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Date: Sun, 1 Feb 1998 21:43:46 -0500 (EST)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Hunger & glycation from cooked starches
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I just ran across a posting made by Douglas Skrecky over 2 years ago
which nicely complements my own recent posting. I am taking the liberty
of "recycling" this gem:
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
On Tue, 19 Dec 1995, Doug Skrecky wrote:
> The Journal of Gerontology (B148-B154 Vol.50A No.3 1995) has an
> article with an interesting title: "Source of Dietary Carbohydrate
> Affects Life Span of Fisher 344 Rats Independent of Caloric Restriction"
> The results were as follows:
> Survival
> Diet Group Mean Upper 10%
> Ad libitum sucrose 659 777 days
> Al libitum cornstarch 720 855
> Restricted sucrose 890 1013
> Restricted cornstarch 726 1095
>
> Substituting cornstarch for sucrose increased the upper 10% survival
> independantly of calories. The researchers eliminated differences in body
> weight, energy absorption, pathological lesions and regulation of glucose
> homeostasis as possible explanations for this difference. They guessed
> that an increase in glycation/oxidation with the fructose derived from
> sucrose accelerates aging with respect to the glucose derived from
> cornstarch. I am particularly impressed with the antiaging result
> obtained with restricted cornstarch fed rats since this did NOT increase
> mean survival. The experimenters may have made a mistake by not adding
> water to the dry starch as many restricted starch fed animals died
> prematurely of intestinal blockages.
> It will be interesting to see the results of an experiment directly
> comparing fructose with glucose and other carbohydrates on lifespan.
> At a guess it seems very likely that galactose feeding would result in
> short lifespans. Increased lactose intake, which is composed of glucose
> and galactose is associated with premature ovarian senescence in humans.
> (Fertility and Sterility 1168-1175 Vol.62 No.6 1994)
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Date: Tue, 3 Feb 1998 13:07:54 -0500
From: "Michael R. Edelstein"
Subject: Bananas for Vitamin B6
To: Ben Best
Cc: CRAN List
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Ben Best wrote:
> Why should I eat bananas at
> 100-calories-a-pop to get B6, when I can get more than enough in my
> Life Extension Mix? =
Intuitively it seems that a nutrient, gotten by eating the food it is in,=
would affect the body differently than when delivered in isolation
as a supplement. However, if you have evidence one way or the other,
your evidence would trump my intuition. =
Michael
Michael R. Edelstein, Ph.D. =
Clinical Psychologist
San Francisco
415-673-2848 (24 hours)
Author of THREE MINUTE THERAPY: =
CHANGE YOUR THINKING, CHANGE YOUR LIFE*
(with David Ramsay Steele, Ph.D.)
FEATURES HELP FOR ANXIETY, DEPRESSION,
RELATIONSHIPS, PANIC ATTACKS AND ADDICTION
*A Quality Paperback Book Club/Book-of-the-Month Club Selection
TO ORDER: www.amazon.com
Or toll free: 1-800-986-4135
DrEdelstein@ThreeMinuteTherapy.com
www.ThreeMinuteTherapy.com
>From owner-cran@ListService.net Tue Feb 3 13:14:20 1998
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Date: Tue, 3 Feb 1998 15:12:46 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Water restriction, second thoughts
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On Sun, 18 Jan 1998, Tim Freeman wrote:
> Ben best said:
> > "Fad diets, such as those very high in
> >protein, however, can hurt your kidneys. Drinking very little water, or
> >an overabundance of water (more than 8 quarts a day), may also damage
> >these organs."
>
> and Tim Freeman said:
> > Thanks for looking this up. Do they give a number for the lower
> > bound? In general I believe that one should aim for the middle.
>
> Silly me, I had a minimum number right here in my hands, in the RDA
> book. Page 249: "For practical puroses, 1ml [of water]/kcal of energy
> expenditure can be recommended as the water requirement for adults
> under average conditions of energy expenditure and envrionmental
> exposure. However, there is so seldom a risk of water intoxication
> that the specified requirement for water is often increased to 1.5
> ml/kcal to cover variations in activity level, sweating, and solute
> load".
>
> Since I'm trying to figure out the "middle" of the safe range, let's
> use the number that isn't already inflated as part of an attempt to
> hit the middle. That's the 1ml/kcal number, guesstimate 2000 kcals,
> thus yielding 2 liters of water/day. 1 liter = 1 quart, close enough,
> and the geometric mean of 2 quarts and 8 quarts is 4 quarts.
I think "intoxication" misrepresents the problem. I think that the
problems with excess water are: (1) overworking the kidney and (2) loss
of electrolytes.
Since early January I have been avoiding baked goods as part of an
experiment to minimize my consumption of starchy carbohydrate (see my
recent post). In the period I have had "cereal" only 3 times (wheat bran,
oat bran & FIBER ONE) and have had occasional beans. Mostly I have been
eating lots of vegetables, especially ones high in water content.
Last weekend I made rough estimates of my urine volume, most of which
I peed into a bottle. It was in the order of 5-6 quarts per day. It has
been very uncomfortable peeing so much and needing to pee so much, and I
even began to suspect that I was having kidney pains and my urine was
becoming cloudy.
This week, I have decided to go back to eating bread. As I cited in my
weight-loss piece, people on carbohydrate-free diets have problems with
electrolyte loss -- and this is probably worstened by excessive water. I
could have chosen to eat less lettace, cabbage, celery, cucumber, etc.
but I was also attempting to reduce my hunger as well as avoid starchy
food. In any case, I did not notice that I finding it any easier or harder
to maintain my weight on a reduced-starch diet than on a diet containing
bread. Glycemic index is another matter, but I have decided not to become
too obsessive about the matter.
On the question of death by kidney disease, there is a good analysis
of cause-of-death in table 3 of an article in THE JOURNAL OF PHYSIOLOGY
[Volume 59 Number 3 pages 826-831 (1985)].
cause of death ( % ) in rats
renal cancer cardiovascular other
disease disease causes
CRAN 67.8 20.6 5.9 5.9
control 41.3 50.0 6.5 2.2
The difference between CRAN and control rats was a dramatic drop
in cancer death and a dramatic rise in kidney death. I think this should
be of concern to humans practicing CRAN, because I think the risk of
cardiovascular disease for a non-smoking human CRAN practitioner might
approach that of rats and the risk of cancer should decline dramatically,
as it does in rats. That means that the risk of death due to kidney
problems becomes increasingly important. Protect your kidneys!
My father officially died because his heart stopped, but actually
he was in the hospital having an operation on his prostate because they
suspected that it might be blocking urine flow and thereby interfering
with kidney function. So although the kidney function was the root cause
of the problem, he officially died of a cardiovascular problem.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Tue Feb 3 13:20:47 1998
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Date: Tue, 3 Feb 1998 15:19:41 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Bananas for Vitamin B6
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On Tue, 3 Feb 1998, Michael R. Edelstein wrote:
> Ben Best wrote:
>
> > Why should I eat bananas at
> > 100-calories-a-pop to get B6, when I can get more than enough in my
> > Life Extension Mix?
>
> Intuitively it seems that a nutrient, gotten by eating the food it is in,
> would affect the body differently than when delivered in isolation
> as a supplement. However, if you have evidence one way or the other,
> your evidence would trump my intuition.
Dr. Walford expresses the same "intuition" in THE 120-YEAR DIET. But he
used intuition for many of his assertions, including the ones on exercise.
He also made intuitive arguments about how fast weight-loss should occur,
but he changed his mind after his Biosphere experience.
I always take my supplements with food. If nutrients are mixed-in
with food in my stomach, why should they be less available than nutrients
contained in the food? I take capsules almost exclusively, and expect
that the coatings dissolve easily and the contents mix readily. Bill
Faloon of the Life Extension Foundation says that they get good results
on bioavailability studies, although I have not seen them. (I was arguing
with him about the fact that I take capsules rather than tablets because
of my concern with bioavailability.)
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Thu Feb 5 05:44:47 1998
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From: "Phil Harris"
To: "Caloric Restriction with Adequate Nutrition Listserver"
Subject: Re: Bananas for Vitamin B6
Date: Thu, 5 Feb 1998 12:35:02 -0000
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>
> > Ben Best wrote:
> >
> > > Why should I eat bananas at
> > > 100-calories-a-pop to get B6, when I can get more than enough in my
> > > Life Extension Mix?
This was followed by Michael Edelstein's and Ben's exchange on intuition
and Ben's citing of Walford's *intuitions*.
