ISSN 0964-5659

Longevity Report 62

Volume 11 no 62. First published November 1997. ISSN 0964-5659.

e-mail: Internet longevityrpt@yahoo.com



Today's The Day Chrissie Loveday

Fly Experiments Douglas Skrecky

Ettinger's Ark Brent Allsop

Nutrition, Lifestyle, Genetics And Longevity Roger L. Bagula

Long-Evans Rat Longevity Database Douglas Skrecky

The Vinpocetine Story OMT



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Today's The Day

by Chrissie Loveday

I read in a book recently,

Every day is for living. Life is to be enjoyed and not a burden to be endured.



I do remember times when the burdens seemed to outweigh the living but those days passed. Now I try to make sure that every day I do something just for me. It may taking a swim, walking the dogs, reading or writing or watching TV. Some days, I manage all of them, so I'm a lucky lady. Naturally, there are always some things that have to be done which are more like the burdens I mentioned. (Cleaning cookers, housework, shopping etc) But if we only ever do things that are pleasurable, they could themselves become burdens. It would be like drinking a special bottle of wine every; very soon it ceases to be special.



My earlier quote came from a book about self-esteem. My work with disability and behavioural problems in children, includes a section on self-esteem. Problems can often be the direct result of low self-esteem, when the child believes itself to be poor at school subjects or unable to read. They then attempt to cover their inability by drawing attention away by unacceptable behaviour.



How often do we say to a child, Not now, we'll do it later? It implies that doing our own thing is more important. We want our children to live up to our own expectations for them and may often show disappointment when they fail. Everyone has been told at some stage in their lives, to go and do something useful, not spend all day reading or watching television. Is this perhaps inflicting own values on others? It certainly doesn't do much for the self-confidence frequently, to be told to do something better than the thing we have chosen to occupy our time.



When he was a young man, Samuel Johnson was asked what was his happiest childhood memory. He replied that it had been a whole day spent fishing with his father. In his father's diary, the entry for that day read:-



Took Samuel fishing. Another wasted day.

One of my able-bodied students recently said that she envied my self-confidence. Little does she know how hard I have worked to appear fully in control of myself. We have all joined groups of people who all look in control of themselves, all wear exactly the right clothes for an occasion, while you are wearing everything wrong and know no-one. Going into a room full of strangers requires as much drive from me, as anyone else. It is never an in-built feature that allows some people the confidence and others to stay outside feeling uncomfortable. I make myself do these things because I know I shall regret wasted opportunities if I don't. I have travelled alone on many occasions. There have been many times when my confidence was very low, but a deep breath and standing tall has usually worked. A simple smile in a waiting room can sometimes lead to an interesting five minutes conversation with someone new, instead of a boring wait.



If we really do extend life or 'have another go at it', following revival after suspension, we need to make certain that we use the extra time, in a way that pleases, and not as time to be endured. But then, I don't expect that I shall ever have a problem ... I never have enough time to do all the things I want to do!



Fly Experiments

by Douglas Skrecky <oberon@vcn.bc.ca>

This is the fifteenth update on my fly experiments. On day 43 all flies were dead in the 4th run. About all that was interesting here was the relative performance of the control, paprika and purple yam bottles. However I am not inclined to regard these results as being significant, since the flies for these 3 bottles were derived from several different old breeding bottles. To be "fair" the control bottle must come form the same breeding bottles as the supplements it is used to compare with. From now on I will be using several control bottles.
Fourth Run

Survival DAY

Supplement 10 24 34 43
Control 100% 56% 0% all 0%
bactine 75 0 0
bactine 4X 50 0 0
garlic 20 0 0
garlic 4X 0 0 0
KCL 100 0 0
KCL 4X 71 0 0
mint listerine 0 0 0
mint listerine 4X 0 0 0
paprika 88 38 0
paprika 4X 50 0 0
pectin 40 0 0
plax 60 0 0
plax 4X 0 0 0
purple yam 86 48 5
purple yam 4X 52 5 0
salt 47 13 0
salt 4X 38 0 0
sterisol 0 0 0
sterisol 4X 0 0 0
viadent 0 0 0
viadent 4X 0 0 0
water reduced 50% 90 30 10











The results of the fifth run were characterized by exceptionally high mortality rates, in comparison with runs from earlier this year. I attribute this difference to the fact that a heat wave hit my native Vancouver, BC and the average temperature the flies were exposed to, rose first above 80 degrees and then on some days to above 90 degrees. A short exerpt from my fly longevity database reveals the strong link between temperature and average life span of drosophilia melanogaster.
Temperature Life Span
oF days
52 152
64 130
68 81
70 86
77 62
81 42
86 25
86 20









Given the above data I should have finished my first census of run #5 a little quicker, while most of the flies were still alive. However even at this late date some useful data emerges, as well as a lesson I will not soon forget.



The lesson is that several control bottles must be used to derive useful data, when temperatures are high. I use several breeding bottles (BBs) to provide enough flies for each run. There will always be some variations in the average age of the flies in each bottle, depending on how much breeding has occurred. These new BBs were "seeded" with parent flies 29 days before run #5 was started. If no offspring were produced all flies inside a breeding bottle will be over 29 days old. If a small amount of breeding occurs the average age will be a little lower, while if a lot of breeding occurs the average age will be much lower. While a difference of (for example) 5 days in average age between BBs will not have much impact if the life span of the flies is several months at cool temperatures, it can have a large impact when high temperature reduces this life span to just a few weeks, as has occurred with run #5. (I have always recorded which BBs are used, but had not included this in my updates as it did not seem to make any difference earlier. I also record the order in which I supply the supplement bottles from a BB. Surprisingly this order does not make any difference; even in the present run.)



Fortunately I created 3 control bottles this time so some usable data emerges. Unfortunately I had to use 4 BBs when breeding bottle #3 (BB#3) ran out of flies before I could create a control from this breeding bottle. Thus the data from the supplement bottles using flies from the BB#3 are of relatively little value. However the total number of flies provided by BB#3 and BB#1 are similar, so control#1 might be used as a "reasonable" substitute. However even if control#2 is used, which problably contains more younger flies, since more flies were bred in BB#2 than in BB#1 or BB#3, it can be seen that the lower dosage of the "nontoxic" bactericide/sugars handily outperformed both control#1 and control#2.



The much higher survival in control#4, I attribute to the huge number of flies that were in BB#4. I did not use all of these. The existence of control#4 is a very valuable check on any misguided enthusiasm on my part regarding carnosine. As I mentioned in the 14th update carnosine is not absorbed intact, but instead is broken down to B-alanine and l-histidine, both of which have proven to be ineffective life-extenders in published experiments. If anyone knows of a source of the stable carnosine precursor acetylcarnosine please let me know. I would give some pretty fair odds that this would significantly increase fly life span.



