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Steven Rose against Nootropics


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#1 gustavo

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Posted 05 October 2003 - 01:12 AM


I've just read a very well written article against nootropics: "No way to treat the mind", by Steven Rose.

http://www.damicon.f...sd-article.html

I would like to know ImmInst's members reactions to, and opinions on, this well written paper. Steven Rose examined over 100 studies, paying attention to issues of methodology, data analysis, and theoretical foundations. He seems more than qualified to write this review. He is a neurobiologist; Professor of Biology and Director, Brain and Behaviour Research Group, The Open University; author of Lifelines; The Making Of Memory; coauthor of Not In Our Genes; editor of From Brains To Consciousness. And he comes to very skeptical conclusions.

what's your opinion on this?

#2 srmann

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Posted 05 October 2003 - 05:03 PM

Just an opinion, I think it varys from person to person if you are getting any results from taking Noots.

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#3 bacopa

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Posted 05 October 2003 - 06:03 PM

I'm also sceptical. It seems to me that these so called smart drugs don't necassarily help one to think better and the whole idea of simply popping a few combination of pills seems to be a bit too simplistic in that our brains are not just sponges that get smarter by putting the right "fuel" in them. I would imagine that it's far more complex than that and taking mental enhacement pills is an unscientific way of doing so. It makes me thing of the whole drug obsessions in the 1960's...the idea of taking an elixir of drugs to have the most "far out" experiences possible! Of course people on LSD had bad experineces just as they had good. and part of that has to do with the mood that their in upon taking the pills. smoking weed ontop of the LSD probably didn't "enhance" the overall experience just changed it a little bit. I've experimented with taking some of the so called mental boosters, only one Notropic so far, but in my experience concentrtation only needs so much focus in that one is either focusing or not! It's pretty simple I think...that's why coffee is still so popular because it must be difficult to prove that some cocktail of pills is that much better than oridnary coffee. But I do feel more stimulated now having taken Vinpocetine, but I feel sufficiently stimulated. I don't see how taking a variety of pills on top of this would help me to feel stimulated or smarter than I feel right now. Of course i could be wrong maybe nootropic combos could put me into a better state of consciousness?

#4 jpars82

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Posted 06 October 2003 - 06:17 PM

I think people take a variety of pills because they all serve different purposes. Some help attention more, some help long-term & some short-term memory. Other's enhance hearing & vision, help you to concentrate better, process thoughts faster. Or for other's there's Dilantin which can help if to calm your thoughts if you have too rapid of thoughts that it actually makes your IQ lower. Not to mention the anti-depressent & anxiolytic effects can help. For me, my "cocktail of pills" has tremendously helped me with my social anxiety & obsessive-compulsive disorder and also increased my IQ. Life is better for me now. Why not take a pill to better yourself as long as it's not harming you?? I don't understand why anyone would be against it.

#5 gustavo

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Posted 06 October 2003 - 06:28 PM

Jparsell, I accept that as a general response.

However, I am interested in someone actually READING what this guy Steven Rose has to say and exactly replying his arguments one by one.

His main points in his article are that:
- The experimental evidence for nootropics is severely flawed.
- Nobody can say that they do not have side effects. The simple fact that you "feel better" is not a criterion for the absence of side effect, which might appear after 10 or 20 years of taking your pills.
- The theoretical point that "increasing neurotransmitter activity is no guarantee of increased mental performance; rather, it can be positively deleterious to throw chemical spanners into the exquisitely balanced biochemical system that is the human brain. More does not mean better. "

plus other points he makes throughout the article. I would be interesting in someone replying those points, one by one.

GF

For Rose's article, visit http://www.damicon.f...sd-article.html

#6 srmann

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Posted 06 October 2003 - 09:00 PM

I say if it works for you then take what ever is helping. I am conducting my own study. It involves one person. srmann

#7 jpars82

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Posted 06 October 2003 - 09:10 PM

"There is no reason to assume that, for most of us at most time, our enzyme and neurotransmitter systems are not working at more or less optimal levels. "

"And even if it did, increasing neurotransmitter activity is no guarantee of increased mental performance; rather, it can be positively deleterious to throw chemical spanners into the exquisitely balanced biochemical system that is the human brain."