In a previous post I queried Ben's earlier rejection of bananas, really, I
think now, for the same reason I queried his argument a while ago about
rejection of fructose and by his implication, fruit. That is, I queried an
approach I saw as intuitively purist.
Purism can be OK, or neccessary, of course. I am not sure that I can keep
to CR if I take caffeine and alcohol (or bread) too regularly. Total
abstention might be easier. I too could eat too many bananas. However I do
not think that in sensible amounts or in the proper context they will do me
any harm. There is some evidence to suggest that fruits in particular, but
not banana especially, will do a lot of good. A little banana is useful
though for adding flavour and texture. We eat neccessarily food not just
nutrients.
I illustrate my understanding of proper context with an extract from a
message of mine to the other list.
>Walford in Biosphere II, on an essentially low fat * Ornish * diet, with
further calory restriction, demonstrated physiological changes in humans
similar to those seen in experimental animal populations that achieved
longevity.<
Diet included bananas, 197 - 375g per day, a little other fruit etc..
Table 1.1 The Anti-Aging Plan.
There seems quite a lot of evidence on benefits of excercise: not just a
Walford intuition: call it interim judgement. I tend to value intuition
quite highly on historical grounds and because of personal experience, but
that is another story.
best wishes
Phil Harris
>From owner-cran@ListService.net Fri Feb 6 16:22:12 1998
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Date: Fri, 6 Feb 1998 15:21:23 -0800 (PST)
From: Jordan Sparks
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Subject: Water intoxication
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> > Ben best said:
> > > "Fad diets, such as those very high in
> > >protein, however, can hurt your kidneys. Drinking very little water, or
> > >an overabundance of water (more than 8 quarts a day), may also damage
> > >these organs."
My physiology book, by Ganong, says that our bodies can process about 24
liters of water a day or about 1 per hour. Water intoxication only
occurs if you significantly exceed this limit. The urine concentration
will compensate so that the salts excreted remain constant and are
completely independent of the volume of water excreted. Water
intoxication has nothing to do with kidney damage, it's just that your
electrolytes get too diluted for your body to function properly. I
prefer to keep my kidneys well flushed, and I need to drink hot or cold
liquid to help regulate my body temperature.
>From owner-cran@ListService.net Sat Feb 7 09:33:10 1998
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Date: Sat, 7 Feb 1998 11:31:57 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Vegetarians and weakness
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On Thu, 29 Jan 1998, Ian Eiloart wrote:
> At 6:15 pm +0000 28/1/98, Ben Best wrote:
> > When John Woodman published his survey of caloric restriction
> >practitioners on the CRSOCIETY last March (25-Mar-1997), one of
> >his results was:
> >
> > "Eight out of nine on 'mild to moderate' CR reported either normal
> >(44%) or increased (44%) energy levels. However, this ranged dropped
> >to normal (60%) and DEcreased (40%) energy levels for the 5 at
> >higher level CR."
> >
> > I get the impression that almost all CRAN practioners are (to some
> >extent) vegetarians. This seems like almost a necessity to me. So I am
> >wondering the following:
> >
> > (1) Is anyone practicing CRAN who regularly includes
> > RED meat in their diet?
>
> I seem to remember running a survey on this, and getting one positive
> response among about 15, but I think that person ate a very limited amount
> of red meat. I'm not sure if I kept the results. I'll check.
Ian,
Sorry for my delay in answering this excellent posting of
yours. I saw no follow-up, so does that mean that you did not find the
results upon checking?
I still think that CRAN would be extremely difficult to
practice while regularly eating red meat -- and the tone of most postings
I have seen from practitioners indicates a strong vegetarian inclination.
> > (2) Is there a correlation between symptoms of decreased
> > energy and the absense of meat from the diet (due
> > to decreased B12 and/or Carnitine)
>
> You'd have to be a vegan to get B12 deficiency, and then you'd have to be a
> vegan for about five years without supplementation, because it is stored
> very efficiently. Daily requirements are around 1 microgram, storage (80%
> in the liver) is around 2-5mg, so that's at least 2000 days. B12 may be
> taken at up to 3mg/day without toxic effects. So, take one of these every
> five years! Seriously though, I have heard that there are limits to the
> possible daily absorption, around 20 micrograms, but I couldn't quote a
> source.
>
> My source for this info is an undergraduate/graduate textbook 'Principles
> of Human Nutrition' by Martin Eastwood pub: Chapman Hall, 1997. The author
> is a retired consultant physician at the University of Edinburgh, UK.
Thank you for providing this information. It served as a stimulus
for me to consult my own nutrition reference: MODERN NUTRITION IN HEALTH
AND DISEASE by M.E.Shils, et.al., Editors, 8th edition, 1994. I tend to
forget these facts fairly easily, for some reason, so I will attempt to
summarize my review (as much for my own sake as for anyone else's).
Both Vitamin B12 and Folic Acid are required for the synthesis of DNA
(Thymidine portion, specifically), which is why they are especially
important in pregnancy. Synthesis of the amino acid methionine from
homocysteine is part of this process, and accumulation of homocysteine
(which is thought to be neurotoxic) in vitamin deficiency states
may contribute to cognitive dysfunction.
Vitamin B12 is also required for myelin synthesis, so further
neurologic damage is seen with deficiency of this vitamin. Both B12 and
Folic Acid can relieve the symptoms of megaloblastic anemia, but if Folic
Acid alone is used, relief of anemia may hide the continued neurologic
damage due to B12 deficiency. B12 is also required for maintenance of
sulfhydryl groups (SH), and Vitamin B12 deficiency is characterized by a
decrease in the free-radical scavenger reduced-glutathione (GSH).
Folic Acid deficiency should not be a problem for vegetarians, since
it is found in fresh green vegetables ("folium" is Latin for "leaf" -- it
was isolated in spinach leaves), although it is easily destroyed by
cooking or canning. Vitamin B12 is not found in fruits, vegetables or
grains, however, because it is synthesized in microorganisms -- usually
only found in animals. Milk & cheese would be adequate sources for
lactovegetarians.
As you pointed-out, both B12 & Folic Acid are stored in the liver,
and it can take decades for vegans to show overt B12 deficiency. My
nutrition book does not say how much B12 can be absorbed at one time,
but I think it must be a limited amount, because absorption occurs
through receptors in the ileum for B12 which is complexed with the
"intrinsic factor of Castle".
> Eastwood says that it is not known whether adult vegans can synthesize
> enough carnitine for requirements, but that it is produced from lysine, a
> limiting amino acid.
[snip]
> The English language abstract includes the claim that adult humans
> synthesise enough carnitine for requirements. Also an ISI search (past 6
> years publications) for keywords 'carnitine' and 'vegan' yields no results,
> although a search for 'vegan' and 'deficiency' does yield 6 results, all
> regarding B12 or iodine. A search on 'carnitine' and 'diet' yields about 6
> results, all talking about carnitine enriched diets as a therapy for
> 'carnitine deficiency', which amounts to a variety of metabolic disorders,
> at least one of which is heritable.
Carnitine has been demonstrated to be significantly lower in plasma &
urine of vegetarians & lactovegetarians [AMERICAN JOURNAL OF CLINICAL
NUTRITION 50:301-306 (1989)], but the levels are not considered to be low
enough to constitute nutritional deficiency. Primary dietary sources of
carnitine (which is a non-essential amino acid) are meat & dairy products,
but carnitine is synthesized by the liver (and by the kidney, to a lesser
extent) from the amino acids lysine & methionine. Carnitive transports
fatty acids into mitochondria -- especially of muscles. It has been used
in the treatment of lethargy & chronic fatigue syndrome -- and it protects
heart muscle [PROGRESS IN CARDIOVASCULAR DISEASES 40(3):265-286 (1997)].
The Acetyl-L-Carnitine form readily crosses the blood-brain barrier,
and is neuroprotective -- retarding loss of pyramidal cells & lipofuscin
accumulation in neurons [EXPERIMENTAL GERONTOLOGY 28:537-548 (1993)]. I
take 500 mg of Acetyl-L-Carnitine every morning, which I get from the
Life Extension Foundation (1-800-544-4440). Unfortunately, the stuff is
very expensive.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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Date: Sat, 7 Feb 1998 11:56:52 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Water intoxication
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On Fri, 6 Feb 1998, Jordan Sparks wrote:
> > > Ben best said:
> > > > "Fad diets, such as those very high in
> > > >protein, however, can hurt your kidneys. Drinking very little water, or
> > > >an overabundance of water (more than 8 quarts a day), may also damage
> > > >these organs."