Of the supplements that did well in run#3, that were retested this time, anise was a disappointment, paba was so-so, while malt and activated charcoal again beat the averages. I could not be sure of the number of dead flies in the high dose activated carbon bottle, but will verify the total number of flies after they are all dead and I can open the bottle without fear of losing some flies.



Although medium 4-24 contains some sucrose already, I suspect that a little more of either this or other sugars reduces pathogen growth and increases life span somewhat. The amino acids were a disappointment as a group, though proline looks to be worth retesting. Proline has been found to increase the life span of the mutant Long Evans Cinnamon rat, which suffers from excessive copper accumulation and is considered an animal model of Wilson's disease. (Pharmacology Biochemistry and Behaviour 52(3): 509-515 1995

Fifth Run

Breed Day 16
Bottle Supplement Alive Dead Survival
1 control #1 2 18 10%
1 l-alanine 2 13 13
1 l-alanine 4X 0 14 0
1 anise 1 9 10
1 anise 4X 0 9 0
1 l-glutamine 2 13 13
1 l-glutamine 4X 0 22 0
1 malt 5 15 25
1 malt 4X 2 20 9
1 paba 2 11 15
1 paba 4X 0 9 0
1 total 16 + 153 = 169

10% (average)

2 control#2 5 18 22
2 l-cysteine 3 14 18
2 l-cysteine 4X 0 15 0
2 l-glycine 2 19 10
2 l-glycine 4X 0 15 0
2 l-isoleucine 3 25 11
2 l-isoleucine 4X 1 30 3
2 l-leucine 2 16 11
2 dl-phenylalanine 2 22 8
2 dl-phenylalanine 4X 3 15 17
2 l-proline 4 11 27
2 l-proline 4X 5 14 26
2 l-threonine 4 14 22
2 l-threonine 4X 0 21 0
2 l-valine 3 20 13
2 l-valine 4X 3 15 17
2 total 40 + 286 = 326

12% (average)

3 activated charcoal 4 11 27
3 activated charcoal 4X 4 6? 40?
3 glucose 6 19 24
3 glucose 4X 5 18 28
3 l-leucine 4X 1 17 6
3 sorbitol 6 18 25
3 sorbitol 4X 3 13 19
3 sucrose 6 13 32
3 sucrose 4X 3 17 15
3 total 38 + 132 = 170

22% (average)

4 control#4 17 9 65
4 l-carnosine 9 14 39
4 l-carnosine 2X 18 15 55
4 l-carnosine 4X 10 20 33
4 l-carnosine 8X 6 33 15











This is the sixteenth update of my fly experiments. The heat wave is over so I expect life spans will be greater in the sixth run than in the fifth run. In the fifth run all that looks interesting is activated charcoal, sucrose and l-proline. Since activated charcoal significantly outperformed controls in the 3rd run, I have shortlisted this as a "probable" life span prolonging supplement for flies.



Since the lower dosage of a supplement almost always results in a greater life span, I am decreasing the dosages I use in the sixth run. I am retesting l-proline as well as sage and paprika here. For the first time I am boiling the water I use. Although flies live longer when live yeast is added to their food, this result was obtained under highly sterile laboratory conditions. This might not apply to my less than completely sanitary home experiments. So I am running two control bottles, one with added yeast from each breeding bottle to test for the effect of live yeast. None of the supplement bottles contains live yeast in this run. The breeding bottles were all created 20 days ago, using boiled water and a high dose (1.04 gm) of activated charcoal added to 20 gm 4-24 medium.
Fifth Run Survival DAY %
B# Supplement 16 23 26 30 36
1 control#1 10 10 0 0 all 0
1 l-alanine 13 0 0 0
1 l-alanine 4X 0 0 0 0
1 anise 10 0 0 0
1 anise 4X 0 0 0 0
1 l-glutamine 13 0 0 0
1 l-glutamine 4X 0 0 0 0
1 malt 25 0 0 0
1 malt 4X 9 0 0 0
1 paba 15 0 0 0
1 paba 4X 0 0 0 0
2 control#2 22 13 4 0
2 l-cysteine 18 0 0 0
2 l-cysteine 4X 0 0 0 0
2 l-glycine 10 0 0 0
2 l-glycine 4X 0 0 0 0
2 l-isoleucine 11 0 0 0
2 l-isoleucine 4X 3 0 0 0
2 l-leucine 11 0 0 0
2 dl-phenylalanine 8 0 0 0
2 dl-phenylalanine 4X 17 0 0 0
2 l-proline 27 13 7 7
2 l-proline 4X 26 5 0 0
2 l-threonine 22 6 6 0
2 l-threonine 4X 0 0 0 0
2 l-valine 13 4 0 0
2 l-valine 4X 17 0 0 0
3 activated charcoal 27 13 0 0
3 activated charcoal4X 40 20 20 0
3 glucose 24 8 8 0
3 glucose 4X 28 9 0 0
3 l-leucine 4X 6 0 0 0
3 sorbitol 25 8 4 0
3 sorbitol 4X 19 6 0 0
3 sucrose 32 21 11 0
3 sucrose 4X 15 0 0 0
4 control#4 65 44 20 8
4 l-carnosine 39 25 13 4
4 l-carnosine 2X 55 27 12 0
4 l-carnosine 4X 33 7 3 3
4 l-carnosine 8X 15 3 3 0





