Volume 10 no 57. First published December 1996. ISSN 0964-5659.
e-mail: Internet firstname.lastname@example.org
New Arrangements for Longevity Report
Accepting the Unacceptable Chrissie Loveday
The Mechanism of Human Longevity Leonid A.Gavrilov et al
What Others Think Alan Hardy, Ian King, Sam Smith
Terror Management Tim Freeman
Liberty versus Freedom Eric Szuter
Brain Geometry Yvan Bozzonetti
Two Photons Interferometers Yvan Bozzonetti
Miscellaneous Round-up Douglas Skrecky
Freeze Drying a Brain,
PBS/Melatonin Extends the Lifespan of Diabetic Mice,
Life Expectancy Statistics
Successful Biotin Treatment of Diabetes
Caloric Restriction, Glycemic Index and Diabetes
Dinh Lang Extends Lifespan,
DNA-RNA Chloroform Injections Increase lifespan 144%,
Variations on a Straight Freeze
Can Lycopene Delay Ageing,
Beware Calcium Channel Blockers,
Can Phosphagain delay age-related frailty?
Beware skin creams with vitamin E.
How Can Ant-Aging Become a National Priority? Tim Freeman
The Scientific Debate Over Cryonics Randy Smith
Ban Dihydroigen Monoxide, the Invisible Killer Eugene Leitl
Single copy rate 3.50. Subscription rates six issues of 20 pages:- 20 (15 by Banker's Order UK only). Cheques in British Pounds should be drawn on a UK bank and should be made payable to "Reeves Telecommunications Laboratories" Alternatively, dollar checks for $34 can be accepted if drawn on a U.S. bank and made payable to "J. de Rivaz". Contents are provided for information only, under the right to free speech. Opinions are the authors' own. No professional advice is intended. If you wish others to be legally responsible for your health, life or finances, then please consult a professional regulated according to the laws of your country.
New Arrangements for Longevity Report
These changes will increase the efficiency of distribution, as people living in the United States can get both Longevity Report and The Immortalist for less money ($25) than they had been paying for Longevity Report alone ($34).
Accepting the Unacceptable
by Chrissie Loveday
This month's obsession in the UK (and possibly elsewhere in the world), seems to be the breakdown in standards of behaviour in schools. As cryonicists we need an ordered world so that we can safely remain in suspension, and a direct link between behaviour of children and the next generation of criminals does not indicate well for the future in this respect.
It seems that many children as young as five are already carrying "statements", which require them to be supported in mainstream education. In effect this means that they have been assessed by a range of professionals, following referrals from school and nursery to reach the conclusion that they need someone to work on a one to one basis for at least part of every school day. Some children of course, need this type of support because of learning difficulties or disability which prevents then from coping normally within the school environment. It is generally accepted that children with special educational needs will integrate in society more readily if they have experienced mainstream education.
So why are some children apparently out of control? Why are they unable to behave in an acceptable manner in society? Many believe it is because of a breakdown in parenting. Too many parents use television or some other electronic dummy to entertain their offspring. Tempting, isn't it? Sit the child down safely in front of some entertainment and you are free to do all those other things that are so vital. In some cases both parents have to work to enjoy a reasonable standard of income; many are one-parent families; some parents lack any skills in parenting, unaware of the need for stimulation and sharing portions of their life with children. Parents who are unwilling to accept their own deficiencies will blame lack of discipline in schools, as the cause. As a long time teacher, I have seen changes in students over the years. They are more assertive and aware of rights. Ceasing corporal punishment in schools removed many of the possible sanctions ... there have even been suggestions that it could be restored, in the current crisis. Kids know that they can instigate action to be taken against the school, well-supported by the very parents who might complain about lack of discipline.
It may be that a convenient label can be attached to the child's behaviour. The latest alphabet soup is ADHD (Attention Deficit Hyper-activity Disorder). This is recognised as a genetic disorder with possible treatments ranging from strict dietary control of certain foods, to the use of drugs to control the behaviour of the child. Great! The child is no longer the parent's problem ... it is a recognisable medical condition. Parents with very good parenting skills still have problem children, so it would seem that the condition of ADHD is very real. As an ancient cynic, I wonder how long it will be before most parents can blame this medical condition for any bad behaviour. I have heard of parents taking their unmanageable child to the doctor and virtually demanding medication.
Doubtless we are entering the age of smart-drugs which can assist with many of today's illnesses or conditions. We need something to blame (besides ourselves) for the problems. I ask, how did all the children in the past cope? There were few counsellors, little medication to solve the problems constructively and little understanding or communication to support parents. Admittedly, many mistakes were made and people institutionalised without reason, but I fear that we are heading too far the other way. More people need to take responsibility for themselves and seek the available help wherever possible. A recent Panorama programme showed a family in shreds. The parents persistently used bad language and spent little time with their child.
"He is an impossible child and I am beginning to dislike him," said the mother. They attended a parenting course and followed the suggestions.
"Brilliant, he just loves it when we play together. He's a different child," said the mother.
Two weeks later:
"He's too demanding. I can't keep playing with him all the time."
Result? Any attention from Mum is better than none, so I'll be naughty. Then she has to take notice of me, even if it's to tell me off and shout obscenities.
(How do you convince a child that some words are unacceptable when they hear them from parents at least twice in every sentence?)
So what of the future? Will the powers that be, control everyone by some form of drugs when they see unacceptable behaviour? Who should be the ones who decide what is acceptable? I certainly hope it isn't the politicians, as many of them need treatment themselves. They have cultivated the art of not listening to a fine degree. Their auto-response of knock the other party does not inspire confidence in a well-thought out plan for the future. I wonder if we shall return to a highly moral society where many things are swept under the proverbial carpet? I doubt it, as international communications are too established, spreading knowledge of all kinds. Perhaps having gone through such an age of change ... more in our lifetime than ever before, we shall be well-adapted to copping with changes we shall see if we succeed in our attempts at cryonic suspension. Think of H. G. Wells' Time machine hero. For him, the distant future was so appealing he gave up his world to enjoy it and what he could bring to a society, apparently devoid of knowledge.
Sounds good to me!
The Mechanism of Human Longevity
by Leonid A.Gavrilov, Natalia S.Gavrilova, Galina N.Evdokushkina, Yulia E.Kushnareva, Victoria G.Semyonova, Anna L.Gavrilova, Evgeniy V.Lapshin, Natalia N.Evdokushkina
Center for Longevity Research at A.N.Belozersky Institute, Moscow State University, Moscow, Russia (electronic mail: email@example.com) and Institute for Systems Analysis, Russian Academy of Sciences, Moscow
The evolutionary theory of longevity predicts that the equilibrium gene frequency for lethal mutations should increase with age at onset of mutation action because of weaker (postponed) selection against later-acting mutations 1-2. According to this mutation accumulation hypothesis, one would expect the genetic variability for survival (additive genetic variance) to increase with age1-2. The ratio of additive genetic variance to the observed phenotypic variance (the heritability of longevity) could be estimated most reliably as the doubled slope of the regression line for offspring life span on paternal age at death . Thus, one would expect this slope to become more and more steep at higher paternal ages, if longevity is indeed determined by late-acting lethal mutations.
In order to check the suggested mechanism of life span limitation, we have computerized and analyzed genealogical data on human longevity in European royal and nobility families published in Genealogisches Handbuch Des Adels 4 and in other professional genealogical sources, listed elsewhere5. Offspring life span was analysed for adults (those who survived by age 30) in order to study the effects of late-acting mutations. The data for offspring born in 20th century were excluded from the analysis in order to have unbiased estimates of longevity for extinct birth cohorts. The data for offspring born before 18th century were also excluded in order to minimize the heterogeneity of population. For each birth cohort the mean expectation of life at age 30 was calculated and used as a dependent variable in multiple linear regression to control for cohort and secular effects on human longevity. Offspring longevity for each particular sex (4,278 records for males and 2,490 records for females) was considered as a dependent variable in multiple regression model (program 1R in BMDP statistical package) and a function of 3 independent predictors: paternal age at death (for estimation of heritability of life span), paternal age at reproduction (control for parental age effects) and cohort life expectancy (control for cohort and secular trends and fluctuations). The F ratio for each multiple regression was higher than 17.0 and all the regressions were statistically highly significant (P<0.0001).