>
> My physiology book, by Ganong, says that our bodies can process about 24
> liters of water a day or about 1 per hour. Water intoxication only
> occurs if you significantly exceed this limit. The urine concentration
> will compensate so that the salts excreted remain constant and are
> completely independent of the volume of water excreted. Water
> intoxication has nothing to do with kidney damage, it's just that your
> electrolytes get too diluted for your body to function properly. I
> prefer to keep my kidneys well flushed, and I need to drink hot or cold
> liquid to help regulate my body temperature.
Thanks for the information, Jordan. But don't forget that the
quotation you cited for me above was taken directly (word-for-word) from
the January-February 1998 issue of FDA CONSUMER magazine.
I didn't mean to imply that electrolyte loss would cause kidney
damage. I was just suggesting that this might be and additional problem
caused by too much water & urination. I was speculating about this, I
admit. Hard evidence about this subject has been difficult for me to
obtain. One of my references on weight loss said that low carbohydrate
intake results in higher electrolyte loss, and I want to know more
about how this happens. My diet was very high in vegetables, but very
low in non-vegetable carbohydrate, since I was trying to avoid grains
(bread & cereal).
The sheer discomfort & inconvenience of my use of high water intake
and high intake of watery vegetables to practice CRAN is a major factor
that is causing me to re-evaluate my latest dietary experiments.
Naturally, though I try to consider all of the possible health
implications as well.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
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Date: Sat, 7 Feb 1998 12:10:09 -0500 (EST)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Bananas for Vitamin B6
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On Thu, 5 Feb 1998, Phil Harris wrote:
> > > Ben Best wrote:
> > >
> > > > Why should I eat bananas at
> > > > 100-calories-a-pop to get B6, when I can get more than enough in my
> > > > Life Extension Mix?
>
> In a previous post I queried Ben's earlier rejection of bananas, really, I
> think now, for the same reason I queried his argument a while ago about
> rejection of fructose and by his implication, fruit. That is, I queried an
> approach I saw as intuitively purist.
I am still unclear about the hazards (high glycation) posed by
fructose and galactose. I intend to learn more about this, but I have
(it seems) hundreds of similar questions I intend to research when I
manage to get around to it. (This in itself is a justification of my
need for a greatly extended lifespan.)
> Purism can be OK, or neccessary, of course. I am not sure that I can keep
> to CR if I take caffeine and alcohol (or bread) too regularly. Total
> abstention might be easier. I too could eat too many bananas. However I do
> not think that in sensible amounts or in the proper context they will do me
> any harm.
What is a "sensible amount"? What is meant my "any harm". These are
all questions of degree. For a person attempting to practice CRAN, eating
high-calorie foods has a potential for undermining the program. But this
is only a potential, and it is difficult to point to any food and say
"don't eat it". Alcohol is 7 calories/gram -- more than protein or
carbohydrate (and only slightly less than fat) -- with little or no
other nutrient value. But if someone is able to drink a glass of wine
a day and still keep total calories under 2000 or 1800, what is the
harm? (I don't drink alcohol mainly because of the effects on the central
nervous system.)
> >Walford in Biosphere II, on an essentially low fat * Ornish * diet, with
> further calory restriction, demonstrated physiological changes in humans
> similar to those seen in experimental animal populations that achieved
> longevity.<
> Diet included bananas, 197 - 375g per day, a little other fruit etc..
> Table 1.1 The Anti-Aging Plan.
>
> There seems quite a lot of evidence on benefits of excercise: not just a
> Walford intuition: call it interim judgement. I tend to value intuition
> quite highly on historical grounds and because of personal experience, but
> that is another story.
Intuition is also often based on familiar beliefs & folklore. In many
cases the results may be correct, but science is full of cases of
discoveries of results that are counter-intuitive. (I still have a hard
time developing an intuitive belief in gyroscopic motion.)
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sun Feb 8 01:39:17 1998
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Date: Sun, 8 Feb 1998 10:36:46 +0200 (WET)
From: Daniel Daboul
To: Caloric Restriction with Adequate Nutrition Listserver
Subject: CR and caffeine (was: Bananas for Vitamin B6)
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> On Thu, 5 Feb 1998, Phil Harris wrote:
>
> > Purism can be OK, or neccessary, of course. I am not sure that I can keep
> > to CR if I take caffeine and alcohol (or bread) too regularly. Total
Can someone explain to me how caffeine intake influences one's
ability to practice CR.
Daniel
>From owner-cran@ListService.net Sun Feb 8 07:02:11 1998
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From: "Phil Harris"
To: "Caloric Restriction with Adequate Nutrition Listserver"
Subject: Re: CR and caffeine (was: Bananas for Vitamin B6)
Date: Sun, 8 Feb 1998 13:51:56 -0000
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> > On Thu, 5 Feb 1998, Phil Harris wrote:
> >
> > > Purism can be OK, or neccessary, of course. I am not sure that I can
keep
> > > to CR if I take caffeine and alcohol (or bread) too regularly. Total
>
> Can someone explain to me how caffeine intake influences one's
> ability to practice CR.
>
> Daniel
Could be purely personal. 9 years ago I was a long term caffeine junky. I
took increasingly a very great deal. It disguised my tiredness and I guess
now, helped mask my serious progressive disease problem which ended with a
coronary. I am not particularly strong willed and I have found for example
that very heavy daily excercise (and recently on business trips, caffeine
again, probably by temporary substitution for food) destabilised my
appetite and routines. I prefer to follow the day's more natural trajectory
with more predictable patterns of hunger, appetite, sleep etc.. Call it
getting old.
Caffeine and booze are diuretics. I feel more comfortable with my minerals
and Vits inside. Diuretics do appear capable of stripping out some useful
substances cf. Jordan's post on electrolyte regulation. (There is a website
of essays for medical students covering some of the mineral regulation;
search under *CSMC NICU teaching files*; sorry not to hand.)
best wishes
Phil Harris
>From owner-cran@ListService.net Mon Feb 9 14:21:10 1998
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Date: Mon, 9 Feb 1998 14:05:24 -0500 (EST)
From: Ben Best
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To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Vegetarians and weakness
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On Sat, 7 Feb 1998, Ben Best wrote:
> On Thu, 29 Jan 1998, Ian Eiloart wrote:
>
> > You'd have to be a vegan to get B12 deficiency, and then you'd have to be a
> > vegan for about five years without supplementation, because it is stored
> > very efficiently. Daily requirements are around 1 microgram, storage (80%
> > in the liver) is around 2-5mg, so that's at least 2000 days. B12 may be
> > taken at up to 3mg/day without toxic effects. So, take one of these every
> > five years! Seriously though, I have heard that there are limits to the
> > possible daily absorption, around 20 micrograms, but I couldn't quote a
> > source.
>
> As you pointed-out, both B12 & Folic Acid are stored in the liver,
> and it can take decades for vegans to show overt B12 deficiency.
As chance would have it, I was speaking to a guy yesterday who had
been a vegan for 6 years and was complaining about his sense of weakness
associated with Vitamin B12 deficiency. He said that he had his blood
levels checked and they were low. It may take decades to develop the overt
symptoms of neurological damage and megaloblastic anemia, but subclinical
manifestations of low B12 can evidently be expressed long before.
-- Ben
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Mon Feb 9 17:46:21 1998
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Subject: Re: Vegetarians and weakness
Date: Mon, 9 Feb 98 23:26:26 +0000
x-mailer: Claris Emailer 2.0, March 15, 1997
From: Ian Eiloart
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Ben Best (benbest@benbest.com) said:
>On Thu, 29 Jan 1998, Ian Eiloart wrote:
>
>> At 6:15 pm +0000 28/1/98, Ben Best wrote:
>> > When John Woodman published his survey of caloric restriction
>> >practitioners on the CRSOCIETY last March (25-Mar-1997), one of
>> >his results was:
>> >
>> > "Eight out of nine on 'mild to moderate' CR reported either normal
>> >(44%) or increased (44%) energy levels. However, this ranged dropped
>> >to normal (60%) and DEcreased (40%) energy levels for the 5 at
>> >higher level CR."
>> >
>> > I get the impression that almost all CRAN practioners are (to some
>> >extent) vegetarians. This seems like almost a necessity to me. So I am
>> >wondering the following:
>> >
>> > (1) Is anyone practicing CRAN who regularly includes
>> > RED meat in their diet?
