dopamine | ADHD Information
Actually it's 2 months on, 1 week off for my med holidays. I can't always manage it that way and have to alter to fit my rotating shifts and the overtime but generally I do my best.
Maxdad I guess you are partially right. I do tend to use the board to journal my path through life with ADHD. But I tend more to think of it as doing my best to help others see that they are not alone. Also I log my goofs and falls so that when I speak of the success they can see that there is no perfect solution. I still feel the urges and the tendencies to slack or make mistakes. I'll always have to work at this so it's no free lunch. But then nothing worthwhile in life is free is it?
and MaxDad - i don't know if you do this but i think it is really sensible to take 'med breaks' ---- i think that helps enormously with not developing tolerance. GlenW has a system i think of one month on a week off (or maybe two/three months i don't remember).here is what one posting on a site said - briefly:
If Adderall were to be used long-term, it would be best to be cycled. Use of NMDA receptor antagonists would be a good idea as well so as to limit the strucutral neurological damage that can occur with chrontic amphetamine use. Repeated use of catecholamine precursors would be essential as well.
(whatever that means - it sounds like he knows what he is talking about but it is the internet.... so you can never be sure that he is not just a complete idiot who knows some long words....)
chjones38847.4958217593
Thanks ch. Good advice. I've considered med holidays. However, just the thought of living a few days in the fog of ADD really brings me down. I'll have to give it some thought.
I also like your idea about a poll. Especially since my profession is market research! LOL I actually have considered conducting a research study on some aspect of ADD with the thought that the findings could be used to develop greater awarness among the public and medical community.
At times I feel like we (adults w/ ADD) are lost in the media hype about our disorder and the treatment strategies used.
[quote]the negative thing about this board - is that the only people who stay here (i think - oops sorry everyone) are those that the meds don't really help 100% so they are still stuck in some sort of glitch - or non-ADDers who have children who are ADD. or those who are trying alternative/complementary methods which take more time. [/quote]
I would add another group -- those that are being treated successfully but find the board a way to "journal" and cope with the everyday aspects of living w/ ADD.
Regardless of the reason, it's also a chance to meet nice folks like yourself! :-)
perhaps you could start a poll/post here. asking whether others thought they developed a tolerance.the negative thing about this board - is that the only people who stay here (i think - oops sorry everyone) are those that the meds don't really help 100% so they are still stuck in some sort of glitch - or non-ADDers who have children who are ADD. or those who are trying alternative/complementary methods which take more time.
but you see people come on here, when they are just starting with the meds and then they never come back (hahahaha because they got a life, at last). which is great. but it slightly means that any poll/post is liable to be skewed. all the people for whom the meds are working fantastically just aren't here any more - i'll exclude glen from that.
they have better things to be doing with their time - like living.
still no harm in asking i guess - as long as one is aware that the data sample is a bit skewed in the first place!
wow! Thank you so much for sharing chjones. This was particularly meaningful to me. I have a son who is rather uncoordinated, has a learning dissability that while not diagnosable as Dislexia , closely mirrors it. He also has many difficulties with focus, attention and impulsivity. This study has opened my eyes to the possibility of one singular cause of his dificulties. I will be putting him on a better EPA/DHA supliment ASAP
thanks spaz for the kind words --- i am sure fish oils are very helpful but i would use them in addition to all the other forms of treatment and accommodations etc. that your ped/psych recommends.
all these studies are in their infancy and so much of the research is still going on -
it is all a bit trial and error to see what works best for you/your son. i only just started looking on the internet about it today, i find it very interesting and am not sure yet what conclusions, if any, i have come to - good luck!
as i'm on the topic - here's some more about fish oils:
Fish oils may help dyslexic children
GUILDFORD, UNITED KINGDOM. Dyslexia is a fairly common condition which involves difficulties in
learning to read and write, mirror reversals of letters and words, and poor short-term memory. Dyslexia
is closely related to dyspraxia (problems with coordination and muscle control) and attention-deficit
hyperactivity disorder. It is estimated that about 10% of the populations of the United States and the
United Kingdom suffer from dyslexia and 4% are severely affected. There was a 3-fold increase in the
prevalence of learning disorders in the USA over the period 1976 to 1993 and 80% of the new cases
involved dyslexia.
Dr. Jacqueline Stordy of the University of Surrey believes that dyslexia, dyspraxia, and attention-deficit
hyperactivity disorder have one common denominator - a deficiency of long-chain fatty acids. She points
to a study which found improved dark adaptation (a problem among dyslexics) after supplementation with
480 mg/day of docosahexaenoic acid (a main constituent of fish oil) for a month. Another study involving
15 dyspractic children found that supplementation with a proprietary mixture of tuna oil, evening primrose
oil, thyme oil, and vitamin E for 4 months markedly improved their motor skills. The mixture provided 480
mg of docosahexaenoic acid, 35 mg of arachidonic acid, 96 mg of alpha-linolenic acid, 80 mg of vitamin
E, and 24 mg of thyme oil daily. Dr. Stordy concludes that long-chain polyunsaturated fatty acid
supplements may benefit children with dyslexia, dyspraxia, and attention-deficit hyperactivity disorder and
notes that large, double-blind, placebo-controlled studies are already underway to verify this hypothesis.
Stordy, B. Jacqueline. Dark adaptation, motor skills, docosahexaenoic acid, and dyslexia. American
Journal of Clinical Nutrition, Vol. 71 (suppl), January 2000, pp. 323S-26S
Your brain needs DHA
NEW YORK, NY. Dr. Barbara Levine, Professor of Nutrition in Medicine at Cornell University, sounds the
alarm concerning a totally inadequate intake of DHA (docosahexaenoic acid) by most Americans. DHA is
the building block of human brain tissue and is particularly abundant in the grey matter of the brain and
the retina. Low levels of DHA have recently been associated with depression, memory loss, dementia,
and visual problems. DHA is particularly important for fetuses and infants; the DHA content of the infant's
brain triples during the first three months of life. Optimal levels of DHA are therefore crucial for pregnant
and lactating mothers. Unfortunately, the average DHA content of breast milk in the United States is the
lowest in the world, most likely because Americans eat comparatively little fish. Making matters worse is
the fact that the United States is the only country in the world where infant formulas are not fortified with
DHA. This despite a 1995 recommendation by the World Health Organization that all baby formulas
should provide 40 mg of DHA per kilogram of infant body weight. Dr. Levine believes that postpartum
depression, attention deficit hyperactivity disorder (ADHD), and low IQs are all linked to the
dismally low DHA intake common in the United States. Dr. Levine also points out that low DHA levels
have been linked to low brain serotonin levels which again are connected to an increased tendency to
depression, suicide, and violence. DHA is abundant in marine phytoplankton and cold-water fish and
nutritionists now recommend that people consume two to three servings of fish every week to maintain
DHA levels. If this is not possible, Dr. Levine suggests supplementing with 100 mg/day of DHA.