I do agree with a lot of what he states. The above statements though... I do not believe everyone's brain is exquisitely balanced. Nor do I believe all our neurotransmitter systems are working how they're supposed to. In my opinion, that's what makes us all different. That's why people are superior or inferior in certain areas. Increasing neurotransmitter activity could be a bad thing but I believe it could also be good depending on the person's brain.

#8 DJS

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Posted 06 October 2003 - 09:28 PM

Here's how I would put it.

Nootropics are, by definition, non-toxic/non-lethal, etc etc. Unless you do something really stupid and mega over dose you are not going to hurt yourself. So why not give nootropics a shot? If they don't work then you're only out $100 or $200. But if they do work...

The main point I am trying to make is that the enhanced cognitive functioning and the subsequent improved mental state that nootropics are suppose to provide is an entirely subjective matter. I have just recently begun my regiment and have noticed a significant jump in my standardized IQ as well as just feeling more clear headed and active. The "clear headed" and "more active" part could be chalked up to subjective experience and/or wishful thinking, but the 10 additional IQ point?? All the wishful thinking in the world can't make you smarter. So, just in my very unexpert opinion, I do think that nootropics can have some positive effects on cognitive function.

Another thing to keep in mind...

I remember reading a critique of nootropics a while back by Michael A. Apparently he found the effects of nootropics to be negligable on him. But he's not even 20 years old!! Judging by his age and the quality/strength of his arguments here on this forum I would say that his brain is already operating at close to peak capacity. :)

I think that is part of the problem here. Individuals who have yet to begin the "slow decline" may have a harder time recognizing the positive effects of nootropics. Whereas older individuals who are already experiencing some level of age related mental decline may experience great gains as a result of using nootropics.

#9 LifeMirage

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Posted 07 October 2003 - 01:37 AM

Steven Rose is not an expert in this area. Most of his statements are overexgatated.

No Way To Treat The Mind
Steven Rose
The idea of memory-boosting pills is appealing. But we should resist the claim that there is automatically a chemical fix for all our psychological fallings.

[There is no automatic fix for any problem, no one has or would claim that. I believe he made that up. ]


Would you like to increase your mental energy, concentration and alertness? PErform better in school or at work? Improve your ability to solve problems? Who could fail to be tempted by these offers adorning the cover of Smart Drugs and Nutrients: How to Improve Your Memory and Increase Your Intelligence Using the Latest Discoveries in Neuroscience? And if you do answer yes, there are, so enthusiasts will tell you, some 140 or more different chemicals, food additives or drugs that will do the job for you.

[Food Additives? Where did he get that? Do the job for you? His statements bolder on ridiculous.]

But the question remains: do any of the substances advertised as so-called ``smart drugs'' work?

[Yes they do work, but like any compound not for 100% of people who try it will see a difference.]

Moreover, if the pharmaceutical industry does come up with an effective treatment for Alzheimer's disease and other senile dementias, will it be of any value to healthy people? Britain's Consumers' Association recently asked me, as a neuroscientist specializing in the biochemical basis of memory, to review the evidence.

[A recent US study on Aricept (a alzheimer’s disease drug) showed it is of value to healthy people.]

It was not a cheering experience. In magazines, books and newsletters, smart drug enthusiasts cite an impressive string of scientific papers to support their claims. Using these and other papers reporting the results of experiments on prototype smart drugs, I examined well over 100 studies, some on animals, some on people with dementia, some on healthy people.

[I examined over 1,000 studies, 1,000 people, and 10 years of my own experience]


Most of these are either misleadingly quoted by advocates of smart drugs or describe experiments that are poorly controlled or extravagantly overinterpreted by the researchers. Worse, some studies use procedures that would not pass ethical scrutiny in Britain, and the most dramatic claims often appear in unrefereed conference proceedings or obscure journals.

[The studies were conducted worldwide including Europe. His statements appear baseless]

This brings us to the first fundamental problem with smart drugs. Most people envision them as improving recall.

[Their are no “problems” with smart drugs. What people envision is not relevant. I could “envision” smart drugs curing cancer, but that would be baseless.]

Yet much of the evidence cited by smart drug enthusiasts comes from animal experiments which can, by virtue of their design, test only a drug's effects on learning, not recall.