>>
>> I seem to remember running a survey on this, and getting one positive
>> response among about 15, but I think that person ate a very limited amount
>> of red meat. I'm not sure if I kept the results. I'll check.
>
> Ian,
> Sorry for my delay in answering this excellent posting of
>yours. I saw no follow-up, so does that mean that you did not find the
>results upon checking?
>
Yes, sorry I seem to have deleted the results.
--
cheers, Ian
http://www.cogs.susx.ac.uk/users/iane
http://www.cogs.susx.ac.uk/users/iane/coops
>From owner-cran@ListService.net Mon Feb 9 20:44:49 1998
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Date: Mon, 09 Feb 1998 19:48:23 -0800
From: Chris Fjell
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Subject: Re: CR and caffeine
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It seems to me there is more going on with caffeine, CR and ageing.
If my memory serves me (I've moved away from academic libraries):
First, my introductory nutrition text says caffeine helps stimulate
conversion of fat to energy.
Also, in the studies of caffeine (actually coffee) toxicity, chronic
high intake in mice caused stunted growth, resistence to some diseases
such as cancer, and survival curve shifted as if the mice were caloric
restricted (all were al lib fed).
And didn't Richard Weindruch have a paper about caffeine causing
molecular changes (phosphorylation patterns in the liver?) similar to
CR, but in ad lib fed mice?
Does anyone have these references? I wasn't able to find them in the
internet search services I use.
--
Chris Fjell
Nanaimo, BC
Canada
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From: "Phil Harris"
To: "Caloric Restriction with Adequate Nutrition Listserver"
Subject: Re: CR and caffeine
Date: Tue, 10 Feb 1998 19:32:55 -0000
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Chris Fjell WROTE
> Date: 10 February 1998 03:48
>
> It seems to me there is more going on with caffeine, CR and ageing.
> If my memory serves me (I've moved away from academic libraries):
>
> First, my introductory nutrition text says caffeine helps stimulate
> conversion of fat to energy.
>
> Also, in the studies of caffeine (actually coffee) toxicity, chronic
> high intake in mice caused stunted growth, resistence to some diseases
> such as cancer, and survival curve shifted as if the mice were caloric
> restricted (all were al lib fed).
>
> And didn't Richard Weindruch have a paper about caffeine causing
> molecular changes (phosphorylation patterns in the liver?) similar to
> CR, but in ad lib fed mice?
>
> Does anyone have these references? I wasn't able to find them in the
> internet search services I use.
>
> --
> Chris Fjell
> Nanaimo, BC
> Canada
Above could all be true, but..... Personally, on the evidence, I prefer CR
as an anti-aging measure, especially as CR appears to favour prevention and
stabilisation of atheroschlerososis. Coffee did not do a lot for me, though
I still enjoy it occasionally.
best wishes
Phil Harris
>From owner-cran@ListService.net Thu Feb 12 05:33:37 1998
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Date: Thu, 12 Feb 1998 04:33:20 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
cc: oberon@vcn.bc.ca
Subject: sham eating & hunger
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"Interactions Between Postprandial Thermogenesis, Sensory Stimulation
of Feeding, and Hunger"
Am. J. Physiol. 271: R936-R940 1996
Abstract:
An early thermogenic response has been described following the
ingestion of palatable food. This study was designed to investigate the
possible relationship between this so-called cephalic response, the
sensory stimulation of feeding, and the declining feeling of hunger as
the meal progresses. O2 consumption, carbohydrate and lipid oxidation, as
well as ratings of hunger were measured in four experimental situations
in which the subjects, after overnight fast, ate either two small caramel
cakes, at one time or the same amount of calories divided in eight
portions that were eaten at 10 min intervals. The third experiment, the
sham-feeding experiment, was similar to the last one except that the food
was spit out instead of being swallowed after being chewed. A control
experiment was added in which no food was given but during which the
subject mimicked the act of chewing as was done in the preceeding
experiment. A small increase in O2 consumed was observed in the control
experiment. After the one-meal experiment, the increase was larger for
the first 90 min and declined thereafter. During the first 40 min of the
sham-feeding experiment, O2 consumption increased more than when the
eight meals were eaten, indicating that during this period the sensory
stimulation per se is responsible for the cephalic thermic response to
food. At 90 min, the ratings of hunger were diminished not only in the
eight meals experiment but in the eight sham meals experiment as well,
showing the role of sensory stimulation in the control of hunger. These
results indicate a possible causal relationship between the cephalic
thermogenesis, the control of hunger, and the prandial sensory
stimulations.
>From owner-cran@ListService.net Thu Feb 12 18:03:42 1998
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Date: Thu, 12 Feb 1998 17:03:27 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
Subject: C57BL/6J Mice Longevity Database (updated)
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C57BL/6J MICE LONGEVITY DATABASE
(Updated by Doug Skrecky February 11, 1998)
The following database lists the effect of various treatments on
average life span of C57 black jax 6 (C57BL/6J) mice. The percent change
in average life span is listed under the %CHANGE columns, relative to
either the CONTROL group used in an individual experiment, or relative to
the Longest Lived Control (LLC) group of all the experiments listed in
this database. The LLC group was one of the control groups from reference
20, which lived an average of 34.3 months. The START column shows the age
when treatment was begun. A ~ symbol means that a number was estimated.
For animals that were calorically restricted, the amount of rat chow
below ab libitum they were allowed to consume is indicated by the number
before the word "chow". Thus -49% chow indicates that the animals were fed
49% less chow, than they would normally consume. Some experiments which
restricted calories by feeding animals only every other day did not
clearly indicate the extent of the reduction. This is indicated by "EOD"
chow. An interesting variant on caloric restriction is to be found in
reference 19. Here the animals were allowed to eat ad libitum of a chow
that was diluted by cellulose. Strictly speaking they were not
"restricted", since the caloric intake was reduced voluntarily.
Some caloric restriction experiments fortified their chows so that
restricted animals did not consume less protein, vitamins, and minerals
than those fed ab libitum. This is indicated by the shorthand PR+, VIT+,
and MIN+. Thus -49% chow PR+ VIT+ MIN+ means that 49% less chow (and
calories) was consumed, but fortification with protein, vitamins, and
minerals eliminated any potential confounding effects of multiple
variations in the intake of these nutrients.
%CHANGE
REF TREATMENT START CONTROL LLC
7 acetaminophen 242 mg/l 9.4+ 2 -33
24 aluminum 10 mM 20.1+ -7 -17
29 antioxidents(beta carotene, 2+ 16 -24
ascorbic acid, alpha tocopherol, 9+ 13 -27
rutin, selenium, zinc) 16+ 4 -27
23+ 2 -22
1 ascorbic acid 1% drinking water 1.2+ 9 -9
7 aspirin 495 mg/l 8.1+ 0 -34
7 242 8.1+ -10 -41
7 113 8.1+-9.3+ 3 -32
4 beta carotene 0.5% 1+ 5 -13
4 0.5% 20.3+ -12 -22
25 brain damage 1+ 1 -18
6 butylated hydroxytoluene 0.5% 2.5+ 26 -18
6 0.2% 10+ 0 -12
7 chloropromazine 16.7 mg/l 9.7+-10.7+ 0 -34
7 chloroquine 39.5 mg/l 10.4+-12.1+ 0 -34
7 13.2 mg/l 9.4+-10.4+ -8 -40
7 chlorpheniramine 2.28 mg/l 9.4+ -2 -34
7 0.762 mg/l 9.4+-10.4+ 0 -34
8 coffee (in place of drinking water) 7+ ~-8 ~-21
8 (in place of drinking water) 4+ ~-17 ~-42
5 copper gluconate 5 mM 1+ -14 -24
5 1 mM 1+ -12 -24
5 0.5 mM 1+ -15 -26
26 -66% chow PR+ VIT+ MIN+ (30 C temp) 1+ 4 -21
26 -54% chow PR+ VIT+ MIN+ 1+ 47 11
23 -49% chow PR+ VIT+ MIN+ 1+ 48 -2
15 -44% chow PR+ VIT+ MIN+ 12+ 20 -13
20 -43% chow VIT+ MIN+ 0+ 12 -16
20 -43% chow VIT+ MIN+ 0+ -9 -9
20 -43% chow VIT+ MIN+ 0+ 5 -3
20 -43% chow VIT+ MIN+ 0.7+ -7 -30
20 -43% chow VIT+ MIN+ 0.7+ -9 -9
20 -43% chow VIT+ MIN+ 0.8+ -11 -17
20 -43% chow VIT+ MIN+ 1+ -1 -38
21 -40% chow VIT+ 1+ 15 -8
21 -40% chow VIT+ 1+ 24 -2
16 -33% chow 1+ 5 -21
28 -26% chow 12+ 16 1
28 -26% chow + dehydroepiandrosterone 12+ 13 -2
18 -25% chow 1+ -33 -43
19 -12.5% chow (50% cellulose) 16+ 8 -21
19 -12.5% chow (50% cellulose) 16+ 11 -16
19 -7.7% chow (33% cellulose) 16+ 5 -23
19 -7.7% chow (33% cellulose) 16+ 4 -22
20 EOD chow (during weaning) 0-0.7 25 -6
20 EOD chow (during weaning) 0-0.7 9 9
(longest lived control (LLC) group here lived 34.3 months average)
17 EOD chow 1.5+ 27 -8
17 EOD chow 6+ 11 -15
17 EOD chow 10+ 0 -21
12 EOD chow 25+ 0 -17
30 cotton seed oil 25% ? 1 -41
28 dehydroepiandrosterone 0.05 mg/day 12+ 2 -11
7 dimethylaminoethyl 8.1+-9.3+ 4 -32
chlorophenoxyacetate
13 exercise 12-24 ~0 ~-13
13 exercise 24+ ~-5 ~-15
14 exposure to 10 C decreases
27 ginkgo biloba (EGb 761 50 mg/day) 15+ 0 ?