Levine, Barbara S. Most frequently asked questions about DHA. Nutrition Today, Vol. 32,
November/December 1997, pp. 248-49
Hyperactive children lack essential fatty acids
WEST LAFAYETTE, INDIANA. Children suffering from attention-deficit hyperactivity disorder (ADHD) are
inattentive, impulsive, and hyperactive. Researchers at Purdue University now report that hyperactive
children have lower levels of key fatty acids in their blood than do normal children. Their experiment
involved 53 boys aged 6 to 12 years of age who suffered from ADHD, but were otherwise healthy and 43
matched controls. Analyses showed that the boys with ADHD had significantly lower levels of
arachidonic, eicosapentaenoic, and docosahexaenoic acids in their blood. The hyperactive children
suffered more from symptoms associated with essential fatty acid deficiency (thirst, frequent urination,
and dry hair and skin) and were also much more likely to have asthma and to have had many ear
infections. The researchers conclude that ADHD may be linked to a low intake of omega-3 fatty acids
(linolenic, eicosapentaenoic, and docosahexaenoic acids) or a poorer ability to convert 18-carbon fatty
acids to longer more highly unsaturated acids. The researchers conclude that supplementation with the
missing fatty acids may be a useful treatment for hyperactivity.
Stevens, Laura J., et al. Essential fatty acid metabolism in boys with attention-deficit hyperactivity
disorder. American Journal of Clinical Nutrition, Vol. 62, No. 4, October 1995, pp. 761-68
[quote=chjones]do ADDers have faulty levels of dopamine - if so, can that be tested. the way they seem to be able to see the lack of dopamine in Parkinson's patients?[/quote]
Reading the article I didn't see a reference to a test for dopamine levels, just observational results. I could be mistaken, but I don't think there are tests that can determine a brains ability to produce and uptake neurotransmitters. I do know that there are encouraging tests being developed with brain scan imaging -- however, these show neural activity versus the level of a particular chemical.
Neurons containing the neurotransmitter dopamine are clustered in the midbrain in an area called the substantia nigra . In Parkinson's disease, the dopamine- transmitting neurons in this area die. As a result, the brains of people with Parkinson's disease contain almost no dopamine.i don't know i thought that the above was maybe something they could actually SEE or test for rather than deduce from the symptoms. but that might not be the case, it might just be, as you say, observational results. too bad.
chjones38846.475787037
chjones,
First post, and I'm having a bad couple of days with meds, so bear with me if I start to ramble. It will get to an end, I promise. Also, apologies if I repeat anything you know already.
First, I have to say I'm really dubious of the UK studies for US AD/HD purposes. Dyslexia is a different diagnosis in the UK, where it serves as a blanket term much like our "learning disability". In the States it refers to a specific disorder, where the dyslexic has specific reading difficulties. Dyspraxia usually seems to refer to the US diagnosis "non verbal learning disability." I never encountered, for instance, anyone diagnosed as "dysgraphic." I did know one guy who had specific problems with maths, and he was diagnosed as dyslexic, not dyscalculic as he would be in the US. I never met anyone diagnosed AD/HD in the UK, though they're clearly out there.
When I was a grad student in the UK, I was having real problems with attention and reading. At first I was sent to psychoanalysis four times a week because it was assumed after a three minute meeting I was just depressed and repressing childhood memories. After six months and no improvement, I took matters into my own hands. I saw a neuropsych (one of only 6 or 7 accepted by my uni) for testing (WAIS). He found that, while I had high verbal and perceptual organisation scores, my working memory was somewhat impared and my speed of processing was significantly below average. His interpretation was that I struggled to remember what I had read, that I had difficulties remembering what I wanted to write or say in my head, and that my fine motor coordination (handwriting) was particularly impared. Bottom line, I couldn't write quickly, read effectively, or write/plan quick and sensible essays. According to him, this was due to a lack of neurological development. The diagnosis was dyslexia.
Back in the States, I sought a second opinion three years later, as I continued to struggle with attention and motivation. This time I saw an expert on attention disorders. The results were through the roof. I told him about the UK diagnosis, and he just rolled his eyes, and declared it a very odd way to explain things to me. What he did explain was that the WAIS results I had were more suggestive of an attention deficit. Simply put, the chemical transportation system in my brain was screwy, so thoughts couldn't get from one place to another. Hence the problems remembering what I had read, getting thoughts onto paper, and getting my hand to write quickly and precisely. The more complicated explanation is this:
Attention deficits are currently thought to be caused in much the same way depression is. That is, your brain has millions of neurons that shoot out certain chemicals (neurotransmitters) when it wants to convey a message to other neurons, which then soak up most of the chemical. This happens like twelve time a second, and any chemical not soaked up by the second neuron is reabsorbed by the first. In certain brains this process doesn't happen correctly, the chemical doesn't seem to pass over and gets taken back in (reuptake) by the original neuron. In brains that are depressed, the chemical involved is called Serotonin. In the AD/HD brain it is thought there is a problem in the transmission of both dopamine and norepinephrine. Because of this, the AD/HD brain is unable to communicate an impulse to focus on one thing and ignore distractions. As a result, the executive functioning system of the brain is short circuited by too much input. Studies have suggested that the AD/HD brain has 70% more receivers for those two chemicals, leading researchers to speculate those brain are trying to get more of the neurotransmitters through. It is very clear that there is significantly less brain activity in people suffering from AD/HD, particularly in the frontal lobes. However, there is no way to effectively measure the dopamine tranmission mechanism in a brain.
What does this have to do with Adderall? Stimulant medications are thought to work because they block the process where the dopamine and norepenephrine are taken back into the original neuron (like Prozac blocks serotonin). Thus they sit in the gap between the brain cells longer, and more of it gets through to the second neuron. The result is that the AD/HD brain, when given psychostimulants actually is able to function more like a normal brain. For the AD/HD person, this means they calm down and can stay on task. This is why doctors say stimulants are effective for AD/HD: If they calm you down, it's pretty certain there's something wrong to begin with. Stimulant meds are not just a relief for the ADDer, they are also partly diagnostic.
So where do omega-3s come into it? This is entirely speculation based on my own experience, but I think the UK studies are targeting something entirely different, for both scientific and cultural reasons. I say culture because in my experience, the UK is far more likely to see psychological problems in environmental terms. This is a gross, gross generalisation, I know, but there is an emphasis on talk therapy and an aversion to meds there. The science bit? No one really knows what causes LD, but I have read that specific learning disabilities are possibly related to areas of the brain being under developed. There is also a possible link between a poorly developed frontal cortex and attention/hyperactivity problems. What I do know is that dyslexia is a catch-all phrase in the UK, so I suspect their fish oil studies are looking at things very broadly, and what they target is the role omega-3 fatty acids play in healthy brain development. This might help promote better psycological health in general, and specifically aid persons with learning diabilities or hyperactivity/frontal cortex problems. I think it's interesting that the Oxford study (on my quick reading) seemed to focus on hyperactivity. Does it say anything about inattention and impulsivity? Is it possible that the fish oils do not aid dopamine transmission?