Sixth Run

BB# Supplement Amount
1 cntl 1
1 cntl 1 +yeast
1 B complex: 1/4 capsule
1 B complex 4X: 1 capsule: (50 mg B1, 50 mg B2, 50 mg B3, 50 mg B5, 50 mg B6, 50 mcg B12, 60 mcg biotin, 1 mg folic acid, 50 mg choline bitartrate, 50 mg inositol, 50 mg PABA)
1 chitosan: 1/4 capsule 75 mg
1 chitosan 4X: 1 capsule 300 mg
1 chondroitin sulfate: 1/4 capsule 100 mg
1 chondroitin sulfate 4X: 1 capsule 400 mg
1 chromium picolinate: 1/4 capsule 125 mcg
1 chromium picolinate 4X: 1 capsule 500 mcg
1 cinnamon: 1/16 teaspoon
1 cinnamon 4X: 1/4 teaspoon
1 DMAE bitartrate: 1/4 capsule 37.5 mg
1 DMAE bitartrate 4X: 1 capsule 150 mg
2 cntl 2
2 cntl 2 +yeast
2 french mushroom: 1/16 teaspoon
2 french mushroom 4X: 1/4 teaspoon
2 kava kava: 1/4 capsule 11.25 mg kavalactones
2 kava kava 4X: 1 capsule 45 mg kavalactones
2 onion: 1/16 teaspoon
2 onion 4X: 1/4 teaspoon
2 paprika, spanish: 1/16 teaspoon
2 paprika, spanish 4X: 1/4 teaspoon
2 l-proline: 1/4 capsule 125 mg
2 l-proline 4X: 1 capsule 500 mg
2 sage: 1/16 teaspoon
2 sage 4X: 1/4 teaspoon
2 sodium citrate: 1/16 teaspoon 375 mg
2 sodium citrate 4X: 1/4 teaspoon 1500 mg
3 cntl 3
3 cntl 3 +yeast
3 St John's Wort: 1/4 capsule 225 mcg hypericin
3 St John's Wort 4X: 1 capsule 900 mcg hypericin
3 sumac: 1/16 teaspoon
3 sumac 4X: 1/4 teaspoon
3 wild yam: 1/4 capsule 125 mg
3 wild yam 4X: 1 capsule 500 mg







Ettinger's Ark

by Brent Allsop

Everyone's familiar with the Noah story right? The one where Noah tries to warn everyone about the impending, yet avoidable doom, trying to get everyone to help build arks so that they might survive the flood. But, unfortunately, no one listens to him, (for what reasons?) and he and his family, along with the animals he has collected, are the only ones that survive.



I was in a Lutheran Church last Saturday (for a friend's wedding) and I noticed a brightly coloured (with rainbow) picture of the inhabitants of the ark coming forth upon the finally dry (and cleansed?) land. It was a large mural covering an entire wall in the children's nursery. It's probably a good thing I resisted the temptation to add a few dead and rotting bodily remains with an ink marker, that surely would have been left over from what, if it really occurred, was one of the most devastating and destructive catastrophes during the history of mankind.

But anyway, I wondered what the chance will be that, maybe 1000 years from now and more, one of the stories we all tell our children (and make children's toys about and paint colourful depictions of on the walls of nurseries...), is how Robert Ettinger, and others, tried to warn and convince the world of the doom they could have avoided by simply taking proper actions. The story would be very similar in that only a relative hand full of people would heed his warning and would make the eternal life saving effort, mostly because of ancient religious ideas contained in stories like that of Noah and the flood... I can imagine toy dewars with little dolls representing people and their pets nicely fitting inside... (and cheesy animated videos...? Nahh!) Obviously, some of the actual survivors will be on hand to retell the story first hand, giving it infinite more significance, as compared to Noah who is, if he was more than a cheesy animated character, long dead and gone.



Religion seems so completely ironic to me, as a cryonaut, in so many never ending ways. Wouldn't it be humorous if it wasn't so tragic?

Nutrition, Lifestyle, Genetics And Longevity

by Roger L. Bagula

The young mother said to her five year old boy at supper: "Eat your peas and broccoli, they are good for you." What is there that is universal about young boys who won't eat their vegetables?



When the person in his fifties goes in after his first mild heart attack, he is told to change his diet and exercise more as if good behaviour after the fact has much of a chance of saving him. We as men and women take our own lifestyle for ourselves from that which our parents offer us as a first alternative and whatever "occurs" to us as desirable. It is usually only as we see death approaching our door step that we reconsider that cigar after supper with the sipping brandy.



In California lettuce may be a death sentence with the insecticide they use to control white flies all through it. We have to take conventional wisdom as only a starting place, since all the conventional thinkers die, just like us. In my youth my girl friend's mother was a trained nutritionist and fed her family for years what she had been taught was the right diet: Last I heard my girl friend's father had just had a bypass operation and his heart condition didn't look good. My own father is several years older and has had a very high cholesterol diet for as long as I can remember and hasn't had any heart trouble that I know of. Is it lifestyle, diet or genetics that makes us die off early or live much longer than others? Jesus said that we should take no thought for what we eat, because life is more than the meat we eat. How we feel about ourselves and what we do, affects how we feel physically. We can not change the genetics we are born with (at this point in history - it may change in the next 20 to 50 years), but we can control two important factors:



diet

2. lifestyle



Of the two lifestyle may be more important and hardest to change and understand.



As basically a kind of primate that turned from a diet of mostly fruit to a hunter's diet of mostly meat back to a diet of mostly grains, we aren't really sure what the proper diet is. One thing that may be true is that five year old boys don't need their vegetables as much as protein from meat and sugar from carbohydrates, but the mother is right as well in trying to establish a long term healthy eating habit that will serve the boy when he becomes a man who does need the fibre and vitamins of vegetables. Today, we find that with processing of food that we must take vitamin pills to get the vitamins and minerals that are taken out of our food by over cooking and milling. If you read the label of any carbonated soft drink, you will find that you are getting water and sugar with only traces of anything else.



Any one that tells you that "sugar" is bad for you is being totally stupid: the major energy your body uses on demand in exercise is from the free sugars of your food. The major component of fruits is natural sugars and fruit is, as being the first food of preference of our primate forefathers, a very important part of our diet. If you give a chimp a banana and a carrot, he may eat them both eventually, but he eats the banana first. If you give a child a hamburger and a carrot, the hamburger gets eaten and the carrot is left. Meat is the second choice for a food for men. We spent a million years after our apehood as predatory hunters. The most natural food for hunting groups has been the grazing animals from which domesticated cattle come (in some ancient cultures the cow became a god of food). It is true that birds have always been part of the hunting diet, but a whole group could not be well fed on a few pigeons alone.



We are told that red meat is "bad" and bird meat (chicken) is good in the sense of how it affects our circulatory system long term. In these terms fish may be better than either, but we have to look at the economy of raising these animals in the modern factory farm. In these terms fish may be better than either, but we have to look at the economy of raising these animals in the modern factory farm . In the crowding of chicken farms more "chemicals" are used to keep the animals healthy and growing to premium size than in beef farming, but in all factory farming hormones and antibiotics are used in the routine care for the animals and they come to us in the tissue we eat. The chemicals used in processed meats like bacon, sausage and lunch meat may be even more deadly. Should we go back to hunting our own, ha, ha?