30 lard 25% ? -9 -47
11 melatonin (night time) 19+ 17 -15
6 2-mercaptoethylamine HCL 1% 10+ 0 -12
6 1% 10+ 0 -18
9 methionine 50 mM 1.4+ ~-17 ~-26
9 50 mM 19.4+ ~0 ~-27
2 pantothenic acid 0.3 mg/day 1+ 18 -36
0.3 mg/day 1+ 20 -37
11 pineal grafting 16+ ~24 ~-24
12 protein 4 to 24% 25+ ~0 ~-15
22 -85% PR 1+ ~19 ~-18
3 pyridoxine HCL 100 mg/kg/day 18+ 11 ?
10 thiazolidine-4-carboxylate 23+ ~9 ~-9
-magnesium 0.07%
12 vitamin level NRC 4X 1+ 19 -28
12 4X 12+ 0 -22
12 4X 17+ 2 -19
12 4X 20+ 0 -24
12 vitamin level NRC 0.5X 1+ -57 -74
12 0.5X 12+ -23 -41
12 0.5X 17+ -18 -34
12 0.5X 20+ 1 -23
31 x-rays 4+ decreases
SPECULATION:
An outstanding effort (reference 26) by a research group led by Akio
Koizumi has finally elucidated the primary mechanism for the life span
increases associated with caloric restriction in C57BL/6J mice. Unlike
humans who suffer greatly from the vissitudes associated with
cardiovascular disease, C57BL/6J mice die primarily of lymphoma cancer.
Also unlike humans, these mice readily experience torpor, especially when
calorically restricted. These reductions in body temperature can be
prevented by housing the mice at 30 C. Doing this virtually eliminates
both the anti-lymphoma effect of caloric restriction, and its associated
life span increases. Stated otherwise, it is body temperature that is the
key determinate of longevity in C57BL/6J mice. (Please note that in order
to equalize body weights the mice housed at 30 C had to have their food
ration slightly reduced: -66% versus -54%.)
The life span of the control groups varies widely, with the LLC group
living longer than virtually all of the calorically restricted groups. It
is apparent that calories are not the only factor influencing torpor. I
speculate that small reductions in housing temperature while the animals
are asleep may promote torpor, independantly of caloric intake.
It would be interesting to see the results of chemically blocking
cancer development in C57BL/6J mice, by adding powerful anticarcinogens
such as curcumin to mouse chow.
1 "Dietary Vitamin C Improves the Survival of Mice" Gerontology
30: 371-375 1984
2 "Effect of Pantothenic Acid on the Longevity of Mice" Proceedings
of the Society for Experimental Biology and Medicine 99(3): 632-633
December 1958 (note mice were referred to only as C57 black mice)
3 "Favorable Effects of Pyridoxine HCL on the Aging Process of C57BL/6J
Mice" AGE 5(4): 143 October 1982
4 "Effect of Dietary B-Carotene on the Survival of Young and Old Mice"
Gerontology 32: 189-195 1986
5 "Excessive Intake of Copper: Influence on Longevity and Cadmium
Accumulation in Mice" Mechanisms of Ageing and Development
26: 195-203 1984
6 "Effect of Antioxidents on Life-Span of C57BL Mice" Journal of
Gerontology 26(3): 378-380 1971
7 "Effects of Various Drugs on Longevity in Female C57BL/6J Mice"
Gerontologia 19: 271-280 1973
8 "The Effects of Prolonged Coffee Intake on Genetically Identical
Mice" Life Sciences 21(1): 63-70 1977
9 "The Effect of Dietary Methionine on the Copper Content of Tissues
and Survival of Young and Old Mice" Experimental Gerontology
19: 393-399 1984
10 "Favorable Effects of the Antioxidents Sodium and Magnesium
Thiazolidine Carboxylate on the Vitality and Life Span of
Drosophilia and Mice" Experimental Gerontology 14: 279-285 1979
11 "The Pineal Control of Aging: The Effects of Melatonin and Pineal
Grafting on the Survival of Older Mice" Annals of the New York
Academy of Sciences" 621: 291-313 1991
12 "The Effect of Dietary Vitamin, Protein and Intake Levels on the
Life Span of Mice of Different Ages" Age 8: 13-17 January 1985
13 "Effect of Exercise on Longevity, Body Weight, Locomotor Performance
and Passive-Avoidance Memory of C57BL/6J Mice" Neurobiology of Aging
6: 17-24 1985
14 "A Longetudinal Study of Tolerance to Cold Stress Among C57BL/6J Mice
Journal of Gerontology 40(1): 8-14 1985
15 "Dietary Restriction in Mice Beginning at 1 Year of Age: Effect on
Life-Span and Spontaneous Cancer Incidence" Science 215: 1415-1418
1982
16 "Effects of Food Restriction on Aging: Separation of food Intake
and Adiposity" Proc. Natl. Acad. USA 81: 1835-1838 1984
17 "Effects of Intermittent Feeding Upon Body Weight and Lifespan
in Inbred Mice: Interaction of Genotype and Age" Mechanisms of
Ageing and Development 55:69-87 1990
18 "Genetic Differences in Effects of Food Restriction on Aging in
Mice" Journal of Nutrition 117: 376-382 1987
19 "Effect of Dietary Cellulose on Life Span and Biochemical Variables
of Male Mice" Age 11(1): 7-9 1988
20 "Survival and Disease Patterns in C57BL/6J Mice Subjected to
Undernutrition" Experimental Gerontology 15: 237-258 1980
21 "Longevity, Body Weight, and Neoplasia in Ad Libitum-Fed and
Diet-Restricted C57BL/6J Mice Fed NIH-31 Open Formula Diet"
Toxicologic Pathology 23(5): 570-582 1995
22 "Dietary Protein, Life-Span and Biochemical Variables in Female
Mice" Journal of Gerontology 31(2): 144-148 1976
23 "Mitotic Activity in Mice is Suppressed by Energy
Restriction-Induced Torpor" Journal of Nutrition 122: 1446-1453 1992
24 "Aluminum in the Organs and Diet of Ageing C57BL/6J Mice"
Mechanisms of Ageing and Development 45: 145-156 1988
25 "Brain Damage, Stress and Life Span: An Experimental Study"
Journal of Gerontology 37(2): 161-168 1982
26 "A Tumor Preventive Effect of Dietary Restriction is Antagonized
by a High Housing Temperature Through Deprivation of Torpor"
Mechanisms of Ageing and Development 92: 67-82 1996
27 "Effect of Long-Term Treatment With EGb 761 on Age-Dependent
Structural Changes in the Hippocampi of Three Inbred Mouse
Strains"
Life Sciences 56(4): 213-222 1995
28 "Effect of Dehydroepiandrosterone Sulfate on Life-Span of
Normally Fed and Calorically restricted C57BL/6 Mice"
The Gerontologist 37(1): 7 1997
29 "The Prolongation of Survival in Mice by Dietary Antioxidents
Depends on Their Age by the Start of Feeding This Diet"
Mechanisms of Ageing and Development 92: 227-234 1996
30 "Osteoarthrosis in Mice Fed Diets Enriched With Animal or
Vegetable Fat"
Archives of Pathology 70: 119-124 1960
31 "Chemical Protection of the Mouse Against Radiation-Induced
Life Shortening"
Radiation Research 47: 537-547 1971
>From owner-cran@ListService.net Tue Feb 17 09:36:23 1998
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Date: Tue, 17 Feb 1998 08:35:43 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
cc: oberon@vcn.bc.ca
Subject: Eat less to live longer to eat more.