[Much of the evidence comes from the 20-30 years these drugs have been prescribed and their effects reported by doctors.
I do not claim smart drugs can or cannot affect recall, because conclusive studies have not been done.]


The animals are trained to perform highly specific tasks and the agents given within an hour or so of the training trials. On this basis, the best a smart drug could do would be to increase the likelihood of the transfer of information from the short-term to long-term memory store. There is little evidence than any of today's smart drugs can do even this much in humans.

[On a basis of his own perception not studies or experience.]

Indeed, the awesome complexity of human memory makes the smart drug creed look suspiciously simple. It is founded on two key assumptions.

[It is not founded on any assumptions except his own speculation]

First, memory loss is not confined to patients with conditions such as Alzheimer's disease but happens to us all as we age. Second, this normal ``everyday'' deterioration is caused by a failure or weakening of the same kinds of biochemical mechanisms that break down in conditions such as Alzheimer's disease. To believers in the faith, the corollary is obvious: drugs developed for patients with senile dementia ought to be made available to the rest of us so that we can crank our memories up to maximum speed and capacity.

[This is apparently his belief and no one else’s.]

The first of these assumptions is by no means confined to smart drug advocates.

[His is right they are confined by him.]

In the US, a vociferous school of thought claims there is a clinically definable condition called Age Associated Memory Impairment (AAMI) - an inexorable loss of memory which, the argument goes, many of us suffer as we move through our fifties. It is true that after the age of 40 performance on standard intelligence tests steadily declines for most people - unless enough time si given to solve the problems. And if speed is taken as the main criterion of memory capacity, then it could be argued that memory grows weaker with age. Yet memory and learning are inextricably bound up with a whole range of other mental and physical abilities. As we age our attention spans, emotions and motivation levels all change. Such effects alone could explain why memory seems to falter and age, without there being any weakening of the molecular and cellular mechanisms of memory itself.

[AAMI and/or similar terms are recognized by various countries, not only the US.]

Furthermore, decline is not inevitable. A recent Dutch study from the University of Limberg, Maastricht, has found that memory decline in otherwise healthy people as they age is associated with mild head injury, general anæsthesia or ``social drinking'' earlier in life. In people without such predisposing ``biological life events'', memory remained unimpaired even into extreme old age.

[Damage does occurring to brain everyday, it may not always affect memory, but it can affect other cognitive functions. Memory is just one aspect of cognition abilites.]

It is extremely difficult to design experiments that test the direct effects of drugs on memory when there are so many indirect influences on mental performance. Elderly people living in institutions who cannot remember what they had for breakfast that morning may be able to recall childhood episodes with great clarity. Have they lost memory, or have they lost interest in institutional food, where one breakfast may be just like another? Recall is not some mechanical process like recovering files from a computer disk, but involves active and interested work on the part of the individual.

Smart drugs are supposed to work in one of two main ways: either by increasing blood flow to the brain, or boosting the levels of one or other of the neurotransmitters thought to play a part in learning and memory. Such drugs are sometimes called ``nootropics'', a term coined by the pharmacologist Cornelius Giurgea in the 1970s from the Greek meaning acting on the mind. To qualify as a nootropic, Giurgea argued, a drug had to:

[Smart drugs work in many ways.]

Enhance learning and memory, especially under conditions of disturbed neural metabolism resulting from a lack of oxygen, electroshock or age-related changes
Facilitate information flow between the cerebral hemispheres
Enhance the general resistance of the brain to physical and chemical injuries
Be devoid of any other psychological or physiological effects
These criteria, though still quoted with zeal by smart drug enthusiasts today, seem absurdly vague by the standards of mainstream neuroscience. I am not sure, for instance, what is meant by ``facilitating information flow between the cerebral hemispheres'', or how to check that it was happening.

[The fact that he does not understand is sad and shows he has little understanding of the brain and did little research.]

The rationale to the belief that agents which affect blood flow or neurotransmitter levels could function as smart drugs came first from research into the effects of stroke.

[Untrue.]

Stroke is one of the common causes of neurological damage in elderly people affecting many aspects of performance including memory and cognition. The damage is often cause by constriction of the arteries supplying blood, and hence oxygen and glucose, to the brain. Therefore, drugs which increase cerebral blood flow and diminish hypertension might be expected to ``improve the performance'' of otherwise energy-starved neurons. This is why propanolol, phenytoin or hydergine are used as smart drugs.