Bottom line, people should be aware they have a life long disorder and use the remedies they find work best. They also shouldn't take anything they feel entirely uncomfortable with. But, to answer your original question, both Adderall and fish oils are chemicals. There is no way to avoid the chemical side of AD/HD or LD because they are chemical processes/differences that happen within the brain. Is it possible the two are affecting different things? Stimulants promote the transmission of dopamine and norepineprine (the specific AD/HD problem), while fish oils develop the basic structure of the brain itself, which improves behaviour and learning?
Wow, that did ramble. Did that help in any way? Or am I just completely wrong?
Forgot to mention, the dopamine transmission deficiency is thought to be why so many ADDers end up using drugs: when they experience the high, the brain craves it because it is providing something normally missing. That would be why ADDers with stimulant scripts end up using drugs less than those who don't. It's also why people with ADD can sleep when on Adderall: the brain is just fuctioning better, and the running commentary gets shut up.[quote=mrdarcey]Wow, that did ramble. Did that help in any way? Or am I just completely wrong?[/quote]
Darcey
That's one of the most insightful and well-explained posts I've read on these board related to meds and the brain. Welcome to the board and keep posting.
MaxDad
[QUOTE=chjones]so roughly speaking, what we have is more than enough receptors but very faulty uptake probably. thanks. [/QUOTE]
Well, it's one theory. It just happens to be the one I buy. Of course, it's also the one my psychologist is trying to advance, so...
http://www.drthomasebrown.com/brown_model/index.html
http://www.drthomasebrown.com/research/index.html
[QUOTE] what i don't understand is if the brain is actively looking to get more dopamine by creating extra receptors why then, do some people still build up a tolerance. why would the brain then delete the amount of receptors in order to maintain what they call a homeostasis - taking them right back to an abnormally low level of dopamine again. [/QUOTE]
I'm not sure it has to do with the receptors. I thought I read somewhere that there was some problem in the original transmittor adjusting the levels of dopamine it produces downward because it is no longer getting back what it used to put out, and the dopamine sits longer in the neural gap. Please don't quote me on that, though, as I've no idea where I read that and can't remember the specifics of it. I've also read I'm exremely inattentive... 
[QUOTE] i actually don't know what properties something has to have in order to be given the term 'drug'[/QUOTE]
Look no further. From quackwatch.org:
"Federal law states that any product (except a device) intended for the diagnosis, prevention, or cure of disease is regulatable as a drug and that it is illegal to market new drugs that have not been recognized by experts as safe and effective for their intended purposes."
[QUOTE] but i remain fairly addled - and am looking to develop some sort of iron-cast self will/discipline in order to be able to combat my sloth/apathy! as opposed to a chemical remedy at the moment.[/QUOTE]
I've heard of this discipline and will power of which you speak. Interesting concept...
and why should the fact that it is receiving less back make it think that it was a good idea to then put less out.... unless it is just being difficult (which wouldn't surprise me with my brain, it hates me). it is not a particularly logical reaction, is it - it might just as well put out more or the same.
or is what you are saying - in the ADD brain, the transmitters are so used to the receptors being faulty and therefore the transmitters receiving back pretty as much as they put out (in which case, you could ask them why bother transmitting anything in the first place dopey git - exercise in futility isn't it) that they have adjusted themselves to this scenario so much and like it so well that they insist on that being the correct mode of being. and will re-adjust the levels to keep it skewed in this way (even though that is faulty logic and will not result in them necessarily getting back the same amount as they put out - they will just put out less and receive even less back, providing the adderall is still blocking re-uptake) so the re-adjustment is a flawed solution which can probably only exacerbate the problem the receptors then being more likely to absorb EVERYTHING and give nothing back at all - the quantities being so minimal.
no, it seems more likely that it is not the transmitters that are at fault or adjusting - but the receptors. it is the receptors who don't absorb what they ought to isn't it (or is it the transmitters who don't produce enough but then blocking re-uptake wouldn't do any good as the quantity would remain insufficient)... and it is probably the receptors that when they get the correct quantity by force almost (ie it has nowhere else to go but the synapse or them) readjust the quantity to a lower amount by simply diminishing the amount of receptors available.
i think i may have confused myself... anyway - thanks v. much for all the info. you are far better and quicker than numerous internet searches! hurrah. will go and read your doctors theory now...
i like the quackwatch definition! just be sure you never market a lemon as a cure for scurvy or you could be in big trouble (that is unless it is already regulated as such - perhaps it is)!
chjones38849.7023611111i don't know why i am posting this here - it has nothing to do with ADD really
but on my vague roundabout way of looking at these things and stims in general - i came across a sort of history of cocaine and i thought it was interesting (although it still doesn't really explain entirely - why it was banned only mentioning drug-crazed soldiers in 1916... and i would have thought conditions at the front were more likely to make you crazed). i hope nobody is offended but if they are i am very happy to delete the post - just post below if you want me to take this off...
i just wanted to find out WHY it was made illegal in the first place. and i guess it must have been due to the addictive qualities. although that is not spelt out here.
Drug That Spans The Ages: The History Of Cocaine By Paul Vallely
I blame the pope. Not the new one. Not the old one either. But one called Leo XIII back in the 19th century. He didn't just take cocaine. He advertised it, appearing on a poster having awarded a Gold Medal to the manufacturer of the "tonic" he carried in a personal hipflask to fortify himself in those moments when prayer was insufficient.
There is, as we shall see, a direct line from His Cokiness to the news that more people in Britain have tried cocaine than anywhere else in the world, according to the announcement by the International Narcotics Control Board yesterday.
Of course, you could go back further than Leo XIII and blame the Incas. The original inhabitants of the area which still produces three-quarters of the world supply -- Colombia, Peru and Bolivia -- chewed the coca leaf for thousands of years.
Officially, coca was reserved for Inca royalty but as archaeological relics of sculptures and ceramics show, it was widely used for mystical, religious, social and medicinal purposes. It was chewed not merely for its stimulant properties -- which warded off fatigue and provided the energy and strength necessary for steep walks in the thin air of their mountainous homeland -- but as a kind of food, for there are vitamins and protein present in the leaves.
The conquistadors didn't like the look of it. Initially the Spanish invaders banned coca as "an evil agent of the devil". But then the incomers discovered that, without what the natives called their "gift of the gods", the locals could barely work the fields -- or mine gold. Suddenly, coca was not only legalised but taxed, with the occupiers taking a tenth of every crop. Coca leaves were distributed three or four times a day to the workers during their breaks. And the Catholic Church began even to cultivate it.
But the leaves did not travel well, so only occasional supplies
were transported to Europe, though tests on 17th century pipes
found in Shakespeare's garden a few years back are said to have
showed up cocaine residues.
By the Victorian era, however, they were on top of the technology. In 1863 an Italian chemist named Angelo Mariani brought onto the market a wine called Vin Mariani which had been treated with coca leaves. He first tried his new tonic on a depressed actress. The results were spectacular. The ethanol in the wine acted as a solvent and extracted the cocaine from the leaves -- creating a compound called cocaethlyene that hugely reinforced the impact of both drugs, much as it has in the systems of Kate Moss and her fellows.
Vin Mariani contained 11 per cent alcohol and 6.5 mg of cocaine in every ounce, which is presumably why Leo XIII gave it his gold medal. He was not the only one.
