise to consume anything that does not
have some *nutritive purpose*.
IMO, advocating or taking Aspartame for weight/calorie reduction is
similar to advocating or taking chitosan. If you simply cannot get
weight/calorie reduction without using such things then perhaps they are
beneficial, but one should always first do ones very best to do without
these non-nutritive and potentially harmful things.
By psychologically contrary to CRAN thinking, I mean that CRAN thinking
should be the most intense application of quality food, nutrient dense
eating, for health promoting purposes and there is simply no room or
place for extraneous non-nutritive chemicals if we can possibly avoid
them.
Hell, smoking will also suppress appetite and cause satiation with fewer
calories, but surely we are not going to advocate *that* as a CRAN
"crutch" for those without the will-power to eat less or to switch to a
diet with sufficient bulk that CRAN is relatively painless.
> Actually, Designer Protein is sold by LEF, but it is not manufactured
> by them and it does not contain stevia.
They now have their own Whey Protein Powder (peach flavored) which is
essentially equivalent to the Designer Protein and which *does* contain
stevia. That is what I was referring to. I expect the Designer Protein
will soon be phased out in favor of this new product made by LEF.
-- Paul --
wakfer@gte.net Voice/Fax: 416-968-6291 Page: 800-805-2870
The Institute for Neural Cryobiology - http://neurocryo.org
Perfected cryopreservation of Central Nervous System tissue
for neuroscience research and medical repair of brain diseases
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From: "Phil Harris"
To:
Subject: Re: Fat versus carbohydrate for energy
Date: Thu, 23 Apr 1998 14:43:52 +0100
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Ben, thanks for your trusty reference store. Your useful clips (below) seem
to bear out what the Sports medicine people are saying. They train so that
they can get energy preferentially from fat store up to 70% of their
maximum
exertion rate. Run the whole marathon on fat I presume.
My point was to try to look at the need for fat as a continuing essential
component in cells, membranes, as a substrate for essential chemistry etc..
as well as part of a dynamic system of fuel use and fuel storage. We
convert and tuck carbohydrate away as fat. Presumably the partition between
use versus storage (conversion in and out of labile storage) goes on the
whole time. How that is modulated is well beyond my knowledge. How the
body can adapt to 'training' is similarly obscure to me. I think your guess
that total fat intake can be very low if essential fatty acids are
available is probably correct. I was trying to say, however, that where
your body was in extreme demand for fuel over long periods ('trained' if
you
like), with consequent very low fat reserves, you were not going to have
much fatty acid of any kind floating about. Essential needs have to compete
perhaps with demands for fuel. That is what I meant by competitive resource
partitioning. You are going to get very efficient for sure, but your
automatic modulation might get into some Hobson's choices. (Not as bad as
the Hobson's choices for a body that is constantly oversupplied with
everything, as in modern SAD).
.
Agree your arrhythmia of over a year ago is intriguing point to hang some
discussions on.
best wishes
Phil Harris
----------
Ben Best WROTE
>
> My copy of MODERN NUTRITION IN HEALTH AND DISEASE (M.Shils, et.al.,
> 1994, page 673) states:
>
> "Theoretically, fat is capable of sustaining light work for long
> periods without supplementation. In contrast, the body's glycogen store
> would be exhausted within half a day if used exclusively. In practice,
> light occupational work relies mainly on fat use delaying considerably
the
> exhaustion of carbohydrate stores. At exceptionally high work loads, the
> capacity to oxidize fats is insufficient to meet the energy needs. At
> these work rates, carbohydrate therefore plays the central role in energy
> provision...SNIP
> An interesting excerpt from REVIEW OF MEDICAL PHYSIOLOGY by William
F.
> Ganong (1993):
>
> "In a 70-kg man, carbohydrate reserves total about 2500 kcal,
> stored in 400 g of muscle glycogen, 100 g of liver glycogen, and 20 g of
> glucose in extracellular fluid. In contrast, 112,000 kcal (about 80% of
> body fuel supplies) are stored in fat and the remainder in protein.