[Phenytoin has little effect on blood flow.]

The second reasoning came from work on the neurochemical deficits in Alzheimer's disease.

[No one I know in the field of Nootropics has these views or “reasonings”.]

One of the characteristic features of Alzheimer's is progressive loss of memory. Postmortem studies of the brains of Alzheimer's patients show a dramatic destruction of neurons, and particularly neurons which secrete or utilize the neurotransmitter acetylcholine. During the 1970s, research with animals also suggested that acetylcholine might be a key neurotransmitter in memory formation; for instance drugs such as scopolamine, which deplete brain acetylcholine also impair memory. In the early 1980s these observations gave birth to the ``colinergic hypothesis'' of memory loss. And if loss of acetylcholine was responsible for memory loss, why not attempt to increase the brain's supply of acetylcholine? In the wake of this argument came one of the first proposed smart drugs, piracetam, along with food additives which are potential metabolic precursors of acetylcholine, such as choline and acetlcarnosine.

[Again with the food additives? Many Factors effect memory Ach merely plays an important role.]

Despite the focus on the role of acetylcholine, nobody seriously believes that any one neurotransmitter dominates the complex processes that underpin cognition and memory. So the search for smart drugs has broadened to include agents that interact with other neurotransmitters, including glutamate, serotonin (5-HT) and dopamine.

[I agree with this statement, this is why many nootropics that has different effects can effect memory. Because memory is a multifaceted process.]

Another class of potential smart drugs are the calcium channel blockers. These, such as verapamil, diltiazem, nifedipine, nitrendipine and nimodipine are not only widely used to treat hypertension, and hence might affect cognition by increasing cerebral blood flow, but also block the entry of calcium ions into neurons. A key stage in the molecular cascade of memory formation appears to be the opening of membrane channels through which calcium ions flow. In old laboratory rodents, the mechanisms that open and close these calcium channels seem to become defective, and so calcium accumulates at dangerous levels inside the cells. The calcium channel blockers might improve memory by countering this effect. Ginseng, that all-purpose elixir of life, contains an agent that blocks calcium channels.

There is some evidence that calcium channel blockers, glutamate agonists, 5-HT antagonists and certain piracetam derivatives can help laboratory animals learn highly specific tasks if the agent is injected around the time of training. Yet in many cases, it is clear [sic; not?] how the drugs act in animal tests. Some may work by interfering with the molecular events leading to memory; others by affecting the animal's general level of physical activity. Testing memory in non-humans presents nearly as many ambiguities as studying it in humans.

[Calcium channels blockers can have some positive effects on memory, but I do not consider them nootropics. While we do not have the current tech to know exactly how memory works or in exact detail nootropics, we do know many nootropics can help us now without side effects of serious nature. Nootropics generally have multiple actions on the brain.]

A popular approach is to measure how effective a drug is in helping rats and mice their way around mazes. In some of these mazes, the animals must run down a series of ``arms'' fanning out from a central area in search of food. Other mazes consist of a large tank of water with a submerged platform, which animals must learn to swim towards and clamber on to to ensure safety. A different kind of test relies on ``passive avoidance.'' If a rat is placed on a narrow shelf above the floor of its cage, its normal tendency is to step down; if the animal is given a mild electric shock every time it does so, however, it will learn to stay put.

Alleviating amnesia

Clearly, such tasks involve many other aspects of performance than merely learning and memory. Drugs that alter sensations of hunger or thirst, or reduce sensitivity to pain, or simply make an animal more active could all improve performance. In some cases animals are trained on tasks and then made amnesiac either by electric shock, or, in one popular test, by administering scopolamine to deplete acetylcholine. Something may be considered a potential smart drug if it can alleviate this kind of amnesia in animals. But there is an obvious flaw: the drug may not necessarily work on less artificially induced amnesia.

There are many other problems with animal studies of smart drugs. The drugs are usually administered by injection, sometimes into the brain, and often at very high doses. In some studies reporting a positive effect on learning, drugs were injected at doses equivalent to inject a human with about 8 grams of the drug. Taken orally, as all smart drugs are, this might scale up to as much as 40 grams - scarcely a realistic proposition. Although it is standard practise in reputable pharmacological papers to publish dose-response curves for any proposed agent, the smart drug literature is remarkably coy on this point. At best two or three concentrations of the drug are tested, often without discernible dose-related effects.