When a dog or cat gets sick, you will see it chewing on grass. Mothers are right in saying that you need what vegetables give you, but beans, corn and potatoes are also vegetables. It is the fibre and vitamins that makes green vegetables desirable in our diet, but we have to have the carbohydrates that our farming ancestors subsisted on in the very bad times of man's recent past. Grains are the staple of our diet and our daily bread. It has been claimed that both milk and eggs are "perfect" foods and they do contain the basics of nutrition, but there is today no "perfect" food.



In our old age the chemical machinery of our bodies begins to break down, and it has been claimed that megavitamins and herbs can help slow this seemingly inevitable deterioration. Ginkgo Biloba is said to help brain chemistry in those with memory problems by promoting microcirculation blood pressure in the brain. I think the best that a modern man can hope for it to choose and eat his food with care and wisdom and hope something doesn't by bad luck kill him early.



As with diet, lifestyle is a matter of individual choice. It has been observed that that many strict religious people may live longer, but what good does it do them if they don't have any fund doing it? I haven't found a religion that tells it's worshippers to exercise or they will go to hell, either. To be an atheist may be reasonable to some intellectuals, but for them to raise their children with no moral self control may be a death sentence. The moral behaviour codes of the major religions were developed over a long history to protect the minds and bodies of people who follow the teachings. No godless ethical code is handed out in standard books with children's stories built in like The Bible. The hard work and virtue of many Christians has led to long lives.



The dangers of "sins" are not just religious in nature, but are lifestyle killers as well. Free sexual practices leads to diseases. Over eating to bad health and over weight. Not working besides keeping you from making the money to stay alive on, also is bad for your body in taking away a reason for exercise. This may not be true in a world where work is pounding a computer keyboard, but it was true historically. As people we seem to "need" reasons like guilt to keep us from a lifestyle that can be a form of suicide. I don't think modern religion is an answer to lifestyle problems, but the humanism of modern science has little hope or guidance for the ordinary person without a very high IQ. In the one "religion" without a god in China good behaviour was still considered the wisest course to a long and healthy life. To tell a child he should be good because he will live longer doesn't seem to have the same weight as saying be good or god will punish you. Even if the end result of a behaviour pattern is the same no matter the motivation.



It seems strange to me that I should be recommending religious behaviour as a lifestyle for prolonging life when it seems aimed at an afterlife. The fact remains that the "golden mean" of behaviour is closer to religious training than it is to "all out do what you damn well please" behaviour of no moral training. Primitive men who did what they wanted died out early and left life and child raising to the those who behaved more rationally. From this came to us wisdom principles as religious teaching in almost all cultures. Reasonably to extend your life you should be moderate in your behaviour and offenses to other men, and get at least a moderate amount of exercise daily. If we look at this as behaviour "blessed" by a god or a the path of a wise enlightened man, it doesn't seem to matter in the end result, does it?



Robert Heinlein wrote a series of science fiction novels about a group of people who married only people whose genetics presupposed long life, and they became a race separate from normal men with very long lives. He recognize that some people just seem to live longer no matter what they do, eat or live through. My mother's side has shorter life span than my Dad's by my observation. Since there are more "hell raisers" and religious both on Dad's side, I take it as a genetic factor more than a diet or behaviour one. As Heinlein suggested we can't seek that form longevity for ourselves, but might by marriage promote it in our offspring. With the hap-hazard marriage customs of modern man where "love" and chance meeting seem to contribute more to who or what is produced in the next generation this may only be the wind coming out of my ears. In a discussion of the methods and causes of long life, I had to mention it.



For most of us who have survived to the point where we begin to see the wisdom of the ages in our culture and see that culture trying very hard to destroy itself in a materialistic "gluttony" it may be too late to change our diets and lifestyles, but it isn't too late to realize that many of the cultural elements that are considered "out" in modern circles are what we should have been doing all along. That we can warn our offspring and try to get them to bring their offspring up in a better and wiser way. For the rational humanist without a god in his life it may mean giving his children the advantage of religion's teachings so they can make their own choices when the come to "reason". (So that they can live long enough to get there.). I myself see that a belief in god makes to me more sense for me than the alternative, but 1 have some very intelligent and "nice" friends for which that is nor true. But most of us who have come to enjoy living also realize that means to live longer may be found just by living a better life as a person and watching what we eat.

Long-Evans Rat Longevity Database



Updated by Doug Skrecky October 10,1997

This is a database listing the effect of various treatments on the average longevity of Long-Evans rats. The percent change in average life span is listed under the %CHANGE columns, relative to either the CONTROL group used in the experiment, or to the Longest Lived Control (LLC) group of all the experiments listed in this database. The LLC group was one of the control groups used in reference #10, which lived an average of 32.6 months. The START column shows the age when treatment was begun. A ~ symbol means that a number was estimated. For animals that were calorically restricted, the amount of rat chow below ab libitum they were allowed to consume is indicated by the number just before the word "chow". Thus -33% chow indicates that the animals were fed 33% less chow, than they would normally consume. One exception to this is in reference 14, where the control rats were themselves mildly restricted by 8%. Note that some animals consumed additional chow, when they were either exercised or exposed to cool water.