The heritability of human life span is equal to 8% +/- 4% for sons and to 16% +/- 4% for daughters born by fathers who survived by age 20 (Table 1). At advanced paternal ages the heritability estimates are much higher: 30% +/- 12% for sons and 60% +/- 16% for daughters born by fathers who lived 70 years and more (Table 1).
Paternal age Regression slopes +/- standard error at death for offspring life span on paternal age at death Sons (number of cases) Daughters (number of cases)
20+ 0.04 +/- 0.02 0.08 +/- 0.02 (4278) (2490) 60+ 0.07 +/- 0.03 0.12 +/- 0.05 (2955) (1704) 65+ 0.13 +/- 0.04 0.19 +/- 0.06 (2402) (1367) 70+ 0.15 +/- 0.06 0.30 +/- 0.08 (1754) (1030) 75+ 0.15 +/- 0.09 0.47 +/- 0.12 (628) (376)
The higher heritability of longevity for daughters might be explained by their specific inheritance of paternal X-chromosome that is more rich in genetic information compared to small paternal Y-chromosome inherited by sons6-7. These results represent the first demonstration to our knowledge of a significant increase in additive genetic variance of human longevity at advanced parental age (above age 60), predicted by the evolutionary theory of life span and by the mutation accumulation hypothesis in particular.
Charlesworth, B. Evolution in Age-Structured Populations (Cambridge Univ.Press, Cambridge, 1994).
2. Partridge, L. & Barton, N.H. Nature 362, 305-311 (1993).
Falconer, D.S. Introduction to Quantitative Genetics (Longman, London, 1989).
4. Genealogisches Handbuch des Adels. Band 75(XI) (C.A.Starke Verlag, Limburg an der Lahn, 1980); Ibid. Band 90(XIII),(1987); Ibid. Band 106(XXIII),(1994); Ibid. Band 107(XVII),(1994).
Gavrilov, L.A. et al. Longevity Report (ISSN 0964-5659), 10(54), 7-15 (1996).
Gavrilov, L.A., Gavrilova, N.S. The Biology of Life Span: A Quantitative Approach (Harwood Academic Publishers, Chur, London, 1991).
7 Gavrilov, L.A., Gavrilova, N.S. Nature 367, 520 (1994).
Acknowledgments. This work was supported by the European Community (grant INTAS-93-1617). In order to continue these studies further, we need now additional funding from any organization or private person. Please contact us for this purpose at E-mail: <firstname.lastname@example.org> or by fax: 7-095-939-0338/3181.
What Others Think
from New Hope International:
Longevity Report (West Towan House, Porthtowan, Truro TR4 8AX) (2O pa) Articles on cryonics and various medical matters, including future medical developments of concern if you plan to be cryonically suspended Incredibly many articles question why cryogenics has remained the obsession of the few and not become of general interest Main explanation given is that the thought of death is so horrific that it triggers in us an automatic averting of eyes, so we miss out on grasping the only life-line by which we could thwart death. We have been warned. (Alan Hardy)
#54 Extremely belligerent, obsessed with death, box numbers in Hollywood and fax-lines in Moscow. It's a fine example of what gypsies call hokinobarri the hypnotic effect of screaming very big words in very big print at very frightened people and getting at their money. It left a bad taste in my mouth and a growing conviction that the articles were, perhaps, nonsensical (Ian W. King)
#55 At 50 I've spent a lifetime accepting my mortality and as a nurse have worked with psychogeriatrics and know that what matters most in life is quality not quantity I came to this as a puritan to pornography and found nothing to change my mind If anyone comes to think they can escape death - either by cryonics or the supernatural - they are instantly less committed to this one-chance life. With vegetarian recipes and drug updates it reads like a hypochondriac's charter. e-mail addresses are given for everything. (Sam Smith)
New Hope International, 20, Wenerth Avenue, Gee Cross, Hyde, SK14 5NL, UK
by Tim Freeman <email@example.com>
Writing in the Internet mailing list Cryonet, David Stodolsky (firstname.lastname@example.org) said:
"Research has shown that mortality salience increases the tendency to conform to culturally acceptable systems of thought. See: Solomon, S., Greenberg, J., & Pyszczynski, T. (1991).A terror management theory of social behaviour: The psychological functions of self-esteem and cultural world views. In M. Zanna (Ed.) Advances in Experimental Social Psychology(Vol. 24, pp. 93-159). New York: Academic Press."
I recently acquired a copy of this, and I agree with David Stodolsky that terror management (TM) explains why so few people are interested in trying to use technology to postpone or prevent death.
Briefly, this is the hypothesis: there is obvious survival value in trying to avoid death in the short term. However, avoiding death in the long term has historically been impossible, so survival has been promoted by any psychological means (a "buffer") that prevents the wasted effort of applying the short-term death-avoidance strategies to the problem of long-term death avoidance. In practice, the usual buffer has two parts:
A firmly-held belief about what makes life valuable. A belief can be more firmly held by a group than by an individual, since the group consensus obscures the essential arbitrariness of the belief. This belief can reasonably be called "culture".
Behaviour that conforms to the values of the culture. Conformity to the cultural value system is a major component of self-esteem.
When people are reminded of death, they must strengthen the buffer, so they defend their culture. Applying this to life extension, technological approaches to life extension remind people of death, and most cultures don't include any useful life extension techniques, so few people do anything intelligent to extend their lives.
This theory makes several predictions that have been born out by experiment:
Remind the experimental subject of death, and remind the control subjects of something inane like television. Ask both groups to determine the appropriate bail bond for a hypothetical arrested prostitute. Of those persons who have a world view that prostitution is bad, the persons who have been reminded of death give a significantly larger number.(Municipal court judges were used as subjects in one run that replicated the result. It is scary that things like this might influence actual court outcomes.)
B. Similar preparation for the subjects, but confront the American subjects with an apparently pro-American interviewer or an apparently anti-American interviewer. The subjects who were recently reminded of death like the pro-American interviewer more and dislike the anti-American interviewer more.
Some time ago I also read Combatting Cult Mind Control by Steven Hassan (Park Street Press, 1988).The author is an ex-Moonie who helps people escape from mind control cults. He did not have the concept of TM, but TM explains why his technique works. It turns out that mind control cults typically give the victim a belief system which the victim adopts as the "culture" to be defended a la TM. Frequently part of the belief system is an exit phobia, a belief that leaving the cult will cause some disaster to happen. TM explains why this is so effective: disasters remind people of death and make people defend their culture (that is, the belief system of the cult).TM also explains why people with low self-esteem tend to be sucked into cults more often. If the existing defence mechanism is broken, a person is more willing to adopt a new one.
The technique used by Hassan to help people leave cults is particularly interesting. He confronts the cult member with someone who is an ex-member of *some other cult*.For example, suppose we're trying to save a Moonie; we go find an ex-EST person to talk to him about cults.(The Moonie does not believe he is in a cult.)The Moonie's belief isn't directly threatened by conversations about how EST works as a cult, so TM does not prevent the ex-EST person from explaining to the Moonie how cults work and detailed things about how EST fit the profile of a cult. Giving the Moonie this knowledge as part of an apparently idle conversation lays the groundwork for a future intervention where his non-Moonie friends and family try to persuade him that he is in a cult that does not help him achieve any reasonable goals.
There are many other details too. Our goal, of course, would be to pull people out of the prevailing deathist mind-set. The difference between this and a cult is merely the size, and that the deathist consensus does not have a strong exit phobia (except some but not all Christians will believe they will burn in Hell if they believe us).
There are also books out there like Virus of the Mind that are explicitly about meme engineering.
At the moment I am reluctant to participate directly in trying to engineer the optimal propaganda technique, since my past experiences where I have accidentally pushed people into TM mode leave me somewhat nauseous and disgusted. Now that I understand why that happened, I may have a different attitude in a few months. Engineering the propaganda technique would definitely be a worthwhile exercise.
Liberty vs Freedom
by Eric Szuter <email@example.com>
I like to make a distinction between the concepts of "liberty" and "freedom".
I think it is useful to view liberty as the societal condition. It can be defined as the societal condition in which everyone has complete control over his own wealth -- which is, of course, an ideal. However, it is one that can be approached. According to this line of thinking, each society has a degree of liberty, and each society can be compared to each other in its degree of liberty. As an example of this concept, consider that the US was approaching liberty in the early 19th century, but has since retreated.