[Untrue again in many studies Nootropics doses do make a difference.]

Studies of smart drugs on human patients are much rarer but no less contentious. Most involve patients in hospitals or other institutions, frequently diagnosed as suffering from Alzheimer's or cerebrovascular disease. Many of the trials are based on small samples of patients, less than 10 in each of the drug and placebo groups. A sizeable number of the human studies come from trials carried out in the south of Italy where the ethical controls and statistical procedures require in British and American trials are often lacking, or at least unspecified. What is more, effects on the patients are often evaluated using subjective criteria. One paper, reporting a study of aniracetam in elderly patients, simply states that doctors and nurses evaluated the drug according to its ``resocialising and revitalizing effects''.

[All countries have differ means of evaluating drugs, I consider the US to be the slowest and unsafest of all countries, all studies are not foolproof, but they are the best we have. Regarding the words most and many is also untrue, this is the problem when you do no research.]

The better research papers supplement such observations with IQ and memory tests, in which subjects try to recall or recognize names or dates associated with past public episodes. Yet often researchers find a drug improves performance in only one or two of a battery of tests. The proper way to avoid error is to then repeat the trial with a different group of patients using only the tests which were found to be significant the first time. I have seen no such reports.

[I agree there are always better ways of conducting tests, but unfortunately few companies’ research drugs in this fashion.]

But even if an experimental drug does help patients with Alzheimer's disease, it may not necessarily be of value to healthy people.

[It may not, but many have shown to do so.]

In addition to suffering memory loss, elderly patients in hospital, especially those with Alzheimer's disease, are often angry, suspicious, anxious or depressed. A drug that reduced such feelings could easily result in an apparent improvement in memory while having no effect on the actual mechanisms of memory.

[This could be true with some people with some drugs. How do you propose we know for sure?]

Clinical trials have yielded some drugs which may be of help in the early stages of Alzheimer's disease. But the claims made by smart drug advocates go far beyond offering treatments for devastating diseases; they offer instant cognitive enhancement to us all.

[This is the most interesting of all his “comments”. No one not even me will say nootropics can or will offer anyone “Instant Cognitive Enhancement to us All”. Why? Everyone is different with all compounds. It’s paramount to saying Lipitor will instantly lower cholesterol in everyone who takes it right away. Now Lipitor is well proven to lower cholesterol in most people in about 3 months. But to go beyond that is meanless and baseless.]

True, at best the research papers on which the claims are based imply that for most of the smart drugs to work, a person should self-administer a massive dose, preferably by intravenous injection, either just before or after learning a particular problem or revising for an examination. Not the most likely of scenarios.

[What? None of the studies on healthy people were injected. Nor a “Massive dose needed”]

But, of course, in addition to claims based on research papers, advocates of smart drugs, such as Dean Morgenthaler, offer personal testimonials as evidence. I am not trying to challenge individual experience and testimony. It is well known that the experience of consuming psychotropic agents varies between individuals, is intensely subjective, depends on mood and expectation, and is often hard to verify by objective scientific criteria. What is abundantly clear, however, is that the primary scientific literature does not justify the claim that smart drugs can be of any therapeutic or ``memory-boosting'' value to healthy humans.

[Actually the weight of evidence, which includes use by doctors and millions of people yearly worldwide show Nootropics are the most important compounds that we have available to use and should be taking if we want to protect our brain, keep it functioning better than normal, and reduce the risk of several neurodegenerative diseases]

Nor should this surprise us. There is no reason to assume that, for most of us at most time, our enzyme and neurotransmitter systems are not working at more or less optimal levels. The brain is well buffered against the effect of arbitrary increases or decreases in circulating chemicals so that simply consuming food additives which are acetylcholine precursors will not normally increase your brain acetylcholine level. And even if it did, increasing neurotransmitter activity is no guarantee of increased mental performance; rather, it can be positively deleterious to throw chemical spanners into the exquisitely balanced biochemical system that is the human brain. More does not mean better.