%CHANGE

REF TREATMENT START CONTROL LLC
2 aluminum 5 ppm 1+ -2 -9
2 aluminum 5 ppm 1+ 2 -12
12 potassium ANTIMONY tartrate 5 ppm ~1+ -12 -22
12 potassium ANTIMONY tartrate 5 ppm ~1+ -12 -18
11 sodium ARSENITE 5 mg/l & chromium 1 mg/l ~1+ -5 -16
11 sodium ARSENITE 5 mg/l & chromium 1 mg/l ~1+ 0 -7
2 Barium 5 ppm 1+ -17 -23
2 barium 5 ppm 1+ -7 -20
2 beryllium 5 ppm 1+ -5 -12
2 beryllium 5 ppm 1+ 6 -9
10 cadmium acetate 5 ppm ~1+ -16 -16
10 cadmium acetate 5 ppm ~1+ -15 -18
13 +44 chow + 23 C water 20 hrs/week 6+ 5 -1
15 +20% chow & exercise 4+ 9 3
5 -8% chow 6+ 1 -5
5 -8% chow & exercise 6+ 10 3
14 -24% chow 3+ 21 8
14 -24% chow & exercise 3+ 14 2
5 -28% chow 6+ 21 14
7 -33% chow 18+ decreases
14 -42% chow 3+ 24 11
10 chromium acetate 5 ppm ~1+ -6 -6
10 chromium acetate 5 ppm ~1+ 1 -3
1 chromium chloride 1 mg/kg diet ~1+ 7
1 chromium dinicotinate 1 mg/kg diet ~1+ 7
1 chromium picolinate 1 mg/kg diet ~1+ 35
14 exercise 3+ 12 0
11 sodium GERMANATE 5 mg/l & chromium 1 mg/l ~1+ -15 -25
11 sodium GERMANATE 5 mg/l & chromium 1 mg/l ~1+ -9 -15
10 lead acetate 5 ppm ~1+ -25 -25
10 lead acetate 5 ppm ~1+ -23 -26
12 lead nitrate 25 ppm ~1+ 1 -10
3 nickel 5 ppm 1+ 0 -12
3 nickel 5 ppm 1+ 6 -6
12 sodium NIOBATE 5 ppm ~1+ 2 -9
12 sodium NIOBATE 5 ppm ~1+ 9 2
4 selenate 2 ppm ~1+ 13 -2
4 selenate 2 ppm ~1+ 16 4
4 selenite 2 ppm ~1+ -93 -94
4 selenite 2 ppm ~1+ -60 -64
11 stannous chloride 5 ml & chromium 1 mg/l ~1+ 0 -11
11 stannous chloride 5 mg/l & chromium 1 mg/l ~1+ -9 -15
9 sugar, brown & vit E deficiency ~1+ -8 -18
9 sugar, brown & vit E deficiency ~1+ -14 -20
9 sugar, raw & vit E deficiency ~1+ -22 -30
9 sugar, raw & vit E deficiency ~1+ -23 -29
9 sugar, white & vit E deficiency ~1+ -15 -24
9 sugar, white & vit E deficiency ~1+ -32 -40
9 sugar, white & vit E deficiency ~1+ -27 -32
9 sugar, white & vit E deficiency ~1+ -31 -36
9 sugar, white, chromium 5ppm & E deficiency ~1+ -31 -39
9 sugar, white, chromium 5ppm & E deficiency ~1+ -30 -35
8 tansy ragwort 2.5% -87
8 tansy ragwort 2.5% & bracken 10% -86
8 tansy ragwort 2.5% & St John's Wort 5% -87
8 tansy ragwort & bracken & St John's Wort -83
4 tellurite 2 ppm ~1+ 1 -14
4 tellurite 2 ppm ~1+ 4 -7
6 -60% trytophan 0.7+ 0 -29
6 -70% trytophan 0.7+ -71 -80
2 tungsten 5 ppm 1+ -9 -16
2 tungsten 5 ppm 1+ 7 -8
12 vanadyl sulfate 5 ppm ~1+ -1 -12
12 vanadyl sulfate 5 ppm ~1+ 5 2
12 zirconium sulfate 5 ppm ~1+ 1 -10
12 zirconium sulfate 5 ppm ~1+ 4 -3

Speculation:

From this database the most interesting treatment is chromium picolinate supplementation. This was added to a chromium replete rat chow at a dosage of 1 mg/kg of chromium. Since standard low fat chow has a caloric density of about 4 cals/gm, a human consuming 2400 calories per day of this chow would be ingesting 600 mcg of chromium. Long-Evans rats are a model of moderate adult onset diabetes. At 200 days of age plasma glucose of rats fed extra chromium picolinate, chromium nicotinate or chromium chloride were 6.6, 7.7, and 7.8 mM. At 1000 days plasma glucose was 6.5, 8.3, and 8.2 mM. So only the picolinate salt prevented age-associated hyperglycemia. Please note that this was only a pilot experiment using just 10 animals per group. It was reported only in abstract form, but subsequently further details were provided by Mark McCarty.1 In humans hyperglycemia is associated with elevated mortality rates and reduced life spans, so preventing this in rats this may account for longevity prolonging effect of chromium picolinate. The greatest maximum life span was 46.6 months for one of two control groups from reference 10. However the maximum life span for some of the treated groups was even longer. The treated groups with the greatest maximum life spans are as follows:
REF INTERVENTION MAXIMUM AVERAGE
    Months months
4 selenate 2 ppm 61 33.8
10 sodium arsenite 5 mg/l & chromium 1 mg/l 53.2 27.5
6 -70 tryptophan 50.9 6.7
2 beryllium 5 ppm 48.8 29.7
14 -24% chow & exercise 48.1 33.2
1 chromium picolinate 1 mg/kg 48 44
10 control group 46.6 31.5

What can we humans expect if the results in Long-Evans rats hold up in humans? Comparing the maximal control group life span of 46.6 months with 95 human years, translates the 44 months for the chromium picolinate group to an equivalent of 90 human years. However since most Long-Evans rats become diabetic and thus live much shorter lives than they should, then perhaps it is the 61 month old selenate doped rat that should be equated with a 95 year old human. Here the average life span of 44 months translates to 69 human years, which is a respectible, but not exceptional figuare. Why does the LLC group live only 32.6 months, when much longer life spans are possible? The glycemic index (GI) or rate that glucose is absorbed from food is known to determine the rate that rodents develop hyperglycemia with age.16Standard rat chow has a high GI, and that may be the reason why Long-Evans develop hyperglycemia and live short lives. Even a small change in GI of chow is now known to alter both average and maximum life span of rodents.17 I speculate here that if fed a sufficiantly low GI chow featuring whole grains, instead of high GI flour or starch, that control rats might live as long as those given chromium picolinate. The standard protein used was casein, which is now also known to decrease rodent life span.18Replacing this with soy protein increases life span, and I suspect using whole cooked soybeans might be even more beneficial. The results from all the other treatments are uninspiring. Selenate showed a slight increase, as does exercise and life long caloric restriction. The later may have been hampered by the finding that caloric restriction imposed gradually starting at 18 months of age actually decreased life span.7As a practical method for increasing human life span, both selenate and caloric restriction get low marks, because of the risk of toxicity. In humans it has been found that after physical fitness is controlled for, that body weight has no effect on mortality, thus strongly suggesting that caloric intake is NOT a significant modulator of human aging.19Moderate exercise gets high marks, and it is this plus consuming a low GI diet and (possibly) chromium picolinate and biotin supplementation that can be recommended. Note: Biotin at a dosage of 9 to 16 mg/day has been found to be effective in treating hyperglycemia in both insulin dependant & non-insulin dependant human diabetics.20,21Chromium picolinate at a dosage of 1000 mcg/day has been found to be much more effective than 200 mcg/day in the treatment of Chinese non-insulin dependant diabetics.22



1 McCarty MF. Longevity Effect of Chromium Picolinate - 'Rejuvenation' of Hypothalmic Function: Medical Hypotheses43: 253-265 1994 (corrections: The maximum life span of Long Evans rats was here incorrectly stated to be 42 months. Also the quoted submitted reference 2 was never published) (but also see) Evans GW, and Meyer L Chromium Picolinate Increases Longevity:Age15: p134 abstract 51 1992