Writers loved it. Henrik Ibsen, Emile Zola, Jules Verne, Alexander Dumas, Sir Arthur Conan Doyle were all mad for it. Robert Louis Stephenson wrote The Strange Case of Dr Jekyll and Mr Hyde during a six-day cocaine binge. Royalty were enthusiasts. Queen Victoria, King George of Greece, King Alphonse XIII of Spain, the Shah of Persia and US presidents William McKinley and Ulysses S. Grant all knocked it back.
The polar explorer Ernest Shackleton took a similar product in tablet form to Antarctica, as did Captain Scott with less happy results. Auguste Bartholdi said that if he had taken Vin Mariani beforehand he would have designed the Statue of Liberty several hundred metres taller. In addition to the general feeling of well-being it induced it was also said to be "a most wonderful invigorator of the sexual organs" -- not a feature which is mentioned in the papal endorsement.
The world's best known coca drink, however, came later. A pharmacist in Atlanta named John Pemberton had made his own coca wine. But when Prohibition outlawed alcohol in the States he had to replace the wine in his recipe with sugar syrup.
He renamed it Coca-Cola: the temperance drink "offering the virtues of coca without the vices of alcohol" and marketed it as the perfect beverage for a "turbulent, inventive, noisy, neurotic new America." Pemberton's ads touted it as "an intellectual beverage" which was "one of the most delightful, cheering, and invigorating of fountain drinks." Very invigorating. Every bottle contained the equivalent of a little line of cocaine.
By that time, cocaine was being sold over-the-counter. In Sears & Roebuck in the US they were, in 1900, selling a Peruvian Wine of Coca which "sustains and refreshes both the body and brain ... may be taken at any time with perfect safety". Cocaine was widely used in toothache cures and patent medicines -- one, Ryno's Hay Fever and Catarrh Remedy, was 99.9 per cent pure cocaine.
In London in 1916, Harrods were selling a kit described as "A Welcome Present for Friends at the Front" containing cocaine, morphine, syringes and needles.
What enabled all that was the development of a technique to isolate the cocaine alkaloid from the leaf. A method was perfected by a German PhD student named Albert Niemann which distilled a crystalline tropane alkaloid from the leaves of the plant. That refined version of the drug brought the user an exhilarating rush by, in effect, tricking the brain into thinking it's been furnished with something pleasurable.
Like heroin and nicotine it taps into the brain's natural reward pathways bringing an enhanced awareness, self-confidence, feeling of strength and sexual prowess.
The effect thrilled the greatest minds. Sigmund Freud in 1884 published Uber Coca in which he wrote cocaine brings: "exhilaration and lasting euphoria, which in no way differs from the normal euphoria of the healthy person ... In other words, you are simply normal, and it is soon hard to believe you are under the influence of any drug ... Long intensive physical work is performed without fatigue ... This result is enjoyed without any of the unpleasant after-effects that follow exhilaration brought about by alcohol ..."
The more rapidly it is ingested the swifter and more dramatic
the effect. So much so that Arthur Conan Doyle had Sherlock Holmes
describe cocaine as "so transcendentally stimulating and
clarifying to the mind that its secondary action is a matter
of small moment".
However, nature, in the words of
one reformed drug-taker, is cruelly parsimonious with pleasure.
The greater the high, the greater the crash when the brain realises
the trick that has been played on it.
Moreover, various doses of cocaine can also produce neurological and behavioural problems including dizziness, headaches, movement problems, anxiety, insomnia, depression and even hallucinations.
Because cocaine stimulates the cells of the central nervous system and the cardiovascular system, in the hour after cocaine is used, the risk of a heart attack rises 24-fold. And many of Freud's patients, to whom he recommended cocaine for a variety of illnesses ended up addicted to cocaine too.
As the century turned, so did the tide of opinion on cocaine.
Its addictive properties had become clear. Cocaine began to appear
in literature as a vice. The pendulum swung in the direction
of moral panic.
In 1904, the manufacturers removed the cocaine from Coca-Cola. The US Government tried to compel the company to change the name of the drink but, after protracted legal argument, the name was saved. The Coca-Cola Company is still sensitive on the subject. Its museum in Atlanta still does not mention the beverage's legacy from the magic bush from Peru, even though the drink is still flavoured with an extract of coca-leaves from which the drug has been removed.
But it persisted among the smart set through the 1920s and 30s. For all Cole Porter's insistence "I'm sure that if I took even one sniff, That would bore me terrific'ly too" he was a user. So was the author William S. Burroughs and the actress Tallulah Bankhead who famously quip-ped: "Cocaine habit-forming? Of course not. I ought to know. I've been using it for years."
Even so, cocaine was, in the decades that followed, overshadowed
on the black market by synthetic stimulants such as amphetamine.
And with the search for greater highs have come greater dangers. Cocaine that is smoked reaches the brain in about five seconds, giving a rush which is much more intense than taking the same amount of cocaine in through the nose. A solvent like diethyl ether can be used to allow the drug to be smoked "freebase".
Cocaine is what pharmacologists call "highly reinforcing". Experiments with animals demonstrate this. When it is made available to mice they will administer it themselves. Indeed they will put up with electrical shocks, and give up food and water, to get the drug.
The evidence is that cocaine is about as addictive as alcohol
but that more users -- about 50 per cent -- end up with an addiction
problem. The trouble is there is no way to predict which 50 per
cent -- - "everyone starts off using cocaine in a non-dependent
fashion," says Dr Adam Winstock of the National Addiction
Centre, "Nobody thinks they'll end up in a dependency unit
in five years." Cocaine dependency develops after about
three years of steady use.
Most recreational users reassure themselves they will not venture into these dodgier areas. They simply pass a china side plate lined with lines of white powder -- " a row of sherbet soldiers" as one regular user put it -- around the table after dinner as their grandparents would have circulated the port, or their parents might have passed a joint.
Many of them will take the same amount over extended periods and not become addicted.
But for some there comes a point when their recreation becomes a preoccupation and then an obsession. Most of their money will go on the drug. Most of their time will be spent thinking about how to get hold of it. Family, friends and workmates will become increasingly alienated by their behaviour. The journey to dependency is an easy carefree path. The one out of it can be a far more difficult uphill struggle.
