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Old 11-07-04, 01:34 AM
DjRyanZ7 DjRyanZ7 is offline
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If you take too much adderall... Advice to not get locked up

You will feel like **** when you come down, its probly nothing i was tweaking yesterday. You cant OD on adderall. I talked to a guy who has been doing that stuff for years, so NEVER call the hospitol, you will get drug charges, lose your medication ect...
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Old 11-07-04, 02:12 AM
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You most certainly can OD on Adderall, it's an amphetamine and it can kill. For example, it can send your heart into arrhythmia, you could pass out and choke on your vomit. You could stop breathing. You better get wise to the game.
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Old 11-07-04, 02:20 AM
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You can't OD on Adderall? Really?

Quote:
OVERDOSAGE

Individual patient response to amphetamines varies widely. While toxic symptoms occasionally occur as an idiosyncrasy at doses as low as 2 mg, they are rare with doses of less than 15 mg; 30 mg can produce severe reactions, yet doses of 400 to 500 mg are not necessarily fatal.

In rats, the oral LD 50 of dextroamphetamine sulfate is 96.8 mg/kg.

Symptoms: Manifestations of acute overdosage with amphetamines include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia and rhabdomyolysis.

Fatigue and depression usually follow the central stimulation.

Cardiovascular effects include arrhythmias, hypertension or hypotension and circulatory collapse.

Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Fatal poisoning is usually preceded by convulsions and coma.
Taken from http://www.drugs.com/PDR/Adderall_Tablets.html

Edit: BTW: LD 50 means a dose that is lethal to 50% of lab animals (usually rats) it is administered to.
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Old 11-07-04, 02:20 AM
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This is dangerous advise DjRyanZ7.

There are worse things than seeking help when I might be taking enough pharmaceuticals that "overdose" becomes part of the conversation regardless of whether it's going to kill me or not.

If my goal is to maintain a steady, uninterrupted supply of dope at all costs maybe this would be a wise strategy but for anyone interested in their health and well being I think not.

If somehow I might be mistaken for someone that requires being charged for the way I unlawfully handle my medication, it might also be time for me to consider there being a thread of truth that needs attending to there.

If I have questions about how to withdraw from meds or think I have abusive or addictive troubles there are many here whom have experience in those matters. My doctor should be my first port of call in all questions regarding the use and abuse of the prescribed and non prescribed dope I might be taking.
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Old 11-07-04, 01:04 PM
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DJ,

People can and do die from ODing on Adderall. There have been several reports in the last year of teens and College students who died from taking too much Adderall.
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Old 11-07-04, 01:25 PM
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Dj, Sweetie...I am speaking from experience here! You take too much of stimulants it will catch up with you in the long run.....U are doing more damage to yourself than you realize.

For one...Too Much adderall(or any stimulant) is a waste.....U are just giving yourself an extra OM-PH but not really solving ADD problems.

#2) I took too much stimulants when I was young too...I know it is hard to resit temptation...self esteem issues making me believe I can not be great unless I had the pills and more of it....It is mentally addictive....

I been there when You have taken way too much and you heart is going to beating so fast and head is going to be tingling.These are two warning signs that you have to slow down cause U are going to get sick....or even worse die. I'd Hate to see ya get to this point if you are not there already!

Please be careful, Babay, and Use this medicine wisely to help yourself with ADD and not to become the energizer bunny on speed!
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Old 11-08-04, 03:35 PM
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eh

Most Fatal ODs are from rittlin, i know a kid who takes 30 adderall 20mg at a time
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Old 11-08-04, 03:42 PM
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Ritalin and Adderall are cousins, Dawlin. Stimulant is A Stimulant and too much can effect the same way. Same as any other stimulant like dexadrine. Again speaking from experience.
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Old 11-08-04, 08:43 PM
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I disagree, there is no case of anyone dying from Ritalin, there is a lot of antidotal evidence from the anti-med squad. Any maybe that one small boy who ate his whole bottle of meds, but that's a more normal toxicology thing.