2 Schroeder HA, and Mitchener M. Life-term Studies in Rats: Effects of Aluminum, Barium, Beryllium and Tungsten: Journal of Nutrition 105: 421-427 1975

3 Schroeder HA, Mitchener M and Nason AP. Life-term Effects of Nickel in Rats: Survival, Tumours, Interactions With Trace Elements and Tissue Levels: Journal of Nutrition104: 239-243 1974



4 Schroeder HA, and Mitchener M. Selenium and Tellurium in Rats: Effect on Growth, Survival and Tumours : Journal of Nutrition 101: 1531-1540 1971

5 Holloszy, JO, Smith EK, Vining M, and Adams S. Effect of Voluntary Exercise on Longevity of Rats : J. Appl. Physiol. 59(3): 826-831 1985

6 Ooka H, Segall PE, and Timiras PS. Histology and Survival in Age-Delayed Low-Tryptophan Fed Rats : Mechanisms of Ageing and Development 43: 79-98 1988

7 Lipman RD, Smith DE, Bronson RT, and Blumberg J. Is Late-Life Caloric Restriction Beneficial? : Aging Clin. Exp. Res. 7: 136-139 1995

8 Garrett BJ, Cheeke PR, Cristobal LM, Goeger DE, and Buhler DR. Consumption of Poisonous Plants (Senecio Jacobaea, Symphytum Offinciale, Pteridum Aquilinum, Hypericum Perforatum) in Rats: Chronic Toxicity, Mineral Metabolism, and Hepatic Drug-Metabolizing Enzymes : Toxicology Letters 10: 183-188 1982

9 Schroeder HA, Mitchener M, and Nason AP. Influence of Various Sugars, Chromium and Other Trace Metals on Serum Cholesterol and Glucose of Rats : Journal of Nutrition101: 247-258 1971

10 Schroeder HA, Balassa JJ, and Vinton Jr. WH. Chromium, Cadmium and Lead in Rats: Effects on Life Span, Tumours and tissue Levels : Journal of Nutrition 86: 51-66 1965

11 Schroeder HA, Kanisawa M, Frost DV, and Mitchener M. Germanium, Tin and Arsenic in Rats: Effects on Growth, Survival, Pathological Lesions and Life Span : Journal of Nutrition96: 37-45 1968

12 Schroeder HA, Mitchener M and Nason AP. Zirconium, Niobium, Antimony, Vanadium and Lead in Rats: Life Term Studies: Journal of Nutrition 100: 59-68 1970

13 Holloszy JO, and Smith EK. Longevity of Cold-Exposed Rats: A Reevaluation of the "Rate-of-Living" Theory: J. Appl. Physiol. 61(5): 1656-1660 1986

14 Holloszy JO, and Schechtman KB. Interaction Between Exercise and Food Restriction: Effects on Longevity of Male Rats: J. Appl. Physiol. 70(4): 1529-1535 1991

15 Holloszy JO. Exercise Increases Average Longevity of Female Rats Despite Increased Food Intake and no Growth Retardation : Journal of Gerontology 48(3): B97-B100 1993

16 Higgins JA, Brand Miller JC, and Denyer GS. Development of Insulin Resistance in the Rat is Dependent on the Rate of Glucose Absorption From the Diet : Journal of Nutrition126: 596-602 1996

17 Mlekusch W, Lamprecht M, Ottl K, Tillian M, and Reibnegger G. A Glucose-rich Diet Shortens Longevity of Mice : Mechanisms of Ageing and Development 92: 43-51 1996

18 Iwasaki K, Gleiser CA, Masoro EJ, McMahan CA, Seo EJ, and Yu BP. The Influence of Dietary Protein Source on Longevity and Age-Related Disease Processes of Fisher Rats : Journal of Gerontology 43(1): B5-B12 1988

19 Barlow CE, Kohl HW, Gibbons LW, and Blair SN. Physical Fitness, Mortality, and Obesity: International Journal of Obesity 19(Suppl 4): S41-S44 1995

20 Coggeshall JC, Heggers JP, Robson MC, and Baker H. Biotin Status and Plasma Glucose in Diabetes : Annals of the New York Academy of Sciences 447: 389-392 1985

21 Maebashi M, Makino Y, Furukawa Y, Ohinata K, Kimura S, and Sato T. Therapeutic Evaluation of the effect of Biotin on Hyperglycemia in Patients With Non-Insulin Dependant Diabetes Mellitus : Journal of Clinical Biochemistry Nutrition14: 211-218 1993

22 McCarty MF. Exploiting Complementary Therapeutic Strategies for the Treatment of Type II Diabetes and Prevention of its Complications : Medical Hypotheses 49: 143-152 1997 (Note the low dose of chromium was quoted as 299 mcg/day. This is a misprint, and the correct figure should be 200 mcg/day)

The Vinpocetine Story.

This article is reprinted from Longevity Report 23

The article, first published in Longevity Report some years ago, refers to the future availability of this product, derived from periwinkle. It is now readily and cheaply available from offshore suppliers. It was originally reprinted from a US based magazine now defunct called Offshore Medical Therapies.



This article explains the effects of a fascinating "new" medicine which is slowly replacing HydergineTMas a drug to both prevent and treat mental decay.



The long story of the development of vinpocetine began as early as 1956. A Hungarian drug company decided to carry out a scientific investigation of local plants in a search for undiscovered chemicals. On analyzing the plant Vinca minorthey discovered the chemical vincamine. Initial investigations showed that vincamine could be successfully used to treat mental decline.



By the early 1960's a drug containing vincamine called DevincanTM, was freely available in Hungary. It was successful, but it had several unwanted side effects which limited its use. Despite this, so successful is vincamine treatment, that the drug is still used today in France, Spain and Korea.



The story might have ended there, were it not for the efforts of Hungarian research scientist Dr. Cs. Lorincz. In 1968, following some extensive experiments carried out on vincamine, Dr Lorincz filed a patent for vinpocetine, a chemically made derivative of vincamine.



Dr Lorincz's work had produced a drug capable of treating the early stages of senile dementia by improving blood flow to the brain, increasing mental energy and improving memory. In fact this "turbo-charged" medicine did everything that vincamine could do and more besides. Best of all, it achieved these improvements without ANY adverse or unwanted side effects. In short Dr Lorincz's work had been nothing short of amazing!



