Longevity Report 91
Steve Harris
<8a2c2731.02092...@posting.google.com>...
>"John de Rivaz" <Jo...@deRivaz.com> wrote in message
news:<5Akk9.1785$q15.1...@newsfep2-win.server.ntli.net>...
>> I have just uploaded Longevity Report 91 to the web.
>> http://www.longevity-report.com/lr91.htm
>>
>> This is unusual in that
>>
>> 1. It contains a single article.
>>
>> 2. none of you will have read this article before.
>>
>> The Role of Enzymic Cofactors in Aging
>> or
>> How to Live to 200
>> Copyright 2002 Michael Clive Price Updated 25/09/2002
>> Feedback to michae...@ntlworld.com
My feedback to Michael Price is that it just ain't that simple. Some years
ago some other researchers looked to see if mice survived longer on 1/2 RDA
vs RDA vs 2 times RDA worth of all conventional vitamins, but the other
nutrients kept controlled, and found that although there was a bit of
difference between 1/2 and 1 RDA, there was no difference in survival in 1
RDA vs 2x RDA. That kicks the cofactor theory of aging in the butt: if
there was any effect there, you should start to be seeing it as you double
the dose from one RDA to 2. Also, it's completely in accord with my own
experience with control groups for CR experiments, which for years I fed on
a much better vitamin regime than the simple AIN-93 levels. They got a
vitamin supplement which was specially made for me and enriched many times
RDA (though not close to toxic levels) in B vitamins, E, and Cr from yeast.
(we didn't bother with beta-carotene because mice turn it into retinol so
fast they don't get any benefti from it. Similar considerations applied to
vitamin C, which mice make on their own in doses far larger than you can
easily give them). But B's and E and Cr made absolutely no drastic
difference. The hybrid strain lived about 3 years mean, and 3.5 years max
under 10-20% restriction, and subtract 6 months from those numbers for ad
lib and add 6 months for max restriction. This is about what rodent
researchers see with the (quite a bit lower) AIN vitamin recommendations,
which are much more in line with the old human RDAs (not even our modern
usually higher DRIs).
Thus, while you can find a lot of old unrepeated (and probably unrepeatable)
reports of life span extension with one B vitamin or another, or E, the
available evidence for "across the board" enrichment of these things
(megadose water solubles and E) absolutely does NOT suggest any kind of
synergy between them when it come to aging.
Sorry. I take Daily One and E for my arteries, and I sure wish that that
kind of thing made mice live to be 5 or 6 years old, or even any difference
that it works at all to lengthen their lives.
SBH
--
I welcome email from any being clever enough to fix my address. It's open
book. A prize to the first spambot that passes my Turing test.
michaelprice
>>> I have just uploaded Longevity Report 91 to the web.
>>> http://www.longevity-report.com/lr91.htm
>>>
>>> This is unusual in that
>>>
>>> 1. It contains a single article.
>>>
>>> 2. none of you will have read this article before.
>>>
>>> The Role of Enzymic Cofactors in Aging
>>> or
>>> How to Live to 200
>>> Copyright 2002 Michael Clive Price Updated 25/09/2002
> >> Feedback to michae...@ntlworld.com
>>
> My feedback to Michael Price is that it just ain't that simple.
> Some years ago some other researchers
Kokkonen and Barrows, 1985 I believe.
> looked to see if mice survived longer on 1/2 RDA vs RDA vs 2 times
> RDA worth of all conventional vitamins,
I had this in mind when I wrote:
"The amounts required to achieve significant life-extension are often
between 30 to 400 times these RDA levels."
> but the other nutrients kept controlled, and found that although
> there was a bit of difference between 1/2 and 1 RDA, there was
> no difference in survival in 1x RDA vs 2x RDA.
Actually 4x RDA, which strengthens your case.
> That kicks the cofactor theory of aging in the butt: if
> there was any effect there, you should start to be seeing it
> as you double the dose from one RDA to 2.
It's a bit simplistic to extrapolate from 1/2x, 1x & 4x RDA, to 30x - 400x
RDA. You're assuming the LE effect follows the same log-linear relationship
across the entire range, which it most assuredly doesn't at the bottom so
why assume it higher up?. For the same cofactor different enzymes reach
maximal activity at different cofactor concentrations. Sometimes new
effects
are known kick in at higher levels (as with selenium and B6 - abs below).
Notice that the B6 temperature reduction effect
has only been observed at the same level that induces the LE. With selenium
"specific Se metabolites, which are produced in significant amounts at
relatively high Se intakes, also discharge antitumorigenic functions."
> Also, it's completely in accord with my own
> experience with control groups for CR experiments,
Published?
Cheers,
Michael C Price
Pharmacol Biochem Behav 1982 Feb;16(2):361-4
Pyridoxine reduces core body temperature in rats.
Lindseth KA, Hicks RA.
A mild hypothermia was produced in female rats during treatment with
pyridoxine HCl (Vitamin B6), 100 mg/kg, administered in the drinking water.
The hypothermic effect appeared by day 3 and persisted through 15 days of
treatment. The reduction in core temperature was greater early in the day,
just following the nocturnal period of maximum food and water consumption of
the rat. Tail tendon temperatures of control and pyridoxine-treated animals
showed no evidence of increased heat loss. Thus the hypothermia appears to
reflect decreased heat production. The implications of a reduced metabolic
rate for gerontological research are discussed.
PMID: 7071086
Pharmacol Ther 1998 Sep;79(3):179-92
Chemopreventive agents: selenium.
Combs GF Jr, Gray WP.
Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.
The element selenium (Se) was recognized only 40 years ago as being
essential in the nutrition of animals and humans. It is recognized as being
an essential component of a number of enzymes, in which it is present as the
amino acid selenocysteine. Se compounds have also been found to inhibit
tumorigenesis in a variety of animal models, and recent studies indicate
that supplemental Se in human diets may reduce cancer risk. The
antitumorigenic activities have been associated with Se intakes that correct
nutritionally deficient status in animals, as well as higher intakes that
are substantially greater than those associated with maximal expression of
the selenocysteine-containing enzymes. Therefore, it is proposed that while
some cancer protection, particularly that involving antioxidant protection,
involves selenoenzymes, specific Se metabolites, which are produced in
significant amounts at relatively high Se intakes, also discharge
antitumorigenic functions. According to this two-stage model of the roles of
Se in cancer prevention, individuals with nutritionally adequate Se intakes
may benefit from Se supplementation. Evidence for chemoprevention by Se and
for the apparent mechanisms underlying these effects is reviewed to the end
of facilitating the development of the potential of Se compounds as cancer
chemopreventive agents.
Publication Types:
Review
Review, Tutorial
PMID: 9776375
michaelprice
>>Steve Harris:
>
>>> That kicks the cofactor theory of aging in the butt: if
>>> there was any effect there, you should start to be seeing it
>>> as you double the dose from one RDA to 2.
>
>> It's a bit simplistic to extrapolate from 1/2x, 1x & 4x RDA,
>> to 30x - 400x RDA.
>
>
> Marcus
Nothing whatsoever. I don't believe we can extrapoate from one dose level
to another - as the refs I cited showed - , especially across two orders of
magnitude, which was what Steve was doing. What I (along with most people)
believe is valid is to extrapolate a dose in one animal to an *equivalent*
dose in another animal.
Of course it would be nice not to have to extrapolate at all, but lifespan
human randomised placebo trials ain't going to happen anytime soon, or
anytime at all, most likely.
Cheers,
Michael C Price
Steve Harris
<97Wk9.2408$sh4.1...@newsfep2-win.server.ntli.net>...
>> Also, it's completely in accord with my own
>> experience with control groups for CR experiments,
>
>Published?
Sure. Medline 2394907 contains a control group eating the mega-vitamin
enriched diet, as does also every life span study done by Walford et al in
the 80's at UCLA (look up Weindruch, Richard and Walford, Roy).
The vitamin formula used in restriction and ad lib control studies at UCLA
was not the stingy AIN-76, but rather (in accord with Walford's prescription
to be SURE you're not malnourished) another more liberal vitamin mix from
earlier times before the AIN started trying to standardize all these lab
diets. We used to put the vitamin and mineral mixes in the diets ourselves
when we made them (I remember the B vitamin smell of the stuff) before we
switched to having Teklad do it. I don't have the precise composition at my
fingertips but IIRC it was the ICN vitamin-mix formula for semi-synthetic
diets, and it had a whopping dose of most of the non-toxic ones, in amounts
of the mix that we used (which are in my paper, or those it references).
Enough that I never seriously considered if further megadosing of these
things would get me anywhere in rodents.
If you're really curious about the stuff you can probably google it from ICN
lab products. Hopefully the same stuff is available now that they offered in
the 80's.
If 4x RDA isn't enough to convince you, I'm sure we exceeded that with many
vitamins in this mix.
michaelprice
>>> Also, it's completely in accord with my own
>>> experience with control groups for CR experiments,
>>
>>Published?
> Sure. Medline 2394907 contains a control group eating the
> mega-vitamin enriched diet,
Thanks for the ref, but since the *controls* received the enriched diet it
can can't cited as a negative mega-vitamin study. (Naturally, since you
were testing for the effects of CR, not 'mega'-dosing.)
> as does also every life span study done by Walford et al in the 80's
> at UCLA (look up Weindruch, Richard and Walford, Roy).
Interestingly this might support the notion that supra-RDA levels (at
sub-megadose levels) extend lifespan, since I remember Walford saying
(as a criticism of earlier experiments) that his control animals outlived
many
other earlier lab animals (of the same strain).
Cheers,
Michael C Price
----------------------------------------
http://www.longevity-report.com/lr91.htm
http://www.hedweb.com/manworld.htm
Joel M. Eichen
michaelprice
"Joel M. Eichen" <joele...@yahoo.com> wrote in message
news:8a2c2731.02092...@posting.google.com...
> "Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
>
> Too simple!
>
> rootcom.com
eh?
Steve Harris
michaelprice wrote in message ...
>"Steve Harris" :
>>>> Also, it's completely in accord with my own
>>>> experience with control groups for CR experiments,
>>>
>>>Published?
>
>> Sure. Medline 2394907 contains a control group eating the
>> mega-vitamin enriched diet,
>
>Thanks for the ref, but since the *controls* received the enriched diet it
>can can't cited as a negative mega-vitamin study. (Naturally, since you
>were testing for the effects of CR, not 'mega'-dosing.)
>
>> as does also every life span study done by Walford et al in the 80's
>> at UCLA (look up Weindruch, Richard and Walford, Roy).
>
>Interestingly this might support the notion that supra-RDA levels (at
>sub-megadose levels) extend lifespan, since I remember Walford saying
>(as a criticism of earlier experiments) that his control animals outlived
>many
>other earlier lab animals (of the same strain).
Comment:
The control group for this one counts, because the controls for IT are the
many historical controls in other trials in other labs in long lived mice
strains were run on AIN doses. To be precise, Walford's the only one I know
of who used his particular hybrid (C57B10 x C3H), and it gave him life spans
better than most labs but not all. Basically, at the high end of what was
being reported—nothing head and shoulders above anybody else who was using
C57B10s (say). As a matter of fact I never saw any of Walford's restricted
mice live longer than 43 months, whereas the record for M. musculus
restriction life span is held by Jackson labs, and is something like 46
months. So Walford's results are good, but by no means good enough to
suspect that his vitamin supplementation of the mice had anything to do with
it. At least one other place got comparable or better results for
restriction without the ICN mix for either restricted animals or controls.
I do now have some vitamin numbers for the Walford controls. The present ICN
vitamin fortification mix 904655 (which I got off the web) is no doubt what
we used historically. It's meant to be used at 2.2% of diet, and we fed it
to controls at 3.5% of "dry" (i.e., no water added) semisynthetic diet, and
to restricted animals at 5% of diet (so it would come out the same vitamin
dose per day per animal, though not per kg diet, per kcal diet, or per kg
body wt mouse—you can have any one of these 4 in a restriction experiment,
but only 1 of 4).
Below are what you get as final diet concentration (mg/kg diet), with the
ICN mix if you use it at 3.5% of final diet, as we did for controls. Next
are how many fold over AIN recommendations this is, using as reference final
concentrations you get with the AIN-76 mix at the recommended 1% of diet. So
"3x" would be 3 times the AIN recommendation. I've rounded everything to 2
significant figures.
