CryoNet #32316 - #32320

CryoNet - Mon 18 Jan 2010

    #32316: Re: Stressing rejuvenation to promote cryonics [David Stodolsky]
    #32317: old question [ettinger]
    #32318: Re: CryoNet #32315 [Eisab]
    #32319: Re: CryoNet #32315 [Michael Smith]
    #32320: synergism between tocotrienol and resveratrol [oberon]

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Message #32316
From: David Stodolsky <[email protected]>
Subject: Re: Stressing rejuvenation to promote cryonics
Date: Sun, 17 Jan 2010 13:52:42 +0100
References: <[email protected]>

On 17 Jan 2010, at 11:00 AM, CryoNet wrote:

> From: Mark Plus <[email protected]>
> Subject: Re: Stressing rejuvenation to promote cryonics
> Date: Sat, 16 Jan 2010 07:34:12 -0800
>
> In Cryonet #32314, Ben Best writes:
>
>>> I was asked to concentrate on the scientific
>>> aspects of cryonics. I will devote the first
>>> half of my presentation to rejuvenation science because
>>> I believe this is an essential part of the cryonics
>>> program that is too often missed, and which provides
>>> so much incentive (a marketing benefit for outreach).
>
>> David Stodolsky wrote:
>
>>> What evidence is there to support this view?
>
>>  I have drawn this conclusion from the hundreds if not
> thousands of conversations I have had with people
> about cryonics.
>
> I've also noticed that several components of the cryonics idea fail  
> to communicate well, including the role of rejuvenation as part of  
> the revival process, and the expectation that progress in trauma  
> medicine will lead to the ability to repair "whole body frostbite,"  
> as someone called cryonic suspension.
>
> Instead I read or hear misconceptions about waking up in Future  
> World with the aged body that killed you in the first place, or  
> "skepticism" that because nobody can revive you from suspension now,  
> the whole cryonics exercise can't possibly work.
>
> Of course, "skepticism" of that sort rationalizes not doing anything  
> to make cryonics better, and therefore guarantees its continuing  
> underperformance. As I feel tempted to say to such people, "Okay,  
> brainiac, tell us your plan for staying alive."
>
> Given that cryonics idea has circulated in the culture for almost 50  
> years, and that people can now easily read about it online, I'd like  
> to know why such misunderstandings about it persist.


I address this issue in my in preparation paper on Marketing Myths:

The Badger (1998) Survey questions examining public knowledge about  
cryonics addressed one of the earliest myths about public acceptance  
of cryonics. This myth was typically expressed, "If people knew that  
cryonics was not that expensive, then it would gain wide-spread  
acceptance". Similar statements questioned knowledge about the  
technology of suspension, number of persons suspended, and the number  
enrolled in suspension programs. The Survey results, while not  
conclusive, suggested that public knowledge was quite accurate on the  
average. As the years have gone by and as cryonics has received more  
and more mass media exposure, this myth has subsided. We will not  
address this myth further here, except to show that attitudes tend to  
be the cause of factual misperceptions. This is widely accepted in  
psychology, where perception is assumed to include a search process,  
except in the simplest, typically laboratory, situations. Powers  
(1973) made this same point from a foundation of control theory, which  
might be more acceptable to many from an engineering background. The  
above mentioned myth presumed the other direction of causality, that  
is, that misperception of facts leads to unfavorable attitudes. This  
is typically referred to as the rational choice model of decision  
making. It tends to dominate virtually all discussions of these issues  
with in the cryonics movement.



Powers, W. T. 1973. Behavior: The control of perception. New York:  
Aldine deGruyter.






dss


David Stodolsky
[email protected]  Skype: davidstodolsky

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Message #32317
From: [email protected]
Date: Sun, 17 Jan 2010 11:21:37 EST
Subject: old question

>Given that cryonics idea has circulated in the culture for almost 
>50 years, and that people can now easily read about it online, I'd 
>like to know why such misunderstandings about it  persist.

>Mark Plus
Wrong question, with an easy answer, capsulized in  Youniverse
and elsewhere as cultural inertia--roughly, most people,  most
of the time, believe and act as they have been taught  or
conditioned.
 
But not always, and in a few cases the conditioning is  positive.
We're gaining on them, albeit still much more slowly  than
we would like.  We are doing some  things right, and if we
maintain and improve the outlook is good.
 
R.E.
 



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Message #32318
From: "Eisab" <[email protected]>
References: <[email protected]>
Subject: Re: CryoNet #32315
Date: Sun, 17 Jan 2010 11:43:55 -0500

In my opinion ideas such as "aging will be conquered in our life time" is 
the main reason people do not sign up for cryonics because it eliminates the 
need for suspension. It has exactly the opposite effect.