In Demand Chewing coca leaves became widespread through South America three thousand years ago. The plant was believed to be a gift from God Restoration poet Abraham Cowley was the first to introduce cocaine into literature, with a 1662 work entitled 'The Legend of Coca' Merck, now one of the world's biggest pharmaceutical companies, began manufacturing cocaine in the 19th century as demand surged for tonics and medicines containing it Cocaine possession for anyone other than medical personnel was made a crime in 1916, following newspaper reports of 'drug crazed soldiers' fighting in the First World War Seven years ago, the drug cost around UKP 70 for a gram. Now it sells for as little as UKP 35 More than 20,000 tonnes of cocaine were seized by UK customs officers in 2004 The world market in cocaine is estimated to be worth as much as 0 billion a yearchjones38846.9676967593
well cheers mr darcey. yes, yes you did help!!!so roughly speaking, what we have is more than enough receptors but very faulty uptake probably. thanks. (the extra receptors developed to try to compensate for the faulty uptake problem... saved me an awful lot of internet research and as maxdad said nicely put in words of one syllable!). what i don't understand is if the brain is actively looking to get more dopamine by creating extra receptors why then, do some people still build up a tolerance. why would the brain then delete the amount of receptors in order to maintain what they call a homeostasis - taking them right back to an abnormally low level of dopamine again. why? or is that only what would happen in those without ADHD?
still gonna take some time to think about it, nonetheless. but it does explain why i am very happy to take the omegas --- (as weirdly enough i am slightly loath to lose my ADD-ness - although it is a pain in the butt... don't ask
it's just the way my brain is working right now, so i have been staying
away from stims and even the 'crawling exercises' just in case they DO
work!) --- but the omegas probably just create a healthy building
blocks for the brain - well that's fine! and i get your point
that they are all chemicals just some are psychotropic (well i have to
look up exactly what that means) but i think anything that starts
playing around with dopamine levels - is probably what constitutes a
(previously) illegal drug somewhere... i actually don't know what
properties something has to have in order to be given the term 'drug' -
as you say why isn't a banana or fish oil a drug what is the specific
property that makes the one a drug and another not. another
internet search i guess.i've been avoiding the fish oils anyway because i am vegetarian but have tried some omegas from veg sources. and some magnesium too.
but i remain fairly addled - and am looking to develop some sort of iron-cast self will/discipline in order to be able to combat my sloth/apathy! as opposed to a chemical remedy at the moment.
chjones38846.9714814815yes, it has a lot to do with parkinsons, in the sense that dopaminergic neurons in the substantia nigra are closely related with the rewards circuitry of the brain (the nucleus accumbens/amygdala/frontal cortex circuit)
by the way: you guys should wiki the disorder for a complete and informative article about it.
brain physiology is really complicated, and it's only explainable at the biological level. No one really knows how certain behavioral patterns are constructed out of certain neuron sectors and no one really knows why certain stimuli have certain effects on the mind of the person--the ever present mind-brain problem!
so understanding why dopamine is not reuptaken...well, that's almost asking to solve the mind-brain problem, which has been a hot issue for philosophers and neuroscientists for the past 200 years.
The drugs themselves bind to the receptor, obv. The way these receptors work are two-fold: they can produce cascades of information to occur in the cell (metabotropic) or open to let certain ions (Na+, Cl-, Ca2+) into the cell to produce an action potential. The receptor is a big protein with certain grooves for its normal neuropeptide but they can have "seats" that will stimulate the openin or closing of these receptor as well (the ones that let in ions,for example). A good example is the GABA-a receptor, which is the receptor for Gamma-Amino-Butiric Acid, and it lets in chlorine when the receptor is opened by its transmitter. Chlorine has an effect in the cell of "stopping" action potentials--less stimulus--less neurons firing--anxiety down. Now, drugs that can act on the GABA-a receptor: benzodiazepines (valium, ativan, klonopin, etc) and phenobarbitals (more anxiolitics/panic attack medicines). Their mechanisms are different, because the receptor has two "seats" for either benzos or barbitals, as well as the GABA "seat" or "pocket" (or lock, if you think of the transmitter as a key).
Ok, so how do they act? benzos stick to their "lock" or "seat" in the receptor--upon stimulus with GABA, the receptor opens with more frequency--more Cl- goes in--people feel chill.
Similar with barbitals: phenobarbital sticks in its "lock" or "groove" or "seat", and when stimulated with GABA, the receptor stays open for a longer period of time--more Cl- goes in, yadda.
the reason why they cause dependency is because the cells using these receptors get used to the frequency of opening and closing, and so when the benzos are not there, less Cl- than before the person started use goes in, and the person is overall more nervous.
amphetamine is both a potentiator for norepi and dopa, as well as a reuptake inhibitor. when the dopa is released into the synaptic cleft, amphetamine makes the "recycling" system work badly--else the dopa doesn't stay around for long, it gets sucked up in the transmitting neuron. Also, it potentiates a bigger secretion of dopa into the synapsis, so more dopamine floating around, with less chance of being re-cycled, then more chance it will find that channel that dopamine binds to and create the response needed. it's like putting leak-protection in a pipe and making sure that there's extra feeding streams so the conduit is never empty...
did that make any sense?
cocaine is a vasoconstrictor, like a really bad one. It leaves permanent constriction in blood vessels after regular use. that's why people who use coke for long periods of time have bad hearts--their coronary arteries are pooped.
I asked a cardiologist once if it's cool to do coke if you pop some viagra (viagra is a vasodilator--opposite effect). he said no :D
Also, coke creates a psychological dependence that is physical the same way nicotine in cigarettes does. nicotine binds to acetycholine receptors (Ach) in the nervous system and produces a calmin effect, but its use has the same problems as the benzos like I said in the previous post. no nicotine around, the receptors where accustomed to have it, so they open less, less synapsis, less tranquility. if you've ever been around a person trying to quit cigarettes cold turkey you'll agree with me.
sorry I deviated from your post, so I post again and then I realize I didnt answer something!! :)
the transmitter is never absorbed into a receptor, it just opens it. it's like a lock-and-key system...dopamine, acetylcholine, etc...they're not sucked into the receptors, they just open the receptors or 'modify" them so that inside the cell another protein notices "hey, this is a signal" and passes it along.it's really weird to think of it like that but it really is like that. either that or the receptor opens and ions come in. The cell always keeps a balance of ions (Sodium=Na, Chlorine=Cl, Potassium=K, Calcium=Ca) and so an influx/outflux of an Ion causes an electrical response-->action potential-->next neuron, and so on. it's really crazy sh*t...
for example, taking a stimulant: a stimulant can bind to adrenergic receptors. these receptors bind to the amphetamine outside of the cell (say, cardiac muscle cell) and on the inside, it's conformation changes--a lock turns. this creates a change in another protein (PhosphoLipase C) and that activates another protein (pip3) which opens calcium storages. Calcium levels are higher than normal, and the cell contracts more strongly. overall response is of more pumping/harder pumping (increased heartbeat is because of something else). the same thing in the blood vessels in your skin constricts the muscle cells in the vessels-->smaller conduits-->less blood flow-->cold hands (blood transports heat in the body)
keep in mind that is just one of many things that get activated by one drug. it's really hard to know every single detail. with stimulants you also have the whole focusing thing, which is because the drug gets into the brain through the blood and as you showed it increases firing in certain zones (the limbic system) which is associated with completion of tasks/rewards/concentration.
Also it goes all the way to the adrenal gland and stimulates the epithelial cells in the cortex there to produce norepi and epi...and cortisol in the medulla...which then creates even more effects. in short, all of those responses are huge and complicated...