> Resting muscle utilizes fatty acids for its metabolism, and so does
muscle
> after exercise. In the fasting human at rest, the brain accounts for
> 70-80% of the glucose utilized, and red blood cells account for most of
> the rest."
>From owner-cran@ListService.net Thu Apr 23 11:38:01 1998
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Date: Thu, 23 Apr 1998 13:37:12 -0400 (EDT)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Is Aspartame useful in the practice of CRAN?
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On Thu, 23 Apr 1998, Paul Wakfer wrote:
> > I'm a little bit surprised by your response however, because it seems
> > to me that you have had arguments with one or more CRAN practitioners who
> > claim that supplements cannot possibly be of additional benefit to CRAN.
> > You, by contrast, seem to support the view that supplements can be of
> > benefit to anyone. Is this a double-standard? What are the relevant
> > physiological parameters?
>
> This does not follow at all. The two things are not the same at all. In
> fact, I don't classify Aspartame in the same category as vitamin/mineral
> supplements since it has no *nutritional* value whatever. It is not even
> "empty calories". Maybe it is simply "empty non-calories", but as a
> general rule I think that it is unwise to consume anything that does not
> have some *nutritive purpose*.
> IMO, advocating or taking Aspartame for weight/calorie reduction is
> similar to advocating or taking chitosan. If you simply cannot get
> weight/calorie reduction without using such things then perhaps they are
> beneficial, but one should always first do ones very best to do without
> these non-nutritive and potentially harmful things.
>
> By psychologically contrary to CRAN thinking, I mean that CRAN thinking
> should be the most intense application of quality food, nutrient dense
> eating, for health promoting purposes and there is simply no room or
> place for extraneous non-nutritive chemicals if we can possibly avoid
> them.
>
> Hell, smoking will also suppress appetite and cause satiation with fewer
> calories, but surely we are not going to advocate *that* as a CRAN
> "crutch" for those without the will-power to eat less or to switch to a
> diet with sufficient bulk that CRAN is relatively painless.
The analogy between smoking & aspartame pushing things a bit. The
evidence that aspartame is harmful is debatable (there is more about this
on my website essay on the subject). Aspartame is the methyl ester of the
two amino acids aspartic acid and phenylalanine. Some methanol can result
from the breakdown, but methanol is normally present in the body anyway,
and the breakdown products are well within normal physiological levels.
Conceivably there is some harm from aspartame, but there may also be
some benefit. If the level of harm is in the 0.000xxx range and the level
of benefit is in the 0.xxx range, then the benefit justifies the harm.
Very few things in life are totally free from any harm. Try reading Bruce
Ames concerning the toxins in fruits & vegetables and you might end-up
thinking of going on a diet of chemically synthesized macronutrients &
micronutrients. But Bruce Ames generally end by saying that we should eat
fruits & vegetables because the benefits exceed the harms.
I think the thrust of your objection is that you don't like the idea of
a benefit that reduces the effort of will power -- and by that standard a
harm of 0.000xxx or even 0.00000000000000xxx is too much. However, if I
have willpower to reduce my calorie intake by 1,000 calories per day, and
I can used aspartame to reduce my calories by 300 calories per day without
willpower, then I may be able to reduce my calories by 1300 calories per
day with both willpower and aspartame. This could conceivably result in a
net extension of my life which greatly in excess of a 0.000000xxx toxic
effect.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Thu Apr 23 13:33:55 1998
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Date: Thu, 23 Apr 1998 14:55:28 -0400
From: Paul Wakfer
Organization: The Institute for Neural Cryobiology
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Ben Best wrote:
> The analogy between smoking & aspartame pushing things a bit.
I agree that this is a stretched because of the harm that smoking has
been proven to cause. Perhaps, an analogy with using cocaine or heroin
would be better. In any case, the difference is only one of degree. One
could well argue also that smoking is beneficial since for those who
smoke it increases daily quality of life.