Basie 

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Message #32319
References: <[email protected]>
Date: Sun, 17 Jan 2010 11:43:49 -0800
Subject: Re: CryoNet #32315
From: Michael Smith <[email protected]>

On Sun, Jan 17, 2010 at 2:00 AM, CryoNet <[email protected]> wrote:
>
> CryoNet - Sun 17 Jan 2010
>
>    #32315: Re: Stressing rejuvenation to promote cryonics [Mark Plus]
>
> Rate This Digest: http://www.cryonet.org/cgi-bin/rate.cgi?msg=32315%2D32315
>
> Administrivia
>
> To subscribe to CryoNet, send email to:
>    [email protected]
> with the subject line (not message _body_):
>    subscribe
> To unsubscribe, use the subject line:
>    unsubscribe
>
>
> ----------------------------------------------------------------------
>
> Message #32315
> From: Mark Plus <[email protected]>
> Subject: Re: Stressing rejuvenation to promote cryonics
> Date: Sat, 16 Jan 2010 07:34:12 -0800
>
> In Cryonet #32314, Ben Best writes:
>
> >> I was asked to concentrate on the scientific
> >> aspects of cryonics. I will devote the first
> >> half of my presentation to rejuvenation science because
> >> I believe this is an essential part of the cryonics
> >> program that is too often missed, and which provides
> >> so much incentive (a marketing benefit for outreach).
>
> >David Stodolsky wrote:
>
> >> What evidence is there to support this view?
>
> >   I have drawn this conclusion from the hundreds if not
> thousands of conversations I have had with people
> about cryonics.
>
> I've also noticed that several components of the cryonics idea fail to communicate well, including the role of rejuvenation as part of the revival process, and the expectation that progress in trauma medicine will lead to the ability to repair "whole body frostbite," as someone called cryonic suspension.
>
> Instead I read or hear misconceptions about waking up in Future World with the aged body that killed you in the first place, or "skepticism" that because nobody can revive you from suspension now, the whole cryonics exercise can't possibly work.
>
> Of course, "skepticism" of that sort rationalizes not doing anything to make cryonics better, and therefore guarantees its continuing underperformance. As I feel tempted to say to such people, "Okay, brainiac, tell us your plan for staying alive."
>
> Given that cryonics idea has circulated in the culture for almost 50 years, and that people can now easily read about it online, I'd like to know why such misunderstandings about it persist.
>
> Mark Plus


At a guess, I would suggest that it's because people are scared of
looking socially deviant.  I think we're all familiar with the
standard litany of illogical arguments against both cryonics and the
whole idea of immortality.  The fact that the same arguments appear in
people who don't collaborate and often clearly haven't put much
thought into the issue suggests that the primary resistance to
cryonics is cultural.  The arguments, I would wager, are completely
secondary to the primary drive to belong to and be accepted by a
community.

There are a few memes in particular that I think compound the problem.
 The two that I think are the most difficult to overcome are (1) the
idea that aging is an integral and therefore inevitable part of life
and (2) the idea that everyone has a proper time to die.  Since being
part of a culture is to a large extent a matter of adopting the memes
of that culture, we immortalists can often appear as though we're not
part of the same "tribe," so to speak, as those whom we would like to
persuade.  I suspect it has absolutely nothing to do with the logic of
life and death and has everything to do with the sense of belonging.

Mind you, this is largely guesswork - well-researched guesswork, but
still very uncertain.  I and a few others who attended the Teens &
Twenties conference in Florida this last weekend are planning on
performing a study to explore this and other hypotheses (e.g. that
people with an inclination towards cryonics have a fundamentally
different psychological constitution than the general populous).  If
I'm right, then that's actually a really good thing.  Yes, it means
people are frustratingly unreasonable - but we already knew that.
What this would tell us is WHY people appear unreasonable by pointing
us to their actual motivations for rejecting cryonics and other
immortalist endeavors.  Once we know that, we can change our tactics
in presenting cryonics so that our presentations come across as more
compelling, meaning that we can really make progress in saving lives.

That's just my personal take on the matter.

 ~Michael Smith

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Message #32320
Date: Sun, 17 Jan 2010 21:10:07 -0800 (PST)
From: [email protected]
Subject: synergism between tocotrienol and resveratrol

[Clinical trials with alpha tocopherol show that this form of vitamin E
offers no mortality benefit in humans. I'd wager that the results would be
different with tocotrienol, particularly in combination with
resveratrol.]