Despite this exceptional breakthrough it was almost ten years before vinpocetine began to appear in the Hungarian marketplace, under the trade name CavintonTM. By 1989 Cavinton had been shown to be more than 70% effective in over 100 medical trials against brain disorders, mental decline due to old age and eye and ear defects.



Vinpocetine will probably be the natural successor to HydergineTM(ergoloid mesylate) as it has produced incredible improvements in all the conditions where Hydergine is usually used. The effects of vinpocetine are more noticeable, they appear more quickly and last longer than those produced by Hydergine. The evidence for hearing improvement with vinpocetine is scientific unlike Hydergine where the "evidence" is mostly anecdotal.



This replacement of Hydergine by vinpocetine is unlikely to happen very quickly for two main reasons:



1) The sales of vinpocetine are very strictly regulated and the product is currently only available in

a) Hungary

b) Japan

c) Korea

d) Czechoslovakia.

At present it is virtually impossible to purchase vinpocetine for export to any other country. Quite why this is so is difficult to determine, although as time passes it is expected that it will become generally more readily available throughout Europe.



2) The cost of vinpocetine is probably going to make it unacceptably high in price to the end user, e.g. the current price being paid in Japan for one month's supply at 4 tablets per day is around $120.



If you are thinking of obtaining vinpocetine for your own use we suggest you wait at least 12 months, as we believe availability and price will have improved considerably by then.



The occurrence of senile dementia and similar kinds of mental decay is increasing rapidly. The development of drugs which can prevent and treat these devastating illnesses is one of the biggest challenges facing medicine. The number of people over 60 years old has doubled in the industrialized countries of the world over the last 100 years.



The cause of senile dementia is still not known. This means that so far it has not been possible to find a way of preventing mental decay. At the present time it is only possible to treat the symptoms.



Drugs called vasodilators, which cause blood vessels to widen allowing a better blood supply have been widely used. Sadly, the effectiveness of this type of drug did not meet expectation. Very often the diseased blood vessels lose the ability to react to vasodilator drugs. Vasodilation may actually be harmful because of the risk of "steal syndrome", i.e. due to the widening of healthy blood vessels, blood is "stolen" from the diseased areas which need it most.



The latest class of drugs have a specific effect on the chemical reactions that go on inside cells, i.e. they invigorate the brain and make it work normally.



Vinpocetine is one of these new type of drugs. When taken regularly, vinpocetine allows the brain to make better use of oxygen and energy. The ability of the brain to withstand the effect of a lack of oxygen is also improved.



Although the brain makes up only 2% of the total body weight, it receives about 15-20% of the blood output from the heart. Energy for the brain is provided by the sugar glucose. The brain only has small energy reserves and these are all gone within 2-3 minutes, if they have to be used. This means that proper brain function depends on good blood flow, oxygen and glucose supply.



Effects.



Vinpocetine is able to intensively and selectively increases blood supply to the brain1,2,3.



Vinpocetine improves the use of oxygen by the brain, it's ability to resist damage due to a lack of oxygen and it's ATP content1,2,4.



Vinpocetine has all the following properties - it



is effective when taken orally.

selectively improves blood supply to the brain.

does not cause slowed heart rate or low blood pressure.

increases oxygen use by the brain.

increases the tolerance of the brain to a total lack of oxygen.

increases vasodilation due to a lack of oxygen.

enhances use of glucose by brain cells.

increases ATP levels in the brain.

stops blood from becoming sticky.

raises the amount of serotonin which has an activating effect on the brain.

is non-toxic even in doses several times higher than those used normally.

is not harmful to the central nervous system.



It has been proven using a wide variety of methods, in many thousands of patients that vinpocetine improves blood circulation, oxygen uptake and glucose utilization by the brain in humans. The degree to which the chemical reactions of the brain are improved depends on the level of oxygen in the brain. Vinpocetine has its first effect on any areas that are damaged. Blood is not stolen from the damaged areas, but is actually increased in the damaged region.



Medical Trials.

Vinpocetine has been found to produce positive results in at least 70% of all users. The main medical fields in which it has been used in are the treatment of brain disorders, treatment of the signs of old age, defects of the eye, and ear, nose and throat problems.



Healthy People.



What is the effect of vinpocetine in healthy people? A study was done on 12 healthy female volunteers. They received vinpocetine 10,20 or 40mg per day for two days in a double blind placebo controlled trial. On the third day the test subjects underwent a battery of psychological tests. Memory was found to be very significantly improved following treatment with 40mg vinpocetine5. It is expected that even better results will be seen if treatment is continued for a longer period.



Brain disorders.



Over 76% of treated patients show improvement. Improvement in the symptoms is seen in 60-70% of cases but at least one month of therapy is necessary to get good results. Regular use can improve all of the following symptoms:

n the healthy older person with no mental decline, vinpocetine can still give very good results. It is usually necessary to use vinpocetine daily for longer than one year to get the maximum effect.



Eyes & Ears.



In the course of treating a group of over 800 patients for eye problems a 71% improvement rate was obtained. The eye problems treated included yellow spot degeneration, diabetic retinopathy and glaucoma.



Vinpocetine is most effective for macula degeneration. Good results are also seen in glaucoma6. Vinpocetine improves the blood supply to the retina of the eye. Eyesight also improves in most patients, e.g. there are reports of improved vision in 88 out of 100 patients. Five to ten percent widening of the visual area in glaucoma patients has been seen6.



Vinpocetine has been used to treat the following ear problems: presbyacusis (hearing loss due to old age), Meniere's disease, acute hypacusis and cochleovestibular neuritis (inflamed nerves in the ear). The beneficial effect of vinpocetine is due to increased blood supply to the inner ear, the nerves which enable us to hear and the cortex. Vinpocetine also inhibits nausea and vomiting7.



Vinpocetine can be used to control any changes in brain structure and function due to the menopause8.



Comparative Studies.

The real value of vinpocetine can only be established by comparing its effect with those of other drugs.



Vinpocetine proved to be better than Hydergine(ergoloid mesylate) in medical tests. Vinpocetine improved over 64% and Hydergine 54% of the patients.



A dose of only 10mg vinpocetine is equivalent to much larger doses of many other brain enhancing drugs9. Vinpocetine was found to be effective in a larger number of cases than centrophenoxine. It has been proven to be better than cyclandelate, difenidol, cinnarizine, nicotinic acid and its derivatives and papaverine.



The effectiveness of vinpocetine has been proved by many double-blind medical trials.



It is superior to all the other drugs which are used for the same purpose.



Japan.



In view of the considerable effectiveness of vinpocetine it was not long before Japanese researchers began to investigate. The tests done by the Japanese scientists confirmed that it improves blood circulation and oxygen and glucose uptake.