> I think the thrust of your objection is that you don't like the idea of
> a benefit that reduces the effort of will power
No. My objection is the "principle" of avoiding the introduction into my
body of chemicals which contribute nothing directly to my biochemical
defenses, repair mechanisms, and energy production, especially when the
harmlessness of such a chemical is not very well proven.
If people *must* use it to obtain CRAN benefits, then I can accept that.
However, one should do everything one can first, to avoid that course of
action. IMO, its of the same order as using potentially harmful
cholesterol lowering drugs instead of lowering cholesterol by proven
dietary methods.
Therefore, IMO, use of aspartame is not in the same category of CRAN
achieving methods/advice as, say, eating more fiberous raw foods.
-- Paul --
wakfer@gte.net Voice/Fax: 416-968-6291 Page: 800-805-2870
The Institute for Neural Cryobiology - http://neurocryo.org
Perfected cryopreservation of Central Nervous System tissue
for neuroscience research and medical repair of brain diseases
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From: Doug Skrecky
To: cran@listservice.net
Subject: interesting bit on salt & calories from longevity digest
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Date: Thu, 23 Apr 1998 09:23:50 -0700
From: Longevity-Digest/Brian Rowley
Subject: CNN - Study finds low salt diets unhealthy - March 13, 1998
****from kaufmnsl@sprynet.com***
Okay, here's a fly in the low-salt ointment.... (Do visit their web site,
this is publicity, not a copyright violation.)
Richard Kaufman
Subject: CNN - Study finds low salt diets unhealthy - March 13, 1998
http://cnn.com/HEALTH/9803/13/salt.reut/index.html
> [CNN logo] [Health banner] [CNNenEspanol.com]
> [Navigation]
> COMMUNITY [rule]
> Message
> Boards Study finds low salt diets unhealthy
> Chat
> Feedback March 13, 1998 [salt shaker]
> Web posted at: 3:58 a.m. EST (0858
> SITE GMT)
> SOURCES
> Contents LONDON (Reuters) -- Low salt diets could be
> Help! hazardous to your health, U.S. doctors warned on
> Search
> Friday.
> CNN
> Networks Contrary to the common belief that eating too much
> salt can lead to heart attacks and strokes,
> SPECIALS lowering your sodium intake may actually be
> Quick harmful, doctors at the Albert Einstein College of
> News Medicine in New York said.
> Almanac
> Video "Cancel current recommendations to reduce salt
> Vault intake, and wait for more data," epidemiology and
> News Quiz social medicine professor Michael Alderman said in
> a statement.
>
> [Infoseek/Big YelloStudy finds mortality inversely related to salt
> intake
>
> [Pathfinder/Warner In a study published in the Lancet medical
> journal, Alderman and his team analysed the diets
> of 11,000 people who took part in the first
> [Barnes and Noble] National Health and Nutrition Examination Survey
> that started in 1971 in the United States.
>
> "Our survey provides no support for
> [Parent Time link] recommendations to lower sodium as a goal of
> dietary policy," Alderman said.
>
> [BHN logo] "Those recommendations are based on data
> indicating that less salt means lower blood
> pressure, which is true for some but not all
> people. Moreover, there are lots of ways to lower
> blood pressure, and not all are good for you;
> indeed, our study suggests that lowering sodium
> may actually be harmful."
>
> Ironically, Alderman and his team found that
> mortality was inversely related to salt intake.
> The more salt people reported eating, the less
> likely they were to die from cardiovascular or
> other diseases.
>
> Study casts doubts on earlier studies
>
> When the team looked at salt intake in relation to
> total calories the results were even more
> interesting. At each level of salt intake people
> who consumed fewer calories were more likely to
> die than those who consumed more calories.