J Cell Mol Med. 2009 Oct 3. [Epub ahead of print]
Co-ordinated autophagy with resveratrol and gamma-tocotrienol confers synergetic cardioprotection.
Lekli I, Ray D, Mukherjee S, Gurusamy N, Ahsan MK, Juhasz B, Bak I, Tosaki A, Gherghiceanu M, Popescu LM, Das DK. Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA.
    ABSTRACT This study compared two dietary phytochemicals, grape-derived resveratrol and palm oil-derived gamma-tocotrienol, either alone or in combination, on the contribution of autophagy in cardioprotection during ischemia and reperfusion. Sprague Dawley rats weighing between 250-300 gm were randomly assigned to one of the following groups: vehicle, ischemia/reperfusion (I/R), resveratrol+I/R, gamma-tocotrienol+I/R, resveratrol+gamma-tocotrienol+I/R. For resveratrol treatments, the rats were gavaged with resveratrol [2.5 mg/kg] for 15 days while for gamma-tocotrienol experiments the rats were gavaged with gamma-tocotrienol [0.3 mg/kg] for 30 days. For the combined resveratrol +gamma-tocotrienol experiments, the rats were gavaged with gamma-tocotrienol for 15 days, and then gavaging co
 ntinued with resveratrol along with gamma-tocotrienol for a further period of 15 days. After 30, days, isolated perfused hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. Our results showed for the first time that at least in part, the cardioprotection (evidenced from the ventricular performance, myocardial infarct size and cardiomyocyte apoptosis) with resveratrol and gamma-toctrienol was achieved by their abilities to induce autophagy. Most importantly, resveratrol and gamma-tocotrienol acted synergistically providing greater degree of cardioprotection simultaneously generating greater amount of survival signal through the activation of Akt-Bcl-2 survival pathway. Autophagy was accompanied by the activation of Beclin and LC3-II as well as mTOR signaling
 , which were inhibited by either 3-methyl adenine (3-MA) or Wortmannin. The autophagy was confirmed from the results of transmission electron microscopy and light microscopy as well as with confocal microscopy. It is tempting to speculate that during ischemia and reperfusion autophagy along with enhanced survival signals helps to recover the cells from injury.
PMID: 19799646

[Here synergism was again noted between tocotrienol and resveratrol.]

Int J Oncol. 2008 Oct;33(4):851-9.
Suppression of cell proliferation and gene expression by combinatorial synergy of EGCG, resveratrol and gamma-tocotrienol in estrogen receptor-positive MCF-7 breast cancer cells.
Hsieh TC, Wu JM. Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.
    Numerous dietary phytochemicals have shown anti-breast carcinogenic activities when tested in vitro; however, in most cases, the demonstrated efficacy of individual phytochemicals requires doses not readily achievable in vivo. Therefore, whether diets might exert translational promises and benefits in clinical settings and prevention of breast cancer remain unclear. Since cancer cells are endowed with complex, redundant, converging and diverging pathways spanning both the genetic and metabolic networks that are not merely replicates of those in normal cells, it is of interest to test whether a multicomponent approach involving lower, physiologically relevant doses of natural dietary agents may be developed as a chemopreventive strategy for breast cancer. Herein, we investigated, using 
 the estrogen receptor-positive MCF-7 breast cancer cells as a model, whether the combination of epigallocatechin gallate (EGCG), resveratrol and gamma-tocotrienol at suboptimal doses elicits synergism in suppressing cell proliferation, modulating gene expression, and increasing antioxidant activity, as compared to each of the three phytochemicals added alone. The results showed that there was a approximately 33, 50 and 58% inhibition of cell proliferation by > or =50 microM EGCG, > or =25 microM resveratrol and > or =10 microM gamma-tocotrienol, respectively, added as a single agent. When a suboptimal dose (10 microM) of each phytochemical was used, a significant additive effect in suppression of cell proliferation was observed with the combination of resveratrol and gamma-tocotrienol wh
 ereas the three phytochemicals added together did not produce more pronounced inhibition of cell proliferation. A significant additive effect in reducing cyclin D1 and bcl-2 expression was found when gamma-tocotrienol was added with either EGCG or resveratrol. Functional synergism among the three phytochemicals was only observed in the induction of quinone reductase NQO1. These results suggest that diet-based protection against breast cancer may partly derive from synergy amongst dietary phytochemicals directed against specific molecular targets in responsive breast cancer cells, and provide support for the feasibility of the development of a diet-based combinatorial approach in the prevention and treatment of breast cancer.
PMID: 18813800