By the way, coke is used in surgery as an anesthetic, just as amphetamines are used to treat narcolepsy and adhd.
also, the body gets used to coke really fast. the rush is supposed to be fantastic. if ritalin turns on a light in your head, and adderall turns on a giant lighthouse, cocaine turns on the whole stadium and the block around it. so people feel more confident and euphoric and love it...so they do it again. by the third time you're doing it, it's already acclimated in your system, so when it wears off it the craving is enormous...that's why coke is so addictive.
I dont know why it's illegal, but it's as illegal as any other drug. why is weed illegal? etc etc.
PS: Freud's patient died of an overdose, which creates extreme sympathetic system excitation so the heart beats like a workhorse and goes into arrythmia really easily...boom, heart attack. and not because of prolonged use.
Sherlock Holmes is killed by his archnemesis, Dean Moriarty, I think. I'm pretty sure he dies in the last book by Conan-Doyle...
Elemental, dear Watson :)
hey kozmik - thanks for that! i'll let my brain process it all for the moment. but thanks really appreciate all the info - it's nice to know what is going on (or what is failing to go on) in my addled brain! cheers
bump
right you are! Mycroft was his name and according to sherlockian.net he was in 2 of the books. His character was rarely used and according to the webpage he was described as intelligent and 7 years his elder - but fat and lethargic rarely going anywhere but his club and home.
Very good memory!
I liked Gene Wilder's playing of him but was definitely not based on doyle's work (I seem to recall they put a notice on at the beginning saying that they very very loosely use doyle's work and was created for comic use rather than to be accurate).
It's been a long time for me too - decades.
Yes he was sick of holmes - I read somewhere he hated writing the books after about the second one (didn't he do them in newspaper format?). He had tried unsuccessfully to kill him off a few times but was thwarted by money LOL.
As for his brother wasn't that a tool used by later writers? I laugh when I remember the Gene Wilder film "Sherlock holmes's smarter brother" and it was and is a classic. Marty feldman was in it too - and I love all his films.
I say testing for anything before drugs is given along with a obsevation. i thought he existed in the books - i think he was called mycroft or something. we were not allowed to watch tv and i remember him as existing (so i can't have got it from any other source but the books - i'm sure).
unless i guess i saw it later and got muddled. it's possible - but i'm pretty sure he was in the books. he almost verged toward the evil though... ah well. memory huh!
hey thanks! i have a good memory - hurrah!
actually they don't use cocaine anymore to my knowledge. They use synthetic derivatives like procaine, novocaine (one of the oldest synthetics) and lidocaine. All slightly modified to do a particular task with nerves. I got novocaine in my finger when I cut it a while back and would love to have them make a whole new group that works better. Ouch.
Oh - sherlock holmes was killed off in the last book. Sort of - a cliffhanger actually. Fell over Reichenbach (sp?) falls with his arch-enemy moriarty. Fans of doyle have written sequels after his death but I stick to the master. I do love the action film "the seven percent solution" with alan arkin as freud. 1976 - based on a Nicholas Meyer film if memory is right.
i thought he fell off the cliff because Conan Doyle wanted to stop writing about him - he was fed up. but then there was such an outcry that he was gently pressured (by his editors and friends i guess) into resurrecting him and Sherlock Holmes miraculously survived the fall.... a year later when the next book came out. there was his even madder, even brighter brother too wasn't there ---it wasn't that - i see (the internet is fantastic). in fact - the hound of the baskervilles was written later but apparently took place before the incident of the falls. so yeah - he died over the falls you're right.
i did have the anthology but i read it when i was about ten and my memory is not quite what it ought to be!
oh well ---
chjones38863.3483912037 [QUOTE=kozmik]yes, it has a lot to do with parkinsons, in the sense that dopaminergic neurons in the substantia nigra are closely related with the rewards circuitry of the brain (the nucleus accumbens/amygdala/frontal cortex circuit)
by the way: you guys should wiki the disorder for a complete and informative article about it.
brain physiology is really complicated, and it's only explainable at the biological level. No one really knows how certain behavioral patterns are constructed out of certain neuron sectors and no one really knows why certain stimuli have certain effects on the mind of the person--the ever present mind-brain problem!
so understanding why dopamine is not reuptaken...well, that's almost asking to solve the mind-brain problem, which has been a hot issue for philosophers and neuroscientists for the past 200 years.
[/QUOTE]
Ok, actually reading the posts, a couple interesting things I knew:
Other drugs are interestingly related to wars. Morphine was made as an anesthesic for soldiers, which then fell into addiction to it. And what do doctors come up with? Heroin haha! Heroin was made to cure morphine addiction...too bad it's much more addictive and destructive, right?
cocaine is really interesting. Freud was a huge coke user, he actually promoted the use of coke with psych patients, and wrote and published a feverish article called "ubercoca", praising its mood elevating effects. then one of his patients died of coke use and...well, he didn't really talk about it anymore.
Sherlock Holmes is a regular cocaine and morphine user, as well as one of the smartest fiction characters ever created. Interesting?
Oh and about the dopamine thing: parkinson's patients are diagnosed by their "tics" not by actually screening to see how much of the substantia nigra neurons are dead. One thing to do with these patients (and I've seen it done, it's really incredible) is a deep brain stimulation, where a neurosurgeon sticks a long thing electrode into a patients brain and zaps at the right place, so that the lost connection is initiated. I saw it once and the patient who was scared to death and completely awake, as in all brain surgeries. He could barely close his hand, it was in a constant state of grip. as soon as the surgeon zapped once, the fingers started moving completely normal, and he said "it's the first time in 5 years I've been able to look at my hand!"
interesting stuff kozmik. And methadone was created to aid heroin withdrawl (and is also addictive). Like a nested russian doll - it's a hard time. The only non-narc med that actually works is I believe called narcanol and totally withdraws receptability of opiates in the body causing instant cold turkey. They use it after putting heavy users in a coma and it works almost 100 percent (if it doesn't kill you first).
The parkinsons treatment you speak of I've been watching carefully. They are using in some cases a pacemaker-type device that sends electrical pulses that keep the synapse pathways active. It's amazing low-tech and they are using it for depression, epilepsy, mental illness and of course parkinsonism. The uses are so widespread and I don't honestly care that they aren't totally sure why it works in so many ways - just as long as it works. A canadian group has made big leaps in depression therapy with it - a good result with long-term recovery.
I had forgotten how the books ended cause I read them so long ago!but yeah I remember the showdown w Moriarty.
FYI: they still use cocaine but only in general anesthetic procedures, and for terminally ill/cancer patients. Obviously they don't make you snort it...it's a liquid solution. I know this because there was a small bottle in my house once. It was never used, so I think it went to the waste...
lucky teh crackhead who found it!
cocaine is really interesting. Freud was a huge coke user, he actually promoted the use of coke with psych patients, and wrote and published a feverish article called "ubercoca", praising its mood elevating effects. then one of his patients died of coke use and...well, he didn't really talk about it anymore.
Sherlock Holmes is a regular cocaine and morphine user, as well as one of the smartest fiction characters ever created. Interesting?
but what did he die of? a heart attack? convulsions?
i still don't understand why cocaine was banned exactly - i found another site (a UK drug recovery site) and here it states that there isn't physical dependency (they think) with cocaine. there are some long-term effects i guess but probably only for absolutely chronic users - so why? why was it ever made illegal in the first place.