[Again nootropics work in multiple ways and have shown no deleterious effects]

The smart thing to do with smart drugs is to resist the claim that there is automatically a chemical fix to any or all social or psychological problems. For most of us who believe that we suffer from a weaker memory than we would like, the old training skills offered by the mnemotechnics of the ancients probably stand at least as good a chance of helping us as does the most fashionable molecule-of-the-moment.

[The Smart thing to do if you have memory problems or not, is to do your own research (or talk to people who are in the field of nootropics) into how the brain works and how different nootropics work and decide if you want to protect you brain from day-to-day damage or try to enhance your cognitive abilities. Memory test can help with memory, but they do not affect the various causes of brain aging.]

#10 shpongled

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Posted 07 October 2003 - 06:13 AM

Well, here are my comments, for what they are worth.

[quote]It was not a cheering experience. In magazines, books and newsletters, smart drug enthusiasts cite an impressive string of scientific papers to support their claims. Using these and other papers reporting the results of experiments on prototype smart drugs, I examined well over 100 studies, some on animals, some on people with dementia, some on healthy people. Most of these are either misleadingly quoted by advocates of smart drugs or describe experiments that are poorly controlled or extravagantly overinterpreted by the researchers. Worse, some studies use procedures that would not pass ethical scrutiny in Britain, and the most dramatic claims often appear in unrefereed conference proceedings or obscure journals.[/quote]

He makes 100 sound like a big number. There are tens of thousands of journal articles on nootropics. This means he only sampled a very small amount of the literature. He is correct that it is common for advocates to misleadingly quote these articles. This is not unique to nootropics, it occurs with every commercial or political enterprise. The fact that something is often quoted incorrectly does not yield the original data irrelevant. The same point can be made to his argument that some of the studies were not methodologically sound - "some" does not mean "all," and there is a great deal of research on nootropics in existence that is very sound.

[quote]This brings us to the first fundamental problem with smart drugs. Most people envision them as improving recall. Yet much of the evidence cited by smart drug enthusiasts comes from animal experiments which can, by virtue of their design, test only a drug's effects on learning, not recall. The animals are trained to perform highly specific tasks and the agents given within an hour or so of the training trials. On this basis, the best a smart drug could do would be to increase the likelihood of the transfer of information from the short-term to long-term memory store. There is little evidence than any of today's smart drugs can do even this much in humans.[/quote]

What he doesn't mention is that if you improve acquistion, you are by definition improving the ability to recall the information at a later date. The two go hand in hand. What nootropics don't do is improve recall of information learned previous to beginning the nootropic regimen. Of course, this would be impossible to do, as you either know something or you don't. So his argument is meaningless.

He says "the best nootropics can do is increase the likelihood of transfer of information from STM to LTM." Well, it is well established that many do this, including in healthy humans (I am not going to bother citing references, this information can easily be found). Additionally many nootropics facilitate working memory.

[quote]Indeed, the awesome complexity of human memory makes the smart drug creed look suspiciously simple.[/quote]

Any physiological process is immensely complex, not just memory. And yet we have drugs that can manipulate all of these processes. Memory is complex, that does not mean we cannot improve it, although we may not know exactly what's going on to the letter, we can determine the end result.

[quote]It is founded on two key assumptions. First, memory loss is not confined to patients with conditions such as Alzheimer's disease but happens to us all as we age. Second, this normal ``everyday'' deterioration is caused by a failure or weakening of the same kinds of biochemical mechanisms that break down in conditions such as Alzheimer's disease. To believers in the faith, the corollary is obvious: drugs developed for patients with senile dementia ought to be made available to the rest of us so that we can crank our memories up to maximum speed and capacity.[/quote]

Nootropics do not just prevent or reduce memory loss, they improve memory. Drugs that are specific to dementia often will not work in healthy individuals, but often drugs that improve memory in those with cognitive impairment will do so in healthy individuals as well, as they are not necessarily condition-specific.