On the other hand, it seems useful to view freedom as the personal condition -- the ability to do anything you want to do, at any time -- again an ideal. And again, it's one that can be approached. For most people, freedom is dependent on the liberty of the society one is living in. Each individual has a degree of freedom, and each individual can be compared to each other in the degree of freedom he has. For example, Ross Perot has more freedom than I do. He can do just about anything he wants to, whenever he wants to. But if he gets seriously ill for a couple of weeks, I would have more freedom than he does during those couple of weeks. (Yet we both live under the same degree of liberty in the US). Even when a society has a low degree of liberty, there are always some who live within it who have a great deal of freedom -- those at the top politically. For example, Mao Tse-Tung had a lot more freedom than most people who ever lived, but his society had very little liberty, almost none.
The greatest freedom for the greatest number of people comes when liberty exists in a high degree. Americans have lived under greater liberty in the past, but still have a great deal of freedom when compared to other societies in the world. Much of Americans' freedom is due to the abundant technology available to the average person. The loss of freedom due to a reduction in liberty has been more than offset by additional freedom due to a huge increase in technology. This explains much of the apathy of Americans with regard to politics. Life is easy in the sense of "labour" for most people.
The growing problem is that there is less and less time available for the individual who works to do what he wants. So the work is easy in the "labor" sense, but there is no time left for living. We'll see what develops as more and more become disgusted with this situation. The solution, of course is more liberty in the society. If the US culture again started to approach liberty, the increase in freedom for most Americans would be staggering. There would be time left for living!
Finally, there is much the individual can do to increase his freedom in most cases. While by comparison, generally, there is not much one can do, as an individual, to increase the liberty of the society.
These are some thoughts I have had over the years, and would be interested in hearing what others have to say on the subject.
Eric Szuter is author of The Return of Common Sense. If anyone is interested The Return of Common Sense, they can fax (001) (504) 888-3241 for more information.
This article is copyright © Eric Szuter 1996, printed here by the author's permission.
by Yvan Bozzonetti
In neurobiology, brain components are studied somewhat as species were classed and indexed in the last century. That may tell how the "technology behaves", but not the logic behind it. From this point springs the need to have a better picture of why all that mechanics works as it does. This may be done only with the tools of modern physics, the most advanced and hardest domain in science (outside General Relativity).
A brain has three functions at least:
1 It commands all other organs, mainly by releasing hormones and some other chemical products.
2 It is too a simulator of the exterior space, at least the part of it can access with its sensory system, this modelling is broadly called intelligence because it allows to test in advance the effect of an action.
3 The last function is the monitoring and capacity to recall its internal state at a given instant, this inward looking "eye" is generally defined as consciousness, its main use is to simulate the behaviour of other similar brains, it is a social function.
Contrary to digital computers where any information is located in a well defined place - an address, brain content seems far more loosely dispersed. Each domain can contain a given kind of information, but more limited becomes the domain, the less specialised it becomes. To get an idea of the process, we can think of two ways to register a picture: We can take a photograph or use a hologram. If we cut out half of the photograph, we have no way of knowing what could be present on the lost part. On the contrary, with a half hologram, we have the full picture but with a reduced definition. Can we use an analysis cleaver than simple interference pattern to recover, at least a part of the original picture sharpness? Fractal modelling can fill in the blanks, but there could be even better way to get back the missing information (missing at the interference level, but present in scrambled form at another level).
For all information we have in hand, brains seem to work somewhat as holograms. So, even a damaged or incomplete brain could be reconstructed in full with minimal loss. That task would ask for heavy computing and a good mastering of the information "space" of the brain. My objective here will be to display what must be that information space.
Here, I'll give a background about the concepts used: Space, function and operators, groups, rings and modulus.
For most of our contemporaries, there is one space: The Euclidean one we see everyday. If we could move at a speed near light velocity (299 972 km/s) another space would reveal itself, the Lorentzian space time in four dimensions. Near a very large mass, a third space, the Schwarzchild one would be worth looking at, if the mass was spinning fast, the Kerr's domain would dominate. At atomic scale, even without large mass quantum space rules the world... Present day physics knows so many spaces but it is hard to think of them as independent realities because we lack a direct experience of them in the everyday life.
There is a general way to build many spaces at will: every time we have a field (think as an example about the electric field) we can define a space for that field and if the field responds to rather loosely defined constraints on differentiability and continuity nearly everywhere, then a space may be built at any given precision by a mesh network. When students learn first of that property, they are given a drawing illustrating a grid and some electrical charges fixed at some intersecting points on the grid. The classical question is then: Compute, from the charge distribution, the electric field at such and such point on the grid. In a continuous space, the task asks for solving some hard integrals with singular points at charge positions. With the grid, the field can be computed everywhere using only the four operations.
Now, assume a small part of the grid is taken out, we can redraw it and compute from the surrounding the field value at any crossing of the wires in the mesh. Doing that, we have created a new complete grid where any new mesh is assumed to be free of electrical charge. But computing what must be the field on the original part of the grid, we find it is not what we are able to measure. Clearly, there must be more charges than we see. Going back from field to charges we can then compute where we need to add charges on the recreated part of the grid to get a full coherent system.
Think neurons in place of grid, neurotransmitter sensitivity in place of electrical field and neuron properties in place of electric charge: There we start to see how a damaged brain could be computed back to its original state. Yes, the picture at that level is very crude and need far more refining. For example there could be different grids giving the same "boundary conditions" on the remaining neurons. A brain could be built back in different way, more there will be damaged parts more the problem will becomes acute. There is a way out, with quantum computing, something seen beyond.
The main result at hand holds in that: A brain is a kind of space, or sum of spaces, made from a mesh structure, something we can both understand and work on. On the geometrical side, that space is a limited portion of the Euclidean space, it is so a representation of the so-called projective plane. There, some words are in order on the projective plane: This is a two dimensional structure folded so that it can't be seen in three dimensions; there are nevertheless two pictures in 3 D of that space: The first is a part of the Euclidean space itself, with some given boundary. The other, is a spherical surface where the equator is a Möebius band (single side ring) and each point in a hemisphere is paired with another in the second hemisphere. That plane is the forerunner of an infinite set of geometries with more than two dimensions. There is a way for the brain to enter in these geometries, but a look at chaos is a necessity here.
Functions and operators.
Quantum mechanics, in Schrödinger's eyes at least, was the introduction of an action (energy X time) constant in a Jacobi formalism of classical physics. Classical physics may be expressed as Newtonian, Lagrangian, Hamiltonian (with four subspecies), Jacobian or Poissonian. Students are taught the Newton form and physicists use the Hamilton or Lagrange formalism, the Schrödinger's wave equation with Jacobi is seen as too complicated.
The quantum mechanics space displays an infinite number of dimensions, each using complex numbers. That space is made from functions, not ordinary geometrical points. A point in a space can be endowed with a value and that value can be altered by a function. In the same way, a function in a function space may be altered by a "function of function", that is an operator. Now we come to the chaos model of quantum space (or Hilbert space):
If an object has one dynamical stability point, for example a simple pendulum, then it is said monostable. More complicated systems can have two or any whole positive power of two stable states. If for example a system demonstrates sixfold stability, it would be the sum of a bistable and a quadristable states. Each power of two behaves as a kind of dimension. When a monostable system goes to chaos, it get all the set of doubling stability states. Chaos is simply the point where the number of stable point get the infinity mark. In the doubling domain, each new dimension is two times larger than the preceding one, it is a kind of double dimension. This is just what complex numbers are, so there is a good incentive to represent these dimensions with complex numbers. If a "distance" is introduced in that space, it is a Hilbert's one.
Now, a brain could be partitioned in a number of elementary domains, each one reserved for a given state of stability. If there are two domains, one doubling is allowed on the chaos road. That is few and seems far from infinity, at least when ordinary number are used. A century ago, Georg Cantor founded the basis of set theory under the name of transfinite numbers, numbers larger than infinity. It followed that number systems with so called "not nil characteristic" can bring back infinity very close. For example the field number with characteristic two contains only two numbers: Zero and one. This is not the binary basis used in computer for number with characteristic zero. In the binary system the set of finite values: 0, 1, 10, 11, 100.. is endless. On the contrary, with the characteristic 2, the only finite number is 0 and the only other number, the infinity, is 1. Beyond that, there are transfinite numbers using the same digits in another order, namely: 1, 0. At this transfinite level, 1 is finite and 0 is infinite.