Tolerance Tolerance to any drug exists when it becomes necessary to take higher doses to achieve the same effects once reached with lower doses. At present there is no evidence to suggest tolerance to cocaine's stimulant effect occurs. Users may keep taking the original amount over extended periods and still experience the same euphoric effects. However, some users do increase their dosage in an attempt to intensify and prolong the effects.
Consequences of cocaine use
Crack cocaine does produce a strong physical dependency. With regular heavy use increasingly unpleasant symptoms occur. Euphoria is replaced by restlessness, over-excitability and nausea. With continued use this can lead to paranoid psychosis. Regular users may appear chronically nervous, excitable and paranoid. Confusion as a result of exhaustion, due to lack of sleep, is common.
Psychological dependence Psychological dependence exists when a drug is so central to a person's thoughts, emotions, and activities that it becomes a craving or compulsion. Among heavy cocaine users, an intense psychological dependence can occur; they suffer severe depression when the supply of cocaine runs out, which lifts only when they take it again. Experiments with animals have suggested that cocaine is perhaps the most powerful drug of all in producing psychological dependence.
When not taking cocaine, many regular users complain of sleep and
eating disorders, depression and anxiety, and the mental craving for
the drug often compels them to take it again.
and i'm just curious about this --- because it seems a cycle.
every time these drugs (or a version of them) are introduced they are
considered miracle drugs/wonder cures (be it cocaine or amphetamines)
and then without fail some years on - they are banned again.
why???? why????
One thing to do with these patients (and I've seen it done, it's really incredible) is a deep brain stimulation, where a neurosurgeon sticks a long thing electrode into a patients brain and zaps at the right place, so that the lost connection is initiated. I saw it once and the patient who was scared to death and completely awake, as in all brain surgeries. He could barely close his hand, it was in a constant state of grip. as soon as the surgeon zapped once, the fingers started moving completely normal, and he said "it's the first time in 5 years I've been able to look at my hand!"
[/QUOTE]
weird! how long does that last anyway --- is it five minutes, a day, a lifetime...?
this is a slightly different thing but it said in the first article too --- that it wasn't the presence of dopamine that was needed exactly. it was just the stimulation of the dopamine receptors (which presumably dopamine does) but that they can also be stimulated with mimickers
direct agonists are more effective because they stimulate dopamine receptors even when dopamine neurons are missing.
so on the one hand you have methylphenidate, amphetamines, cocaine, adderall etc. blocking re-uptake, keeping the dopamine in the synapse for longer and/or promote release of dopamine from the neuron in the first place and/or bond with the protein that is the dopamine transporter (normally takes it back for re-uptake in the original neuron) stopping it getting reabsorbed.
otherwise you can have a chemical that becomes the neurotransmitter itself (weird idea!) - capable of stimulating the receptor and mimicking the actions of dopamine (i think they were in fact not referring to cocaine/amphetamines but other direct-acting agonists) like the l-dopa or levadopa. i think i find it weird because i don't yet understand whether the receptor merely needs to be stimulated or whether it needs to ABSORB a certain amount of dopamine. everything seems to imply that the receptor merely needs to be stimulated and i don't quite get that yet.... or what i don't know is what happens to the dopamine that gets transmitted/absorbed by the receptor?? i understand that the bit that is not absorbed gets re-uptook and broken down by MAO in part. but does the same thing happen to the bit that gets absorbed/transmitted - or does it not get absorbed?? does it just sit in the synapse tickling the receptors until re-absorption by the original transmitting neuron?
anyway! i am definitely sure that i have faulty receptors! i have a feeling for me - it is NOT the production but the uptake that is my fault-line. perhaps that is the difference between ADHD and ADD - one has the faulty (not enough) production and the other normal enough production but faulty uptake.
(i guess that would be too obvious to work out tho - because all ADHDers would prefer methylphenidate/ritalin type drugs and all ADDers would prefer ADDerall/dexedrine type drugs --- so if it was that simple i am sure it would have been noticed by now!).
but it might go some way to explaining what i perceive as the RADICAL difference between ADDers and ADHDers. and the fact that they both suffer from a dopamine imbalance but in entirely different ways.
chjones38862.663587963
[quote=chjones]why then, do some people still build up a tolerance[/quote]
That's an interesting question because I have wondered if I am experiencing increased tolerance. I keep reading however that the scientific community believes otherwise.
From "Highlights of the Attention Deficit Hyperactivity Disorder (ADHD) News Media Briefing" from Medscape Psychiatry & Mental Health. Posted 06/10/2005"During Dr. Bright's presentation, it was asked if patients develop a tolerance or resistance to stimulant drug therapy. According to Dr. Bright, individuals do not develop tolerance to these drugs." I don't know what studies support this view (which I have read elsewhere), but if it is accurate, then I wonder what other factors are giving me the impression that I might be developing a tolerance. I suspect they relate to coping issues and behaviorial modifications that I need to deal with.
Wow mrdarcey! That was great! Feel free to share anytime. You provided me with a wealth of information.
i've never bothered to look too much into the chemical side of ADD (not taking any meds why should I?) but i was surfing and found this article which although not directly related, being about Parkinsons, i thought was interesting:Dopamine - A Sample Neurotransmitter
One of the neurotransmitters playing a major role in addiction is dopamine. Many of the concepts that apply to dopamine apply to other neurotransmitters as well.
As a chemical messenger, dopamine is similar to adrenaline. Dopamine affects brain processes that control movement, emotional response, and ability to experience pleasure and pain.
Dopamine
Regulation of dopamine plays a crucial role in our mental and physical health. Neurons containing the neurotransmitter dopamine are clustered in the midbrain in an area called the substantia nigra . In Parkinson's disease, the dopamine- transmitting neurons in this area die. As a result, the brains of people with Parkinson's disease contain almost no dopamine. To help relieve their symptoms, we give these people L-DOPA, a drug that can be converted in the brain to dopamine.
Drugs can stimulate or fail to stimulate dopamine receptors
Some drugs are known as dopamine agonists. These drugs bind
to dopamine receptors in place of dopamine and directly stimulate those receptors. Some
dopamine agonists are currently used to treat Parkinson's disease. These drugs can
stimulate dopamine receptors even in someone without dopamine neurons.
An example of agonist drug action
In contrast to dopamine agonists, dopamine antagonists are drugs that bind but don't stimulate dopamine receptors. Antagonists can prevent or reverse the actions of dopamine by keeping dopamine from attaching to receptors.
Dopamine antagonists are traditionally used to treat schizophrenia and related mental
disorders. A person with schizophrenia may have an overactive dopamine system.
Dopamine antagonists can help regulate this system by "turning down" dopamine
activity.
Cocaine and other drugs of abuse can alter dopamine function. Such drugs may have very different actions. The specific action depends on which dopamine receptors the drugs stimulate or block, and how well they mimic dopamine.
