What Happened to Oden's Study?
chris zell
doses of DNA. His results were called "inconclusive".
Has no one ever attempted to replicate these findings?
michaelprice
Cheers,
Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm
"chris zell" <chri...@clearchannel.com> wrote in message
news:dcea6927.04012...@posting.google.com...
Manfred Bartz
There is a LEF article which mentions Oden:
New Studies Reinforce Older Ones . . .
RNA Therapy May Slow Down Aging
http://www.lef.org/magazine/mag97/aug97-research.html
A Google search turned up a sales brochure:
http://www.vpnutrition.com/pdfs/Quantum_Nucleotide_Complex.pdf
The only mention Max Oden gets:
"Nucleotides may help us live longer, fuller lives
according to the late English physician Max Oden."
However, there are references. Where possible, I have replaced the
original reference with the PubMed one, I hope it will save someone
some time: :)
Bustamante SA, Sanches N, Crosier J, Miranda D, Colombo G, Miller MJ.
Dietary nucleotides: effects on the gastrointestinal system in swine.
J Nutr. 1994 Jan; 124(1 Suppl): 149S-156S.
PMID: 8283306 [PubMed - indexed for MEDLINE]
Carver JD.
Dietary nucleotides: cellular immune, intestinal and hepatic system
effects.
J Nutr. 1994 Jan; 124(1 Suppl): 144S-148S. Review.
PMID: 8283305 [PubMed - indexed for MEDLINE]
Jyonouchi H.
Nucleotide actions on humoral immune responses.
J Nutr. 1994 Jan; 124(1 Suppl): 138S-143S. Review.
PMID: 8283304 [PubMed - indexed for MEDLINE]
Marshall, RJ and Forbes, LL.
The overlooked role of chronic infection in neurodegeneration and its
reversal using nutraceutical agents,
JANA, Spring, 2003.
Uauy R.
Nonimmune system responses to dietary nucleotides.
J Nutr. 1994 Jan; 124(1 Suppl): 157S-159S. Review.
PMID: 8283307 [PubMed - indexed for MEDLINE]
Van Buren CT, Kulkarni AD, Rudolph FB.
The role of nucleotides in adult nutrition.
J Nutr. 1994 Jan; 124(1 Suppl): 160S-164S. Review.
PMID: 8283308 [PubMed - indexed for MEDLINE]
Walker WA.
Nucleotides and nutrition: role as dietary supplement.
J Nutr. 1994 Jan; 124(1 Suppl): 121S-123S. No abstract available.
PMID: 8283300 [PubMed - indexed for MEDLINE]
Weimann A, Bastian L, Bischoff WE, Grotz M, Hansel M, Lotz J,
Trautwein C, Tusch G, Schlitt HJ, Regel G.
Influence of arginine, omega-3 fatty acids and nucleotide-
supplemented enteral support on systemic inflammatory response
syndrome and multiple organ failure in patients after severe trauma.
Nutrition. 1998 Feb; 14(2): 165-72.
PMID: 9530643 [PubMed - indexed for MEDLINE]
So far, I have only glanced over the abstracts, and it looks very
interesting. But maybe it would be more productive to search
Pubmed for nucleotide and longevity....
--
Manfred
Delete the D
in 1997 that its Foundation would attempt to repeat Oden's provocative finding
as the second part of a so called "Rejuvination Project"[1], I called the
Foundation, perhaps about a year or so ago, and after some rooting
around was told that they simply didn't follow through. <sigh>
Thanks,
Kingsley
Reference
[1] http://www.lef.org/magazine/mag97/may-proj97_2.html
--
Kingsley G. Morse Jr.
No...@none.none
"Your membership dues, donations and product purchases support
research that could significantly extend your lifespan." They
*simply* didn't follow through? Lol.
Tim
X-Message-Number: 7160
Date: Mon, 18 Nov 1996 20:31:57 -0800 (PST)
From: Doug Skrecky <obe...@vcn.bc.ca>
Subject: Why the DNA-RNA experiment was never replicated
All those who emailed their addresses have now been sent copies of
the incredible report on increasing rat life span by 144%. This actually
understates things slightly. After looking at the report again I saw that
the maximum life span of the DNA-RNA injected rats was 2250, not the 2200
days previously reported. Sorry for this typo. The increase is then 150%,
not the 144% previously stated. If anyone is still interested in
recieving the report just email your address.
After rereading the report it is apparent that the author Max Odens
was not a life extensionist. This is perhaps not surprising given the
conservative nature of many in the medical profession. Dr. Odens seemed
to be mostly interested in proving a viral theory of cancer. The fact
that he did not state the exact day of death of the remaining four
injected rats suggests he may have found this embaressing, since this was
almost certainly not what he was looking for. Indeed the 2250 figuare is
suspect, since the chances of the exact day of death being a multiple of
50 are 1 in 50. I suspect the real figuare may be something like 2263.
The fact that this experiment was not replicated is not hard to
explain. Dr. Odens and his colleagues almost certainly had no interest in
doing so, since they had little or no interest in extending the lifespan
of humans.