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This pithy saying was from the February 16'th 1998 edition of the
Vancouver Sun newspaper.
>From owner-cran@ListService.net Wed Feb 18 02:25:21 1998
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Date: Wed, 18 Feb 1998 01:25:22 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
Subject: Risk Factors in the Oldest-Old
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"Risk Factors for All-Cause and Coronary Heart Disease Mortality in the
Oldest-Old: The Adventist Health Study"
Arch Inern Med 157: 2249-2258 1997
Abstract:
Background: The oldest-old population ( >= 84 years of age) is growing
rapidly and consumes a disproportionate amount of health care dollars.
Risk factors for disease have not been extensively studied in this
group.
Methods: A cohort study of non-Hispanic white Seventh-Day Adventists
from California allowed follow-up for mortality from 1976 through 1988.
Associations between tradional risk factors, consumption of selected
foods, and both coronary heart disease (CHD) and all-cause mortality were
evaluated in the oldest-old portion of this population, using
proportional hazards regression analyses.
Results: we observed 364 cases of CHD and 1387 total deaths during
11,828 person-years of follow-up. Men had higher risk of both all-cause
mortality and mortality from CHD. The relative risks (RRs) associated
with diabetes mellitus were 1.51 for all deaths amd 1.95 for mortality
from CHD. The apparent effects of hypertension were small unless subjects
were currently taking antihypertensive medications. Compared with those
with no regular vigorous activity, subjects who exercised at least 3
times each week had RRs of death of 0.80 and 0.74 for mortality from CHD.
Subjects who consumed nuts 5 times per week had RRs of death of 0.82 and
0.61 for death from CHD compared with those consuming nuts less than
weekly. In men, regular consumption of donuts appeared hazardous for both
all-cause mortality (RR, 1.40) and mortality from CHD (RR, 2.10), and
consumption of beef 4 times weekly was associated with a 2-fold RR for
CHD compared with vegetarians, but there was no increase in risk for
women.
Conclusions: Even in the oldest-old, certain traditional risk factors
and dietary habits are associated with mortality.
>From owner-cran@ListService.net Thu Feb 19 21:13:09 1998
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Date: Thu, 19 Feb 1998 23:11:21 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
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cc: Ben Best
Subject: Re: Risk Factors in the Oldest-Old
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On Wed, 18 Feb 1998, Doug Skrecky wrote:
> Subjects who consumed nuts 5 times per week had RRs of death of 0.82 and
> 0.61 for death from CHD compared with those consuming nuts less than
> weekly.
Douglas,
Your epidemiological studies are interesting, but they must never be
taken at face value. Remember that epidemiological studies are usually
concerned with the general population which generally eats mostly junky
food. I mostly avoid nuts because they are so high in fat. Unfortunately,
epidemiological studies do not tell us WHAT ingredient in the nuts might
be reducing the risk of heart disease (and it may be NO ingredient -- but
something else associated with why people eat nuts, when they eat them or
what they eat them with.)
One guess: some nuts are high in vitamin E (for example almonds,
filberts and, to a much lesser extent, peanuts). Perhaps the crummy diet
of most people is such that they mainly get vitamin E from peanuts -- and
those who don't eat nuts get little or none of this vitamin.
My belief is that a person practicing CRAN and who is taking
supplements such as Life Extension Mix and a source of essential fatty
acids (such as linseed capsules or a multi-essential fatty acid capsule),
such as I do, is better-off without nuts (which are FAT, FAT, FAT !!!).
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Fri Feb 20 09:58:18 1998
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Date: Fri, 20 Feb 1998 08:57:40 -0800 (PST)
From: Doug Skrecky
To: Ben Best
cc: Caloric Restriction with Adequate Nutrition Listserver
Subject: Re: Risk Factors in the Oldest-Old
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On Thu, 19 Feb 1998, Ben Best wrote:
> One guess: some nuts are high in vitamin E (for example almonds,
> filberts and, to a much lesser extent, peanuts). Perhaps the crummy diet
> of most people is such that they mainly get vitamin E from peanuts -- and
> those who don't eat nuts get little or none of this vitamin.
>
In this study of aged Adventists (who already outlive the average American
by about 7 years I beleive), supplemental vitamin E offered no benefit.
> My belief is that a person practicing CRAN and who is taking
> supplements such as Life Extension Mix and a source of essential fatty
> acids (such as linseed capsules or a multi-essential fatty acid capsule),
> such as I do, is better-off without nuts (which are FAT, FAT, FAT !!!).
>
The amount of fat in 5 nuts per week is negligible.
>From owner-cran@ListService.net Fri Feb 20 16:27:13 1998
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Message-ID: <34EE0CF0.8345D897@gte.net>
Date: Fri, 20 Feb 1998 15:08:32 -0800
From: Paul Wakfer
Reply-To: wakfer@gte.net
Organization: Full Length Life Society
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To: Caloric Restriction with Adequate Nutrition Listserver
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Doug Skrecky wrote:
> On Thu, 19 Feb 1998, Ben Best wrote:
>
> > One guess: some nuts are high in vitamin E (for example almonds,
> > filberts and, to a much lesser extent, peanuts). Perhaps the crummy diet
> > of most people is such that they mainly get vitamin E from peanuts -- and
> > those who don't eat nuts get little or none of this vitamin.
> >
> In this study of aged Adventists (who already outlive the average American
> by about 7 years I beleive), supplemental vitamin E offered no benefit.
With the recent information about alpha tocopherol displacing gamma tocopherol
in cell membranes with negative effects, I think any non-positive results of
any study of supplemental vitamin should be suspect, if it uses only alpha
tocopherol (which most do/did).
> > My belief is that a person practicing CRAN and who is taking
> > supplements such as Life Extension Mix and a source of essential fatty
> > acids (such as linseed capsules or a multi-essential fatty acid capsule),
> > such as I do, is better-off without nuts (which are FAT, FAT, FAT !!!).
> >
> The amount of fat in 5 nuts per week is negligible.
But the abstract you quoted said: "Subjects who consumed nuts 5 times per
week", not 5 nuts per week. I don't think that anyone consumes only one nut at
a time and I can't believe that 5 nuts per week (even the largest types) would
have any significant effect at all.
However, I agree with you that eating moderate amounts of a variety of nuts is
beneficial and I disagree with Ben's constant attempt to optimize things but
eliminating important food variety in favor of supplements.
-- Paul --
wakfer@gte.net Voice/Fax: 909-481-9620 Page: 800-805-2870
The Prometheus Project -- http://prometheus.morelife.org
Perfected Suspended Animation for Patient Stabilization
until Cures for Their Terminal Diseases are Available
>From owner-cran@ListService.net Mon Feb 23 02:57:35 1998
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Date: Mon, 23 Feb 1998 01:57:26 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
Subject: Herbal Hope may be in store for insomniacs
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From the February 12, 1998 edition of the Province newspaper in
Vancouver, BC.:
Herbal Hope May be in Store for Insomniacs
The nightmare may soon be over for Canadian insomniacs who rely on
melatonin, a hormone they can't legally buy in this country.
Researchers at the University of Guelph have discovered that at least
three herbs available in health-food stores contain significant levels of
the hormone.
Melatonin, naturally produced at night by the brain's pineal gland,
regulates the body's sleep patterns. Synthetic melatonin, which has
become one of the top-selling drugs in the United States, duplicates the
effect, topping up the body's supply and acting as a sleep aid.
But Health Canada classifies all hormones as drugs and refuses to
approve melatonin for use here. So people are forced to cross the border
or use mail order.
That may soon be over if the herbs feverfew, St. John's Wort and
hunag-qin prove to contain sufficient quantities of melatonin to work
effectively.
The discovery was made by a team led by Prof. Praveen Saxena. The
horticulture professor says the amount of melatonin in some samples of
the herbs tested higher than commercial preparations.
However, University of Toronto's Prof. Greg Brown, who has studied the
hormone for 25 years, says: "What we don't know ias whether the quantity
is there. If you have to take 100 (herb capsules) to get the same dose as
one melatonin (pill), that wouldn't be much use."
Brown and others are looking into it; he hopes to have a clear measure
in weeks.