ICN at 3.5%, final vitamin concentrations in mg/kg diet
B1 16 mg/kg = 2.7 x AIN
B2 16 2.7 x
niacin 68 2.3 x
B5 48 3.0 x
B6 16 2.3 x
folate 1.4 0.7 x
biotin 0.32 0.1 x
B12 0.022 (2.2 mcg/kg) 2.2 x
A 29 (7200 IU) 1.8 x (13,000 IU)
C 716 mg/kg -- (no AIN rodent value)
E 350 (87 IU) 1.8x (150 IU)
D2 2.0 (800 IU) 4x (3200 IU)
(K is present in the AIN mix, but not in the ICN so we never fed it). AIN
recommendations for rodents don't include vitamin C, which we did feed.
Comments: it's interesting that the only vitamins fed less in ICN than AIN
are folate and biotin. I suppose folate had been upped in AIN due to
reproductive problems (AIN was formulated as not as a geriatric formula, but
more of a general husbandry formula supplement). Biotin was skimped on in
the old ICN no doubt due to price, and AIN fixed that.
I was surprised when I actually did the numbers that most of these ICN
numbers in our formula are really only in the 2 to 3 x AIN range, not "5x"
as I'd remembered. The difference is probably due to the fact that I'd once
compared them to human RDAs on a mg/kcal basis, which is a fairer comparison
of humans to rodents. The rodent AINs recs are liberal-- about twice the
human DRIs in terms of mg/kcal, as you can see from the fact that the diets
above are about 4,000 kcal/kg, meaning that human dietary need (depending on
body size) would be somewhere about 0.6 to 0.75 kg of this kind of diet, so
multiply the vitamin doses by that, to get the human equivalent dose if you
were living on mouse diet. That DOES come out to be more like 5x RDA or DRI,
or a bit more. You get numbers like 10 mg for B1 and B2, 30 mg for B5, and
500 mg C and 100 IU vitamin E. These are "therapeutic multivit" type dosage
numbers, though of course far less than what you find in lots of
supplements.
Yes, you can argue that optimal health doses of these vitamins could be far
higher, but that certainly cannot be the case of SOME of them. For example,
there's a limit of about 20 mg in how much B1 or B2 you can absorb in a
meal, so it's rather silly to take much more of them in a day than that.
Similarly, your body stores of vitamin C will probably be well saturated at
500 mg, so taking more than that and expecting to live any longer because of
it, is just not realistic.
Steve
michaelprice
thanks, I appreciate the effort you've put into supplying the
viatmin breakdown of lab feed figures, they'll prove invaluable.
At the end you say:
> Yes, you can argue that optimal health doses of these vitamins
> could be far higher, but that certainly cannot be the case of SOME
> of them. For example, there's a limit of about 20 mg in how much
> B1 or B2 you can absorb in a meal, so it's rather silly to take much
> more of them in a day than that.
But larger amounts of B1 are less efficiently absorbed by passive
diffusion, over and above the gut's load-limited but more efficient
active transport mechanisms.
(See page 281, The Vitamins: Fundamental Aspects in Nutrition
and Health, 2nd Edition.Gerald F Combs, Jr (1998)
ISBN 0121834921.)
(Digression: for the apparent benefit 3-8 gm/d over 3 gm/d of oral B1
see the [*] Alzheimer refs at end.)
And 20mg of B2 is already way over 10x RDA and actually
more than my guess for the optimal amount at 10mg/d, based
PMID: 3213264 [Effect of riboflavin (vitamin B2) on spontaneous
gonarthrosis in the mouse] So even if B2 absorption is load
limited (which I suspect may be a myth, as with B12[**]) to
20mg/meal it wouldn't bother me.
> Similarly, your body stores of vitamin C will probably be well
> saturated at 500 mg, so taking more than that and expecting
> to live any longer because of it, is just not realistic.
500mg is already nearly 10xRDA. I reckon 2500mg is a better
guess, based on Michael Colgan's work, but close enough, I guess.
(I can't get that excited by vitamin C, anyway.)
Rheumatol 1988 May-Jun;47(3):166-72
Z Rheumatol 1988 May-Jun;47(3):166-72
[Effect of riboflavin (vitamin B2) on spontaneous gonarthrosis in the mouse]
[Article in German]
Wilhelmi G, Tanner K.
Biologische Forschungslaboratorien, Division Pharma, Ciba-Geigy AG, Basel.
Male mice of the C57 black strain were given 1 mg/kg body weight of
riboflavin (vitamin B2) in their drinking water daily for 4 months, in
addition to the vitamin B2 contained in their standard pellet feed. Controls
received the standard feed only. Histological examination of the joints at
the end of the experiment showed that the incidence of gonarthrosis in the
group given supplementary riboflavin was less than half that found in the
controls; the number of mice with bilateral gonarthrosis was also
considerably smaller, and the severity of the lesions less marked. Signs of
physiological degeneration in the epiphyseal cartilage of the femoral and
tibial condyles were only marginally less pronounced than in the controls.
The notable inhibitory effect of riboflavin, which is known to promote
regenerative processes, on osteoarthritis was compared with that of drugs
stimulating wound healing, e.g. flavonoids, tribenoside, and zinc sulfate.
These latter substances were also found to exert a similar inhibitory effect
on spontaneous gonarthrosis in the mouse.
PMID: 3213264
[*] B1 and Alzheimer's
J Geriatr Psychiatry Neurol 1993 Oct-Dec;6(4):222-9
Preliminary findings of high-dose thiamine in dementia of Alzheimer's type.
Meador K, Loring D, Nichols M, Zamrini E, Rivner M, Posas H, Thompson E,
Moore E.
Department of Neurology, Medical College of Georgia, Augusta 30912-3200.
Thiamine is important not only in the metabolism of acetylcholine but also
in its release from the presynaptic neuron. Pathologic, clinical, and
biochemical data suggest that thiamine deficiency is detrimental to the
cholinergic system and that thiamine-dependent enzymes may be altered in
Alzheimer's disease. Two previous studies reported contradictory results in
patients with dementia of Alzheimer's type treated with 3 g/day of thiamine.
In the present study, we examined the effects of 3 to 8 g/day thiamine
administered orally. Our results suggest that thiamine at these
pharmacologic dosages may have a mild beneficial effect in dementia of
Alzheimer's type. The mechanism of the observed effect is unknown, but the
findings warrant further investigation, not only for their therapeutic
implications but for their possible etiologic clues. In addition, the
results suggest long-term carry-over effects that should be considered in
the design of future studies.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 8251051
Arch Neurol 1991 Jan;48(1):81-3
A trial of thiamine in Alzheimer's disease.
Nolan KA, Black RS, Sheu KF, Langberg J, Blass JP.
Altschul Laboratory for Dementia Research, Cornell University Medical
College, Burke Rehabilitation Center, White Plains, NY 10605.
Because a previous short-term study demonstrated a statistically
significant, but not clinically important, improvement in cognitive test
scores during thiamine treatment in patients with dementia of the
Alzheimer's type, a 12-month, double-blind, parallel-group study was
conducted to examine whether long-term administration of thiamine at 3 g/d
might slow the progression of dementia of the Alzheimer's type. Fifteen
subjects were enrolled and 10 completed the 1-year study. Data are available
for two additional subjects through the first 9 months of study. No
significant differences were found between the placebo and thiamine groups
at any point during the study. In both groups, overall means for the
Mini-Mental State Examination, verbal learning, and naming scores decreased
significantly over the 12-month study period. These results do not support
the hypothesis that long-term administration of thiamine at 3 g/d might slow
the progression of dementia of the Alzheimer's type.
Publication Types:
Clinical Trial
Controlled Clinical Trial
PMID: 1986730
Arch Neurol 1988 Aug;45(8):833-5
Thiamine and Alzheimer's disease. A pilot study.
Blass JP, Gleason P, Brush D, DiPonte P, Thaler H.
Will Rogers Institute, White Plains, NY.
As a test of the significance of previously described biochemical
abnormalities in thiamine-dependent enzymes in brains and other tissues in
patients with Alzheimer's disease, a double-blind, placebo-controlled,
crossover, outpatient pilot study compared the effects of 3 g/d of oral
thiamine hydrochloride for three months with those of a niacinamide placebo.
Eleven moderately impaired patients with "probable Alzheimer's disease" by
the National Institute of Neurological and Communicative Disorders and
Stroke-Alzheimer's Disease and Related Disorders Association criteria
completed the study. All patients were well nourished and had no stigmata of
dietary thiamine deficiency. Their initial mean +/- SEM Mini-Mental State
Examination score was 14.2 +/- 1.4, and the mean age was 72 years. Global
cognitive rating by the Mini-Mental State Examination was higher during
three months with 3 g/d of oral thiamine hydrochloride than with niacinamide
placebo. Behavioral ratings, however, did not differ significantly, nor did
clinical state when it was judged subjectively.
Publication Types:
Clinical Trial
Controlled Clinical Trial
PMID: 2969232
This went out on a earlier thread on just sci.life-extension,
so for the other cross-posted groups:
[**] ----------- repost ---------
"Hua Kul" <g...@adres.nl> wrote in message
news:3da4c6e5.02092...@posting.google.com...
> I believe I am B12 deficient and I want to try a transdermal solution
Best - and easiest - bet is to take mega-doses (i.e. a mg or two or ten)
orally. The medical consensus (recently revised) is that large amounts
*will* correct deficiencies in people lacking the intrinsic factor. It is a
myth that people with absorption problems can't acquire enough by simple
saturation - you just have to take mega-RDA amounts [which are
absorbed by passive diffusion, as opposed to active transport].
Vitamin B12 absorption test and oral treatment in 14 children with selective
vitamin B12 malabsorption.
"This study lends further support to the use of megadoses of VB12 as an
alternative treatment for selective VB12 malabsorption." PMID: 10100276
&
Did we learn evidence-based medicine in medical school? Some common medical
mythology.
"Medical myths occur for many different reasons. A common thread is that
they all make some pathophysiologic sense. A good example is the concern
about using oral cobalamin when treating pernicious anemia. The difficulty
in absorbing vitamin B12 when intrinsic factor is not available does not
make oral replacement impossible; the dose just needs to be higher. " PMID:
10220238
In full:
J Am Board Fam Pract 1999 Mar-Apr;12(2):143-9
Did we learn evidence-based medicine in medical school? Some common medical
mythology.
Paauw DS.
Division of General Internal Medicine, University of Washington School of
Medicine, Seattle 98195-6420, USA.
Medical myths occur for many different reasons. A common thread is that they
all make some pathophysiologic sense. A good example is the concern about
using oral cobalamin when treating pernicious anemia. The difficulty in
absorbing vitamin B12 when intrinsic factor is not available does not make
oral replacement impossible; the dose just needs to be higher.
Pathophysiologic concerns have also been a key reason why physicians have
avoided using beta-blockers in patients with diabetes. They fear that
beta-blockers will block adrenergic symptoms, and patients will not know
when they are hypoglycemic. In studies addressing this issue, there appears
to be no real problem with increased severe episodes of hypoglycemia in
patients on beta-blockers or increased hypoglycemic unawareness. Several
studies commented on the unanticipated symptom of increased sweating
associated with hypoglycemia in diabetic patients who are taking
beta-blockers. Another important concept behind some medical myths is the
overreliance on case reports or authoritative text. The concern about
depression associated with beta-blocker use grew out of one widely
referenced case report. Subsequent studies have not shown convincing
evidence for a strong association with beta-blocker use and depression. The
strong position taken against narcotic use in Cope's Early Diagnosis of the
Acute Abdomen is probably the reason for the perpetuation of the myth of
avoiding narcotics for pain relief in patients with undiagnosed acute
abdominal conditions. The only two studies addressing this issue showed no
problems with diagnosis caused by providing narcotic pain relief. Newer
therapies usually undergo closer scrutiny before being accepted, often
including placebo-controlled trials to show the efficacy of a medication.