Here's a few quotes from the report:
"ABSTRACT: To test the effect of RNA-DNA in preventing the
deleterious effects of old age, an experiment was conducted that involved
10 rats with a normal life span of 800-900 days. All were fed the same
diet; 5 rats were not treated, and 5 were given weekly injections of DNA
+ RNA. After twelve weeks the difference in appearance, weight and
alertness was remarkable. The 5 untreated rats died before 900 days. Of
the treated rats, 4 died at ages of 1600-1900 days, and 1 at 2250 days. A
parallel cannot be drawn with aging in human beings fed RNA-DNA, but the
findings on rats may have some application to cellular studies on
cancer."
(Later on in the body of the report Dr. Odens mentions:)
"Although it is tempting to think in terms of the possibility of an
equivalent prolongation of the life span of human beings accomplished by
injections of DNA and RNA, it should be emphasized that the parallels
between aging in rats and aging in humans are not only unknown but are
entirely outside the scope of this experiment."
Tim Tyler
Nucleotides are just upstream from many
of the coenzymes he is interested in -
as he explains on:
http://www.quantium.cwc.net/lr91.htm
The chorella sales-folk will also be
pleased if the tale pans out - they've
been banging on about eating RNA for years.
--
__________
|im |yler http://timtyler.org/ t...@tt1lock.org Remove lock to reply.
michaelprice
perhaps Max Oden's work has been replicated?
According to Secrets of Life Extension (page 68)
by John A Mann, Dr Hans J Kugler injected nucleic acids
and doubled the lifespan of Snell-Bagg dwarf mice,
reported as "three to five months". Doubled from 3 to 5
or doubled from 3-5 to 6-10 months? I'm not sure, but
there is a reference given:
Hans J Kugler
American Laboratory 8 (Nov 1976), 24
Tim Tyler is correct that the only explanation that makes
sense to me -- apart from incompetence or fraud -- is that
the RNA was broken down and resynthesised as coenzymes
and ribozymes (enzymes formed from nucleotide, not amino
acids). It hardly needs restating, though, that the LE
(especially in Oden's case) does seem implausibly high.
However another deceased physician, Max Wolf, -- also
reported in Secrets of Life Extension (page 68)-- claimed to
have doubled the lifespan of rats by feeding them a protein,
nucleic acid and B-vitamin enriched yeast extract.
Unfortunately I suspect that the subject of dietary nucleic
acid supplementation has been tainted by association with
fetal cell injections in Swiss clinics and so is unlikely to seriously
investigated in the foreseeable future. Which is a shame, since
ribozymes are believed to be the most ancient part of our
metabolism and may hold many important secrets.
Thanks for the references, Manfred.
Cheers,
Michael C Price
----------------------------------------
http://mcp.longevity-report.com
http://www.hedweb.com/manworld.htm
"Manfred Bartz" <spam...@dev.null> wrote in message
news:m28yk14...@logi.cc...
mrogara
Hmmm...replicating this would be a great "Methuselah Mouse prize" entry,
wouldn't it?
-- Mike O'Gara
Thomas Carter
Hi,
I do happen to have some evidence that remotely suggests nucleic
acid injections could be very beneficial. Research on this is
proceeding slower than I'm aging, I'm afraid.
Thomas
The effective dose could be as high as 100 gms/day (2) Purines may
not be absorbed. (3) If purines are not absorbed, yet nucleotides are
beneficial, injection of purines along with pyrmidines could be MUCH
more beneficial. This would be a long shot.
J Nutr. 2000 Dec; 130(12): 3085-9. Related Articles, Links
(1) A nucleoside-nucleotide mixture may reduce memory deterioration
in old senescence-accelerated mice.
Chen TH, Wang MF, Liang YF, Komatsu T, Chan YC, Chung SY, Yamamoto S.
Department of Nutrition, School of Medicine, The University of
Tokushima. Tokushima 770-8503, Japan.
We investigated the effects of a mixture of dietary
nucleosides and nucleotides (NS + NT) on memory in 1- and 7-mo-old
senescence-accelerated mice (SAM). Memory retention was studied with
passive avoidance (step-through) and active avoidance (shuttle) tests.
For 14 wk, mice in the control groups were fed a 20 g of casein/100 g
diet, whereas the NS + NT groups were fed this diet supplemented with
a 0.5 g of NS + NT mixture/100 g. All mice were killed at wk 14, and
we studied the brain histopathology. Lipofuscin, monovacuoles and
multiple vacuoles of various brain regions were measured. Body weight,
food intake and ambulatory activity did not differ between the control
and NS + NT groups. In old mice, the time of passive avoidance was
significantly higher in the NS + NT group than in the control group at
d 1 and 7 (P: < 0.05). However, such an effect of NS + NT was not
observed in young mice. In the active avoidance test, the incidence of
successful avoidance in old mice was higher in the NS + NT group than
in the control group at d 1 and 2 (P: < 0.05). The percentages of
specific brain cells containing lipofuscin were lower in NS + NT
groups than in the control groups in both young and old mice (P: <
0.05). The number of monovacuoles and multiple vacuoles in specific
brain regions tended to be lower (P: = 0.1-0.25) in NS + NT than in
control groups, with significant differences in the microvacuoles of
the middle cortex of young mice and in the multiple vacuoles in the
hind cortex of old mice (P: < 0. 05). These results suggest that
increased dietary NS + NT may be associated with decreases in the
age-induced deterioration of brain morphology and certain memory
tasks.PMID: 11110874………………
From the full text
Dietary sources of nucleic acids and their components have not been
considered essential for normal growth and development because it was
generally assumed that living organisms, including humans, could
synthesize adequate amounts of the compounds required for normal
growth and development and that dietary sources are not used. However,
some cells and tissues, such as erythrocytes, polymorphonuclear
leukocytes, intestinal mucosa, bone marrow, hematopoietic cells and
brain, are incapable of de novo synthesis of purine and pyrimidine
bases due to their reduced content of pyrophosphorylribosyl-phosphate
amidotransferase (Victor 1993 ). The supply of nucleosides (NS)2and
nucleotides (NT) to these organs for normal growth comes mainly from
the liver via a salvage pathway. Recent studies indicate that the
endogenous supplies of NS and NT are not adequate for the optimal
function in these tissues under certain clinical conditions, such as
infection and damage of intestinal mucosa through surgical stress
(Adjei et al. 1995 , Carver 1994 , Kulkarni et al. 1994 , Yamamoto et
al. 1997 ).