>
> Heart disease is the leading cause of death in
> most developed countries and high blood pressure
> is a major risk factor. Specialists, convinced
> that high salt intake increased blood pressure,
> had advised people to cut down on it.
>
> An earlier study, also published in the Lancet,
> linked a high salt diet to osteoporosis, stomach
> cancer, asthma and fluid retention.
>
> But Alderman is not alone in his beliefs.
>
> Canadian hypertension expert Alexander Logan
> reached similar conclusions in research published
> in The Journal of the American Medical Association
> nearly two years ago. He concluded that the
> harmful effects of restricting salt intake were
> not fully appreciated, and doctors should not
> assume a low-salt diet was harmless.
>
> Alderman said the relationship between salt intake
> and other dietary components may be so complex
> that across-the-board guidelines may never be
> possible.
>
> Copyright 1998 Reuters Limited. All rights
> reserved.
-Richard Kaufmans
------------------------------
End of LONGEVITY-DIGEST Digest - 22 Apr 1998 to 23 Apr 1998
***********************************************************
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Date: Sat, 25 Apr 1998 21:00:13 -0400 (EDT)
From: Ben Best
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It is now currently believed that early studies showing extended
lifespan due to protein restriction were, in fact, demonstrating effects
of calorie-restriction. However, concern remains about demonstrable kidney
damage due to high levels of dietary protein -- and about death rates due
to kidney problems in animals with reduced rates of cardiovascular &
cancer deaths. For these reasons, an CRAN diet could be improved-upon
by the use of high quality (complete) protein in moderate amounts.
A regular diet of *complete* protein (ie, containing all essential
amino acids in good proportions) is necessary because surplus amino acids
are not stored in the body. Adequate Nutrition for protein can be achieved
with lesser amounts of high quality protein than with greater amounts of
low quality protein (quality being a function of completeness and
essential amino acid proportions).
Egg white (albumin) is often given as a standard for high-quality
protein. Whey protein, however, is not only more complete than egg
albumin, it may offer additional benefits. It is high in branch-chained
amino acids, which means it is good for preventing muscle-wasting during
weight-loss programs.
Whey protein (also known as "lactalbumin") constitutes 18% of cow milk
and 67% of human milk protein (which are 82% & 33% casein, respectively).
Cow and human lactalbumin (whey) can be broken-down into constituents as
follows:
COW HUMAN
beta-lactoglobulin 57 % small
alpha-lactalbumin 21 % 42 %
immunoglobulin G 11 % 1 %
serum albumin 7 % 9 %
immunoglobulin A 2 % 15 %
lactoferin small 30 %
[CLINICAL AND INVESTIGATIVE MEDICINE 14:296-309 (1991)]
Lactoferrin is an iron-binding protein which has been shown to reduce
uptake of LDL cholesterol by macrophages -- and hence reduce the foam-cell
formation of atherosclerosis. [BIOCHEMICA ET BIOPHYSICA ACTA 1213:82-90
(1994)]. Rats fed high levels of whey protein showed reduced plasma VLDL
cholesterol & liver cholesterol in contrast to diets of casein & soya-bean
protein. Lower levels of whey only reduced liver cholesterol. The effect
of whey protein was explained by reduced whey-protein binding of bile
acids. Interestingly (to a person attempting CRAN), the whey-fed rates
ate less than the casein-fed rats. [BRITISH JOURNAL OF NUTRITION
70:139-146 (1993)]
A 6-month study on mature mice showed a 30% increase in mean survival
time of whey-fed mice, in contrast to those fed "nutritionally-equivalent
Purina mouse chow" [CLINICAL AND INVESTIGATIVE MEDICINE 12:343-349
(1989)]. Full-lifespan studies on Syrian hamsters showed a dramatic
increase in lifespan with animals on varying levels of lactalbumin, in
contrast to a commercial diet:
% Lifespan Increase
males females
10 % lactalbumin (whey) 43 54
20 % lactalbumin (whey) 52 46
40 % lactalbumin (whey) 39 62
[JOURNAL OF NUTRITION 112:2151-2160 (1982)]
Although protein-calorie restriction experiments extended the life of
animals kept in highly sterile conditions, resistance to infection was
depressed in these animals. The humoral immune response of a 20-gram
(protein)/100-gram (dietary total) whey-protein diet was demonstrated to
be significantly higher than that of a 20-gram/100-gram portion of protein
from either of casein, soy, wheat, corn, egg-white, fish, beef, Spirulina
maxima, Scenedesmus algae or Purina mouse chow [noted in CLINICAL AND
INVESTIGATIVE MEDICINE 11(3):213-217 (1988)]. The clonal expansion &
antibody production required for the humoral immune response demands
availability of amino acids for protein synthesis.