Now, getting back to brains with two domains, right and left brain respectively, there is room for zero or one doubling state in the function space. With the characteristic 2 field ( ON2 for short), this is sufficient to get a Hilbert's space. That space has only one dimension, but that is infinity here. With an infinite number of dimensions, there is the possibility to get an infinity of geometries in the function space. Going beyond the first geometry of the projective plane is no more a problem, simply there will be an intensive use of transfinite quantities at the ON2 level, but that is allowed by the mathematical structure.
At this level, the brain is a Hilbert's space with potentially an infinite number of geometries. If one is chosen and there is some destroyed areas, the reconstructed sector may take many forms (in the worst case). The same can then be done with another geometry where the destroyed zone will fall elsewhere. There too, will be many possible build back solutions, but not the same as in the first case. The only common solutions will reduce the choice to select the good one. With the use of a sufficient number of geometries, there will be in the end only one common build back solution: The good one.
This result is potentially very important: Using geometries in Hilbert's ON2 space allows to reconstruct the full content of a partly destroyed brain.
In mathematics, a group is a set of elements: a, b, ... and an operation symbolized by a sign, say: *. There is an unique unit element u and each element has one inverse: if b is the inverse of a, then a*b = b*a = u.. The inverse element is comprised in the set a, b, ... All of that is very dry and seems very far from brain structure, indeed some explanations will be in order before getting back to groups.
Up to now, a brain is a mesh-based space with limited three dimensional extension so that it is a representation of the projective plane. Mathematicians call this kind of space a manifold because to "navigate" in it asks for a set of charts, each one giving a not too distorted Euclidean picture of a portion of the full space. The manifold has a dual space made from functions or hyperplanes. When the function is simply a multiplication by a number, the hyperplane is simply a flat space with one dimension less than the manifold. For a three dimensional manifold as a brain, the hyperplane is simply a plane in two dimensions.
Now, in a brain, everything in the information process takes place at the surface of cell membranes. The hyperplanes of the function space are then simply the neuron membrane, the plane is far from a flat surface and the associated functions will be far more complicated than simple multiplication. Contrary to M, that dual space M* can be extended at an infinite number of dimensions because there is a doubling of possible stable states with the left-right brain. Without that particularity, M* has the same number of dimensions than M itself.
In a schizophrenic brain, with many independent domains, there is room for many doubling and so, use of field numbers larger than ON2 . Infinite may be indeed far away in these systems and the number of geometries is large, contrary to the normal ON2 case. So, there is an incentive to look at more structures so that there is a sufficient number of possibilities to choose between in the reconstruction process.
Beyond M and M* there is the mathematical possibility to introduce, for each element of M a tangent space E and its dual E*. The classical illustration of the situation is to take a sphere for M and put it on a table. The table top forms the tangent space E to the sphere at the contact point. It remains to think at such a surface at each point on the sphere. The table top is flat, the tangent space needs not to be so, a marble surface could do well in the role of the tangent space. The Mandelbrot set, with "buds" on its border at all scales is a better picture of a set of tangent spaces. Another way to think about that structure is to take a object with a rough surface at all scales, a kind of fractal, and smooth it by rejecting all roughness to tangent space.
Brain has no such roughness forming a tangent space, so there is two solutions: or take it at face value and discard the idea or introduce something able to cancel tangent space on a global scale. What is interesting in tangent objects is not E itself, but its dual E*. This is a differential structure and, as such can be cancelled by its opposite: An integral object, a fibre bundle. The simplest fibre bundle is a distorted ring as a Moebius band. At each element of M can be fixed such a ring. In the quantum world, when such a ring needs to be turned about a certain angle from one place to another, this is equivalent to say a photon has been emitted or absorbed. Electromagnetism is so reduced at the rotation of a ring about a single axis. All these rotations form a group called U(1), the value 1 says there is only one axis used.
What about brains? The mesh structure defines readily a loop at each place, the U(&) fibre bundle is so built in brain structure. What is then E*? Mathematics say E* is a space made from 1-forms. If the vectors of E are seen as arrows, then 1-forms are pudding slices or more abstractly, a set of parallel surfaces. Each such surface is a 0-form or function seen before. In the brain, such functions are materialized by the global surface of all neurons. The corresponding 1-form structure will be a stack of such surface. Because there surfaces come into play throughout the neural receptors at their surface, if there is different neuromediator receptors on the same physical surface, that surface will be counted as many time as there are kind of receptors for different neuromediators. More than one neuromediator is so required to build E*.
In more than one dimension, there may be forms other than 0 or 1-forms, in a space with n dimensions, everything up to the n-form is allowed. A p-form contains p differential operators, each one can be integrated so that there may be a p parameter fibre bundle. In the simplest case that translate into a p independent axis of rotation. If p = 2, the fibre bundle is a ring rotated about a direction perpendicular to its axis, this give a sphere. The simplest group with this symmetry is SU(2). In the quadri- dimensional world with three dimensional space, the largest form is a 3-form and the associated fibre bundle uses the hypersphere S3 symmetry with group SU(3). The corresponding force field, the colour force rules, the inner part of nuclear particles. The so called strong nuclear force is a leakage of the colour outside particles.
In a brain, the manifold M is the projective plane, a two dimensional space. At most, E will be two dimensional, so is E*. Nothing is allowed beyond 2-forms and the fibre can display only two parameters, the larger group is so SU(2). Brain has no colour at its basis. SU(2) is a spherical rotation, the corresponding object in the brain is the surface of a single neuron. This is hardly a geometrical sphere but it is topologically equivalent to it. That is to say, beyond geometrical properties, there will be necessary to introduce topological ones to complete the picture.
With ON2, the number of dimensions remain low and that limit the SU(n) set at a small value, nevertheless that value is linked to the infinity in the number field used. Because 2 in SU(2) is a transfinite quantity, SU(n) has the so called power of the continuous: It forms its own one dimensional space. Because that space has, as its largest element SU(2), the symmetry of angular momentum in three dimensions, it is a good idea to name it the spin dimension.
Because fields must vary smoothly if there is no singular points (particles), the no particle condition in the field brain allows us to reconstruct some piece of missing information. Dendrite loops in present neurons display a state near the one found originally on now missing neurons (U(1) field). The number, state and position of neural receptors on a neuron speak about what has been destroyed on nearby missing places. One would find a tool able to do the same work on more distant place so that larger destroyed area could be handled.
In mathematics, a ring is nearly two groups, simply the unit element of the second group has no inverse. It is common to note the operation in the first group with the + sign and assume it is commutative ( a+b = b+a). On the contrary, the second group operation is noted multiplicatively and a x b often is unequal to b x a ( non Abelian groups ). The neutral element in a multiplication is 0 and that component has no finite inverse. When there are two groups, in the second, the neutral element u and its inverse u'=u can be exploited to form two rings. In the first, u=0 and its inverse is infinite. That infinite element is the 0 of the multiplicative law in the second ring. In some way, the second ring is the transfinite picture of the first. ON2 has permeated until that level.
If there is a law giving a "ticket travel" from the tangent space E to its dual E*, the same law must allows to go from E* to the dual-dual E**. If E is finite dimensional and flat, E** is simply E itself, in the infinite dimensional case, E** is a so-called tensor space, something where the unit length is different of what it is in E. If the unit in E is taken to be 1, it will be 2 for an "ordinary" tensor and one half for so called spinors. Tensor and spinors have both the possibility to pile up many spaces such E or E*. The number of spaces is the tensor (or spinor) rank. That property is often taken as the only one defining a tensor, it is not the case, outside spinors, matrix direct product generate too multilinear systems (with unit length in the natural unit); Few texts on tensors make this clear so that we don't know if we are speaking about a brain function or the gravitational pull of a neutron star. There will be only direct products (called too matrix's block product) on continuous spaces.
From E* there is a choice: Going back to E or jumping on E**, in fact the two options are selected at the same time so that the arrival space contain two indices: one for numbering the E dimensions and another for the E** ones, this is a rank two multilinear object, in fact, a bilinear direct product.