After injury to tissues, including the central nervous system,
extracellular purine NS and NT may interact synergistically with other
growth factors to stimulate the glial proliferation, capillary
endothelial cell proliferation and sprouting of nerve axons (Rathbone
et al. 1992 ). We first demonstrated the effects of an NS + NT mixture
on memory with the passive avoidance test in normal, demented and aged
mice (Chen et al. 1996 ). In the present study, we further
investigated the effects of a dietary NS + NT mixture on memory by
using both passive (step-through) and active (shuttle) avoidance tests
in young and old mice. In addition, we studied brain histopathology.
Changes in brain morphology may be important factors in memory
impairment. Some studies of the SAMP8 report that the age-related
morphological impairments of the brain begin at 6–8 mo of age. In
SAMP8, the spongy degeneration (vacuolization) in the brain stem and
spinal cord, especially in reticular formation, is closely related to
learning and memory deficits (Yagi et al. 1989 ). The vacuole number
was much higher in the old mice than in the young mice, indicating the
rapid development of sponge caused by aging in SAMP8. In both young
and old mice, the vacuole numbers in brain were 20% lower in the NS +
NT groups than in the control groups, with significant differences
only in a few portions of the brain (P < 0.05). This suggests that NS
+ NT somewhat reduced spongy production.
Lipofuscin accumulation is one of the best-documented
age-related changes in postmitotic cells (Brizzee and Ordy 1979 ,
Brunk and Ericsson 1972 , Mann et al. 1978 ). Sohal and Brunk (1989)
reported that lipofuscin could be used as a marker of oxidative stress
and aging, and it has been suggested that lipofuscin deposits
represent the accumulation of the peroxide active action of free
radicals (Dormandy 1982 , Katz and Robison 1986 ). Kadar et al. (1990)
reported that lipofuscin accumulation may be a good histochemical
marker for central nervous system cell degeneration, because it was
correlated with memory impairment in brain of aged rats. In addition,
lipofuscin deposits increase in the hippocampus of SAMP8 (Flood et al.
1993 ). The preventive effect of NS + NT supplementation on lipofuscin
accumulation was observed in various portions of the brain in both
young and old mice. We found a significant decrease due to NS + NT in
lipofuscin accumulation in the hind hippocampus, which plays a key
role in learning and memory.
NS + NT also have strong antioxidant properties. Purines, NS + NT and
bases are degraded to uric acid in humans. Uric acid is a strong
antioxidant, and the concentration in plasma is higher than that of
vitamin E (Ames et al. 1981 ). Monji et al. (1994) reported that a
vitamin E–supplemented diet decreased lipofuscin accumulation due to
age in rat brain. In light of these findings, prolonged
supplementation of NS + NT might decrease the production of lipofuscin
in SAMP8.
Other possible mechanisms that explain the present findings should be
considered as well. For example, NS + NT play an important role in
lipid metabolism. Sato et al. (1995) reported that dietary NT may
influence lipid metabolism of the cerebral cortex and contribute to
the rise in the learning ability of rats. They proposed that dietary
NT intake may increase the phosphatidylcholine content and 20:4(n-6)
and 22:6(n-3) levels of the cerebral cortex and contribute to
increased learning ability of rats……………………….
(2) Zhonghua Yu Fang Yi Xue Za Zhi. 2003 May; 37(3): 158-60. Related
Articles, Links
[Effect of yeast RNA on physical functions, morphology of hepatic
cells and brain neurons in aged rats]
[Article in Chinese]
Pan HZ, Zhao X, Chu WF, Li R.
Department of Health Chemistry and Microbiology, Public Health College
of Harbin Medical University, Harbin 150001, China.