J Neurochem. 2009 Dec 17. [Epub ahead of print]
Nanomolar vitamin E alpha-tocotrienol inhibits glutamate-induced activation of phospholipase A(2) and causes neuroprotection.
Khanna S, Parinandi NL, Kotha SR, Roy S, Rink C, Bibus D, Sen CK. Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, OH 43210.
    ABSTRACT Our previous works have elucidated that the 12-lipoxygenase (12-Lox) pathway is directly implicated in glutamate-induced neural cell death, and that such that toxicity is prevented by nM concentrations of the natural vitamin E alpha-tocotrienol (TCT). In the current study we tested the hypothesis that phospholipase A(2) (PLA(2)) activity is sensitive to glutamate and mobilizes arachidonic acid (AA), a substrate for 12-Lox. Furthermore, we examined whether TCT regulates glutamate-inducible PLA(2) activity in neural cells. Glutamate challenge induced the release of [(3)H]AA from HT4 neural cells. Such response was attenuated by calcium chelators (EGTA and BAPTA), cPLA(2)-specific inhibitor (AACOCF(3)) as well as TCT at 250 nM. Glutamate also caused the elevation of free polyunsa
 turated fatty acid (AA and docosahexaenoic acid) levels and disappearance of PL-esterified AA in neural cells. Furthermore, glutamate induced a time-dependent translocation and enhanced serine phosphorylation of cPLA(2) in the cells. These effects of glutamate on fatty acid levels and on cPLA(2) were significantly attenuated by nM TCT. The observations that AACOCF(3), transient knock-down of cPLA(2) as well as TCT significantly protected against the glutamate-induced death of neural cells implicate cPLA(2) as a TCT-sensitive mediator of glutamate induced neural cell death. This work presents first evidence recognizing glutamate-induced changes in cPLA(2) as a novel mechanism responsible for neuroprotection observed in response to nanomolar concentrations of TCT.
PMID: 20028458

[Below tocotreinols, but not alpha tocopherol suppress tissue damage.]

Drug Chem Toxicol. 2009;32(4):319-25.
Effect of tocotrienols on iron-induced renal dysfunction and oxidative stress in rats.
Gupta A, Chopra K. Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.
    Ferric nitrilotriacetate (Fe-NTA) is a well-established nephrotoxic agent. This study was designed to investigate the modulatory effect of the subacute administration of tocotrienol-rich fraction (T3), a product from palm oil, and alpha-tocopherol (T) on Fe-NTA-induced renal injury and oxidative stress. Fe-NTA administration markedly increased blood urea nitrogen (BUN) and serum creatinine level, which was coupled with a marked lipid peroxidation, reduced activity of glutathione levels, and morphological alterations in rat kidney. Pretreatment with T3 (50 mg/kg/day) and T (50 mg/kg/day) for 7 days before Fe-NTA administration significantly reduced the serum creatinine and BUN levels, reduced lipid peroxidation in a significant manner, and restored levels of reduced glutathione and supe
 roxide dismutase. T3 pretreatment also attenuated the serum tumor necrosis factor-alpha levels, as compared to pretreatment with T, and restored normal renal morphology. These findings suggest a strong correlation between iron-induced oxidative stress and renal dysfunction and point toward the protective effects of T3 in Fe-NTA-induced renal injury.
PMID: 19793023

Eur J Appl Physiol. 2009 Nov;107(5):587-95. Epub 2009 Aug 25.
Effects of tocotrienol-rich fraction on exercise endurance capacity and oxidative stress in forced swimming rats.
Lee SP, Mar GY, Ng LT. Ping Tin Enterprise Co., Ltd., Kaohsiung, Taiwan.
    The present study aimed to examine the effects of tocotrienol-rich fraction (TRF) on exercise endurance and oxidative stress in forced swimming rats. Rats fed on isocaloric diet were orally given 25 (TRF-25) and 50 (TRF-50) mg/kg of TRF, or 25 mg/kg D-alpha-tocopherol (T-25) whilst the control group received only the vehicle for 28 days, followed by being forced to undergo swimming endurance tests, with measurements taken of various biochemical parameters, including blood glucose, lactate and urea nitrogen, glycogen, total antioxidant capacity, antioxidant enzymes, thiobarbituric acid-reactive substances (TBARS), and protein carbonyl. Results showed that the TRF-treated animals (268.0 +/- 24.1 min for TRF-25 and 332.5 +/- 24.3 min for TRF-50) swam significantly longer than the control 
 (135.5 +/- 32.9 min) and T-25-treated (154.1 +/- 36.4 min) animals, whereas there was no difference in the performance between the T-25 and control groups. The TRF-treated rats also showed significantly higher concentrations of liver glycogen, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as of muscle glycogen and SOD than the control and the T-25-treated animals, but lower levels in blood lactate, plasma and liver TBARS, and liver and muscle protein carbonyl. Taken together, these results suggest that TRF is able to improve the physiological condition and reduce the exercise-induced oxidative stress in forced swimming rats.
PMID: 19705143

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