Your brain can only use so much Ritalin (since it is basically a dopamine uptake inhibitor) it doesn't send your brain into overdrive.
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Old 11-09-04, 01:26 AM
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Ok, I found something today..should be particular interest....http://www.mnpoison.org/mnpoison/pdfs/DOA.pdf

BTW......It most certainly does send brain and heartrate into maximum overdrive if taken too much at one time. Ando....may I ask have u ever experienced the effects of over medicating yourself?
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Old 11-09-04, 02:42 AM
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I don't get why you posted that web-page, Ritalin wasn't mentioned. As for abuse, yea I have abused the hell out of it. (in the past) I've researched it extensively but I'm not interested in digging up all the links. If you avoid all the scare tactics and hidden motives and stick to medical studies you get a much clearer picture.

Adderall is amphetamine, Ritalin is not - huge difference.
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Old 11-09-04, 03:28 AM
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Np.....I was reading that website and I happened to see ridalin mentioned in the same sentence as all other stimulants....but If You want more elaboration...lucky for me I have time on my hands.....

http://www.acnp.org/G4/GN401000166/CH162.htm <~~~~~~States...(Direct quote so ya know where to look)

Neurotoxic Effects of Stimulant Drugs

Sustained high-dose administration of amphetamines (especially methamphetamine) to experimental animals produces a persistent depletion of DA which is associated with terminal degeneration (62, 182, 195), as well as neuronal chromatolysis in the brain stem, cortex and striatum (42, 182). In contrast, continuous dosing with extremely high doses of cocaine (100250 mg/kg/day i.v.) did not induce terminal degeneration in frontal cortex and striatum (62, 183). Recently, Cubellis et al. (36) presented evidence that amphetamine, in contrast to cocaine, induces redistribution of DA from the vesicles into the cytosol; thus, the loss of the protection of the vesicles' relatively reducing environment results in cytosolic oxidative stress that may initiate amphetamine neurotoxicity. The DA depletion is reported to be permanent in the caudate of monkeys (196). The main hypotheses for underlying mechanisms have included 1) the conversion of DA into a hydroxy oxidative metabolite (195, 196); and 2) glutaminergic stimulation of toxicity, which can be inhibited by N-methyl-D-aspartate antagonist MK-801 (200).

Methamphetamine toxicity is inhibited by a variety of drug treatments, including: 1) DA synthesis inhibitor alpha-methyl-para-tyrosine; 2) DA receptor antagonists; 3) NMDA receptor antagonists, e.g., MK-801; 4) DA and serotonergic reuptake inhibitors protecting against DA and serotonin toxicity respectively (195). Even though most studies have found that serotonergic and DA reuptake inhibitors specifically protect these two sites, certain reuptake blockers (such as benztropine) do not (195). On the other hand, mazindol, a non-specific blocker, protects against both DA and serotonergic neurotoxicity. Ali et al. (1994) have further demonstrated in mice that a major factor for neurotoxicity is hyperthermia which is highly correlated with the degree of long-term DA depletion (21). Furthermore, haloperidol, diazepam and MK-801, all of which can reduce methamphetamine-induced hyperthermia, protect rats against DA depletion (4). They also demonstrated that reducing the ambient temperature (4C) reduced neurotoxicity to the same levels found when phenobarbital, diazepam and MK-801 were present to protect the cell. Tolerance to methamphetamine induced by increasing doses also reduces the hyperthermic response and as well protects against neurotoxicity (89, 188).

An important caveat is that not all protective mechanisms act by preventing the hyperthermic effect; the monoamine uptake blockers inhibit neurotoxicity in the absence of inhibition of hyperthermia, e.g., fluoxetine blocks methamphetamine serotonin toxicity without reducing temperature (140). The monoamine protection from neurotoxicity by reuptake inhibition is emphasized by the unexpected discovery that even massive and 24-hour continuous dosing of cocaine, e.g., 100 mg/kg/day, does not result in DA system neurotoxicity (119, 182, 183). Hyperthermia has been well documented to increase amphetamine stereotypy (93, 220). Hyperthermia alone is well known to result in neuronal chromatolysis and has been previously proposed as a significant contributor to amphetamine-induced DA depletion and neuronal damage in clinical as well as experimental animal histopathology (52). Hyperthermia may have been one of the factors resulting in deaths among athletes taking moderate doses of amphetamine in the 1960s and 70s (145). Even in mild hyperthermia, increased body temperature induces a linear decrease in the inhibitory feedback of stimulants on somatodendritic autoreceptors (130). Thus, body temperature changes induced by amphetamine should be considered as one of the contributors to toxicity.