-Southam Newspapers.
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Mon, 23 Feb 1998 08:56:44 -0500 (EST)
Date: Mon, 23 Feb 1998 08:56:44 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: OBESITY AT THE 1997 A4M CONFERENCE
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I previously mentioned that I attended the 1997 American Academy
of Anti-Aging Medicine (A4M) conference in Las Vegas, Nevada in December.
I didn't attempt to detail much of the information in the lectures because
the speakers would go through their slides too quickly. In frustration, I
bought some videos of the presentations, but even watching these is
inferior to a review in a journal. Citations of sources is often either
sketchy or omitted. Nonetheless, I will attempt to give a brief summary
of information of the two lectures on obesity.
One lecture on obesity was by Denise Brunner and the other was by
Henry Anhalt. Brunner concentrated on adults & therapeutics, whereas
Anhalt concentrated on children. Both speakers began by giving
statistics on the increase in obesity in the USA. Brunner said that
obesity in adults had been stable for decades at about 24% for men and
28% for women, but since 1980 these figures have increased to 32% and
35%, respectively. Anhalt said that from 1965-1980 obesity in the 6-11
year age group increased 54% and in the 12-17 age group increased 39%.
Only 25% of people exercise on a regular basis. For children, there
is a linear correlation between obesity and hours spent watching TV.
Brunner said that 80% of adult-onset diabetics (non-insulin dependent)
are obese. Anhalt said that the number of adult-onset diabetics in the US
increased from 1 million in 1958 to 8 million in 1996.
Anhalt gave a formula for determining Ideal Body Weight & Obesity --
an alternative to the usual BMI approach. For males, add 6 pounds per inch
to 106 pounds for every inch over 5 feet height. For females, add 5 pounds
per inch to 100 pounds for every inch over 5 feet. By this formula, I am
25-30 pounds below my "ideal". According to Brunner, the average American
female model is 5'9" & 120 pounds -- which is also about 25 pounds under
"ideal". Obesity is defined as a weight 20% or more above "ideal".
Brunner had some interesting things to say about appetite. A study of
500 college students (no other reference information given) showed that
taste preference for increasing sugar content rises sharply to a peak and
then falls sharply. For fat, below a threshold there is little increase
in preference, but at the threshold there is a sharp increase and then a
long plateau. (I suppose to optimize fat-pleasure while minimizing fat,
one should find the point where the plateau begins -- although I think
I will pass on this pleasure, if I can manage.) (Unfortunately, her charts
did not label the units of the axes.)
Brunner noted several peptides that hold promise for appetite
manipulation. Cholecystokinin (CCK), which is secreted in the gut, decreases
appetite. Neuropeptide Y stimulates appetite, whereas the peptide galanin
increases fat intake. Although leptin is high in obese people, its actual
role is more ambiguous than the first impressions -- and is yet to be
elucidated.
Brunner said that obesity is 40% genetics and 60% environment. Anhalt
said that obesity is 90-95% heredity and was emphatic that "will power"
is not an issue. The speakers seemed to contradict each other and
themselves on this point -- probably because it is so "politicized". One
study Brunner cited showed that the weight of adopted twins correlated
with biological parents, but not with adopted parents. Anhalt's recipie
for weight control was entirely concerned with food choices, exercise and
thoughts about eating -- "will power", I'd call it.
Anhalt did, however, refer to the success of surgical removal of fat.
He described the proliferation of fat cells in obese children, which
remain for a lifetime once formed. From his remarks I conclude that
(1) surgical removal of fat cells could be of benefit for adults
practicing CRAN and (2) even if CRAN might be harmful for a pre-pubescent
child, "overweight" should still be arduously avoided. More research on
both these points would be useful. I would like to know by what mechanism
an increased number of fat cells could worsen one's weight profile --
especially for a fixed caloric intake. And I would like to know how one
could optimize the weight of a pre-pubescent child so as to minimize
fat cell formation while also minimizing the harm which calorie restriction
might have on growth & development.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Tue Feb 24 01:13:22 1998
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Date: Tue, 24 Feb 1998 00:12:46 -0800 (PST)
From: Doug Skrecky
To: cran@listservice.net
cc: crsociety@lists.csn.net
Subject: Caloric Restriction Does not Slow Aging in Humans
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There has been some speculation that caloric restriction might be able
to retard the rate of aging, and extend maximum human life span beyond
120 years of age. (For example see the book "The 120 Year Diet" by Roy
Walford)
Recent evidence indicates that the anti-aging effect of caloric
restriction, which has been documented in rodents, is not operative in
humans.
A low body-mass index does have a positive association with reduced
mortality rates in humans. However recent research indicates that this is
due to a negative association between BMI and physical fitness. After
physical fitness is accounted for, there exists no further effect of BMI
on mortality. See the following table from (International Journal of
Obesity 19 Suppl: S41-S44 1995.
All Cause Death Rates
BMI Fitness
Low Moderate High
<27 52.1 28.6 20.0
27-30 49.1 29.8 19.7
>30 62.1 18.0 (moderate & high together)
While the above data indicate that the body mass index itself is not
a primary driving factor for mortality in humans, the case it makes
against caloric restriction exerting an anti-aging effect is not
air-tight. What is needed is a false prediction from a postulated
anti-aging effect of caloric restriction that could then be used in turn
to falsify that hypothesis. I believe there exists one such prediction.
Lower BMI is associated with reduced mortality in young and
middle-aged humans. If caloric restriction retards the rate of aging and
extends maximum life span in humans one must expect that a lower BMI
would be significantly associated with reduced mortality in aged humans.
If such an significant association is not found then caloric intake is
not operative in modifying the rate of aging in humans and life spans
beyond 120 will not be possible by reducing caloric intake.
In humans over 84 years of age BMI has not been found to exert any
significant effect on mortality. (New England Journal of Medicine 338:
1-7 1998 & Arch Intern Med 157: 2249-2258 1997) Therefore since no
association has been found between BMI and mortality in aged humans, then
caloric restriction is not operative in modifying the rate of aging in
humans.
The fact that caloric restriction dramatically extends life span in
mice, but not apparently in humans requires some explanation. Here is
one. In mice caloric restriction is associated with torpor, which can act
to reduce tumor growth. In C57BL/6J mice blocking torpor, by increasing
housing temperature to 30 C reduced the increase in average life span
associated with caloric restriction from 47% to just 4%. Since humans
neither experience torpor, nor suffer from cancer to the degree that mice
do the effect of caloric restriction in mice can not be generalized to
include humans. For example in human centenarians only 4% die from
cancer. By comparison cardiovascular disease accounts for 63% of deaths
in those aged 95 and over. (Epidemiology 8: 501-504 1997) Thus it is
cardiovascular disease and not cancer that is the major longevity
limiting factor in humans.
It is possible that potassium intake may be a major dietary modulator
of human longevity. A high potassium intake has been found to reduce
stroke associated mortality to zero. (New England Journal of Medicine
316: 235-240 1987)
>From owner-cran@ListService.net Wed Feb 25 11:15:25 1998
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Date: Wed, 25 Feb 1998 13:14:38 -0500 (EST)
From: Ben Best
X-Sender: benbest@shell1.interlog.com
To: Caloric Restriction with Adequate Nutrition Listserver
cc: Ben Best
Subject: Re: Caloric Restriction Does not Slow Aging in Humans
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To give a thorough reply to Douglas I should go to the library and get
copies of his references and read them. I would also give references for
my counter-information. I will probably do this within the next few weeks,
but I am much too busy to do this right now. However, I want to give a few
replies off the top-of-my-head rather than allow his assertions to go
completely unchallenged.
On Tue, 24 Feb 1998, Doug Skrecky wrote:
> Recent evidence indicates that the anti-aging effect of caloric
> restriction, which has been documented in rodents, is not operative in
> humans.
CRAN has been proven to extend the maximum lifespan of hundreds of
species -- every species tested, in fact, except two: Drosophila (fruit
flies) and amoeba. Rodents are only noteworthy insofar as they are the
species that have been most thoroughly-studied due to the fact that they
are mammals and their lifespans are not unreasonably long.
Naturally, there is a problem in testing long-lived species and the
only reasonable way of doing so within a human generation would be if we
have biomarkers of aging. But again, to validate biomarkers would require
more than a generation.
Nonetheless, there are some highly plausible candidates for
biomarkers, a very noteworthy one being insulin-resistance. Both the
monkey studies at the University of Wisconsin and those at the NIH have
demonstrated a slower acquisition of insulin-resistance in CRAN monkeys in
comparison with controls.