OBJECTIVE: To study the effect of exogenous nucleic
acid on physical functions, morphology of hepatic cells and brain
neurons in aged rats. METHODS: Thirty two aged Wistar rats (20
month-old) were divided randomly into four groups (one aged control
group and three aged experimental groups) and eight young rats (3
month-old) was set as young control group. Control groups were fed on
standard chow and experimental groups were fed on standard chow
supplemented with 93.75 mg/kg (high-dosage group), 46.88 mg/kg
(middle-dosage group) and 9.38 mg/kg (low-dosage group) of yeast RNA
respectively. SOD, MDA, HDL, sex hormone and growth hormone were
determined at the end of a 4-week observation. The microcosmic images
of the hepatic cells and brain neurons using the image-pro plus
(V.4.0) were also observed. RESULTS: SOD, serum HDL and growth hormone
levels in the high dosage group were significantly higher (P < 0.05)
than that in the aged control group, and the levels were not different
from that in the young control group. MDA level of all yeast RNA
supplemented groups was significantly lower than that of aged control
group (P < 0.05) and that was not different from the young control
group. Serum testosterone of the high and middle dosage groups reached
the level of young control group, and that was much higher than the
aged control and low dosage group (P < 0.05). Estradiol levels among
the aged rats were not different, and those were much lower than the
young control group (P < 0.05). Much more number of brain neurons were
observed in the high-dose group than other aged rats (P < 0.05). Brain
neurons, hepatic cells and karyons in the high-dose group were bigger
than that in other aged rats (P < 0.05). CONCLUSION: Exogenous yeast
RNA might play an important role in physical functions, the morphology
of brain neurons and hepatic cells in natural aged rats. There might
have a dose-effect relationship in the process.PMID: 12880559………………….
(3) Evidence for incorporation of intact dietary pyrimidine (but not
purine) nucleosides into hepatic RNA.
Proc Natl Acad Sci U S A. 1995 Oct 24; 92(22): 10123-7.
PMID: 7479738 full text
chris zell
> age in rat brain. In light of these findings, prolonged
> supplementation of NS + NT might decrease the production of lipofuscin
> in SAMP8.
> Other possible mechanisms that explain the present findings should be
> considered as well. For example, NS + NT play an important role in
> lipid metabolism. Sato et al. (1995) reported that dietary NT may
> influence lipid metabolism of the cerebral cortex and contribute to
> the rise in the learning ability of rats. They proposed that dietary
> NT intake may increase the phosphatidylcholine content and 20:4(n-6)
> and 22:6(n-3) levels of the cerebral cortex and contribute to
> (3) Evidence for incorporation of intact dietary pyrimidine (but not
> purine) nucleosides into hepatic RNA.
> Proc Natl Acad Sci U S A. 1995 Oct 24; 92(22): 10123-7.
> PMID: 7479738 full text
ARRRRGHHH! Can you feel the frustration with this?
Do we have the solution to aging almost in our grasp and
nobody does anything about it?????!!! I'm appalled!
Can humans really eat RNA and get the benefit? I thought it
wasn't absorbed ( digested?). I think Oden injected his mice.
Also, are mice kinda short
lived creatures, mostly designed for mass reproduction?
So that small changes might cause a bigger life extension than in
people?
Could we clone 'perfect' DNA/RNA and inject ourselves with it?
questions, questions.....
Tim
Could nucleotide supplementation be augmenting synthesis of
ribose-5-phosphate?
Energy seems to be diverted between NADPH synthesis and
ribose-5-phosphate synthesis depending on current cellular demands via
the nonoxidative pentose phosphate shunt or to glycolysis. G6PDH does
become less active during aging.
So shifts in energy demand or supply could unfavorably effect this
biosynthetic pathway.
The Metabolism of Glucose 6-phosphate by the Pentose Phosphate Pathway
Is Coordinated with Glycolysis
Only the nonoxidative branch of the pathway is significantly active
when much more ribose 5-phosphate than NADPH needs to be synthesized.
Under these conditions, fructose 6-phosphate and glyceraldehyde
3-phosphate (formed by the glycolytic pathway) are converted into
ribose 5-phosphate without the formation of NADPH. Alternatively,
ribose 5-phosphate formed by the oxidative branch can be converted
into pyruvate through fructose 6-phosphate and glyceraldehyde
3-phosphate. In this mode, ATP and NADPH are generated, and five of
the six carbons of glucose 6-phosphate emerge in pyruvate. The
interplay of the glycolytic and pentose phosphate pathways enables the
levels of NADPH, ATP, and building blocks such as ribose 5-phosphate
and pyruvate to be continuously adjusted to meet cellular needs.
In regards to Thomas's article on nucleotides/nuclweosides on memory.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6738601&dopt=Abstract
Tim
Tim Tyler
> Can humans really eat RNA and get the benefit? I thought it
> wasn't absorbed ( digested?). I think Oden injected his mice. [...]
It doesn't look as though that's a problem.
``Dietary nucleotides, found in normal diets, have been recently
determined to be required for normal immune defenses. Rejection of
cardiac transplants, graft-vs.-host disease, and delayed cutaneous
hypersensitivity in animal models are all suppressed by a diet deficient
in nucleotides. T lymphocytes seem to require dietary nucleotides for
normal maturation and function. Host resistance to bacterial and fungal
infections is decreased in mice on nucleotide free diets; addition of
RNA or uracil prevents this vulnerability to infection. Dietary RNA
is required to restore lost immune function after protein deprivation.''
- http://calorierestriction.org/pmid/?n=8283308
This seems to be suffering rather from too many negatives -
but the first sentence seems clear enough.
Manfred Bartz
> tcar...@elp.rr.com (Thomas Carter) wrote in message news:<a7b55247.04012...@posting.google.com>...
> ARRRRGHHH! Can you feel the frustration with this?
> Do we have the solution to aging almost in our grasp and nobody does
> anything about it?????!!! I'm appalled!