One set of groups, the SU(n) one, was tied to E*, the same thing works for E and E** so that the relevant structure on the bilinear space is a ring. What are these groups? The SU(n) set is a particular class of groups: The finite simple ones, that is each group in the set cannot be broken into more smaller groups, all fundamental symmetries are built from finite simple groups, the question is then: how many of them are there? The answer is: There is an infinite number of such groups, but all of them fall in seven sets. The prime number set giving SU(n), is the simplest set, at the other limit is the seventh set made from 26 finite simple sporadic groups.
Because the seventh set is not homogenous it is difficult to work with it in the same way than the other group sets. That leaves six sets: In ring building, one group will comes from the SU(n) set and the second from one of the five remaining ones. For example the set 2 will goes to E**, the set three to E*** and so on. This produce 5 set pairing with groups coming from different sets. Each double group generates two rings, so there are ten ring kinds built in this way. Each kind of ring is an twofold infinite ring set using two group sets. A kind of ring forms a dimension. The ring world is then ten dimensional. This may look complicated but the constraints are hard: No two groups in a ring come from the same set and the prime number set is always present.
What is the material counterpart of that theoretical structure? With U(1), the material objects was dendrites loops: A dendrite going from neuron A to neuron B and then a B neuron dendrite going back to A in the simplest case. SU(2) was a topological sphere, a neuron body. With rings there are two groups, one of them comes from the SU(n) set as before, but there is another group too. This group will be associated to more complex brain structures. These larger structures must repeat themselves without a singularity point (no particles in the brain fields). That allows us to deduce the structure and content of a destroyed domain larger than one neuron or a small group of them.
Ring pairing opens another possibility: There are two identical rings but the nature of the second group unit element is transfinite. At this level, SU(n) is most probably never in this position, but it displays a simple pattern useful for a first explanation. In the ON2 field, 2 is transfinite and writes as 1. If there is a neuron whose dendrites have survived, its U(1) structure can be detected, it will be possible to find what was the neuron inputs. On the contrary, the neuron body has been destroyed, so that the SU(2) symmetry is no more present: It is impossible to know how this information will be worked out. Now going to the transfinite ring, SU(2) reads as U(1), what was in the neuron body can now be read in the dendrite membrane, the full neuron will never work any more, but all its information content will be at hand for building back a new one.
A modulus is a mathematical structure made from three groups. This is a very complicated and large domain, only the basic entry can be explored here. The main modular symmetry is of the form up-down or heaven-hell: There is an unit element and everything larger than it has a corresponding one smaller than the unity.
In the flip-flop game adding more and more stars to E-like spaces, there is no limitation, a multilinear quantity can display any rank value. But each new space cannot be created without its fibre counterpart, and this one display a well defined symmetry pattern. When there are no more groups, the only solution is to use more of them simultaneously. Numbers are build in the same way, after 9 comes 10... after 99 comes 100.. After two group rings come the modular structure with three groups. The smallest possible group here is the two element permutation group: With the first group element nothing is moved and with the second, in a set A, B, the order is reversed: A takes the B place and B the A one. The ordered set A, B becomes B, A.
The first effect on rings, is to find SU(n) in the upper place, no more the basic one. That gives 6 x 2 - 1 = 11 new rings set. The minus one comes from the fact that a permutation on two copies of the same group set produce the same result. The ring set: SU(n), SU(n) counts for one. Outside that special case, elementary space elements are no more made from neurons bodies and dendrites loops. The basic component is now more complex. There is then naturally an upper space with even larger elements and a lower space with object smaller than the space unity, but larger or equal to a single neuron.
The usefulness of that property is evident: If a brain retains its general structure at large but remains pocked with small destruction zones, the large structure allows to build back the fine one. On the contrary, if a large chunk of the brain is missing, the fine structure in the remaining portion can be used to build back the missing part.
There is a very big price to pay for that high flying technology: The permutation group is not included in a simple groups set. It is simply the sub element, a factor of the trivial representation of a group. The knocked door is somewhat awful, it is the seventh set domain, the one of finite simple sporadic groups. The first, the Janko 1 group is the permutation of all the transformation of the seven dimensional matrix. Its order, or number of elements is 177560. Using two of them in a permutation law is very few, but the whole group is not very large when looked against some of its neighbours. It seems these groups are linked to topological discontinuities and string spaces. There is a long way to explore all the possibilities...
Two Photons Interferometers.
By Yvan Bozzonetti
In the BOson New ZOne, intensity interferometers are a first step worth to look at. The first systems of that kind was build by the astrophysicist Robert Hanbury Brown in UK and then in Australia at the Narrabri site. They are a subclass of four waves interferometers where wave are detected in a time independent way on two receivers, each one mixes two wave so that it gets from occupation state a Hamiltonian density without time variable. This is a probability density or, on a given surface in a given time an energy or photon count. The intensity interferometer, as applied to photons, works by looking at correlations in the arrival time of different photons on the two detectors. The square root of that correlation is an energy, similar to the one encountered in fringe patterns seen on ordinary, two waves interferometers.
The main interest of that system comes from the possibility to trade between integration time, sensibility and resolving power without limit. The intensity interferometer is a "particle-property" interferometer, that is, it does not matter what is the wavelength used to get information. For technological reasons, astronomical instruments work with light and handle it as radio waves. A radio wave could as well be used with sub wavelength definition.
The current project uses a three step approach : First, two telescopes will be used in remote access operation, one in France the second in western US. The objective is to get a common observation from both sites. They will produce CCD pictures, photometric data and spectra (at least for the French unit). This system must enter into function on INTERNET next year. The first trial coming this winter. At the same sites, a second instrument made from many plastic mirrors with a total surface near 100 square metres will be devoted to photon counting photometry and spectrography. That system is in the component procurement stage. It must work two years after the first system. An upgrade will be to add a clock and register to the photon counter. That will turn the photometer into a transcontinental intensity interferometer. All of that is closely related to astronomy and has nothing to do with cryonics.
Now, if the photomultiplier tube in the photometer head is removed and a sound detector put at its place, we have a sonar intensity interferometer(if their is a sound source).The idea is to use a multi channel version of the system to get a brain scanner at the 100 nm level. The astronomical part of the project is there to develop, and finance the electronics and computer parts. A brain reader working on that principle could start to function five years from now on an experimental basis.
I am looking for electronics specialists able to build the clock and amplifier for the intensity interferometer.
The first "reader system" would be able to scan a frozen rat 's brain in one year or so. More advanced systems could scan a man brain many time a second, using radio waves.
Intensity interferometers was first used at the end of World War two, but forty years later they remain uncommon systems, largely ignored from many, including optical specialists. There are some general references on the subject :
W . H . STEEL (1983) : Interferometry, 2nd ed. Cambridge Studies in Modern Optics; Camb. Univ. Press, see ch. 6 -6.8 : Higher-order correlations, p. 85 and ch. 14 -14.3.2 : Stellar intensity interferometer, p. 279.
Collective book : Modern Technology and its Influence on Astronomy, ed. by: J. V. WALL and A. BOKSENBERG. Cambridge University Press 1990 p. 6 to 11,51, 91, 92, 95, 96, 101 - 103.
Gordon WALKER (1987) : Astronomical Observations : An optical perspective. Camb. Univ. Press, p. 37 and 180.
by Douglas Skrecky
Freeze-drying a brain
Freeze-drying a brain should reduce storage costs quite significantly since liquid nitrogen cryostats would no longer be needed for storage. How much would it cost to freeze-dry a brain? Probably not very much as the following information shows.
In his book Freeze-Drying Biological Specimens: A Laboratory Manual Rolland O. However from the Smithsonian Institution details his experiences in freeze-drying a wide variety of biological specimens. Freeze-drying of a formalin fixed 1386 gram human brain took just 28 days at -30 C. Weight loss was 1145 grams or 83%. Slicing the brain reduced drying time to 14 days. Increasing the storage temperature to -5 C reduced drying time of an intact brain to 7 days, though numerous cracks were evident. Considering its size the human brain seems to be remarkably quick and easy to freeze-dry. A barn owl weighing 1369 grams took 130 days to freeze-dry at -20 C. A tortoise took 132 days, while an alligator took 9 months at -20 C. The absence of either a thick epidermis or bone which can act as vapour barriers may be the reason why the human brain was so quick to dry.