The human experience at Biosphere also demonstrated a great
improvement in risk factors (blood glucose, blood pressure, blood
cholesterol, etc.) for cardiovascular disease, cancer and adult onset
diabetes. This would indicate a likely increase in mean lifespan, if not
maximum lifespan.
> A low body-mass index does have a positive association with reduced
> mortality rates in humans. However recent research indicates that this is
> due to a negative association between BMI and physical fitness. After
> physical fitness is accounted for, there exists no further effect of BMI
> on mortality. See the following table from (International Journal of
> Obesity 19 Suppl: S41-S44 1995.
>
> All Cause Death Rates
> BMI Fitness
> Low Moderate High
> <27 52.1 28.6 20.0
> 27-30 49.1 29.8 19.7
> >30 62.1 18.0 (moderate & high together)
>
> While the above data indicate that the body mass index itself is not
> a primary driving factor for mortality in humans, the case it makes
> against caloric restriction exerting an anti-aging effect is not
> air-tight. What is needed is a false prediction from a postulated
> anti-aging effect of caloric restriction that could then be used in turn
> to falsify that hypothesis. I believe there exists one such prediction.
Far less than air-tight. I will need to read the paper to do a
reasonable evaluation. However, the first thing I notice is that the
lower limit of BMI that you cite is 27 -- but this is the lower limit
for OBESITY! This study compares very obese with moderately obese with
non-obese. BMI is problematic insofar as it does not distinguish an obese
person from a muscle-bound person of the same height & weight. I am
curious as to how the study defines "fitness".
We know from Framingham and countless other studies that people with
lower blood pressure, lower cholesterol and who do not smoke are far less
likely to experience death from cardiovascular disease. We also know that
obesity correlates with high blood pressure and high cholesterol, whereas
people who exercise have lower blood pressure, lower cholesterol (and more
importantly a better HDL/LDL cholesterol ratio). Moreover, people who are
"fit" are less likely to smoke. This gives us the result we should know
from the beginning: that people who are more fit have a lower risk factor
for cardiovascular disease. But this only means that they have a longer
MEAN lifespan (squaring the curve), but it has no effect on MAXIMUM
lifespan -- something we only see with CRAN.
If people were completely free from cardiovascular disease they would
live (on average) 13 years longer -- but their MAXIMUM lifespan would not
be increased at all. Nor would their rate of aging. CRAN is what extends
MAXIMUM lifespan and slows rate of aging.
> Lower BMI is associated with reduced mortality in young and
> middle-aged humans. If caloric restriction retards the rate of aging and
> extends maximum life span in humans one must expect that a lower BMI
> would be significantly associated with reduced mortality in aged humans.
> If such an significant association is not found then caloric intake is
> not operative in modifying the rate of aging in humans and life spans
> beyond 120 will not be possible by reducing caloric intake.
> In humans over 84 years of age BMI has not been found to exert any
> significant effect on mortality. (New England Journal of Medicine 338:
> 1-7 1998 & Arch Intern Med 157: 2249-2258 1997) Therefore since no
> association has been found between BMI and mortality in aged humans, then
> caloric restriction is not operative in modifying the rate of aging in
> humans.
The major studies which established the inverse correlation between
BMI & longevity were landmark studies which corrected for smoking &
underlying disease. Other studies rarely do this. Even if these studies
corrected for smoking, it would be very difficult to correct for
underlying disease, since so many elderly people are, indeed, suffering
from underlying disease.
More important, however, is the fact that many elderly people lose
their appetite and do not eat properly. Their low BMI may indicate Caloric
Restriction, but it does NOT indicate Adequate Nutrition. The malnourished
elderly are numerous.
> The fact that caloric restriction dramatically extends life span in
> mice, but not apparently in humans requires some explanation. Here is
> one. In mice caloric restriction is associated with torpor, which can act
> to reduce tumor growth. In C57BL/6J mice blocking torpor, by increasing
> housing temperature to 30 C reduced the increase in average life span
> associated with caloric restriction from 47% to just 4%. Since humans
> neither experience torpor, nor suffer from cancer to the degree that mice
> do the effect of caloric restriction in mice can not be generalized to
> include humans. For example in human centenarians only 4% die from
> cancer. By comparison cardiovascular disease accounts for 63% of deaths
> in those aged 95 and over. (Epidemiology 8: 501-504 1997) Thus it is
> cardiovascular disease and not cancer that is the major longevity
> limiting factor in humans.
I have said many times before that cardiovascular disease is a more
important cause of mortality in humans than in rodents. And from this I
conclude that CRAN may be of even MORE benefit to humans than it is to
rodents from the point of view of MEAN lifespan. Douglas repeatedly fails
to distinguish between MEAN and MAXIMUM lifespan.
Cancer is only such an important cause of death (relatively speaking)
for rodents because cardiovascular disease is a relatively less important
cause. But as the death-rate from cardiovascular disease declines in
humans, the relative importance of cancer increases. It is estimated that
sometime within the next decade cancer will become the leading cause of
death for humans.
Even without reading the papers Douglas cites (which I intend to do),
and even without citing the numerous papers giving evidence for the
effectiveness of CRAN, I see serious problems with the interpretation he
places on literature he cites.
--------------------------------------------
Ben Best (benbest@benbest.com)
http://www.benbest.com/
>From owner-cran@ListService.net Sat Feb 28 21:23:09 1998
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From: "Doug Younkin"
To: CRAN@ListService.net, crsociety@lists.sni.net
Date: Sat, 28 Feb 1998 22:28:18 +0000
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Subject: Re: Lowfat Diets - my experience
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I have found that when I reduce my fat intake to below about
10% of total calories, within one week I start to develop symptoms of
easily damaged skin (especially on my hands - just brushing up
against something slices my skin open easily) and quickly develop
hemorrhoid discomfort and eventual rectal bleeding. When I resume
fat intake in the 25% of calorie range, these symptoms disappear
after about two weeks. I have tried several variables besides fat
intake (protein, fiber, water) but the weakened tissue response
seems to track with the lower fat intake for me.
My daily caloric intake is around 2000 calories and I am maintaining
about 125 pounds (I am 6 ft. 1 in.) and will be 44 years old next
month. I have previously posted my blood test profile. I take one
teaspoon flax oil (or equivalent flax seeds) and eat fish about once
weekly to assure adequate omega-3 intake. I eat about one teaspoon
each of sunflower seed and pumpin seed, and 1/4 cup each of oat bran
and rolled oats (all raw) daily of assure adequate omega-6 intake.
The remainder of my fat intake tends to be dominant in
mono-unsaturated oils. I take about 1500mg Vit C daily divided
between meals and 400IU of Vit E with the omega-3 and -6. I take
these vitamins to help prevent oxidation of LDL. I also take Alpha
Lipoic Acid to help recycle Vit C and E. (I take other vitamins too,
but these in particular relate to lipid protection.)
For some reason, I tend to forget about the necessity of maintaining
my fat intake at about 25% (maybe from reading something about
Ornish-type low fat diets, or wanting to make it easier to keep my
caloric intake at my target by relying on the larger volume of a
low-fat diet to make me feel full more easily). When the
uncomfortable side-effects eventually come, I remember and have to
suffer for about two weeks until my body can heal from the damage. I
think I may have been near to the severly harmful situation that Ben
Best described when I once was down to 119 pounds and 1600 (low-fat)
calories per day and I would frequently feel my heart pounding hard
with what seemed an unusual rhythm. After reading Ben's warning, I
gradually brought my weight up to 125 and have kept it there since.
Has anyone had similar (or opposite) experiences relating to fat
intake?
Doug Younkin
====================================
> Date: Wed, 18 Feb 1998 10:20:57 -0800 (PST)
> To: crsociety@lists.sni.net
> From: Gary Ditta
> Subject: Lowfat Diets
> There's been some discussion here about lowering fat intake. The following
> work indicates that individual genetics play an important role in
> determining how each of us will respond to a low fat diet, and that beyond
> a certain point, lowfat can actually be counterproductive.
>
> Heart Disease? Blame Genes and What You Eat
> By Maggie Fox, Health and Science Correspondent
>
> PHILADELPHIA (Reuters) - People who are overweight or who have heart
> disease can blame their genes but their behavior is also a factor,
> scientists said Saturday.
snip
> The research has already turned up one surprise result -- some people do
> not do well on very low-fat diets meant to cut the risk of heart
> disease, and their genes almost certainly hold the secret.
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