Such might not be the case with newer technologies. It is harder to evaluate
the benefit of a new technology in the face of noncomparable previous
technologies. Catheterization of the right side of the heart (Swan-Ganz
catheter) was a technology that became widely used before any outcome
studies became available. Multiple reports in the last decade have shown
increased mortality and increased utilization of resources in patients who
received catheterization of the right side of the heart. Most new drug
therapies require randomized data to show effects before widespread use and
acceptance occur. Older therapies that have been widely accepted for a long
time might not have had controlled trial data behind recommendations for
their use, and once practice patterns become widespread, it is hard to
change. It is always good to ask the question, "Will this help my patient
live better or longer?" when prescribing a therapy. These myths underscore
the importance and utility of outcome-based research to help guide
physicians in their practices.
Publication Types:
Review
Review, Tutorial
PMID: 10220238
Pediatr Hematol Oncol 1999 Mar-Apr;16(2):159-63
Vitamin B12 absorption test and oral treatment in 14 children with selective
vitamin B12 malabsorption.
Altay C, Cetin M.
Department of Pediatrics, Ihsan Dogramaci Children's Hospital, Faculty of
Medicine, Hacettepe University, Ankara, Turkey.
Oral vitamin B12 (VB12) absorption was studied in 12 patients with selective
VB12 malabsorption and in 6 age-matched healthy controls. Serum VB12 level
was measured before and 3 h after oral administration of VB12 100 or 1000
micrograms. After administration of 1000 micrograms of VB12 an appreciable
increase in the serum VB12 level was observed in patients as well as in
controls. The mean of the increase in the serum VB12 level did not differ
between patients and the controls (273 +/- 203 pg/mL, 180 +/- 71 pg/mL,
respectively P > .05). Twelve patients previously treated by parenteral VB12
were switched to, and 2 newly diagnosed patients were started on, oral VB12
treatment of 1000 micrograms given every 2 weeks. Hematological parameters
and serum VB12 levels remained stable after switching to oral therapy in the
12 patients. In the two newly diagnosed patients anemia was cured by orally
administrated VB12. This study lends further support to the use of megadoses
of VB12 as an alternative treatment for selective VB12 malabsorption.
PMID: 10100276
Hua Kul
> "Hua Kul" <g...@adres.nl> wrote in message
> news:3da4c6e5.02092...@posting.google.com...
> > I believe I am B12 deficient and I want to try a transdermal solution
>
> Best - and easiest - bet is to take mega-doses (i.e. a mg or two or ten)
> orally. The medical consensus (recently revised) is that large amounts
> *will* correct deficiencies in people lacking the intrinsic factor. It is a
> myth that people with absorption problems can't acquire enough by simple
> saturation - you just have to take mega-RDA amounts [which are
> absorbed by passive diffusion, as opposed to active transport].
>
by external (transdermal) diffusion and internal diffusion? I'm
getting the picture that my body will safely tolerate a large dosage
range for B12 but I'm trying to calculate the dosage I should apply to
correlate with an optimal body level, assuming 100% gets into my
serum. This started out with B12 but if it works I may try to
administer other vitamins this way and need to determine good dosage
levels. Thanks for reposting to this thread.
--Hua Kul
michaelprice
>>
>> Best - and easiest - bet is to take mega-doses (i.e. a mg or two or
>> ten) orally. The medical consensus (recently revised) is that large
>> amounts *will* correct deficiencies in people lacking the intrinsic
>> factor. It is a myth that people with absorption problems can't
>> acquire enough by simple saturation - you just have to take mega-
>> RDA amounts [which are absorbed by passive diffusion, as opposed
>> to active transport].
>>
> Is there any significant difference in effectiveness between entrance
> by external (transdermal) diffusion and internal diffusion? I'm
> getting the picture that my body will safely tolerate a large dosage
> range for B12 but I'm trying to calculate the dosage I should apply to
> correlate with an optimal body level, assuming 100% gets into my
> serum. This started out with B12 but if it works I may try to
> administer other vitamins this way and need to determine good
> dosage levels. Thanks for reposting to this thread.
>
> --Hua Kul
I don't know of any evidence that intramuscular injection is superior to
oral ingestion for any vitamin (although it is for CoQ10). I've made a stab
at estimating (with refs) optimal values for B12 (and other B-vitamins) in
http://www.longevity-report.com/lr91.htm
See what you think.
Steve Harris
>I don't know of any evidence that intramuscular injection is superior to
>oral ingestion for any vitamin (although it is for CoQ10).
Not for vitamin C, most B, vitamins, or A. However, you certainly retain a
larger % of the dose with IM B12 and IM vitamin E. For B12 the liver
receptors saturates after you retain 10 to 20 mcg of an injected dose, but
you wouldn't absorb that much orally if you took 100 mcg or even 1000 mcg.
You do retain that much from a shot of either 100 mcg or 1000 mcg. Now, the
entire healthy loaded liver may contain 5000 mcg of B12, but it takes 20
injections or so to load it. It can't be done in a day.
Much the same kind of thing is true for solubilized forms of vitamin E,
which are given to calves with deficiencies. You can't do this nearly as
well PO as you can with a few IM doses. It takes weeks to saturate body
pools with oral vitamin E, but it can be done in one or two injections IM.
Toni
> book. A prize to the first spambot that passes my Turing test.
>
I doubt anyone is that interested...
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:MEqm9.3909$lV3.3...@newsread1.prod.itd.earthlink.net...
David Lloyd-Jones
> Steve,
> thanks, I appreciate the effort you've put into supplying the
> viatmin breakdown of lab feed figures, they'll prove invaluable.
Michael & Steve, (two of the people I most admire on the Net),
All this talk of rat chow (Michael, you say rat "pellets," but I always
thought pellets came out the other end :-) ) reminds me that in Africa
the UN sometimes delivers a "human chow," pellets which are mixed with
water and dished out as mush to the starving. (My partner is Sudanese,
so this stuff is important to me; many of our family are on faculties of
medicine all over Africa and Europe. Others are trapped in refugee camps
in Uganda, Chad and Kenya, if they are still alive.)
Here is my question: can you give me a pointer -- perhaps a sensible
Google entry -- to find out who makes this human chow. My instinct is we
could get a couple of million North American students paying maybe $4
for a bowlfull once a week or so -- particularly if we gave 'em the
choice of Kikkoman shoyu, Wit Fowler's sauce, or Heinz ketchup to get it
down -- and raise a few million a week for UNRRA. (No, it has not
escaped my attention that Kikkoman, Wit Fowler and Heinz might be good
sponsors, with sales forces available to deliver all the stuff to the
campuses...)
Best to you both.
-dlj.
David Lloyd-Jones
> michaelprice wrote in message ...
>>I don't know of any evidence that intramuscular injection is superior to
>>oral ingestion for any vitamin (although it is for CoQ10).>
> Not for vitamin C, most B, vitamins, or A. However, you certainly retain a
> larger % of the dose with IM B12 and IM vitamin E.
Michael,
What's your theory: all the Doctor Feelgoods on Park Avenue are
hypnotizing their clients into thinking the injection was what did it?
-dlj.
michaelprice
>
> What's your theory: all the Doctor Feelgoods on Park Avenue are
> hypnotizing their clients into thinking the injection was what did it?
? I'm not saying that injections don't work, just that mega-dosing
orally is a viable alternative. It's ironical that B12 is often injected
as a 'placebo'.
michaelprice
>
> All this talk of rat chow (Michael, you say rat "pellets," but I always
> thought pellets came out the other end :-) ) reminds me that in Africa
> the UN sometimes delivers a "human chow," pellets which are mixed
> with water and dished out as mush to the starving.
I'm afraid I have no specialist knowledge of chow. I don't think
I mentioned "pellets" either, but LEF mix, as tablets, springs to mind
- it looks like pellets.
michaelprice
> michaelprice wrote in message ...
>
>> I don't know of any evidence that intramuscular injection is
>> superior to oral ingestion for any vitamin (although it is for CoQ10).
>
> Not for vitamin C, most B, vitamins, or A. However, you certainly
> retain a larger % of the dose with IM B12 and IM vitamin E.
True, absorption by passive diffusion must be less efficient than injection.
> For B12 the liver receptors saturates after you retain 10 to 20 mcg
> of an injected dose, but you wouldn't absorb that much orally if you
> took 100 mcg or even 1000 mcg.
But you might if you take 10 000 mcg in the active coenzyme form. An
experiment on mice demonstrates the superiority of oral methyl-B12 10mg/d
over 1mg/d (if we accept allometric scaling, which, provisionally, I do).
[101b] [Effects of mecobalamin [methyl-B12] on testicular dysfunction
induced by X-ray irradiation in mice]
Oshio S, Yazaki T, Umeda T, Ozaki S, Ohkawa I, Tajima T, Yamada T, Mohri H.
Department of Urology, Teikyo University School of Medicine, Tokyo, Japan.
Experimental testicular dysfunction were produced by X-ray irradiation to
the testes in mice. Mecobalamin (CH3-B12) was orally administered at a daily
dose of 0.01, 0.1 or 1 mg/kg six times a week for 8 weeks from the next day
after the irradiation. The control mice received physiological saline in the
same manner. On 4th- and 6th-week after the irradiation, the weights of
testes and epididymides were decreased, although those of the body and
accessory sex glands (seminal vesicle, coagulating gland and prostate) were
nearly equal to those of non-irradiated mice. At the same time, the diameter
of seminiferous tubules decreased and sperm parameters (sperm count, sperm
motility and sperm abnormality) deteriorated. When CH3-B12 (1 mg/kg) was
administered, the diameter of seminiferous tubules increased and sperm
parameters improved as compared to those of the control. The results
indicate that CH3-B12 improved the experimental testicular dysfunction in
mice induced by the irradiation. These results suggest that CH3-B12 might
accelerate testicular function.
PMID: 1783330
> You do retain that much from a shot of either 100 mcg or 1000 mcg.
> Now, the entire healthy loaded liver may contain 5000 mcg of B12,
> but it takes 20 injections or so to load it. It can't be done in a day.
>
> Much the same kind of thing is true for solubilized forms of vitamin E,
> which are given to calves with deficiencies. You can't do this nearly as
> well PO as you can with a few IM doses. It takes weeks to saturate body
> pools with oral vitamin E, but it can be done in one or two injections IM.
Agreed. For rapid correction of a deficiency, injection would be superior
to the oral route.
Steve Harris
spambot ever has.
Toni wrote in message ...
Sheila Winterstone
> >"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
sbha...@ix.netcom.com
sbha...@ix.netcom.com
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George W. Cherry
LOL! Alan Turing would be proud of you, Sheila.
George
Maleki
<sbha...@ix.RETICULATEDOBJECTcom.com> wrote in
<lVJm9.5038$OB5.4...@newsread2.prod.itd.earthlink.net>
that:
>
>I had an epiphany back about 1990 that the worst starving/dying people of
>the world should actually be sent generic dry cat chow or dog chow. Both are
>complete nutrition, and for humans may be short only of (perhaps) vitamin C.
>For that matter, many of them weirdly even have the vitamin C-- don't ask me
>why. They aren't absolutely perfect for humans-- for example cat chows and
>even dog chows have more protein than humans need, but none of their
>differences would be unhealthy, AFAIK. If anything, cat or dog chow as a
>high protein supplement, along with the little bits of carbos that starving
>Africans get from other sources, may be JUST the thing.
>
>If you go to COSTCO you can see bags of Newco or Diamond dog chow (made out
>of mostly chicken byproduct and corn, with supplemental stuff) at prices
>like $16 for 40 lbs, which is 40 cents a pound or less than a buck a kilo.
>And this is 26% protein food, which delivers 3850 kcal/kg. So you could
>feed a person completely for 50 cents a day, and that includes fat, protein,
>vitamins, fiber, essential fatty acids (hell the stuff has omega-3's
>added)-- the whole shebang. And that's figuring the American retail price---
>price from the manufacturer will be a lot less, and probably offset some of
>the shipping.
>
>I have the horrid feeling that a lot of malnutrition in Africa happens
>because sending them dogfood is politically untenable. but not because it
>doesn't make nutritional sense, in terms of bang per buck.
But cat and dog food also has animal feces in it. I
would expect the manufacturers to be including that as
part of protein, fat etc. They don't miss a thing.
If it was not for the feces in them, American people
themselves would probably be the number one consumers
of such products as human food, forget the Africans.
Gym Bob
I bet the pet food manufacturers would have much to say about your feces
comment. have any references to back that one up?
"Maleki" <male...@hotmail.com> wrote in message
news:f4nqpugckkse28451...@4ax.com...