PBS/melatonin Extends Lifespan of Diabetic Mice
Melatonin would seem to be an unlikely therapy for type 1 diabetes, since it can increase autoimmune responses. However when given to female non-obese diabetic (NOD) mice it was found that despite increasing insulin auto antibodies, both oral & injected melatonin increased survival. Treatment was from 3 to 37 weeks. After 50 weeks survival was 34.5% of the controls, 58.8% of the oral melatonin group,.2% in the phosphate buffered saline (PBS) subcutaneous injected group and 90% in the PBS/melatonin injected group. The positive effect of both PBS and PBS/melatonin injection is astonishing and quite unexpected. Hopefully more research will clarify the mechanisms involved.
Reference: Role of the Pineal Gland and Melatonin in the Development of Autoimmune Diabetes in Non-obese Diabetic Mice J. Pineal Res. 20: 164-172 1996
Life Expectancy Statistics
Present Age Average Years Remaining Year of Death
0 75.7 2071
25 52.2 2048
30 47.5 2043
35 42.8 2038
40 38.2 2034
45 33.7 2029
50 29.3 2025
55 25.1 2021
60 21.1 2017
65 17.5 2013
70 14.1 2010
75 11.1 2007
80 8.4 2004
85 6.3 2002
Data are derived from the National Center for Health Statistics as reported in: International Journal of Bio-Medical Computing 39: 209-217 1995
Sometimes it seems that life is too short. However humans have a pretty good go at it in comparison to most other animal species. The following data are taken from How and Why We Age" by Leonard Hayflick, PhD. If you are over 46 years of age for example you have outlived all horses and shorter lived animals in the entire planet for all time.
The maximum life span for humans is currently subject to revision. The record holder is Jeanne Calment, who is still alive at 121 years young. We'll see a year from now whether the new record is to be 122. Note that humans are unusually long lived for mammals, the runner up being African Elephants at 69 years. All animal species with similar life spans are cold blooded. Humans live twice as long as their closest cousins, the great apes.
SPECIES MAXIMUM LIFE SPAN
Zebra, Chapman's 40
Rhinoceros, Great Indian 40
Terrapin, Diamond-Backed 40
Vulture, King 40
Pelican, Rough-Billed 41
Terrapin, Speckled 42
Macaw, Blue & Yellow 43
Rhinoceros, African Black45
Eagle, Golden 46
Crane, Australian 47
Whale, Humpback 47
Gorilla, Western Lowland 47
Elephant, African 48
Echidna, Australian 49
Parrot, Golden-Napped 49
Snail, Haliotis Cracherodi 51
Bivalve, Pismo Clam 53
Hippoptamus, River 54
Parrot, Vasa 54
Eagle, Bateleur 55
Chimpanzee, Troglodytes 56
Cockatoo, Sulfer-Crested 56
Tortoise, Snapping 58
Orangutan, Sumatran 59
Owl, Eagle 68
Elephant, Asian 69
Tortoise, Galapagos 100
Bivalve, Margaritifera 116
Tortoise, European Pond 120
Tortoise, Carolina Box 129
Tortoise, Marion's 152
Tortoise, Giant 180
Bivalve,Arctica Islandica 220
*[Editorial comment: there has been some speculation that the lifespan of lobsters is determined purely bu accidents, ie they do not age.]
Pbs/Melatonin Extends Lifespan of Diabetic Mice
Melatonin would seem to be an unlikely therapy for type 1 diabetes, since it can increase autoimmune responses. However when given to female non-obese diabetic (NOD) mice it was found that despite increasing insulin autoantibodies, both oral & injected melatonin increased survival. Treatment was from 3 to 37 weeks. After 50 weeks survival was 34.5% of the controls, 58.8% of the oral melatonin group, 68.2% in the phosphate buffered saline (PBS) subcutaneous injected group and 90% in the PBS/melatonin injected group. The positive effect of both PBS and PBS/melatonin injection is astonishing and quite unexpected. Hopefully more research will clarify the mechanisms involved.
Reference: Role of the Pineal Gland and Melatonin in the Development of Autoimmune Diabetes in Non-obese Diabetic Mice J. Pineal Res. 20: 164-172 1996
Successful Biotin Treatment of Diabetes
Biotin has been found to be a potent inhibitor of neuropathy in both uremic and diabetic patients. Biotin at a dosage of 10 mg/day effected a marked improvement in neurological status for patients with kidney failure. Within 3 months disorientation, speech disorders and memory failure almost disappeared. Myoclonic jerks, flapping tremor, restless legs, abnormal skin sensations and difficulties in walking were all greatly improved. (1) After this success with uremic patients 6 years later, 5 mg/day biotin was used to treat three insulin dependant diabetics suffering from neuropathy. Within 4-8 weeks there was a marked lessening of muscle cramps and abnormal skin sensations as well as an improvement in the ability to walk. Restless leg syndrome was also eliminated over this time period. After 1 year of treatment all three patients were free of abnormal skin sensations and could walk over 300 meters unassisted. Nerve conduction velocity was improved in 2 of 3 patients. Fasting blood sugar was unchanged. (2) At a sufficent dosage biotin significantly reduces plasma glucose levels in diabetics. In a double blind placebo controlled trial of 16 mg/day biotin plasma glucose levels were found to be reduced in insulin dependant diabetics, even after they had been removed from insulin therapy! Plasma glucose fell from an average of 266 mg/dl to 126 mg/dl after 1 week of insulin free, oral biotin therapy. Placebo treated patients saw an increase in glucose levels, as expected. (3)
In a placebo controlled study 9 mg/day biotin normalized hyperglycemia in non-insulin dependant diabetics after 1 month of treatment. (4) After a further 1 month washout period serum glucose was found to have climbed back to its initial levels. (5)
The mechanism for the potent antidiabetic effect of megadose biotin has been theorized to be by the enhancement of the activity of biotin-dependant pyruvate carboxylase, which promotes glucose utilization. There exists a possibility that biotin monotherapy is all
that many diabetics would require to normalize their condition.
1 Biotin in the Management of Uremic Neurological Disorders Nephron 36: 183-186 1984
2 Biotin for Diabetic Peripheral Neuropathy Biomed. & Pharmacother 44: 511-514 1990
3 Biotin Status and Plasma Glucose in Diabetics" Ann. NY Acad. Sci. 447: 389-392
4 3 gm/day anti-microbial drug Miya-BM was also given to prevent growth of biotin degrading bacteria in the intestines during this period. However there is no proof that this aided in the therapeutic effect of biotin.
5 Therapeutic Evaluation of the Effect of Biotin on Hyperglycemia in Patients With Non-Insulin Dependant Diabetes Mellitus" J. Clin. Biochem. Nutr. 14: 211-218 1993
Caloric restriction, glycemic index & diabetes
One of my coworkers just developed adult onset non-insulin dependant diabetes. This fellow was decidedly overweight, never exercised and ate a diet that would scare any life extensionist. His doctor told him to either mend his ways or look forward to daily needle injections for the rest of his life starting fairly soon. Never have I seen such an abrupt turnaround in lifestyle. This fellow now nibbles on fruit all day long and is losing weight at a fair clip. After this I became interested in ascertaining whether caloric restriction or even a low glycemic index diet fed ab libitum could prevent the development of diabetes in experimental animals. Here are the results of my search:
Caloric restriction is highly effective in preventing the development of diabetes in the Otsuka Long Evans Tokushima Fatty rat. At 20 weeks of age incidence of diabetes was 67% in ab libitum fed rats, 13% in 15% restricted rats and 0% in 30% restricted rats. (Diabetes Research and Clinical Practice 97-106 Vol.27 1995)
Lower glycemic index diets fed ab libitum to Australian Albino Wistar rats delayed the onset of hyperinsulinemia. The rats were becoming diabetic after 8 weeks of glucose feeding, 16 weeks on amylopectin starch and 26 weeks on 60% amylose/40% amylopectin starch. Unfortunately 100% amylose starch was not tested. (Journal of Nutrition 596-602 Vol.126 1996)
A high fat & sucrose diet induces hyperinsulinemia in Fisher 344 rats. At 24 months of age serum insulin was increased by 400%. By comparison insulin levels were unchanged in 24 month old Fisher rats fed a high complex carbohydrate diet. (Gerontology 205-211 Vol.41 1995)
Replacement of just 200 g sucrose/kg diet with sorbose prevented the development of diabetes in genetically diabetic C57BL/KsJ mice. (Journal of Nutrition 59-65 Vol.123 1993)
In is suggestive that maximum lifespan is increased by 10% when cornstarch is substituted for sucrose in the diet of Fisher 344 rats. When rats were 40% calorie restricted cornstarch beat sucrose with a 41% increase as opposed to 30% for sucrose. (Journal of Gerontology B148-B154 Vol.50A No.3 1995)
One can't help but wonder if an extremely low glycemic index diet would offer the same age retarding effects as caloric restriction and whether their combination would offer still further benefits. If anyone reading this message knows of any professional researchers in the field of caloric restriction I urge them to forward this message to them for their consideration.