Whey protein contains 8 times more of the amino-acid cysteine than
casein. Cysteine administered directly into cells increases the synthesis
of the tripeptide glutathione -- which, in turn, enhances lymphocyte DNA
synthesis. But the humoral response of mice fed a whey protin diet was
found to be 5 times greater than for a diet of either pure casein or
casein enriched with cysteine [CELLULAR IMMUNOLOGY 97:155-163 (1986) and
CLINICAL AND INVESTIGATIVE MEDICINE 11(4):271-278 (1988)].
Glutathione (GSH) is a tripeptide composed of the amino acids
cysteine, glycine and glutamic acid (gamma-glutamyl-cysteinyl-glycine).
Cysteine is toxic outside of cells, and is not readily transported into
cells. Inside cells, cysteine alone does not increase synthesis of
glutathione as much as the dipeptide glutamyl-cysteine. Dietary
glutamyl-cysteine is also believed to increase cellular cysteine much more
than dietary cysteine. The whey proteins beta-lactoglobulin, serum albumin
and lactoferrin are especially rich in glutamyl-cysteine. Liver
glutathione concentrations have been shown to be more than twice as high
in whey & casein-fed rats than in soyabean-protein fed rats. [JOURNAL OF
NUTRITION 125:809-816 (1995)].
Reduced glutathione is often written as GSH to indicate the importance
of the thiol (-SH, sulfhydryl) group. GSH accounts for 90% of total
non-protein sulfhydryl in cells. GSH represents one of the most powerful
celluar defenses against DNA damage from hydroxyl radicals (HO*) by the
transformation:
GSH + HO* --> GS* + H2O
The thiyl radical (RS*) is not reactive enough to damage DNA.
Glutathione can even react with DNA peroxyl radicals (DNA*) before
they lead to DNA damage:
GSH + DNA* --> GS* + DNA
[PHARMACOLOGY & THERAPEUTICS 39:101-108 (1988)]
Glutathione concentration in liver, kidney, heart and brain are 30%,
34%, 20% and 30% lower (respectively) in elderly mice than in mature mice
[CLINICAL AND INVESTIGATIVE MEDICINE 14(4):296-309 (1991)]. Glutathione
concentrations in the eye are normally very high, and the lens even
possesses a transport mechanism to facilitate GSH uptake. Decreasing
glutathione levels in the lens due to aging is associated with cataract
formation [CURRENT EYE RESEARCH 3(1):83-87 (1984)]. In an experiment on
the induction of colon cancers in mice, all animals fed whey protein were
still alive at the end of the experiment, in contrast to only 66% still
living of those who had been fed casein or Purina diet [TUMOR BIOLOGY
11:129-136 (1990)].