John 'the Man'
rambled on about "Re: Longevity Report 91."
Our champion De-Medicalizing in sci.med.nutrition retorts, thusly ...
Here is a post worth repeating. :-)
Steve 'the Stiff' never paid up on his 'public' wager. I bet Steve
will stiff you too. :-(
--
John Gohde
Email: N...@NaturalHealthPerspective.com
((((((((((( Left-Brain Mode ON ))))))))))))
Richmond, Virginia, USA, Planet Earth, The Sun, Milky Way galaxy
Chris Jain
> Once upon a time, our fellow Sheila Winterstone
> rambled on about "Re: Longevity Report 91."
> Our champion De-Medicalizing in sci.med.nutrition retorts, thusly ...
> will stiff you too. :-(
Following up only to sci.med.nutrition
Is this an implicit admission that you are a SPAMBOT?
Please note that Steve offered a prize to the FIRST spambot that
solved his Turing test. So it would seem that you are disqualified.
Steve Harris
>Steve 'the Stiff' never paid up on his 'public' wager. I bet Steve
>will stiff you too. :-(
Which public wager was that?
SBH
Steve Harris
>But cat and dog food also has animal feces in it.
Show your evidence. It's not on the package list of ingredients.
Gym Bob
US. nutrition content and all are totally controlled as much as human foods.
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:z0on9.8771$OB5.8...@newsread2.prod.itd.earthlink.net...
Steve Harris
>In article <AH2n9.7256$lV3.6...@newsread1.prod.itd.earthlink.net>,
>Steve Harris <sbha...@ix.RETICULATEDOBJECTcom.com> wrote:
>
>>I've had dozens of people interested enough to see if they got it. No
>>spambot ever has.
>
>(Stetson-estimate) who do not speak english as their first language. Cool
>and wise, or not?
>
>Marcus
I'm ruling out all the people who don't speak English as primary language,
and who don't know anybody who does. AND who are using the internet and want
to email me badly.
Must be zillions of them. Not.
SBH
John 'the Man'
Once upon a time, our fellow Chris Jain
rambled on about "Re: sbha...@ix.netcom.com (Re: Longevity Report
91)."
Our champion De-Medicalizing in sci.med.nutrition retorts, thusly ...
>John 'the Man' <DeMan[89]@hotmail.com> wrote in message news:<39kqpu07cv007mpca...@4ax.com>...
>> Once upon a time, our fellow Sheila Winterstone
>> rambled on about "Re: Longevity Report 91."
>> Our champion De-Medicalizing in sci.med.nutrition retorts, thusly ...
>> Steve 'the Stiff' never paid up on his 'public' wager. I bet Steve
>> will stiff you too. :-(
>
>Following up only to sci.med.nutrition
>
>Is this an implicit admission that you are a SPAMBOT?
>
>Please note that Steve offered a prize to the FIRST spambot that
>solved his Turing test. So it would seem that you are disqualified.
The way I figure it. The more replies to this post, the more Steve's
'the Stiff' private email address becomes not so private. :)
John@getstev.com Sir John
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:CZnn9.8765$OB5.8...@newsread2.prod.itd.earthlink.net...
dolores
Pet food is not required to be manufactured under the same sanitary
standards as human food. Before you send kibble to some third world
country I suggest you try eating it for a week.
America could feed the world without resorting to dog food. The
political situations in so many of these countries make it impossible
to distribute food.
Dolores
David Lloyd-Jones
> Pet foods are under very strick government controls in Canucksville and the
> US. nutrition content and all are totally controlled as much as human foods.
Reply to various:
To Gym Bob:
There's a saying among health and food professionals that "there are
more fecal bacteria in the kitchen than any place else in the house, the
bathroom included." I treat my kitchen like a lab, and wash it down
with one-to-five bleach, i.e. 1% sulphite, any time the beasties get big
enough to cart the eggplants away.
To Steve:
Your epiphany is rather like mine, though mine has become somewhat more
focused through my partner's participation in one of the most vicious
civil wars that has occurred (and is occurring) in the post WWII period.
(During the recent reign of the right-wing Bill Harris in Ontario, I
toyed with the idea of putting out a "The Common Sense Revolution
Cookbook," which would have been various ways of gussying up dogfood.
Golfer Bill is history before I could get around to it. [But this is
small-time humour compared to the Sudan thing, about which I am serious.])
There is no starvation in Africa except that caused by war or deliberate
political policy by madmen, a near-equivalent to war. There will be
starvation in Zimbabwe befor the spring (they're in the southern
hemisphere) because their thug dictator has deliberately disrupted
everything.
The truly humungous starvation in Sudan is a weapon of war by the
Khartoum "government."
There will no doubt be starvation in Sierre Leone and throughout West
Africa, unless the French airlift in hundreds of tons of everything, not
because the land has stopped producing, but because the wars have
disrupted the mechanisms of trade and communication.
* * *
"Human chow" is necessary only when you have a crowd-
at-the-front-of-the-C-130 sort of emergency. Everybody in Africa has
food, given only a year of peace.
I think you have taught me an important point, which is that if there is
to be any campaign of having Canadian and American students eat this
stuff, it must *not* convey the idea that Africans can't feed themselves.
We should be sending money to UNRRA to help very viable people -- like
my in-laws in muddy stinking camps -- in the same way we helped the
French, Germans and Poles in the post-war 1940's.
-dlj.
Maleki
<sbha...@ix.RETICULATEDOBJECTcom.com> wrote in
<z0on9.8771$OB5.8...@newsread2.prod.itd.earthlink.net>
that:
>Maleki wrote in message ...
>>But cat and dog food also has animal feces in it.
>
>
>Show your evidence. It's not on the package list of ingredients.
Smell it.
Maleki
<no...@spam.com> wrote in
<ODen9.1603$EA4.18...@radon.golden.net> that:
>I belive the ratio is about 40% of the pet food is consumed by humans.
>
? It is hard for me to believe that. Frozen chicken is
almost always available in USA at prices below cat
food. People there don't have to eat cat food for
saving money. But for convenience they _would_ if only
it didn't have animal feces in it.
>I bet the pet food manufacturers would have much to say about your feces
>comment. have any references to back that one up?
Wet your dry cat food and wait an hour or so, then
smell it. It smells of chicken shit. Even dry form of
it if you have good nose will smell that. I bet the
whole innards of chickens when taken out are sent to
the cat food processing sections in the factories
without further separating the feces from the
intestines, etc. Cats don't mind that at all of course
and indeed the innards together with feces are the most
interesting part of the kill for them to eat. But for
humans it is a different story.
Gym Bob
food to help control our ever out of control pet population but cannot
because of the high pet food consumption by humans.
"Maleki" <male...@hotmail.com> wrote in message
news:7ultpu8meise32oa2...@4ax.com...
Gym Bob
Smell your turkey before the oven. Can you smell the salmonella?
"Maleki" <male...@hotmail.com> wrote in message
news:4cltpuk84irp4otcq...@4ax.com...
Steve Harris
Can't smell a thing. Pet foods are manufactured to smell good to human
owners, since they're not being sold to pets (ever seen a cat pushing a
grocery cart in supermarket?). Petfood that smelled like feces, wet or
dry, immediately, or after delay, would quickly be pushed off the market by
others that didn't.
SBH
Steve Harris
<52rn9.3300$ue4.1...@bgtnsc04-news.ops.worldnet.att.net>...
>"A prize to the first spambot that passes my Turing test."
No spambot ever has.
SBH
Steve Harris
It is well that you use the frowny face emoticon, you toothless wonder.
You'll be a skull long before I'm a popsicle. And without a grin you won't
even be a competent skull. Perhaps they'll bury you with dentures for future
archeologist comic relief.
Steve Harris
>To Steve:
>
>Your epiphany is rather like mine, though mine has become somewhat more
>focused through my partner's participation in one of the most vicious
>civil wars that has occurred (and is occurring) in the post WWII period.
>
>(During the recent reign of the right-wing Bill Harris in Ontario, I
>toyed with the idea of putting out a "The Common Sense Revolution
>Cookbook," which would have been various ways of gussying up dogfood.
>Golfer Bill is history before I could get around to it. [But this is
>small-time humour compared to the Sudan thing, about which I am serious.])
>
>There is no starvation in Africa except that caused by war or deliberate
>political policy by madmen, a near-equivalent to war. There will be
>starvation in Zimbabwe befor the spring (they're in the southern
>hemisphere) because their thug dictator has deliberately disrupted
>everything.
>
>The truly humungous starvation in Sudan is a weapon of war by the
>Khartoum "government."
>
>There will no doubt be starvation in Sierre Leone and throughout West
>Africa, unless the French airlift in hundreds of tons of everything, not
>because the land has stopped producing, but because the wars have
>disrupted the mechanisms of trade and communication.
COMMENT:
While I disagree with none of this, arguing about it on an "instead of"
basis is rather like doctors arguing about smoking when the immediate
problem is the patient who is dying of pneumonia and needs antibiotics,
oxygen and/or a ventilator. The basic idea is that if you don't save him
now, you certainly can't cure him of his bad habits later, since he'll be
dead. Treating pneumonia and emphysema does not mean you've given up on
smoking education.
>"Human chow" is necessary only when you have a crowd-
>at-the-front-of-the-C-130 sort of emergency. Everybody in Africa has
>food, given only a year of peace.
And if my grandmother had wheels, she'd be a trolley car. Human chow is
necessary in all situations in which society has been disrupted, and people
with guns are interfering with people growing and distributing food. People
with guns always eat. Until you've eliminated bad governments (which tends
to be frowned on by the UN, for political reasons) the problem continues.
The only way to treat it is to drop food directly to people without guns,
and bypass the corrupt middle men.
My objection is that we're doing this inefficiently. As I've noted, you can
get 2,200 Kcal of dog food wholesale for less than 50 cents. That feeds a
starving adult for a day.
What are we dropping to starving populations (as in Afghanistan) instead?
Why, prepackaged "culturally sensitive" (see politically correct) vegetarian
2,200 kcal rations which cost $4 to produce, and that's just the marginal
cost, not counting the millions wasted in developing something with five
entrees containing lentils, beans, rice, bread, fruit bars, fortified
biscuits, peanut butter, spices, utensils, and for all I know, a little Kron
chocolate to be put on the pillow.
So to be politically correct we are feeding 1 person and letting 7 starve,
when for the same money we could feed all 8.
And the people who make this kind of nonsense happen? Why, politicians who
worry about "cultural sensitivity" when people are dying,and the academics
on the Left and the Right whose opinions drive them. (Neither Jewish nor
Muslim dietary laws demand that starving people comply with them-- both
religions have been around far too long to have such rigid rules). And
bigots like you see right here, suggesting that pet food might have feces in
it. The sorts of Hindu and Muslim fanatics who brought you the Sepoy riots
(Google it if you don't know your history). And the sorts of people who
brought you the mindless wars between religious factions that make the
starvation happen in the first place. The obsessive compulsive zealots and
the power hungry bastards.
The intelligent first-aid solution is drop them dog chow. That's it. But
it's way too obvious and simple to ever be done.
The second thing is to inform the UN that unless they start getting serious
about peacekeeping in countries where mass starvation is being caused by
civil war, that we're going to simply stop supporting them, sell that stupid
blue building that sits on the old slaughterhouse site in NYC, and take on
the job ourselves. Screw politically correct opinion. People are dying.
>I think you have taught me an important point, which is that if there is
>to be any campaign of having Canadian and American students eat this
>stuff, it must *not* convey the idea that Africans can't feed themselves.
African's can't feed themselves. If they could, they would. Let me quote
from American philosopher Mae West: "If the guy who really wants to do
something isn't doing it, it's because he really doesn't want to do it."
Too many people in Africa don't really want to do what has to be done.
They'd rather play with guns, because power gets you women, and that's
written into the genes. The starving kids and the starving losers are not
provided for by Mother Nature. It's the same everywhere in the world.
SBH
Maleki
<sbha...@ix.RETICULATEDOBJECTcom.com> wrote in
<pAFn9.10668$lV3.1...@newsread1.prod.itd.earthlink.net>
that:
>Maleki wrote in message <4cltpuk84irp4otcq...@4ax.com>...