>
> Can humans really eat RNA and get the benefit? I thought it wasn't
> absorbed ( digested?).
AFAIK, during digestion all NAs are broken down into their nucleotide
components before absorbtion. The nucleotides can then readily be
used by human cells to synthesize their own NAs.
Good sources of NAs are meat and eggs. As a supplement, a spoon full
of brewers yeast twice a day should make an excellent, additional
source of NAs (and vitamin B). No need for expensive
"Nutraceuticals". :)
> I think Oden injected his mice. Also, are mice kinda short lived
> creatures, mostly designed for mass reproduction? So that small
> changes might cause a bigger life extension than in people?
I think that is very likely.
> Could we clone 'perfect' DNA/RNA and inject ourselves with it?
Not a good idea IMHO. Short RNA sequences can cause RNA interference
(RNAi) which potentially suppresses some genes. Longer, matching NA
sequences can trigger apoptosis. If you mess with your genes you
better know *exactly* what you are doing.
Maybe Oden hit a lucky RNA combination which altered genetic
expression by RNAi. The exact same RNA may do something quite
different in humans.
Scientists Develop New Technique for Silencing Human Genes:
http://www.sciam.com/article.cfm?articleID=00064349-E65F-1C5E-B882809EC588ED9F&pageNumber=1
Killing the Messenger
Turning off RNA could thwart cancer and AIDS
By Carol Ezzell
http://www.sciam.com/article.cfm?articleID=0006F940-DDC2-1D29-97CA809EC588EEDF&pageNumber=1
--
Manfred Bartz
Tim
resulting nucleotides are apparently absorbed. An explanation for the
effects that were noted in Thomas's study may be that supplementation
with nucleotides and nucleosides allows for an allocation of energy
into other biosynthetic or reducing pathways rather than expending the
energy in the synthesis of nucleotides. That may account for the
decvreased lipofuscin etc.
Tim
michaelprice
> The effective dose could be as high as 100 gms/day (2) Purines
> may not be absorbed.
Or at least, not absorbed and processed as intact nucleotides.
> (3) If purines are not absorbed, yet nucleotides are
> beneficial, injection of purines along with pyrmidines could be
> MUCH more beneficial. This would be a long shot.
>
> (3) Evidence for incorporation of intact dietary pyrimidine
> (but not purine) nucleosides into hepatic RNA.
> Proc Natl Acad Sci U S A. 1995 Oct 24; 92(22): 10123-7.
> PMID: 7479738 full text
The full text article (free PDF available) is quite enlightening
and I'still digesting the contents. It may be that uraecil
is the key component of dietary RNA.
In the meantime I'm copying something Doug Strecky
has just posted to cryonet, which includes more on
Max Oden's (or Max Odens'?) study:
**********************************
Message #23318
Date: Sun, 25 Jan 2004 20:32:56 -0800 (PST)
From: Doug Skrecky <obe...@vcn.bc.ca>
Subject: Prolongation of the Life Span in Rats
Here's a quote from Saul Kent's article entitled
Can nucleic acid therapy reverse the degenerative processes of aging?
Geriatrics October 1977 130-136
" Of particular note is a study by English physician Max Odens in which
weekly injections of DNA and RNA were given to five rats with a normal
maximum life span of 800 to 900 days; treatment began at the age of 750
days. All the untreated rats died before the age of 900 days, while four
treated rats survived to ages of 1,600 to 1,900 days, and one rat survived
2,250 days. This degree of prolongation of the life span is unparalleled
in gerontological research. But few investigators have paid attention to
this study - despite the remarkable conclusion - because of its small
size and limited data."
Although lifespan studies on rodents treated orally with nucleotides
have been completed, with largely negative results, no follow-up
experiment using injectable DNA & RNA has ever been done. Back in 1997 I
made an attempt at this, when I spent $253.45 to purchase a 2 year old
Fisher 344 rat from Harlan Sprague Dawley, Inc. A local graduate
gerontology student, from the university of British Columbia obtained
some injectable salmon testes DNA & some torula yeast RNA from Sigma (for
$91.70), and tried to repeat this experiment. Unfortunately, due to a
mistake in mixing the DNA, & RNA with solvent, the subject rat
immediately died, after being injected for the first time. That was the
end of the experiment!
In retrospect it is unlikely that our attempt to replicate the
experiment could have succeeded, since we did not know what type of DNA,
or RNA was used by Max Odens. In an incredible omission, he never
mentioned the source of the DNA or RNA he used in his report. He only
mentioned that the RNA was "ordinary", whatever that means. However since
he quoted a lifespan study in C3H/HEJ mice, which used yeast RNA, then a
reasonable assumption would be that yeast RNA was used for his
injections. This still leaves the source of the DNA used, as an complete
unknown. Any attempt to replicate his experiment would first have to
resolve this omission. Injectible (but not oral) DNA vaccines are an
extremely effective means for inducing an immune response against
pathogen DNA, as well as inducing autoimmune disorders, and even
paradoxically inducing immune tolerance.
A brief review of the Max Odens experiment appeared in Nutrition Reviews
Vol 32, No. 10 October 1974 316- 317.
Quote:
"The Stuff on Which Quackery Thrives?