An example of antagonist drug action
Drugs can act directly or indirectly on dopamine receptors
Drugs such as cocaine and amphetamine produce their effects by changing the flow of neurotransmitters. These drugs are defined as indirect acting because they depend on the activity of neurons. In contrast, some drugs bypass neurotransmitters altogether and act directly on receptors. Such drugs are direct acting.
Use of these two types of drugs can lead to very different results in treating the same disease. As mentioned earlier, people with Parkinson's disease lose neurons that contain dopamine. To compensate for this loss, the body produces more dopamine receptors on other neurons. Indirect agonists are not very effective in treating the disease since they depend on the presence of dopamine neurons. In contrast, direct agonists are more effective because they stimulate dopamine receptors even when dopamine neurons are missing.
MAO affects dopamine levels
Once returned to the sending neuron by the reuptake system, dopamine is subject to an enzyme named monoamine oxidase (MAO). MAO usually breaks down dopamine.
If no other factors were at work, MAO would keep the amount of "used" dopamine fairly low. However, dopamine taken back into the nerve ending can return to the vesicle for storage. Once inside the vesicle, dopamine is protected from MAO.
A drug named reserpine prevents the reuptake of dopamine and some other neurotransmitters. Administering reserpine causes dopamine to remain exposed within the cell and broken down by MAO. This profoundly reduces the available dopamine.
Changing the action of MAO can help us treat diseases that involve dopamine transmission. For instance, the drug deprenyl inhibits MAO. This increases the stores of dopamine and slows the progression of Parkinson's disease. In higher doses, deprenyl enhances the effects of dopamine on behavior.
Interestingly, one form of MAO actually protects dopamine. This form of MAO, found in dopamine neurons, acts on substances in the neuron other than dopamine. Here MAO protects the "purity" of neurotransmission by breaking down other neurotransmitters. Inhibiting this form of MAO can increase levels of neurotransmitters such as serotonin, which seems to help people diagnosed with depression.
Drugs can also affect dopamine levels
Dopamine binds to its receptors quickly. This neurotransmitter is also quickly removed from its receptors as long as dopamine levels in the synapse are sufficiently high.
However, drugs can affect dopamine levels. Some drugs increase dopamine by preventing dopamine reuptake, leaving more dopamine in the synapse. An example is the widely abused stimulant drug, cocaine. Another is methylphenidate, used therapeutically to treat childhood hyperkinesis and symptoms of schizophrenia.
It's interesting that amphetamine and cocaine produce affect behavior and heart function in similar ways. Furthermore, both drugs increase the amount of dopamine in the synapse. However, cocaine achieves this action by preventing dopamine reuptake, while amphetamine helps to release more dopamine. So, these drugs with similar effects produce their actions through entirely different processes. In turn, addiction to the two drugs may call for somewhat different types of treatment.
Neurons can become sensitized or desensitized to dopamine
One important aspect of drug addiction is how cells adapt to previous drug exposure.
For example, long-term treatment with dopamine antagonists increases the number of dopamine receptors. This happens as the nervous system tries to make up for less stimulation of the receptors by dopamine itself. Likewise, the receptors themselves become more sensitive to dopamine. Both are examples of the same process, called sensitization.
A type of sensitization.An opposite effect occurs after dopamine or dopamine agonists repeatedly stimulate dopamine receptors. Here overstimulation decreases the number of receptors, and the remaining receptors become less sensitive to dopamine. This process is called desensitization.
Desensitization is better known as tolerance, where exposure to
a drug causes less response than previously caused. Tolerance reflects the actions of the
nervous system to maintain homeostasis -a constant degree of
cell activity in spite of major changes in receptor stimulation. The nervous system maintains
this constant level in an attempt to keep the body in a state of equilibrium, even when
foreign chemicals are present.
Sensitization and desensitization do not take place only after long-term understimulation or overstimulation of dopamine receptors. Both sensitization and desensitization can occur after only a single exposure to a drug. In fact, they may develop within a few minutes.
A type of desensitization.Disease and drugs can produce faulty sensitization
Sensitization or desensitization normally occur with drug exposure. However, addiction or mental illness can tamper with the reuptake system. This disrupts the normal levels of neurotransmitters in the brain and can lead to faulty desensitization or sensitization. If this happens in a region of the brain that serves emotion or motivation, the individual can suffer severe consequences.
Consider an example. Cocaine prevents dopamine reuptake by binding to proteins that normally transport dopamine. Not only does cocaine "bully" dopamine out of the way-it hangs on to the transport proteins much longer than dopamine does. As a result, more dopamine remains to stimulate neurons, which causes a prolonged feelings of pleasure and excitement. Amphetamine also increases dopamine levels. Again, the result is over-stimulation of these pleasure-pathway nerves in the brain.
i realise now i post that the above doesn't make much sense - but there is a connection to Adderall if i paste together a few other bits of surfy-nonsense (all from the internet so sources are as reliable as you want to think they are - generally Wikipedia etc.) maybe it will be clearer that i was interested in the connection between dopamine and adderall and thought it might be of interest to others - i suppose you all know it backward anyway but i don't know anything about it.
do ADDers have faulty levels of dopamine - if so, can that be tested. the way they seem to be able to see the lack of dopamine in Parkinson's patients? or is it just our levels of sensitization - we don't got enough receptors... and if not, why not? seeing as the brain can obviously make more if it chooses to - (re. tolerance/sensitization).
and how does this fit in with fish oil omegas and/or crawling? hmmm... more internet surfing i think. unless someone wants to save me the bother and just spell it out in words of one syllable for me?
Dopamine is released as part of the brain's reward system, and is either directly or indirectly involved in the addictive properties of every major drug of abuse.
Cocaine in the brain - In the normal communication process, dopamine is released by a neuron into the synapse, where it can bind with dopamine receptors on neighboring neurons. Normally dopamine is then recycled back into the transmitting neuron by a specialized protein called the dopamine transporter. If cocaine is present, it attaches to the dopamine transporter and blocks the normal recycling process, resulting in a buildup of dopamine in the synapse which contributes to the pleasurable effects of cocaine.
While the exact mechanism is unknown, it is believed that Adderall works by blocking the reuptake of dopamine and norepinephrine into the presynaptic neuron and increasing their release from the presynaptic neuron into the extraneuronal space. In other words, Adderall reverses the reuptake mechanism, turning it into a pump instead of a vacuum. Sources note that amphetamine and related compounds (ephedrine, etc.) displace noradrenaline from the presynaptic neuron and do not act as reuptake inhibitors as referenced above. [citation needed]
The increased flow of dopamine and norepinephrine into the extraneuronal space causes the brain, as one psychiatrist explains, to experience a more intense level of concentration, causing an increased ability to focus for extended periods of time, and a heightened interest in performing mental tasks.
Though rare, it is possible for Adderall to cause psychotic episodes at recommended doses in patients with a history of psychosis.
In Parkinson's disease, the dopamine- transmitting neurons in this area die. As a result, the brains of people with Parkinson's disease contain almost no dopamine. To help relieve their symptoms, we give these people L-DOPA, a drug that can be converted in the brain to dopamine.
chjones38845.5978819444BUMPED FOR ANTEROS - hope it is of some use???