>>On Fri, 04 Oct 2002 21:48:15 GMT, "Steve Harris"
>><sbha...@ix.RETICULATEDOBJECTcom.com> wrote in
>><z0on9.8771$OB5.8...@newsread2.prod.itd.earthlink.net>
>>that:
>>
>>>Maleki wrote in message ...
>>>>But cat and dog food also has animal feces in it.
>>>
>>>
>>>Show your evidence. It's not on the package list of ingredients.
>>
>>Smell it.
>
>
>Can't smell a thing. Pet foods are manufactured to smell good to human
>owners, since they're not being sold to pets (ever seen a cat pushing a
>grocery cart in supermarket?). Petfood that smelled like feces, wet or
>dry, immediately, or after delay, would quickly be pushed off the market by
>others that didn't.
>
>SBH
Are you familiar with the smell of chicken shit (or
pigeon shit)? I am, and I can smell it in any brand of
cat food. It doesn't smell like human shit at all, it
has its own special odor. It is easier to feel the
smell in dry cat food especially when it's moist.
Maleki
<no...@spam.com> wrote in
<AZDn9.1687$AQ3.19...@radon.golden.net> that:
>Thirty or so years back they wanted to put sterilizing agents in the pet
>food to help control our ever out of control pet population but cannot
>because of the high pet food consumption by humans.
Interesting. Well, about feces I don't think they have
a choice. Either they'd have to throw away lots of bird
innards or introduce some bird feces into cat food.
John@getstev.com Sir John
:) Steve "the patient's Doctor" :)
Ha, ... Hah, Ha!
Don't quit your day job Steve, no patient would every put up with your
mannerisms. :)
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:NLFn9.10687$lV3.1...@newsread1.prod.itd.earthlink.net...
John@getstev.com Sir John
You are just a cheap stiff, ... Steve.
And, a Dumb-Ass to boot. :)
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:cFFn9.10676$lV3.1...@newsread1.prod.itd.earthlink.net...
Steve Harris
Maleki wrote in message <15gupuk13maono90d...@4ax.com>...
>On Sat, 05 Oct 2002 17:47:01 GMT, "Steve Harris"
>Are you familiar with the smell of chicken shit (or
>pigeon shit)?
Yes. Possibly your nose is better than mine for this, however.
> I am, and I can smell it in any brand of
>cat food.
That's remarkable, since some brands have no chicken products in them of any
kind.
I will admit that many (perhaps most) brands of both dog and cat food do
have "chicken by product meal" and (upon examination) I find that this is
indeed ground up dried and sterilized chicken stuff, including heart liver
and intestines-- just about everything but the feathers-- so it's bound to
have some chicken shit in it. It's sterile if canned, and the bacterial
count is low if dry. But it's in there.
It's hard to know what to make of this. You're going to get a little feces
in your diet even if you're a vegetarian. The more organic you are, the more
you'll get. Most of the nutrition in by product meal is NOT from the feces.
Steve Harris
<39kqpu07cv007mpca...@4ax.com>...
>Steve 'the Stiff' never paid up on his 'public' wager.
Liar.
John@getstev.com Sir John
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:r5Kn9.10606$OB5.1...@newsread2.prod.itd.earthlink.net...
A spambot is nothing but a web-crawler allegedly designed to extract email
addresses from web pages, which are then allegedly used as targets for spam.
Examples of spambots would be bumblebee/1, Gigabot/1, webcollage/1,
Scooter/3, Scooter-W3.1.2, Jonzilla/666, Scooter-3.2.EX, libwww-perl/5, and
W3C_Validator/1.
About 5% of the hits to my website are from spambots. I have made
absolutely no attempt to hide my email addresses from spamots. To date, I
have yet to receive a single piece of spam from any spambot. :)
Your signature is, thus, totally stupid. And, you are indeed a cheap-skate
who stiffed me. :(
And, you are nothing but a paranoid fool. :)
Gym Bob
<taur...@pacbell.net> wrote in message
news:l0tupuo6vlnnt2ei9...@4ax.com...
> On Sat, 05 Oct 2002 22:47:40 GMT, "Steve Harris"
> <sbha...@ix.RETICULATEDOBJECTcom.com> wrote:
>
> >I will admit that many (perhaps most) brands of both dog and cat food do
> >have "chicken by product meal" and (upon examination) I find that this is
> >indeed ground up dried and sterilized chicken stuff, including heart
liver
> >and intestines-- just about everything but the feathers--
>
> The feathers are probably there too - in the form of feather meal.
>
> Ora
>
>
>
>
>
> so it's bound to
> >have some chicken shit in it. It's sterile if canned, and the bacterial
> >count is low if dry. But it's in there.
> >
> >SBH
>
Gym Bob
Must be the Christian morals that have destroyed their food
knowledge.....LOL
"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
news:qBGn9.10763$lV3.1...@newsread1.prod.itd.earthlink.net...
dolores
There may or may not be feces in cat food because pet foods are not
held to the same sanitary standards as are human foods. However, cat
food does smell like rotten fish because the manufacturers spray it
with fermented fish so that the cats will eat it. Have you noticed
that if you put more food in the bowl than your cat will eat, that the
cat will not eat the rest of the food until you add more food fresh
from the bag. That is because the odor dissipates and the cat isn't
interested until he smells that nice rotten fish odor.
I don't know why anyone would be surprised that there might be feces
in cat food. Twenty Twenty or some other show like it once had a
camera in a slaughter house (where the meat was destined for human
consumption ) and recorded sloppy butchering practices that resulted
in feces on the meat. Imagine in a pet food place where government
regulations are less stringent as far as sanitation is concerned.
Dolores
Doug Brooks
> About 5% of the hits to my website are from spambots. I have made
> absolutely no attempt to hide my email addresses from spamots. To date, I
> have yet to receive a single piece of spam from any spambot. :)
You're lucky. Perhaps things have changed, perhaps your ISP blocks
spam, I don't know. My previous experience was that when I posted with
a legit address, spam started almost immediately, having previously been
zero. Over time, it eventually became about 20 to 1 spam to real email,
and I had to get a new email address.
The fact that some have published Steve's actual email address, when it
was clear by design that he wished to hide it from spambots, I find
unconscionable.
John 'the Man'
rambled on about "Re: sbha...@ix.netcom.com (Re: Longevity Report
91)."
Our champion De-Medicalizing in sci.med.nutrition retorts, thusly ...
>The fact that some have published Steve's actual email address, when it
>was clear by design that he wished to hide it from spambots, I find
>unconscionable.
Ha, ... Hah, Ha!
Not when the clown is just begging people to do same. And, his warm
personality demands public disloseure.
Ha, ... Hah, Ha!
And, I still maintain that you clowns don't have a clue about
spambots. You are just paranoid and grossly misinformed about
reality.
You get spam from posting on newsgroups. As far as I know, Steve has
no webpage, ego his comments are just plain stupid and inflammatory.
Maleki
(dolores) wrote in
<7e9164f6.0210...@posting.google.com> that:
>There may or may not be feces in cat food because pet foods are not
>held to the same sanitary standards as are human foods. However, cat
>food does smell like rotten fish because the manufacturers spray it
>with fermented fish so that the cats will eat it. Have you noticed
>that if you put more food in the bowl than your cat will eat, that the
>cat will not eat the rest of the food until you add more food fresh
>from the bag. That is because the odor dissipates and the cat isn't
>interested until he smells that nice rotten fish odor.
>
>I don't know why anyone would be surprised that there might be feces
>in cat food. Twenty Twenty or some other show like it once had a
>camera in a slaughter house (where the meat was destined for human
>consumption ) and recorded sloppy butchering practices that resulted
>in feces on the meat. Imagine in a pet food place where government
>regulations are less stringent as far as sanitation is concerned.
>
>Dolores
The somewhat equivalent to "cat food" but for humans is
beef (or chicken) franks. Same stuff are used but the
feces have carefully been removed. For cat food they
don't have to go that extra mile especially when cats
indeed prefer their food to have that smell.
Paul Rogers
<gwch...@alum.mit.edu> wrote:
>"Sheila Winterstone" wrote:
>
>"> >
>> >"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in message
<snip email address>
>LOL! Alan Turing would be proud of you, Sheila.
Huh! Google turns that up in about 20 seconds. :-)
PR
Max Watt
> The intelligent first-aid solution is drop them dog chow. That's it. But
> it's way too obvious and simple to ever be done.
>
I think Zupreen primate chow would be better balanced nutritionally,
and cost about the same as dog-food.
bogus address
>> But cat and dog food also has animal feces in it.
> Show your evidence. It's not on the package list of ingredients.
I have worked in a slaughterhouse (one of the biggest in the world)
shovelling spare sheep organs down the catfood chute. No way in hell
was there any faeces on them. *Everything* got hosed down all the
time; the wastewater from the factory had the volume of a small river.
Minced spleen, lung and labia wouldn't be my ideal meal but they
hardly have a hygiene problem.
: There is no starvation in Africa except that caused by war or
: deliberate political policy by madmen, a near-equivalent to war.
Malawi hasn't a war since independence and it's the worst threatened
country in the region.
What it *does* have is (a) rampaging capitalism that has thrown almost
all farmers off food-producing land to grow tea for British companies,
(b) ecological disaster induced by American energy policy. I guess
you could describe those as acts of war if you wanted, but there are no
diamond-company goon squads running around Malawi shooting up villages
with AK-47s.
========> Email to "jc" at this site; email to "bogus" will bounce. <========
Jack Campin: 11 Third Street, Newtongrange, Midlothian EH22 4PU; 0131 6604760
http://www.purr.demon.co.uk/purrhome.html food intolerance data and recipes,
freeware logic fonts for the Macintosh, and Scots traditional music resources
michaelprice
experiment that Steve and I have been discussing:
"Only a single and limited study has addressed this problem. While mice fed
1/2 RDA levels of (all) vitamins lived 12% less long than controls, there
was no difference in survival between mice fed regular RDA and those fed 4x
RDA amounts of (all) vitamins (Kokkonen and Barrows, 1985). "
A clear and conclusive statement. Walford is saying, hey you need the RDAs,
but this experiments shows that any supra-RDA amounts are wasted excess.
Calories restriction is the only thing proven to work etc etc
I looked the study up and found - to my amazement - that the life-extension
was :
1/2 x RDA = -43% (that right, not the -12% Walford reports)
1 x RDA = 0 (i.e. controls)
4 x RDA = +19% (a statistically significant extension)
for animals receiving the diet over their whole life.
For animals that started the dietary vitamin regimes in middle age onwards
there was a non-statistically-significant increase in lifespan (remaining LE
for 4xRDA = 3% & 6%, approx -50% for 1/2 RDA).
I shall never trust anything Walford says again.
Cheers,
Michael C Price
----------------------------------------
http://www.longevity-report.com/lr91.htm
http://www.hedweb.com/manworld.htm
Hua Kul
> Walford (The 120 year diet, page 392) cites the Kokkonen & Barrows
> experiment that Steve and I have been discussing:
>
> "Only a single and limited study has addressed this problem. While mice fed
>
I assume the experiment did not imply anything about the impact of
vitamin C supplementation in species which do not make their own. Am
I correct?
--Hua Kul
michaelprice
>> Walford (The 120 year diet, page 392) cites the Kokkonen &
>> Barrows experiment that Steve and I have been discussing:
>>
>> "Only a single and limited study has addressed this problem. While
>> mice fed 1/2 RDA levels of (all) vitamins..."
>>
> I assume the experiment did not imply anything about the impact of
> vitamin C supplementation in species which do not make their own.
> Am I correct?
>
> --Hua Kul
I don't know the mix or amounts. The graduated tests were done on multiples
or fractions of the amount set by the National Academy of Sciences National
Research Council. I presume it is similar (identical?) to the RDAs then
established since the NRC sets RDAs also, but I don't know how they handled
vitamin C, since there was no breakdown published.
michaelprice
> Barrows experiment that Steve and I have been discussing:
I forgot to give the reference if anybody wishes to check the report
Its AGE, vol 8, pages 13-17, Jan 1985
"The Effect of Dietary Vitamin, Protein, and Intake Levels on the Life Span
of Mice of Different Ages."
by Gertrude C Kokkonen and Charles H Barrows.
Only mean lifespan data reported.
Cheers,
Michael C Price
Steve Harris
book chapter things that isn't peer reviewed? Does it have an abstract?
Somewhere I've seen this paper or something like it, and I'm wracking my
brains as to where.