Dinh Lang Extends Lifespan
Alcoholic extracts from the Vietnamese herb dinh lang has been proven to be effective in extending rodent maximum lifespan.
Here's some data.
Dinh lang extract and deprenyl have some additive effects on prolonging the lifespan of OFA-1 mice. (Acta Physiologica Hungarica 79(2): 119-124 1992)
Group Maximum Lifespan
control 133 weeks
dinh lang 170
This also works in Wistar rats as well. (Acta Physiologica Hungarica 75: 301-302 1990)
Group Average Maximum
control 147 164 weeks
dinh lang 180 194
dinh lang & 206 239
The life extending effect of dinh lang extract appears to be quite real as it has been demonstrated in two strains of rodents. Moreover dinh lang appears to be more effective than deprenyl.
n addition the dosage used was probably suboptimal. Only 10 mg/kg extract was used in the life extension experiments, while maximal effects of passive avoidance performance in young OFA mice was found at 20 mg/kg. (Acta Physiologica Hungarica 75(1): 69-76 1990) In Wistar rats aged 22-24 months 20.8% resumed full scale sexual activity at a dosage of 20 mg/kg, 11.5% at 10 mg/kg, 7.7% at 5 mg/kg and 0% for controls. (Acta Physiologica Hungarica 75(1): 61-67 1990)
It would be interesting to see more research on dinh lang, especially at the 20 mg/kg dosage.
DNA-RNA-Chloroform Injections Increase Life Span 144% (fwd)
Weekly injections of DNA solution in water saturated with chloroform (3 mg/ml) plus ordinary RNA have dramatically increased the life span of rats. Ten rats from an unidentified strain with a reported maximum life span of 900 days were selected for the experiment when they were 750 days old. The five control animals all died before 900 days, as expected. It was reported that after 84 days (12 weeks) the five injected rats looked remarkably "younger", were more "lively" and had gained weight. Of the injected rats 4 died aged between 1600 and 1900 days, while the fifth lived to 2200 days1. An increase of maximum life span by 144% from 900 to 2200 days with a treatment which was only commenced in old (750 day) animals is (to be frank) simply unbelievable. A weighted average life span for the five injected animals of about 1850 days is likewise unprecedented. If these results can be replicated they would constitute the most effective anti-aging intervention in rodents by a large margin. For example one experiment investigating the effect of life long 40% calorie restriction in Fisher 344 rats found that maximum life span was increased by 38% from 941 to 1296 days. A copy of the DNA-RNA-CHLOROFORM injection experiment using humans would mean that injections were started in five 75 year olds and four of them died at between 160 to 190 years of age, while the final survivor lived to 220 years of age. This experiment needs to be replicated in rats first!
Prolongation of the Life Span in Rats Journal of the American Geriatrics Society 21(10) 450-451 October 1973
2. Nutritional Influences on Aging of Fisher 344 Rats: I. Physical, Metabolic and Longevity Characteristics Journal of Gerontology 40(6) 657-670 1985
Variations on A Straight Freeze
With the circulatory system being unavailable in many cases for cryoprotective perfusion what are the available options? The brain could be dipped in cryoprotectant, but this would benefit only a very thin layer of tissue on the surface. The major arteries could be injected with cryoprotectant, but with the capillaries being blocked by coagulated blood no circulation is possible. Something better is needed. Based on my expectations of the quality of the treated tissue I group the following 8 techniques in order of increasing merit:
(Worst) Blender technique: Homogenize brain in a blender with cryoprotectant. Pour into a brain shaped mold and freeze.
2. Embalming technique: Inject methanol into arteries and veins. Immerse brain in methanol for 24 hours at 0 C. (Methanol is the fastest penetrating fixative. It penetrates cell membranes 20 times as fast as glycerol. ref: The Journal of General Physiology Vol.62 714-736 1973)
Hamburger technique: Pretend that cryoprotectant perfusion was done and do the usual slow freeze. The result is hamburger.
4. Microwave technique: Microwaves can rapidly penetrate and fix tissue. Pack the brain with ice and place in a microwave with a turntable, which has been top rated by Consumer's Reports for uniformity of heating. Cook using pulses of radiation until well done. Treat brain with cryoprotectants by storing it in a concentrated cryoprotectant solution for a week. Store in freezer until needed. (Journal of Neuroscience Methods 53:81-85 1994)
Freeze Substitution technique: Freeze brain slowly to -10 C to limit ice crystal damage. Pickle brain in an anhydrous silica gel desiccant packed alcohol based cryoprotectant solution till ice has all melted. Baste in liquid nitrogen. (Note the main difference between this and the embalming technique is the temperature used.)
6. Quick Freeze technique: Freeze brain slowly to -10 C to partly dehydrate cells and reduce subsequent intracellular ice crystal formation. Then dunk in liquid propane/butane cooled with dry ice. Rapid freezing limits extracellular ice crystal growth. Then slowly cool further with liquid nitrogen vapour to limit the formation of cracks due to increased tissue brittleness. (Biophysical Journal Vol.64 1908-1921 1993 & Cryobiology Vol.31 506-515 1994)
Salami technique: Cut the brain into slices 5 mm thick. Cryoprotectants can rapidly diffuse into thin slices of tissue, thus preserving them well when they are frozen. The result is a Dagwood sandwich. (eg: see Cryobiology 24:120-134 1987)
(Best) Pin Cushion technique: Immerse brain in a cryoprotectant bath. Inject cryoprotectant into the brain via many very fine needles which are first slowly inserted into the brain, then slowly removed. Then do a quick freeze.
One strategy for avoiding hunger on a reduced calorie diet would be to bulk up with foods which possess a very low caloric density. Here is a list of all foods listed in appendix B of Roy Walford's book The 120 Year Diet which yield no more than 250 calories per kilogram. (1 kilogram = 2.2 lbs) I think the recommendation to eat less and exercise more to lose weight should be changed to both eat and exercise more.
Celery 170 (associated with allergic reactions)
Longevity Books still has some copies of 120 Year Diet left at 9.50 post paid to UK or Europe. This is not to be repeated once sold!
Can Lycopene Delay Aging?
Lycopene is the red coloured carotenoid found in tomatoes and pink grapefruit. While the earlier enthusiasm for beta carotene has waned, the prospects for lycopene look "healthier" than ever. Although no lifespan study has been completed with lycopene, there exists some data which indicate that this pigment may be able to slow the aging process.
When fed a very small amount of lycopene, SHN mammary tumour prone mice start developing such tumours at the age of 9 months, instead of 7 months.1
Cancer deaths were halved in those over 66 years of age, when at least 1 serving per week of tomatoes was consumed. Carrots (beta carotene) offered no benefit.2
In 77-98 year old nuns plasma lycopene levels were positively related to the degree of independence in self care tasks. Plasma beta carotene had no relationship.3
1 Effects of Lycopene on Spontaneous Mammary Tumour Development in SHN Virgin Mice: Anticancer Research 15: 1173-1178 1995
2 Increased Green and Yellow Vegetable Intake and Lowered Cancer Deaths in an Elderly Population: American Journal of Clinical Nutrition 41: 32-36 1985
3 Antioxidants and Reduced Functional Capacity in the Elderly: Findings From the Nun Study: Journal of Gerontology 51A(1): M10-M16 1996
Beware Calcium Channel Blockers
Lets assume you have high blood pressure. You go to the doctor and ask about OTC garlic extracts or drug company sponsored calcium channel blockers to control your blood pressure. Which will he recommend? You got it, the drug company stuff gets the go-ahead every time. The only trouble with is that some studies have shown that calcium channel blockers increase cardiovasular disease mortality. To matters even worse it has recently also been found that calcium channel blockers increase the risk of cancer by 72%.