[quote]The first of these assumptions is by no means confined to smart drug advocates. In the US, a vociferous school of thought claims there is a clinically definable condition called Age Associated Memory Impairment (AAMI) - an inexorable loss of memory which, the argument goes, many of us suffer as we move through our fifties. It is true that after the age of 40 performance on standard intelligence tests steadily declines for most people - unless enough time si given to solve the problems. And if speed is taken as the main criterion of memory capacity, then it could be argued that memory grows weaker with age. Yet memory and learning are inextricably bound up with a whole range of other mental and physical abilities. As we age our attention spans, emotions and motivation levels all change. Such effects alone could explain why memory seems to falter and age, without there being any weakening of the molecular and cellular mechanisms of memory itself.

Furthermore, decline is not inevitable. A recent Dutch study from the University of Limberg, Maastricht, has found that memory decline in otherwise healthy people as they age is associated with mild head injury, general anæsthesia or ``social drinking'' earlier in life. In people without such predisposing ``biological life events'', memory remained unimpaired even into extreme old age.[/quote]

Age-related mental impairment is well established. It may happen to varying degrees depending on the person and obviously lifestyle factors make a difference. However it is impossible to be in "perfect" health. Thus anything that is protective against physical and chemical insults is beneficial to a degree.

[quote]It is extremely difficult to design experiments that test the direct effects of drugs on memory when there are so many indirect influences on mental performance. Elderly people living in institutions who cannot remember what they had for breakfast that morning may be able to recall childhood episodes with great clarity. Have they lost memory, or have they lost interest in institutional food, where one breakfast may be just like another? Recall is not some mechanical process like recovering files from a computer disk, but involves active and interested work on the part of the individual.[/quote]

This is why studies are controlled.

[quote]Smart drugs are supposed to work in one of two main ways: either by increasing blood flow to the brain, or boosting the levels of one or other of the neurotransmitters thought to play a part in learning and memory. [/quote]

He obviously did not do his research. Nootropics can have many more mechanisms of action that do not involve either of these processes. Some examples: hormonal changes, neuropeptide changes, altered membrane fluidity, effects on ion channels, changes of enzyme concentrations/activity, increased receptor density and various other changes at the receptor site, and decreasing levels of certain pigments. And that's just off the top of my head, there are many others.

[quote]To qualify as a nootropic, Giurgea argued, a drug had to:

Enhance learning and memory, especially under conditions of disturbed neural metabolism resulting from a lack of oxygen, electroshock or age-related changes
Facilitate information flow between the cerebral hemispheres
Enhance the general resistance of the brain to physical and chemical injuries
Be devoid of any other psychological or physiological effects
These criteria, though still quoted with zeal by smart drug enthusiasts today, seem absurdly vague by the standards of mainstream neuroscience. I am not sure, for instance, what is meant by ``facilitating information flow between the cerebral hemispheres'', or how to check that it was happening.[/quote]

I agree that these criteria are quite vague, but so are the criteria by which we define many other drugs (for example, hallucinogens). Determining the flow of information between hemispheres can be done by EEG.

[quote]And if loss of acetylcholine was responsible for memory loss, why not attempt to increase the brain's supply of acetylcholine? In the wake of this argument came one of the first proposed smart drugs, piracetam, along with food additives which are potential metabolic precursors of acetylcholine, such as choline and acetlcarnosine.[/quote]

Piracetam's mechanism of action is not dependant on cholinergic mechanisms, he does not know what he is talking about. Choline supplementation is not only beneficial by providing substrate for acetylcholine, but phosphatidylcholine and others.

[quote]A popular approach is to measure how effective a drug is in helping rats and mice their way around mazes. In some of these mazes, the animals must run down a series of ``arms'' fanning out from a central area in search of food. Other mazes consist of a large tank of water with a submerged platform, which animals must learn to swim towards and clamber on to to ensure safety. A different kind of test relies on ``passive avoidance.'' If a rat is placed on a narrow shelf above the floor of its cage, its normal tendency is to step down; if the animal is given a mild electric shock every time it does so, however, it will learn to stay put.

Alleviating amnesia

Clearly, such tasks involve many other aspects of performance than merely learning and memory. Drugs that alter sensations of hunger or thirst, or reduce sensitivity to pain, or simply make an animal more active could all improve performance. In some cases animals are trained on tasks and then made amnesiac either by electric shock, or, in one popular test, by administering scopolamine to deplete acetylcholine. Something may be considered a potential smart drug if it can alleviate this kind of amnesia in animals. But there is an obvious flaw: the drug may not necessarily work on less artificially induced amnesia.[/quote]

Of course screening tests aren't perfect, nor does every drug that passes screening prove useful in the real world. But there is a good corellation. Also, many nootropics have been tested in a wide variety of paradigms in a wide variety of conditions with multiple species, which voids these arguments.