I begin every morning with a large glass of 100-grams broccoli,
100-grams strawberries, a 22-gram scoop of Natural Flavor Designer Protein
(a whey-protein product), a teaspoon of Herbal Mix, and a 1-mg drop of
Deprenyl -- all mixed in my Vita-Mix blender. This gives me about half of
my daily requirement of protein, plus lots of phytochemicals -- without a
lot of carbohydrates. I am very sensitive to the soporific
(sleep-inducing) effect of carbohydrates, and I have learned to avoid
eating much carbohydrate any time before evening. My other major protein
source is skim milk cheese, which is also currently my prime trigger for
overeating. I have considered trying to drop cheese from my diet, but I
worry about the loss of calcium and the increased dependency on Designer
Protein.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sun Apr 26 13:59:43 1998
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Date: Sun, 26 Apr 1998 01:43:06 -0700 (PDT)
From: Doug Skrecky
To: cran@listservice.net
Subject: potassium protects humans from fatal strokes
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Authors
Khaw KT. Barrett-Connor E.
Title
Dietary potassium and stroke-associated
mortality. A 12-year prospective population study.
Source
New England Journal of Medicine. 316(5):235-40, 1987 Jan 29.
Abstract
Hypertension is the most important known risk factor for stroke. Clinical,
experimental, and epidemiologic evidence suggests that a high dietary intake
of potassium is associated with lower blood pressure. In
hypertensive rats, a high intake of
potassium is reported to protect against stroke, even though
blood pressure is not affected. We examined the relation between the 24-hour
dietary potassium intake at base line and subsequent
stroke-associated mortality in a population-based cohort of
859 men and women (aged 50 to 79 years) in Southern California. After 12
years, 24 stroke-associated deaths had occurred. The relative risks of
stroke-associated mortality in the lowest tertile of
potassium intake, as compared with that in the top two
tertiles combined, were 2.6 (P = 0.16) in men and 4.8 (P = 0.01) in women. In
multivariate analyses, a 10-mmol increase in daily potassium
intake was associated with a 40 percent reduction in the risk of
stroke-associated mortality (P less than 0.001). This effect
was independent of other dietary variables, including the intake of calories,
fat, protein, fiber, calcium, magnesium, and alcohol. The effect was also
apparently independent of known cardiovascular risk factors, including age,
sex, blood pressure, blood cholesterol level, obesity, fasting blood glucose
level, and cigarette smoking. These findings support the hypothesis that a
high intake of potassium from food sources may protect
against stroke-associated death.
>From owner-cran@ListService.net Tue Apr 28 18:50:48 1998
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Date: Tue, 28 Apr 1998 20:50:48 -0400 (EDT)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Dietary fat composition and arrhythmia
In-Reply-To: <199804191657.JAA00210@infoscreen.com>
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On Sun, 19 Apr 1998, Tim Freeman wrote:
> > rat monkey
> > --- ------
> > sheep fat (saturated) 42 % 45 %
> > olive oil (mono-unsaturated) 36 % N/A
> > sunflower seed oil ( w-6 ) 8 % 13 %
> > fish oil ( w-3 ) 0 % 0 %
>
> Did your diet include any fish or other obvious source of w-3 fatty
> acids when you had the heart palpitations?
Sorry for the delay in answering this message, but I just received it!
It now appears to me that I was having problems from all 3 of my ISPs at
the time this was sent: my listserver provider, my domain name provider
and my local account provider. And this was a time of very active CRAN
list postings! Some messages got to me only because they had bounced off
of the sites of subscribers!
No, I had no fish oil and ate no fish in any form at this time. I
still don't, but this is subject to review. I would be more inclined to
take fish oil supplements (less danger of mercury).
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Wed Apr 29 16:36:40 1998
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Date: Wed, 29 Apr 1998 15:36:36 -0700 (PDT)
From: Doug Skrecky
To: cran@listservice.net
Subject: satiety of foods
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Authors
Holt SH. Brand Miller JC. Petocz P.
Institution
Department of Biochemistry, University of Sydney, NSW, Australia.
Title
Interrelationships among postprandial satiety, glucose and
insulin responses and changes in subsequent food intake.
Source
European Journal of Clinical Nutrition. 50(12):788-97, 1996 Dec.