SBH
michaelprice wrote in message
<4eKp9.4343$345.2...@newsfep2-win.server.ntli.net>...
--
michaelprice
> book chapter things that isn't peer reviewed? Does it have an abstract?
>
> Somewhere I've seen this paper or something like it, and I'm wracking
> my brains as to where.
>
> SBH
>
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=journals&list_
uids=27580&dopt=full:
Age. Links
pISSN: 0161-9152
MEDLINE Abbr: Age (Omaha)
Publication Start Year: 1978
Publication End Year: 1999
Publisher: American Aging Association
Language: eng
Country: United States
NLM ID: 7801686
http://locatorplus.gov/cgi-bin/Pwebrecon.cgi?DB=local&v2=1&ti=1,1&Search_Arg
=7801686&Search_Code=0359&CNT=20&SID=1
but the congress abstracts are not available, prior to 2002
http://www.americanaging.org/past_meetings/.
To get my paper copy I had to pay a visit to the (central) British Library.
Cheers,
Michael C Price
----------------------------------------
http://www.longevity-report.com/lr91.htm
http://www.hedweb.com/manworld.htm
> michaelprice wrote in message
Michael
"michaelprice" <michae...@ntlworld.com> wrote in message news:<o9xp9.1496$345....@newsfep2-win.server.ntli.net>...
> Walford (The 120 year diet, page 392) cites the Kokkonen & Barrows
> experiment that Steve and I have been discussing:
>
> "Only a single and limited study has addressed this problem. While mice fed
> 1/2 RDA levels of (all) vitamins lived 12% less long than controls, there
> was no difference in survival between mice fed regular RDA and those fed 4x
> RDA amounts of (all) vitamins (Kokkonen and Barrows, 1985). "
This is a perfectly accurate summary of the study's results. Indeed,
it's just what the paper's abstract says: "Feeding one half the amount
of vitamins recommended by the [NRC] statistically significantly
reduced the life span of animals, starting at 17 months of age or
younger. Increasing the vitamin level four fold did not increase the
life span of adult animals." Presumably, that's why they reported it
in AGE, instead of a higher-impact journal.
>
> I looked the study up and found - to my amazement - that the life-extension
> was :
>
> 1/2 x RDA = -43% (that right, not the -12% Walford reports)
> 1 x RDA = 0 (i.e. controls)
> 4 x RDA = +19% (a statistically significant extension)
>
> for animals receiving the diet over their whole life.
>
> For animals that started the dietary vitamin regimes in middle age onwards
> there was a non-statistically-significant increase in lifespan (remaining LE
> for 4xRDA = 3% & 6%, approx -50% for 1/2 RDA).
The above does not reflect the actual findings of the study. The av'g
LS data are given thus [ignoring te SEMs] in Table 1:
Starting Age 0.5 NRC 1.0 NRC 1.0 AIN76 4.0 NRC
[mo]
---------------------------------------------------------------
1 8.8 20.7 23.3 24.6
12 20.3 26.3 26.5 26.7
17 22.5 27.3 27.2 27.9
20 26.4 26.2 27.6 26.0
The NRC and AIN76 diets are intended to be rodent RDA diets.
What Michael Price SEEMS to have done in his reporting above, is
something like to take the most short-lived 1-RDA cohort in the study,
taken them as the standard, and compared all the other cohorts thereto
(ignoring the 6 or 7 other 1-RDA cohorts, which all had av'g LSs
considerably longer, & most of them ~31% longer). As Steve, Aubrey,
and myself keep trying to point out, this isn't a meaningful way to
make comparisons. If one wants to do life extension studies, one has
to start with a control group that is well-nourished (in a simple RDA
sense), well-cared-for, not crippled by some genetic disorder, and not
full of nasty pathogens, etc. It's neither relevant to biogerontology
nor of interest more broadly for an essentially well-nourished (in a
simple RDA sense), genetically typical person of average socioeconomic
status and access to health care to know that giving Substance X to
rodents who are malnourished, or victims of poor genetic dice-rolls,
or infected with pathogens, or subjected to nasty toxins, or otherwise
at high risk of early death results in them living lives closer to the
norm for the species when properly cared for.
Clearly, from Table 1, the av'g LS for this lab's animals are ~26-27
mo. Thus even the MOST longevous group is in no way "life extended:"
aside from the lack of max LS data (which can certainly be taken to be
unremarkable -- no one in biogerontology is going to just neglect an
increase in max LS, even if it were just for the cohort), 27.6 mo =
849 days, whereas well-cared-for, non-genetically-fucked-up,
undiseased mice can live 900 days on average (1, summarizing previous
data from lab mice). And if we're gonna talk AGING, we wanna see, at
LEAST, extended species max LS (for mice, ~1200 days (eg (2,3)), &
preferrably some convincing Gompertz data to go with it. And, of
course, we want frank or crypto-CR ruled out by seeing that neither
food intake nor body weight are reduced by the intervention.
Characterizing anything of the above as a life extension effect is the
same error previously reported for B vitamins, RNA, etc. If Elixir
Pharmaceuticals runs a controlled trial of a putative anti-aging
drug, and the controls die, on average, at age 60 and the oldest of
'em is dead at 80, whereas the group taking their pill lives a
perfectly normal average age of 78 years and manages one centenarian,
no one sensible is going to declare that the control of biological
aging is at hand.
What is seen above is that (a) these guys don't know how to care for
weanling mice, with the result that all of the animals in their care
from 1 mo on are short-lived, and that (b) as Walford summarizes,
"While mice fed 1/2 RDA levels of (all) vitamins lived 12% less long
than controls, there was no difference in survival between mice fed
regular RDA and those fed 4x RDA amounts of (all) vitamins."
Walford's usual, simple challenge stands: "Show me the 45-month-old
mouse."
-Michael
1: Miller RA, Harper JM, Dysko RC, Durkee SJ, Austad SN.
Longer life spans and delayed maturation in wild-derived mice.
Exp Biol Med (Maywood). 2002 Jul;227(7):500-8.
PMID: 12094015
2: Pugh TD, Oberley TD, Weindruch R.
Dietary intervention at middle age: caloric restriction but not
dehydroepiandrosterone sulfate increases lifespan and lifetime cancer
incidence
in mice.
Cancer Res. 1999 Apr 1;59(7):1642-8.
PMID: 10197641 [PubMed - indexed for MEDLINE]
3: Weindruch R, Walford RL.
Dietary restriction in mice beginning at 1 year of age: effect on
life-span and
spontaneous cancer incidence.
Science. 1982 Mar 12;215(4538):1415-8.
PMID: 7063854 [PubMed - indexed for MEDLINE]
--
http://www.sciam.com/print_version.cfm?articleID=000F3D47-C6D2-1CEB-93F6809EC5880000
(Climate change is real). http://www.climatechangesolutions.com
(Real choices) http://www.fueleconomy.gov/feg/hybrid_news.shtml
(Car choices) http://www.janeholtzkay.com/AsphaltNation (Another car
choice).
michaelprice
>> Walford (The 120 year diet, page 392) cites the Kokkonen & Barrows
>> experiment that Steve and I have been discussing:
>>
>> "Only a single and limited study has addressed this problem. While
>> mice fed 1/2 RDA levels of (all) vitamins lived 12% less long than
>> controls, there was no difference in survival between mice fed regular
>> RDA and those fed 4x RDA amounts of (all) vitamins (Kokkonen
>> and Barrows, 1985). "
>
> This is a perfectly accurate summary of the study's results.
No it isn't. The 12% is either a complete fiction or confusion of the NRC
(=RDA) with the AIN76 regime, which aren't comparable. And it totally
ignores the actual whole-life 1x NRC and 4xNRC survival differences,
even though they were statistically non-significant. "no difference" is not
the same as "no statistical difference"..
> Indeed,
> it's just what the paper's abstract says: "Feeding one half the amount
> of vitamins recommended by the [NRC] statistically significantly
> reduced the life span of animals, starting at 17 months of age or
> younger. Increasing the vitamin level four fold did not increase the
> life span of adult animals." Presumably, that's why they reported it
> in AGE, instead of a higher-impact journal.
My statement (follows), unlike Michael Rae's, was a completely accurate
summary of the comparable NRC = RDA vitamin regimes. If the abstract
chose to emphasis the negative aspects and completely ignore the positive
effects of whole life 4xRDA over 1xRDA that's not my problem.
>> I looked the study up and found - to my amazement - that
>> the life-extension was :
>>
>> 1/2 x RDA = -43% (that right, not the -12% Walford reports)
>> 1 x RDA = 0 (i.e. controls)
>> 4 x RDA = +19% (a statistically significant extension)
>>
>> for animals receiving the diet over their whole life.
>>
>> For animals that started the dietary vitamin regimes in middle age
>> onwards there was a non-statistically-significant increase in
>> lifespan (remaining LE for 4xRDA = 3% & 6%, approx
>> -50% for 1/2 RDA).
>
> The above does not reflect the actual findings of the study.
On the contrary it is a *completely* accurate summary.
> The av'g
> LS data are given thus [ignoring te SEMs] in Table 1:
>
> Starting Age 0.5 NRC 1.0 NRC 1.0 AIN76 4.0 NRC
> [mo]
> ---------------------------------------------------------------
> 1 8.8 20.7 23.3 24.6
> 12 20.3 26.3 26.5 26.7
> 17 22.5 27.3 27.2 27.9
> 20 26.4 26.2 27.6 26.0
>
> The NRC and AIN76 diets are intended to be rodent RDA diets.
Crap. You can't compare the NRC with AIN76.
I'm amazed that Michael Rae can go to the trouble of typing in the raw
data and then not bother to process it sufficiently to see that it is
entirely compatible with my summary above. This negates the
remainder of his analysis, which we've all heard before anyway.
Steve Harris
michaelprice wrote in message
<0pKq9.14537$345.7...@newsfep2-win.server.ntli.net>...
>> This is a perfectly accurate summary of the study's results.
>
>No it isn't. The 12% is either a complete fiction or confusion of the NRC
>(=RDA) with the AIN76 regime, which aren't comparable. And it totally
>ignores the actual whole-life 1x NRC and 4xNRC survival differences,
>even though they were statistically non-significant. "no difference" is
not
>the same as "no statistical difference"..
Well, actually it is. If there's no statistical difference, that means that
any difference you see is possibly due to shear chance (toss of the coin)
with a probability which is too high for you to say with any confidence that
it isn't. Thus, there's a reasonable chance (at least 1 in 20 by convention)
that there's no effect at all. If I flip a coin 20 times and you do too,
there's very likely going to be a difference between our results. But we
don't CARE that there is, because the question we're interested in is not
whether there's a difference, but in whether or not the difference ill
persist (one of us doesn' have a fair coin, or is telekinetic, or is
cheating, or whatever).
>My statement (follows), unlike Michael Rae's, was a completely accurate
>summary of the comparable NRC = RDA vitamin regimes. If the abstract
>chose to emphasis the negative aspects and completely ignore the positive
>effects of whole life 4xRDA over 1xRDA that's not my problem.
It's your problem if you choose to think of "whole life" survival data as
having anything to do with gerontology or aging! If clean drinking water and
vaccinations for kids raises the average life expectancy in Uganda from 40
to 60, do you think that has to do with the antiaging effects of the Peace
Corps? Come ON.
>> The av'g
>> LS data are given thus [ignoring te SEMs] in Table 1:
>>
>> Starting
Age 0.5 NRC 1.0 NRC 1.0 AIN76 4.0 NRC
>> [mo]
>> ---------------------------------------------------------------
>> 1 8.8 20.7 23.3 24.6
>> 12 20.3 26.3 26.5 26.7
>> 17 22.5 27.3 27.2 27.9
>> 20 26.4 26.2 27.6 26.0
Okay, just stop right there. Ignore the life expectancies starting at 1
month-- they have nothing to do with aging. Now, look at the rest of the
table. And yawn.
That's it.
SBH
michaelprice
>> The 12% is either a complete fiction or confusion
>> of the NRC (=RDA) with the AIN76 regime, which aren't
>> comparable. And it totally ignores the actual whole-life 1x NRC
>> and 4xNRC survival differences, even though they were
>> statistically non-significant. "no difference" is not the same as
>> "no statistical difference"..
>
> Well, actually it is.