Quackery in nutrition and medicine is discouraged vigorously by ethical,
competent health professionals because of actual or potential health
hazards, economic factors, or the possibility that adherents to such
practices may bypass successful orthodox treatment. One device by which
misinformation can be combatted by scientists is educating the public to
demand documentation of claims.
A recent issue of the Journal of the American geriatrics Society
included a report by M. Odens that weekly injections of DNA and RNA more
than doubled the life span of rats. Ten 750-day old rats of a strain said
to ahve a usual life span of 800 to 900 days were fed the same diet
(composition unspecified). Five received weekly injections of DNA and RNA
(concentration, source, and purity unspecified). The five untreated rats
were said to have looked old, moved slowly, failed to eat much, and lost
weight after 12 weeks while the treated rats looked younger and were very
lively. The untreated rats were all dead by 900 days of age. The untreated
rats were all dead by 900 days of age; the injected rats died between
1600 and 2250 days of age.
Doubling the life span of any mammal is dramatic, and potentially
significant. Unfortunately, this paper contains insuffient information
for evaluation or repetition. Absent from the report are all data
concerning prior nutritional and health status, strain, sex, and weight
of the experimental animals, caging conditions, criteria of assignment to
treatments, full description of either the injection solution or the
experimental diet, and information on the cause of death.
The study of aging and longevity is difficult even under the best
experimental conditions. The publication in recognized professional
journals of startling claims based upon uncritically designed and
described experimental results constitutes a disservice to science and
the public by both the authors and the editors."
Despite extreme reservations about the format of Max Odens' research
report, I can find no serious reason to doubt his results. In think Odens
probably did produce a 2250 day old rat. Due to copywrite, it is
generally considered that one should not quote an entire research
article. However I'm willing to take a chance that the Journal of the
American Geriatrics Society is not going to overtly object to my quoting
the entire text from the "uncritically designed and described
experimental results" obtained by Max Odens .
For the first time, here in its unabridged from, is the complete text from:
Journal of the American Geriatrics Society Vol. XXI No.10 1973
Prolongation of the Life Span in Rats
Max Odens, MD, DTM*
London, England
* Deputy President, International Society for Research in Diseases of
Civilization & Vital Substances, 26 Weimers Hof, Luxembourg.
Address: 2 Devonshire Place, London W1, England.
Abstract: To test the effect of RNA-DNA in preventing the deleterious
effects of old age, and experiment was conducted that involved 10 rats
with a normal life span of 800-900 days. All were fed the same diet; 5
rats were not treated, and 5 were given weekly injections of DNA + RNA.
After twelve weeks the difference in appearance, weight and alertness was
remarkable. The 5 untreated rats died before 900 days. Of the treated
rats, 4 died at ages of 1600 - 1900 days, and 1 at 2250 days. A parallel
cannot be drawn with aging in human beings fed RNA-DNA, but the findings
on rats may have some application to cellular studies on cancer.
Several theories have been proposed concerning the role of DNA and RNA
in aging (1-5). Certain qualitative changes occur in DNA with aging (6),
and also changes in RNA synthesis and metabolism (7,8). The conflicting
results of many investigations (9-13) challenge as well as support these
theories.
The link between RNA synthesis and vitamin A (14), the hormonal
influence over RNA synthesis (15), further indicate the complexity of the
processes active in aging.
The effect of RNA supplementation on the memory and well-being of old
people has been the subject of many conflicting findings. It has been
reported (16,17) that supplementation of elderly patients' meals with
exogenous RNA (measuring in grams) for a relatively long period (measured
in months) enhances well-being and, if continued, improves memory. These
conclusions are supported by the results of work with rats (18). However,
the results of another study (19) in which old people were given RNA daily
(measured in milligrams) for shorter periods (measured in weeks) indicate no
improvement.
RNA is metabolized and enters the bloodstream in physiologically
significant amounts when ingested after food intake (20). It is specific
in restoring nucleic protein synthesis in isolated cell nuclei (21).
The foregoing observations led to a consideration of the possible role
in aging of the accumulated cellular insult from repeated virus
infections incurred over a lifetime, and the prevention of these
deleterious effects in rats by weekly injections of exogenous DNA and
RNA.
MATERIALS AND METHODS
Ten rats of a strain, in which the life span varies between 800 and 900
days, were selected for the experiment when they were each 750 days old.
They were given the same diet.
Group A, the controls, were not treated.
Group B recieved weekly injections of DNA solution in water saturated
with chloroform (3 mg per ml) plus ordinary RNA.
All necessary determinations such as temperature and weight were made.
The charts were compared every day. After twelve weeks of injections,
Group B rats looked younger, were very lively, and had gained weight
(1.5-2.3 gm). Group A rats looked old, moved slowly, did not eat much,
and had lost weight. the difference was remarkable.
All the untreated rats died before 900 days. Of the treated rats, 4 died
aged between 1600 and 1900 days. One rat lived 2250 days.
DISCUSSION
Many of the tissues of aged persons have characteristics which seem to
have stemmed from a process of cell replication that alters slowly but
surely over the years. Nevertheless, the aging process at the cellular
level can vary so remarkably between individuals that it is not always
possible for pathologists to grade unidentified tissue specimens according
to age.
If a virus takes over the cells, the production of protein is changed
and the cell begins to die slowly. Evidence of the original virus
infection can be carried over into daughter cells through mitotic
division (22).