The Japanese carried out a special study to find out the best way of using vinpocetine10. The study included over 50 patients suffering from senile dementia with the major complaint of dizziness. Doses of 15mg and 30mg were compared. Their results showed that the development of the effect is slower in patients treated with 15mg per day, than in the 30mg per day group. However, if the treatment is continued for more than 4 weeks, then there is no difference between the two groups. The number of side effects - mainly gastrointestinal symptoms - was considerably lower in patients treated with 15mg per day. This means that the best oral dose is 15mg per day.



In Japanese medical trials vinpocetine has been found to be better than all other products and improvement was 70-75% after only 4 to 8 weeks of use.



In a trial including 40 hospitals the effect of 4 weeks treatment with vinpocetine 3X5mg daily or Hydergine 3mg per day was studied. Vinpocetine was found to be more effective in the improvement of general condition, and in all other symptoms than Hydergine11.



Interactions.

So far vinpocetine has not been found to interact with other drugs and so it can be taken in combination with other medicines.



Safety Studies.

In one year toxicity studies no ill effects were seen. Studies carried out to find out whether vinpocetine could cause cancer revealed that it was completely safe.



No change in male or female fertility was seen. No teratogenic (ability to cause defects in the unborn child) effects were seen. Vinpocetine cannot cause mutation or damage normal cells12.



Dosage.



The usual oral dose is 1 to 2 tablets three times a day. A maintenance dose for longer periods of time, i.e. one year is 1 tablet three times daily.



Side Effects.

Side effects which may be due to vinpocetine are only experienced by a small number of people, most of them are mild and disappear after the drug has been taken for some time. Side effects are much more common with the injectable form of the drug. A brief drop in blood pressure or faster heart rate may occur in some people.



Overview.



Each tablet contains 5mg of the active ingredient vinpocetine.



Vinpocetine works in a complex way, however, it has three main effects.

1) Improving brain chemistry:

It increases the glucose and oxygen uptake and use by the brain, improves the brain's tolerance to a lack of oxygen, allows glucose to be used in a more favorable way, raises the ATP level of the brain, increases turnover of the brain chemicals serotonin and noradrenaline, and has an antioxidant effect13,14. All these effects mean that vinpocetine protects the brain against damage.



2) Improving blood circulation in the brain:

It stops the blood from becoming sticky, stops dangerous thickening of blood, promotes oxygen transport into the brain.



3) Selectively and intensively increasing cerebral blood flow:

It reduces the brains resistance to blood circulation, has no effect on blood pressure or heart rate, improves blood supply to the impaired areas of the brain while the circulation of the intact area remains unchanged.



Vinpocetine is truly unique in having ALL these effects. None of the other drugs used to treat the same conditions as vinpocetine have this multiple effect.



Of all these effects the stimulation of brain chemistry is the most important. The condition of the delicate brain tissue is improved and so it becomes more resistant to blood deficiency and a lack of oxygen. The brain is able to use its reservoirs of nutrients and energy much more efficiently.



The brain protecting and activating effects of vinpocetine explain how it protects and enhances memory and thought processes.



Summing up: the research data collected so far shows that the most important effects of vinpocetine are the selective improvement of brain chemistry, blood circulation and blood flow. All three of these effects work together in a synergistic way. As a result the blood, oxygen and nutrient supply of the brain improves. The removal of waste material is also promoted. Increased permeability of the brains blood vessels means that nerve tissues use more nutrients and the efficiency of the energy making system increases. All these processes create better conditions for brain cells.



Vinpocetine can be used to treat the signs of senile dementia or mental decay, e.g. memory problems, dizziness, headache etc. It can be used in all forms of poor blood circulation in the brain such as TIA (transient ischemic attack), progressive stroke, completed stroke, post-apoplectic conditions, multi-infarct dementia, cerebral arteriosclerosis etc. Some symptoms of the menopause syndrome respond well to treatment with vinpocetine. It can be used to treat eye problems such as vascular disorders of the choroid and retina due to arteriosclerosis or vasospasm, also for the treatment of macula-degeneration and secondary glaucoma due to partial thromboses or vascular obstructions. Ear disorders like impaired hearing of vascular or toxic origin, sensorineural hearing loss and dizziness of labyrinth origin.



In common with all drugs, vinpocetine should never be administered to children or pregnant or lactating women.



We would repeat at this point that vinpocetine may prove virtually impossible to obtain at this time, however, we thought it to be such an important chemical we would bring it to your attention right now. We would certainly be interested if any of our readers could advise us of a supplier, we will of course pass this information on to our subscribers at the earliest possible opportunity. We believe this product to be an exceptional weapon in the armory of any would-be life extender. We hope this item will become much more readily available in the near future.



References.

  1. Kawakami H et al; Pharmracometrics 10:199 (1975).
  2. Karpati E et al; Arzneim-Forsch (Drug Res.) 26 10/a :1908 (1976).
  3. Karpati E et al; Paper, 7th International Congress on Pharmacology of Cerebral Vascular Diseases Symposium. Reims, 23rd July (1978).
  4. Caravaggi A; Symposium on Pharmacology of Vinca alkaloids. Ed. by Gy Fekete, Akademiai kiado, Budapest pp. 27-30 (1976).
  5. Subban Zeta!; Eur. J. Clin. Pharmacol 28:567-571(1985).
  6. Albert B; Paper XIth International Congress of Angilology, Prague, July 6th (1978).
  7. Bodo Cy et al; Evaluation of the efficacy of Cavinton in prevention and treatment of vestibular and vegetative disturbances occurring during space flight. RGD 23 983.
  8. Vero T et al; Possibilities of the treatment of some symptoms of menopause with Cavinton. RGD 13 381.
  9. Takeda Chemical Industries, Ltd. A Comparison between TCV-3B and Lucidril. RGD 14 113.
  10. 10) Nukata T; Dose finding study on TCV-3B (Vinpocetine) tablets for treatment of the various symptoms of Cerebrovascular Disorders. RGD 26909.
  11. Ohtomo E et al; Evaluation of Usefulness of TCV-3B tablets in Cerebrovascular Disorders. Comparison with Ifenprodil tartrate tablets or Dihydroergotoxine tablets (sublingual) by the cross-over method. RGD 2862
  12. Cholnoky E et al; Arzneim-Forsch (Drug Res.) 26 10/a: 1938(1976).
  13. Suno, M et al; I. Takeda Res. Lab. 42 (3/4) 249-252 (1983).
  14. Banga et al; Gyogyszereink 30:170-176(1980).

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