No it isn't. I shouldn't have to explain this to you Steve, but a number of
non-statistically significant results can amount to a statistically
significant result, whereas any number of no-difference results is still no
difference. Come ON.
[.......]
> Okay, just stop right there. Ignore the life expectancies starting at 1
> month-- they have nothing to do with aging.
Maybe, maybe not. Since the next age is nearly halfway through their
lifespans, this is hardly conclusive.
> Now, look at the rest of the table. And yawn.
Yawn all you like. Walford was still spouting crap.
Steve Harris
>"Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in part:
. "no difference" is
>>not
>>>the same as "no statistical difference"..
>>
>>
>>Well, actually it is. If there's no statistical difference, that means
that
>>any difference you see is possibly due to shear chance (toss of the coin)
>>with a probability which is too high for you to say with any confidence
that
>>it isn't. Thus, there's a reasonable chance (at least 1 in 20 by
convention)
>>that there's no effect at all
>I don't have a whole lot to offer on nutrition science, but I am a
statistical
>consultant and the above (by Steve Harris) is absolutely wrong. A
difference
>that is found in a study ALWAYS may be the result of chance alone and
ALWAYS
>may be the result of a true treatment effect.
Yes, I never said otherwise. Go back (see above) and read what I DID say
carefully.
> The term "statistically
>significant difference" only means that, if the study is repeated many
times,
>the proportion of times you will find such an observed difference WHOLLY BY
>CHANCE is 5% (or whatever cookbook choice of alpha has been selected).
Yes, I said this above (and I've put it above so people reading this message
can see what I wrote).
Are you having trouble with the English language?
>If you are really interested in the probability distribution over a
difference
>being a true measure of a population difference (true treatment effect),
then
>you will find that you should indeed, as the original poster indicated,
infer
>a somewhat higher probability for a difference in the direction of the
>observed difference, no matter how statistically insignificant it may be.
We're having a problem with you use of the term "somewhat higher." If I flip
a coin 10 times and get 6 heads, according your your philosophy the
probability is "somewhat higher" than I have a biased coin which gives more
heads than tails than that I have an unbiased coin, because you say this is
true "for a difference in the direction of the observed difference, no
matter how statistically insignificant it may be." But you're wrong. This is
a two tailed test. Anybody who makes a judgement about the bias of a coin
because they got 6 heads out of 10 tosses, would be a damn fool. You cannot
"infer a somewhat higher probability for a difference in the direction of
the observed difference," in this case.. You cannot legitimately infer
ANYTHING. Is there a "somewhat higher" probability, based on this test, that
you have an unfair coin that gives more heads than tails? No. If you do this
test, you're going to get 5 heads out of 10 only 24.6% of the time, and
75.4% of the time, you'll get something else. Therefore, getting something
else is more than 3 times as likely as getting 5 out of 10, and in fact even
getting 6/10 of either heads or tails is more than 66% more likely than
getting 5/10, so if you don't get exactly 5 out of 10, you can conclude
exactly nothing.
Gym Bob
"Jim Chinnis" <jchi...@SPAMalum.mit.edu> wrote in message
news:jfqoquopoa2kr7od1...@4ax.com...
> "Steve Harris" <sbha...@ix.RETICULATEDOBJECTcom.com> wrote in part:
>
> >If I flip
> >a coin 10 times and get 6 heads, according your your philosophy the
> >probability is "somewhat higher" than I have a biased coin which gives
more
> >heads than tails than that I have an unbiased coin, because you say this
is
> >true "for a difference in the direction of the observed difference, no
> >matter how statistically insignificant it may be." But you're wrong. This
is
> >a two tailed test. Anybody who makes a judgement about the bias of a coin
> >because they got 6 heads out of 10 tosses, would be a damn fool.
>
> I'm not having any trouble understanding English. But you are having
trouble
> with statistics.
>
> You are lost in classical hypothesis testing, and are not addressing the
> question you think you are.
>
> Let's cut through the USENET idiocy that I see I have so quickly found in
this
> newsgroup. Let's propose a simple question:
>
> Take two coins, A and B. Flip each five times. Suppose coin A gives 2
heads
> and coin B gives 3. We both agree that any conventional classical
hypothesis
> test would conclude that the null hypothesis cannot be rejected. The null
> hypothesis is, of course, that the two coins have the same probability of
> producing heads.
>
> Now let's propose a gamble:
>
> We agree to flip one of the coins 1000 times. Further, we agree that each
time
> the coin comes up heads, you pay me $10 and each time it comes up tails I
pay
> you $10.
>
> Now you say "Anybody who makes a judgement about the bias of a coin
> because they got 6 heads out of 10 tosses, would be a damn fool." So you
don't
> care which coin we toss. I'll offer to pay you $10 for us to use coin B.
>
> So which are you, a damn fool or a sucker? You have to be one or the
other.
> (Both is a distinct possibility.)
>
>
>
>
> --
> Jim Chinnis Warrenton, Virginia, USA
Michael
g...@adres.nl (Hua Kul) wrote in message news:<3da4c6e5.02101...@posting.google.com>...
You are. Fortunately, the highly intuitive and plausible-sounding
'hypoascorbemia' theory has been tested, by (1).
"The current experiment was designed to assess the influence of
dietary ascorbic acid on the [LS] of guinea pigs, a species, like man,
dependent upon dietary sources of the vitamin."
"Fifty male ... guinea pigs were used. ... When five weeks old they
were divided into two groups: 25 received a daily supplement of 0.5 mg
ascorbic acid/ 100 g body weight and 25 received 1% [C] in their
drinking water. Previous studies indicated that intakes of this order
produced tissue saturations of circa 10% and 100 % respectively. In a
parallel experiment two groups of eight identically-treated guinea
pigs were killed after 12 months to confirm that substantially
different tissue concentrations of [C] were preesent in the 2 groups."
"There was no evidence that a sustained 'megadose' of [C] increased
[LS]; in terms of the first six deaths the low [C] group had a
significantly greater [LS] than the 'megadose' group."
==========================================
Table 1.
---------
Mean LS (days) of:
-----------------------------------------------------
Daily C intake Total Cohort First 6 deaths Last 6
deaths
-------------------------------------------------------------------------
0.5 mg/100 g BW 864 564 1251
1% in water 783 315 1179
====================================================
Table 2 shows that the high dose resulted in ~ 10-20-fold increases in
plasma C compared to the lower dose.
So much for "hypoascorbemia." In humans, an extensive review of the
epidemiology (2) shows pretty clearly that there is a protective
effect of a daily intake of ~ 90-100 mg/day as opposed to less (2).
Hence, these Linus Pauling Institute investigators suggest a new RDA,
designed to "optimally protect against" "cancer, cardiovascular
disease, and cataract" of 90-100 mg/day, except in those specifically
exposed to C-depleting circumstances such as smoking, pregnancy, and
biological old age.
The same essential evidence led the IOM to set the new RDA of 90
mg/day.
A decent diet can readily provide 500 mg of C/day.
-Michael
1: Davies JE, Ellery PM, Hughes RE.
Dietary ascorbic acid and life span of guinea-pigs.
Exp Gerontol. 1977;12(5-6):215-6. No abstract available.
PMID: 604083 [PubMed - indexed for MEDLINE]
2. Carr AC, Frei B.
Toward a new recommended dietary allowance for vitamin C based on
antioxidant and health effects in humans.
Am J Clin Nutr. 1999 Jun;69(6):1086-107. Review.
PMID: 10357726
http://www.ajcn.org/cgi/content/full/69/6/1086
Michael
In the post I just fired off, I wrote:
"Table 2 shows that the high dose resulted in ~ 10-20-fold increases
in plasma C compared to the lower dose."
This should've read, "Table 2 shows that the high dose resulted in ~
10-20-fold increases in VARIOUS ORGANS' C compared to the lower dose."
Sorry for any confusion.
-Michael
michaelprice
>
> "There was no evidence that a sustained 'megadose' of [C]
> increased [LS]; in terms of the first six deaths the low [C]
> group had a significantly greater [LS] than the 'megadose'
> group."
Yes, I'd be quite worried if vitamin C was a B-vitamin.
Thomas Carter
> All:
As far as I know this is the only controlled study which evaluates hi
vs. low intake of vit. C in animals which do not synthesize it. Any
others?
This is the third paper I have seen that indicates no benefit
of antioxidants to young animals, two of which suggest a detriment.
There is also a slight indication of a U shaped curve for
antioxidant balance and that older animals can get out of the sweet
spot by extreme supplementation.
I append below the other two.
Thomas
1) FASEB J 1999 Feb;13(2):411-8 (R)-alpha-lipoic acid-supplemented
old rats have improved mitochondrial function, decreased oxidative
damage, and increased metabolic rate. Hagen TM, Ingersoll RT,
Lykkesfeldt J, Liu J, Wehr CM, Vinarsky V, Bartholomew JC, Ames AB.
Department of Molecular and Cell Biology, University of California at
Berkeley, Berkeley, California 94720, USA. A diet supplemented with
(R)-lipoic acid, a mitochondrial coenzyme, was fed to old rats to
determine its efficacy in reversing the decline in metabolism seen
with age. Young (3 to 5 months) and old (24 to 26 months) rats were
fed an AIN-93M diet with or without (R)-lipoic acid (0.5% w/w) for 2
wk, killed, and their liver parenchymal cells were isolated.
Hepatocytes from untreated old rats vs. young controls had
significantly lower oxygen consumption (P<0. 03) and mitochondrial
membrane potential. (R)-Lipoic acid supplementation reversed the
age-related decline in O2 consumption and increased (P<0.03)
mitochondrial membrane potential. Ambulatory activity, a measure of
general metabolic activity, was almost threefold lower in untreated
old rats vs. controls, but this decline was reversed (P<0.005) in old
rats fed (R)-lipoic acid. The increase of oxidants with age, as
measured by the fluorescence produced on oxidizing
2',7'-dichlorofluorescin, was significantly lowered in (R)-lipoic acid
supplemented old rats (P<0.01). Malondialdehyde (MDA) levels, an
indicator of lipid peroxidation, were increased fivefold with age in
cells from unsupplemented rats. Feeding rats the (R)-lipoic acid diet
reduced MDA levels markedly (P<0.01). Both glutathione and ascorbic
acid levels declined in hepatocytes with age, but their loss was
completely reversed with (R)-lipoic acid supplementation. Thus,
(R)-lipoic acid supplementation improves indices of metabolic activity
as well as lowers oxidative stress and damage evident in aging. PMID:
9973329 full text available (The abstract fails to mention that the
R form almost doubles the MDA content of the cells. Border line
significant in young rats)
2) An identical supplemental diet fed to young rats did not enhance
the resistance to t-BuOOH, indicating that antioxidant protection was
already optimal in young rats. Thus, this study shows that cells from
old animals are more susceptible to oxidant insult and (R)-lipoic
acid, after reduction to an antioxidant in the mitochondria,
effectively reverses this age-related increase in oxidant
vulnerability. PMID: 11229361
michaelprice
> This is the third paper I have seen that indicates no benefit
> of antioxidants to young animals, two of which suggest a detriment.
> There is also a slight indication of a U shaped curve for
> antioxidant balance and that older animals can get out of the sweet
> spot by extreme supplementation.
Vitamin E also exhibits a U curve (whole-life this time) LS . Comparison
20, 40 and 400 mg/kg diet were compared and 40mg/kg had the shortest LS for
mice:
Biogerontology 2001;2(2):109-12
Lack of an effect of vitamin E on lifespan of mice.
Morley AA, Trainor KJ.
Department of Haematology and Genetic Pathology, Flinders University of SA
and Flinders Medical Centre, Bedford Park, South Australia, Australia.
alec....@flinders.edu.au
It has been speculated that ageing results from accumulation of damage to
macromolecules, particularly DNA, owing to the action of oxidising free
radicals. This possibility would predict that administration of
anti-oxidants might prolong lifespan, but previous data on this prediction
are conflicting. Three groups of mice were exposed throughout life, from the
time of conception until death, to 20, 40 and 400 mg/kg of vitamin E in the
diet. No effect on lifespan was observed and the median lifespans in the
three groups were 804, 830 and 801 days, respectively. The design of the
study also enabled an effect of parental age on lifespan of female progeny
to be sought, but no effect was detected.