Possibly one of the characteristics of cells in aging is the
accumulation of viral debris as imprints of prior viral infection,
regardless of how trivial or how serious the effect of the original
infection on the well-being of the host.
If such be the case, it is reasonable to assume that protein synthesis
by DNA and RNA for cell renewal is somehow interfered with by such viral
debris. On the other hand, exogenous RNA greatly improves the life span
C3H/HEJ mice challenged by a syngeneic tumor, when given after the tumor
challenge and preceded by immunization. The mechanism by which yeast RNA
influences this process is unknown (23).
The life span of laboratory rats is normally 800-900 days, although it
varies slightly in different countries. The results of the present
investigation on 5 untreated and 5 treated rats show that, with weekly
injections of DNA and RNA, and life span of 4 rats was doubled on the
average, and the life span of the fifth rat was more than trebled.
Although it is tempting to think in terms of the possibility of an
equivalent prolongation of the life span of human beings accomplished by
injections of DNA and RNA, it should be emphasized that the parallels
between aging in rats and aging in humans are not only unknown but are
entirely outside the scope of this experiment.
Postmortem results must still be evaluated by the electron microscope,
and will form the basis of another paper. There is one question to be
answered. Can supplementary exogenous DNA and RNA strenghten cellular
resistance to the invasion of viruses implicated in the etiology of
cancer? Cancer researchers should consider experiments along these lines.
Acknowledgment
My thanks to Professor Dr. An der Lan of the Zoological Institute of the
University of Innsbruck for his useful advice concerning the animal
experiments.
REFERENCES
1. Alexander P: The role of DNA lesions in the processes leading to aging
in mice, Symp Soc Exper Biol 21: 29 1967.
2. Medvedev ZhA: Aging at the molecular level and some speculations
concerning maintaining the functioning of systems for replicating
specific macromolecules, in Biological Aspects of Aging, ed. by N. W.
Shock. New York, Columbia Univ. Press 1962.
3. von Hahn HP: The role of desoxyribonucleic acid (DNA) in the aging
process, Gerontologia 8: 168, 1968.
4. Sinex FM: Genetic mechanisms of aging, J Gerontol 21: 340 1966
5. Wulff VJ Quastler H and Sherman FG: An hypothesis concerning RNA
metabolism and aging, Proc US Nat Acad Sci 48: 1373, 1962.
6. von Hahn HP: Age-dependant thermal denaturation and viscosity of crude
and purified desoxyribonucleic acid prepared from bovine thymus,
Gerontologia 8: 123, 1963.
7. Mainwaring WIP: Changes in the ribonucleic acid metabolism of aging
mouse tissue with particular reference to prostate gland, Biochem J
110: 79, 1968.
8. Devi A, Lindsay P, Raina PS et all: Effect of age on some aspects of
the synthesis of ribonucleic acid, Nature 212: 474 1966.
9. Enesco HE: A cytophotometric analysis of DNA content of rat nuclei in
aging, J Gerontol 22: 445, 1967.
10. Geary S and Florini JR: effect of age on the rate of protein
synthesis in isloated perfused mouse hearts, J Gerontol 27: 325 1972
11. Sobel H: Effect of age on cardiac metabolism. Proc 3rd Annual Meeting
of International Study Group for Research in Cardiac Metabolism,
Stowe, Vermont, June 29-July 1, 1970.
12. Britton VJ, Sherman FG and Florini JR: Effect of age on RNA synthesis
by nuclei and soluable RNA polynerases from liver and muscle of
C57BL/6J mice, J Gerontol 27: 188 1972.
13. Beauchene RE, Roeder LM and Barrows CH Jr: The effect of age and of
ethionine feeding on the ribonucleic acid and protein synthesis of
rats, J Gerontol 22: 318, 1967.
14. Kaufman DG, Baker MS, Smith JM et all: RNA metabolism in tracheal
epithelium: alteration in hamsters defient in vitamin A, Science 177:
1105, 1972.
15. Zolakar M: Hormonal control of RNA synthesis as a developmental
problem, J Gerontol 22 (II): 17, 1967.
16. Odens M: R.N.A. effects on memory, Vitalstoffe 14: 144, 1969.
17. Odens M: R.N.A. effects on memory (continues), Vitalstoffe 15: 172,
1970.
18. Solyon L, Enesco HE and Beaulieu MA: The effects of RNA on learning
and activity in old and young rats, J Gerontol 22: 1, 1967.
19. Britton A, Bernstein LL, Brunse AJ et al: Failure of ingestion of RNA
to enahnce human learning, j Gerontol 27: 478, 1972.
20. Allfrey V and Mirsky AE: Some DNA-dependent synthetic systems of
isolated cell nuclei, Tr New York Acad Sci 21: 3, 1958-59.
21. Rigby PG: The effects of "exogeous" RNA on the improvement of
syngeneic tumor immunity, Cancer Res, 31: 4, 1971.
22. Odens M: Can We Delay Old Age? Lecture given at the 18th Internat.
Congress, Internat. Soc. for Research on Diseases of Civilization,
Berlin, Berlin, Sept. 1972.
23. Rigby PG: The effect of "exogenous" RNA on the improvement of
syngeneic tumor immunity, Cancer Res 31: 4, 1971.