Don't use calcium channel blockers. If your doctor insists on you using them, get another, better informed doctor.
Calcium-Channel Blockade and Incidence of Cancer in Aged Populations: Lancet 348: 493-497 August 24,1996
Can Phosphagain Prevent Age-Associated Frailty?
One of the hazards of old age is muscle wasting. Unfortunately many old people are such couch potatoes that it is not possible to get them to do much exercise. A nutritional supplement called Phosphagain might be of some help here. At the very least it works very well in enhancing lean tissue growth in young weight lifters after 28 days, in comparison to other supplements. (see table)
Supplement Lean Tissue Fat Mass
Maltodextrin +1.5 lb -0.1 lb
Gainers Fuel 1000 +1.5 +1.6
Phosphagain +4.4 -0.2
Further research will be needed before the anabolic ingrediants in phosphagain can be identified. Possible candidates include creatine monohydrate, yeast derived RNA, taurine and l-glutamine.
Effects of Ingesting Supplements Designed to Promote Lean Tissue Accretion on Body Composition During Resistance Training: International Journal of Sport Nutrition 6: 234-246 1996
Beware Skin Creams with Vitamin e
Although unesterfied vitamin E can help prevent skin cancer, most sun screens contain the acetate ester of vitamin E. Unfortunately experiments have found that both vitamin E acetate and vitamin E succinate increased the risk of skin cancer due to UVB exposure.1) In a recent survey of 191 sun screens, 119 (62%) contained some form of vitamin E. Of these 72 (61%) contained the acetate ester, 24 (20%) did not specify the form, while only 23 (19%) stated that unesterfied vitamin E was used.2
If a sunscreen is purchased make sure that only unesterfied alpha-tocopherol is used!
1 Importance of the Form of Topical Vitamin E for Prevention of Photocarcinogensis: Nutr Cancer 26: 183-191 1996
2 Disposition and Metabolism of Topically Administered Alpha-tocopherol Acetate: A Common Ingredient of Commercially Available Sunscreens and Cosmetics: Nutr. Cancer 26: 193-201 1996
How Can Anti-aging Become
a National Priority?
by Tim Freeman <firstname.lastname@example.org>
Thomas Hotz Jr. <email@example.com> asked this question on the Internet.
First, I suppose, it would have to become a priority for a lot of individuals in the given nation, then they'd have to organize and get the attention of the relevant politicians.
What would have to happen for preventing aging to become a personal priority for a bunch of people? The obstacle is terror management. People have short-term strategies for staying alive, and in an environment where staying alive in the long term is impossible, some cognitive strategy is necessary to prevent the wasted effort of applying these short term strategies to the unsolvable long-term problem. So there is a wide variety of entrenched belief systems that give life meaning despite inevitable death. There are specific psychological things that happen when people are reminded of death: people reinforce their own entrenched comforting belief system to avoid feeling bad. Reference: A Terror Management Theory of Social Behaviour: The psychological Functions of Self-Esteem and Cultural World-views, by Sheldon Solomon et al, pp 93-159 of Advances in Experimental Social Psychology, volume 24, 1991. (Thanks to David Stodolsky for the reference.)
Some of the entrenched belief systems even twist things around to say that inevitable death is good; this made no practical difference when the death really was inevitable. Expect these people to wobble more than others as the problem of aging is solved. For instance, in the Immortality on Ice special on TV lately, a cryobiologist who knew he was lying implied that cryonics organizations don't use cryoprotectant.
Now that preventing aging appears to be a difficult, not-yet-solved problem instead of an obviously impossible problem, thinking about aging and death is a practical, useful activity instead of a waste of effort that must be prevented by psychological defense mechanisms. The entrenched belief systems will eventually change to reflect this. For anti-aging to become a national priority before it becomes a solved problem, they have to change sooner rather than later. I don't know how to make this happen. Since workable anti-aging techniques threaten many of the world-views people use for terror management, it will be significantly harder for workable aging prevention to become a national priority than, say, defeating the Warsaw Pact or visiting the moon. Those other activities do not contradict the beliefs people hold that keep them from worrying about death.
There is an obvious opportunity for Darwinian evolution here. Within at most a few generations, the people who wish death on themselves will succeed, and those who take intelligent persistent action to avoid it will also succeed, so there will be more of the latter. The difference in outcome will be obvious enough to persuade the majority of people who are somewhere in between. I hope the consensus changes more quickly than this scenario implies, though, both because my personal biological clock is ticking and because it would be nice if all those people didn't have to die from something preventable.
The Scientific Debate Over Cryonics
by Randy Smith
A scientific debate was exactly what I was looking for when I first began investigating cryonics. Over the years many have criticized cryonics on the net, a couple with far greater scientific credentials that poor anonymous here; I wanted to see some harsh scientific criticisms of cryonics, and looked in the Internet news group <sci.med> debates section of Cryonet archives. The cryonics critic with the best scientific credential was a fellow named Terence Ma. This guy was an MD with a PhD in physics who worked as a neuroscientist for the prestigious University of Chicago. He posted many times arguing against cryonics. In all those posts the only thing he ever said against cryonics which could vaguely be considered "scientific" was that it wouldn't work because of "autolysis," this despite the fact that he was asked many times to give valid reasons. There was only the one word, autolysis, with no elaboration whatsoever.
Dr Ma did also say that he thought there might be a slim chance of workability if preservation was attempted immediately upon legal death. Again, he gave no reasons, despite the fact that there were many debating him with their own credentials, including Ralph Merkle (btw, Merkle also posted his excellent pro-cryonics brief on nanotech and its role in data recovery application for reviving cryonics; Ma just brushed this off without saying why).
Dr. Ma's strongest objection to cryonics was moral grounds and he did mention organized religion. I later came on his web page and found references to the Mormon church therein. I can only conclude that he felt, no doubt without even articulating his feelings, that cryonics was somehow against God's plan or had some other deeply felt emotional --but *not* scientific--objections. Another case of rationalizing against cryonics: giving reasons other than the real ones for dislike of cryonics.
One other person with an MD posted many times during the sci.med debates, Dr Gordon Banks. He really had in for us. But again, his posts were woefully deficient in real scientific reasons. The closest he ever came was this (somewhat paraphrased):
"It'll never work, etc... what if there's some delicate protein essential for long term memory that would be shattered by the freezing process; it would be randomized like a log cabin made of Leggo that you kicked.."
Not exactly my idea of a valid scientific objection. He must have posted 40 times and that was the *only* time he ever came close to anything like a scientific objection.
Yes, the world is the best place of all ...
but then right in the middle of it comes the smiling mortician
do not go gentle into that good night
rage, rage against the dying of the light
Ban Dihydrogen Monoxide!
The Invisible Killer
Anonymous, found by Eugene Leitl <firstname.lastname@example.org>
Dihydrogen monoxide is colourless, odourless, tasteless, and kills uncounted thousands of people every year. Most of these deaths are caused by accidental inhalation of DHMO, but the dangers of dihydrogen monoxide do not end there. Prolonged exposure to its solid form causes severe tissue damage. Symptoms of DHMO ingestion can include excessive sweating and urination, and possibly a bloated feeling, nausea, vomiting and body electrolyte imbalance. For those who have become dependent, DHMO withdrawal means certain death.
Contamination Is Reaching Epidemic Proportions!
Quantities of dihydrogen monoxide have been found in almost every stream, lake, and reservoir in America today. But the pollution is global, and the contaminant has even been found in Antarctic ice. DHMO has caused millions of dollars of property damage in the midwest, and recently California.
Despite the danger, dihydrogen monoxide is often used:
Companies dump waste DHMO into rivers and the ocean, and nothing can be done to stop them because this practice is still legal. The impact on wildlife is extreme, and we cannot afford to ignore it any longer!
The Horror Must Be Stopped!
The American government has refused to ban the production, distribution, or use of this damaging chemical due to its "importance to the economic health of this nation." In fact, the navy and other military organizations are conducting experiments with DHMO, and designing multi-billion dollar devices to control and utilize it during warfare situations. Hundreds of military research facilities receive tons of it through a highly sophisticated underground distribution network. Many store large quantities for later use.
It's Not Too Late!
Act NOW to prevent further contamination. Find out more about this dangerous chemical. What you don't know can hurt you and others throughout the world.
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