PMID: 11708376
Thomas Carter
Indeed,
And the effects might be immunologically mediated perhaps thru
interference with CoQ10. I'm taking mixed E's and tocotrienols plus
CoQ to hopefully avoid this putative down side of hi E doses.
Here are three items from my archives.
Thomas
A study 88 people age 65 or over showed about 50 % more immune
response for those who took only 200 IU's. 60 IU's showed no help, nor
did the placebo group. a forth group who took 800 IU's showed a mixed
response but basically not much better than the placebo group. Tuft
Univer. Health and Nutrition June '97.
Why does extra vit E kill the increased immune response?
) J Nutr 2000 Sep;130(9):2343-8 Dietary coenzyme Q10 and vitamin E
alter the status of these compounds in rat tissues and mitochondria.
Ibrahim WH, Bhagavan HN, Chopra RK, Chow CK. Department of Nutrition
and Food Science, and Kentucky Agricultural Experiment Station,
University of Kentucky, Lexington, KY 40506, USA.
Vitamin E (VE) and coenzyme Q (CQ) are essential for maintaining
functions and integrity of mitochondria, and high concentrations of
these compounds are found in their inner membranes. This study was
conducted to examine the interaction between exogenously administered
CQ10 and VE in rats. Male Sprague-Dawley rats (12 mo old) were fed a
basal diet (10 IU VE or 6.7 mg RRR-alpha-tocopherol equivalent)
supplemented with either 0 or 500 mg CQ10, and 0, 100 or 1310 IU VE/kg
diet for 14 or 28 d. Liver, spleen, heart, kidney, skeletal muscle,
brain and serum were analyzed for the levels of CQ10, CQ9 and VE. CQ10
supplementation significantly (P: < 0.05) increased CQ10 concentration
in the liver and spleen (total and mitochondria) and serum, but not in
other organs. Interestingly, rats supplemented with CQ10 plus 100 IU
VE/kg diet had significantly higher CQ10 levels in the liver and
spleen, whereas those supplemented with CQ10 plus 1310 IU VE/kg diet
had lower levels, compared with those supplemented with CQ10 alone.
JPEN J Parenter Enteral Nutr 1991 Jul-Aug;15(4):433-6 Survival in
septic guinea pigs is influenced by vitamin E, but not by vitamin C in
enteral diets. Peck MD, Alexander JW. Department of Surgery,
University of Miami School of Medicine, Florida.
Oxygen-free radicals are produced during sepsis, and may contribute to
cell injury and dysfunction. We studied the effect of different levels
of vitamins E and C in the diet fed enterally to septic guinea pigs.
Sixty-four female guinea pigs were provided with gastrostomies and
allowed to recover. Intraperitoneal osmotic pumps were then implanted
that provided effusion of Escherichia coli and Staphylococcus aureus
for the next 7 days. Three days after pump implantations, the animals
were started on one of nine diets. The diets were isocaloric and
isonitrogenous, and differed only in the amounts of vitamins E and C.
Three levels of each vitamin were used, based on the Recommended Daily
Allowance (RDA). The feedings were continued for 2 weeks, during which
time mortality was observed. The amount of vitamin C had no effect on
outcome, with mortality rates of 68% (15/22) in the 1 x RDA group, 73%
(16/22) in the 5 x RDA group, and 65% (13/20) in the 25 x RDA group.
However, vitamin E altered outcome significantly, with mortality rates
of 86% (18/21) in the 1 x RDA group, 45% (10/22) in the 3 x RDA group,
and 76% (16/21) in the 9 x RDA group. Mortality in the 3 x RDA group
was significantly lower than that in the 1 x RDA group and in the 9 x
RDA group.(ABSTRACT TRUNCATED AT 250 WORDS) PMID: 1910107 This is the
third abstract I have seen that indicates a U shaped curve for Vit E
supplementation.
Thomas Carter
> There is also a slight indication of a U shaped curve for
> antioxidant balance and that older animals can get out of the sweet
> spot by extreme supplementation.
>
Hi,
I had remembered a paper giving some indication of this, but could not
find it until now. It is supposed that a major mechanism of CR is a
reduction in ROS production. If true, a combination of CR and
antioxidant supplementation could put even an older animal out of the
sweet spot and onto the wrong side of the redox balance. That is to
say in more danger from antioxidants than free radicals. While I think
this very unlikely the appended paper does give such an indication.
And by the same reasoning implies that the redox sweet spot is at
about the level of a 30% reduction in free radicals which is evendent
in CR. This would also imply that there will be no more that a 30%
increase in lifespan possible by reduction or interception of free
radicals. In this case greater lifespan extension would have to come
from inhanced repair mechanisms or other effects. AFAIK this is the
only paper that bears on the coeffects of CR and antioxidant
supplementation. Steve is one of the authors, maybe he will give some
insights.
Thomas
J Gerontol 1990 Sep;45(5):B141-7 Dietary restriction alone and in
combination with oral ethoxyquin/2-mercaptoethylamine in mice. Harris
SB, Weindruch R, Smith GS, Mickey MR, Walford RL. Department of
Pathology, University of California, Los Angeles. To
investigate effects of dietary caloric restriction (DR) combined with
antioxidant feeding, long-lived hybrid mice were divided into four
dietary groups at weaning, and followed until natural death. Groups
"C" and "R" received control (97 kcal/wk) and restricted (56 kcal/wk)
diets respectively. Groups "C+ alpha ox" and "R+ alpha ox" received C
or R diets supplemented with an antioxidant mixture
(2-mercaptoethylamine plus ethoxyquin). R mice (mean life span 41
months) significantly outlived the other three groups (mean life span
30-34 months). Hepatic degeneration and increased hepatoma in the R+
alpha ox group suggested unusual hepatotoxicity of this regimen.
Antioxidants had little effect on splenic cell mitogen response in
similarly fed mice sacrificed at 12-15 months. Gompertz analysis
suggests that the beneficial effect of DR may be due to reductions in
initial vulnerability or rate-of-aging parameters, or both, and that
the relative influence of each factor may vary with animal strain and
DR protocol used. PMID: 2394907 (Both of these substances are
well known to be beneficial antioxidants. The combination of the two
plus CR apparantly caused liver damage. This result is probably an
abberation of some sort, but it can't be ruled out that the result was
due to a redox imbalance caused by the combination of CR and
antioxidant supplementation)
Steve Harris
COMMENT:
I agree this probably doesn't same much about antioxdative status per se.
Some antioxidants are fairly toxic, and mice under CR have little tiny
livers which really don't have the same capacity to deal with metabolism of
them. Mouse livers under chronic duress are extremely sensitive to hepatoma,
also, and there are many examples of ethical pharmaceuticals which are
"known carcinogens" in mice, except that when you look at the data, it's all
hepatoma. Mostly such things are ignored, even by the FDA.
A couple of things that aren't in print relative to the study above.
Hepatoma was the main cause of increased deaths in the antiox mice, but I
also found a couple of mice that had died in a very odd way, with body
cavities full of blood. It wasn't clear why. I thought this might be a
cysteamine effect. Aortic rupture has been seen in animals fed cysteamine
while growing, and I guessed that this was due to copper deficiency and loss
of effectively strong collagen synthesis. I thought the same thing might be
happening to my animals, but Walford didn't want to be that speculative (a
double speculation, here), so this never made it to the paper.
Later, in a study never published, I fed control and restricted mice
ethiophos (WR-2721), a pretty good sulfur-based antioxidant. It fed it at
doses about half of that required to cause weight loss, figuring that was
toxicity point. It didn't work-- life span wasn't increased, nor decreased,
except in the CR animals. However, again I saw increased mortality only in
the restricted group with it (relative to plain restricted without it)--
another indication that restricted mice are bad at tolerating near toxic
doses of things. No sign of the aortic problem, but I didn't do all the
autopsies, and it could have been missed.
Restricted mice tolerate huge doses of chromium, folate, and CoQ10 fine in
life span studies, I found. But these all have big margins of safety even at
the doses I was feeding. CR mice I found were more sensitive to the toxicity
of 13-cis retinoic acid, and I think I did publish this. The general rule,
if I had to guess, seems to be that the substance has to be fed at doses on
the edge of toxicity anyway, for CR to uncover the increased toxicity
effect. I would guess that we are NOT particularly seeing evidence of an
"over-antioxidative" effect. The first place I'd expect that to show up
would be infectious disease resistance, and we never got the opportunity to
test this. So far as I can tell, very little work has been done in this
direction in CR.
michaelprice
http://www.longevity-report.com/lr91.htm
Apart from general tidying up, expansion of some points, clarification etc I
have down-graded the benefit of chromium on humans by a factor of 4,
principally because I suspect the controls were prediabetic.
Cheers,
Michael C Price
----------------------------------------
http://www.longevity-report.com/lr91.htm
http://www.hedweb.com/manworld.htm
slipstream
your introduction here. - You downgrade the benefit of Chromium by a factor
of 4 because you SUSPECT .......
What is this? How can you change a recommendation based on a suspicion????
Please tell me your introduction was sloppy.....
"michaelprice" <michae...@ntlworld.com> wrote in message
news:7KGs9.5548$eg6.3...@newsfep2-win.server.ntli.net...
michaelprice
Thank you
> However IMHO you kill it with your introduction here. - You downgrade
> the benefit of Chromium by a factor of 4 because you SUSPECT .......
> What is this? How can you change a recommendation based on a suspicion????
How can I not????
All recommendations are based on probabilities; any new relevant information
(even when it falls far short of certainty (p=1)) may alter the
probabilities and hence the expected cost/benefit ratios. In this case I
came across (strong) evidence (but not a certainty) that the Long-Evans rats
used were exhibiting age-related insulin resistance, 4x as much as exhibited
by typical non-diabetic humans, as measured by glycated haemoglobin levels.
Further circumstantial evidence (which I should have also mentioned) is that
a sub-strain of Long-Evans (LE) rats is used as an animal model of type2
diabetes (the OLEM strain of rats).
What I said still seems sound:
"Part of the reason why chromium deficiency is so common is that plants do
not require chromium, like selenium; plants can thrive in chromium poor
soils, leading to chromium poor diets. Chromium optimises insulin function,
which, in turn, lowers fasting glucose levels, improves glucose tolerance
and reduces glycation. Chromium's anti-glycation, glucose-regulatory action
is mediated entirely via the protein insulin (a hormone); chromium,
therefore, is a proteonomic cofactor with a single target protein, unlike
the enzymic cofactors, which, typically, operate in conjunction with number
of target enzymes. Therefore we have to be cautious in extrapolating the
chromium rodent lifespan extension of 27% to humans; the control rats tested
showed evidence of pre-diabetic, sub-clinical insulin resistance - their
glycated haemoglobin levels increased almost 4-fold more as they aged[5a,
5c] (as a proportion of their lifespan) than in non-diabetic humans[83i];
the anti-aging effect on non-diabetic humans will probably be only a quarter
as much, about 7%."
[5a] Composition and Biological Activity of Chromium-Pyridine Carboxylate
Complexes. GW Evans and DJ Pouchnik, Journal of Inorganic Biochemistry 49,
pg 177-187 (1993). Describes the action of dietary chromium picolinate
(relative to chromium chloride and chromium nicotinate) in reducing
glycation & plasma glucose levels in rats as they aged.
[5c] Chromium picolinate increases longevity. Evans GW, Meyer LK in AGE
(the Journal of the American Aging Association) Oct 1992; 15(4), 134.
[83i] The effects of ageing on glycation and the interpretation of glycaemic
control in Type 2 diabetes. Kilpatrick ES, Dominiczak MH, Small M in QJM
1996 Apr;89(4):307-12
"In 232 non-diabetics, there was a linear relationship between HbA1C and
age (r = 0.49, p < 0.0001). Mean HbA1C rose from 3.82% to 4.44% between the
ages of 20 and 70."
>
> "michaelprice" <michae...@ntlworld.com> wrote in message
> news:7KGs9.5548$eg6.3...@newsfep2-win.server.ntli.net...
>> I have updated my monograph at:
>>
>> http://www.longevity-report.com/lr91.htm
>>
>> Apart from general tidying up, expansion of some points,
>> clarification etc. I have down-graded the benefit of
slipstream
"michaelprice" <michae...@ntlworld.com> wrote in message
news:xtat9.1805$R24....@newsfep1-win.server.ntli.net...