*************************************--
Aubrey de Grey
I would like to make sure that a detail in the Nutrition Reviews piece
that Michael Price just posted does not go unnoticed: that the rats in
Odens's experiment were injected not from weaning but only from age 750
days, which is stated to be only 50-150 days short of their mean lifespan.
The idea that lifespan could be doubled by a treatment as simple as this
is highly dubious, but the idea that remaining lifespan can be increased
by a factor of ten -- yes, ten -- is, quite frankly, absurd. I think
this is probably the main reason there was no followup.
Aubrey de Grey
michaelprice
Hi Aubrey,
sadly, I'm sure this is the reason for no follow-up (along with
the Swiss-clinic-foetal-cell-injections association I mentioned
elsewhere). Yes, Oden's claims are absurd, but that's no reason
for not following them up - after all plenty of "absurd" things have
turned out to be true. And even if it only produced a 10% extension,
that would still be worth knowing.
Oden claimed (if I've understood it correctly) to have demonstrated
rejuvenation, not just retardation. As you may remember I am sceptical
about rejuvenation (perhaps more so than you, Aubrey, I think) and
am more interested in aging retardation (on which I am more optimistic,
of course). None of this alters what Mike O'Gara said - it would make
an ideal "Methuselah Mouse prize" entry!
BTW, Aubrey, I haven't thanked you for IABG10 - thanks! As a
followup to our discussion in The Eagle, do you still think that if 2
genes are altered (e.g. in a transgenic strain of mice), and produces
no change in lifespan (over "wild-type" controls) that we can conclude
that neither gene has an effect on LS? Perhaps I misunderstood you
(the pub was *very* noisy and I was dog tired), but it seems to me that
this can only be concluded if there is no LS increase as both genes are
*independently* varied, which didn't seem to be the case under discussion.
Aubrey de Grey
Michael Price wrote:
> Yes, Oden's claims are absurd, but that's no reason
> for not following them up - after all plenty of "absurd" things have
> turned out to be true. And even if it only produced a 10% extension,
> that would still be worth knowing.
>
> Oden claimed (if I've understood it correctly) to have demonstrated
> rejuvenation, not just retardation. As you may remember I am sceptical
> about rejuvenation (perhaps more so than you, Aubrey, I think) and
> am more interested in aging retardation (on which I am more optimistic,
> of course). None of this alters what Mike O'Gara said - it would make
> an ideal "Methuselah Mouse prize" entry!
All absolutely true. Specifically, even if one only got half the effect
that Odens got, one would be able to win the Reversal Prize by a mile,
and with only a few mice at that. Any volunteers? If not, why not?
> BTW, Aubrey, I haven't thanked you for IABG10 - thanks! As a
> followup to our discussion in The Eagle, do you still think that if 2
> genes are altered (e.g. in a transgenic strain of mice), and produces
> no change in lifespan (over "wild-type" controls) that we can conclude
> that neither gene has an effect on LS? Perhaps I misunderstood you
> (the pub was *very* noisy and I was dog tired), but it seems to me that
> this can only be concluded if there is no LS increase as both genes are
> *independently* varied, which didn't seem to be the case under discussion.
I imagine I was even more tired, because I don't recall this conversation
at all. Certainly what you say is correct. In practice one might say
that it would be pretty unlikely to pick a gene alteration that increased
lifespan and then, by bad luck, to combine it with one that nullified
that increase, but in principle, sure.
Aubrey de Grey
rs
What would this suggest then... that Odens fabricated his data, or
perhaps a mischevious colleague replaced the rats on Odens without him
noticing?
Tim
> Aubrey de Grey wrote:
> >
> > I would like to make sure that a detail in the Nutrition Reviews
> > piece that Michael Price just posted does not go unnoticed: that
> > the rats in Odens's experiment were injected not from weaning
> > but only from age 750 days, which is stated to be only 50-150
> > days short of their mean lifespan. The idea that lifespan could be
> > doubled by a treatment as simple as this is highly dubious, but the
> > idea that remaining lifespan can be increased
> > by a factor of ten -- yes, ten -- is, quite frankly, absurd.
> > I think this is probably the main reason there was no followup.
>
> Hi Aubrey,
> sadly, I'm sure this is the reason for no follow-up (along with
> the Swiss-clinic-foetal-cell-injections association I mentioned
> elsewhere). Yes, Oden's claims are absurd, but that's no reason
> for not following them up - after all plenty of "absurd" things have
> turned out to be true. And even if it only produced a 10% extension,
> that would still be worth knowing.
As I mentioned it may be supplying some synthetic products produced by
the pentose phosphate pathway that are not only decreased by aging but
may also be generally deficiently synthesized for longevity purposes.
I've always been pretty skeptical of the results. In my mind I think
the fact that Oden's was neither interested in longevity, looking for
a longevity effect, or interested in marketing RNA/DNA injections
lends some credibility to the study.
None of this alters what Mike O'Gara said - it would make
> an ideal "Methuselah Mouse prize" entry!
Indeed, a shame no one foillowed it up. More seemingly absurd things
have proved to be true. But then arguably it could be as important as
reducing ROS as the cell seems to have to expend energy either for
reducing power or biosynthesis and we know that certainly isn't as
efficient as it could be.
Tim