Abstract
OBJECTIVE: The aim of this study was to investigate whether postprandial
glucose and insulin responses were related to concurrent changes in
satiety. DESIGN: Thirty-eight common foods, grouped into six
food categories, were tested in total. Each food category was fed to a
separate group of subjects. A within-subjects repeated-measures design was
used such that within each food category each subject consumed all of the
test foods in random order. SETTING: The study was conducted at the Human
Nutrition Research Unit, Sydney University. SUBJECTS: Separate groups of
11-13 healthy young subjects, who were unrestrained eaters, were recruited
for each of the six food categories. INTERVENTIONS: Isoenergetic 1000 kJ (240
kcal) portions of the test foods were fed to fasting subjects. Fingerprick
blood samples and satiety ratings were obtained every 15 min
over 120 min after which a standard meal was presented and ad libitum food
intake was recorded. A glycaemic score, insulin index and
satiety index score was calculated for each
food by dividing the area under the 120 min response curve (AUC) for the test
food by the AUC for white bread and multiplying by 100. Expressing the
results of the test foods relative to those for white bread minimised the
confounding influence of inherent differences between the subjects. RESULTS:
Among the 38 test foods, there were no significant relationships between
satiety and plasma glucose or insulin responses. However, a
negative correlation was found between insulin AUC responses and ad libitum
food intake at 120 min which suggests that test foods producing a higher
insulin response within 120 min were associated with less food intake and
thus indirectly greater satiety. This result is consistent
with previous findings that carbohydrate-rich foods are more satiating than
fat-rich foods. Thus, total carbohydrate content appears to have been a
stronger determinant of short-term satiety, in conjunction
with the foods structural characteristics, than the foods glycaemic impact.
CONCLUSIONS: The total amount of carbohydrate consumed at a meal and
subsequent insulinaemia may partly determine the degree of hunger arising
within the next 2 h.
Authors
Holt SH. Miller JC. Petocz P. Farmakalidis E.
Institution
Department of Biochemistry, University of Sydney, Australia.
Title
A satiety index of common foods.
Source
European Journal of Clinical Nutrition. 49(9):675-90, 1995 Sep.
Abstract
OBJECTIVE: The aim of this study was to produce a validated
satiety index of common foods. DESIGN AND
SUBJECTS: Isoenergetic 1000 kJ (240 kcal) servings of 38 foods separated into
six food categories (fruits, bakery products, snack foods, carbohydrate-rich
foods, protein-rich foods, breakfast cereals) were fed to groups of 11-13
subjects. Satiety ratings were obtained every 15 min over
120 min after which subjects were free to eat ad libitum from a standard
range of foods and drinks. A satiety index
(SI) score was calculated by dividing the area under the
satiety response curve (AUC) for the test food by the group
mean satiety AUC for white bread and multiplying by 100.
Thus, white bread had an SI score of 100% and the SI scores of the other
foods were expressed as a percentage of white bread. RESULTS: There were
significant differences in satiety both within and between
the six food categories. The highest SI score was produced by boiled potatoes
(323 +/- 51%) which was seven-fold higher than the lowest SI score of the
croissant (47 +/- 17%). Most foods (76%) had an SI score greater than or
equal to white bread. The amount of energy eaten immediately after 120 min
correlated negatively with the mean satiety AUC responses (r
= -0.37, P < 0.05, n = 43) thereby supporting the subjective
satiety ratings. SI scores correlated positively with the
serving weight of the foods (r = 0.66, P < 0.001, n = 38) and negatively with
palatability ratings (r = -0.64, P < 0.001, n = 38). Protein, fibre, and
water contents of the test foods correlated positively with SI scores (r =
0.37, P < 0.05, n = 38; r = 0.46, P < 0.01; and r = 0.64, P < 0.001;
respectively) whereas fat content was negatively associated (r = -0.43, P <
0.01). CONCLUSION: The results show that isoenergetic servings of different
foods differ greatly in their satiating capacities. This is relevant to the
treatment and prevention of overweight and obesity.
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