[quote]There are many other problems with animal studies of smart drugs. The drugs are usually administered by injection, sometimes into the brain, and often at very high doses. In some studies reporting a positive effect on learning, drugs were injected at doses equivalent to inject a human with about 8 grams of the drug. Taken orally, as all smart drugs are, this might scale up to as much as 40 grams - scarcely a realistic proposition. Although it is standard practise in reputable pharmacological papers to publish dose-response curves for any proposed agent, the smart drug literature is remarkably coy on this point. At best two or three concentrations of the drug are tested, often without discernible dose-related effects.[/quote]

Once again showing that he didn't do his research. The dose-response curves for many nootropics are well established (for example, optimal dosage of piracetam in rats is 100-300 mg/kg, in healthy humans 2.4-4.8 g). Bioavailability can easily be taken into account, and piracetam, for example, is almost 100% orally bioavailable, making the dosage the same whether injected or taken in pill form. Again, he uses the word "sometimes," as though bad methodology in some studies automatically means the same thing in all of them. In this case, we have to dismiss every study ever published on anything.

[quote]Studies of smart drugs on human patients are much rarer but no less contentious. Most involve patients in hospitals or other institutions, frequently diagnosed as suffering from Alzheimer's or cerebrovascular disease. Many of the trials are based on small samples of patients, less than 10 in each of the drug and placebo groups. A sizeable number of the human studies come from trials carried out in the south of Italy where the ethical controls and statistical procedures require in British and American trials are often lacking, or at least unspecified. What is more, effects on the patients are often evaluated using subjective criteria. One paper, reporting a study of aniracetam in elderly patients, simply states that doctors and nurses evaluated the drug according to its ``resocialising and revitalizing effects''.[/quote]

Same as above, you can find poorly done research on any topic. Also, multiple (small) studies with similar designs can undergo meta-analysis, and this has been done in many cases. Small studies with positive results can actually be seen as being more promising, as it takes quite significant results for such studies to have statistically significant results.

[quote]The better research papers supplement such observations with IQ and memory tests, in which subjects try to recall or recognize names or dates associated with past public episodes. Yet often researchers find a drug improves performance in only one or two of a battery of tests. The proper way to avoid error is to then repeat the trial with a different group of patients using only the tests which were found to be significant the first time. I have seen no such reports.[/quote]

This problem is not unique to nootropics, it can be seen with any class of drug. Many studies on nootropics improving certain clinical subscales have been replicated.

[quote]Nor should this surprise us. There is no reason to assume that, for most of us at most time, our enzyme and neurotransmitter systems are not working at more or less optimal levels. The brain is well buffered against the effect of arbitrary increases or decreases in circulating chemicals so that simply consuming food additives which are acetylcholine precursors will not normally increase your brain acetylcholine level. And even if it did, increasing neurotransmitter activity is no guarantee of increased mental performance; rather, it can be positively deleterious to throw chemical spanners into the exquisitely balanced biochemical system that is the human brain. More does not mean better. The smart thing to do with smart drugs is to resist the claim that there is automatically a chemical fix to any or all social or psychological problems. For most of us who believe that we suffer from a weaker memory than we would like, the old training skills offered by the mnemotechnics of the ancients probably stand at least as good a chance of helping us as does the most fashionable molecule-of-the-moment.[/quote]

One cannot define "optimal," one can define "better" or "worse." The idea that we cannot constantly improve is absurd, there is always room for improvement, and humanity is by no means perfected. He is completely correct that it is not so simple as increasing neurotransmittor levels, but I discussed this above. The "quick fix" argument is a problem with people, which does not deny the efficacy of these substances.

I skipped some stuff, but addressed everything.

#11 gustavo

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Posted 07 October 2003 - 12:24 PM

Thanks so much, LifeMirage and Shpongled! Your comments do help me put Rose's article in a different perspective.

Gustavo

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#12 LifeMirage

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Posted 08 October 2003 - 01:22 AM

shpongled, great reply.




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