One of the hallmarks of amphetamine-induced neurotoxicity is the loss of DA uptake sites in the striatum and accumbens. These studies of transporters after chronic amphetamine have reported decreases in the range of 3040% (158). Recently, Silvia et al. (198) addressed the functional significance of changes in transporters on amphetamine's behavioral effects. After seven days of infusion of transporter RNA antisense ODN into the SN/VTA nuclei, mazindol binding was reduced 32% in the caudate. Administration of 2 mg/kg of amphetamine at this time resulted in robust contralateral turning (an increase of 400%); in contrast, 10 mg/kg of cocaine induced no changes in the turning response. The lack of turning response to cocaine after transporter reduction contrasts with the substantial cocaine-induced contralateral turning after unilateral SN/VTA D2 ODN to reduce D2 autoreceptors in the striatum (199). Thus, the amphetamine-induced loss of DA uptake sites could have two consequences: 1) a protective mechanism reducing further neurotoxicity, and 2) reverse tolerance to subsequent amphetamine administration, perhaps resulting in adverse symptoms such as paranoid psychosis (see also the discussion on neurotoxicity in the habenular interpeduncular track and its possible relationship to augmentation amphetamine-induced adverse effects).

Recently, Fleckenstein et al. (68) reported that methamphetamine induced a dose-response sensitive reduction in [3H] DA uptake in washed striated synaptosomes which lasted for at least three hours; at 24 hrs the response had returned to normal. Since the decrease in intake was at maximum as early as 30 minutes after methamphetamine, this decrease in DA uptake is probably augmenting the amphetamine behavioral response and certainly not inducing tolerance. The decrease in DA uptake at doses up to 15 mg/kg could also provide some protection from neurotoxicity due to oxidative species.

These marked neurotoxic effects on the DA systems may underlie the mild Parkinson-like symptoms or "burned out" clinical picture in chronic, high-dose amphetamine abusers. These same individuals have a readily activated stimulant psychosis response. Similar re-activation of psychosis by L-dopa and direct agonists in Parkinson patients raises the question of whether the more severe psychosis resulting from amphetamine vs. cocaine abuse may have a partial basis in the greater toxicity induced by amphetamine.

Fatal Toxicity

Deaths directly attributable to the pharmacological response to amphetamines relate to several phenomena, including: 1) hypertensive cerebrovascular hemorrhage (confirmed pathologically); 2) cardiovascular collapse secondary to ventricular fibrillation (46, 154), with the majority of these cases in individuals less than 30 years of age with no evidence of pre-existing heart disease; 3) hyperpyrexia in the range of 40C and 4) miscellaneous causes, such as septicemia with bacterial endocarditis or necrotizing angiitis (154). In general, acute fatal drug reactions to amphetamine are more common in the occasional user than in the tolerant, chronic, high-dose abuser. This is particularly true of the hyperthermic and convulsive cascade that precedes many fatalities. This may be related to the observation that experimental animals rapidly develop tolerance to the hyperthermic effects of amphetamine. Although hyperthermic conditions associated with convulsions are seen more frequently with amphetamine, convulsions are more frequent antecedents in acute toxicity from cocaine (76). In contrast to amphetamine, cocaine has the capacity to induce potentially toxic reactions in those tolerant to its use (76). These differences may be related to the differential local anesthetic potency, resulting in arrhythmias, convulsions, and depression of the medullary respiratory center. Although the exact interrelationship of hyperthermia, hypertensive crisis and convulsions, and the sequence of these events in the toxic cascade, is still unknown, both types of stimulants induce a similar fatality (154).

The multifactorial nature of stimulant toxicity requires careful control of experimental conditions in order to study the effects of these agents in the intact animal. When lethality is used as the dependent variable, this endpoint may result from different contributing factors based on the experimental design. For example, aggregation of rodents dramatically increases the toxic and lethal effects, based either on an increase in locomotor activity or hyperthermia (154). Although hyperpyrexia is often fatal to rodents treated with any pharmacological agent, temperature elevation observed in cocaine-treated animals (in contrast to amphetamine-treated ones) is usually not sufficiently high to completely explained the observed mortality. Thus, in experimental studies of toxicity, even in the absence of lethality, control over the acute convulsive as well as the hyperthermic effects of stimulants is a necessary prerequisite. Clearly, catecholamine release and activation of receptors are important in acute toxicity. This statement is supported by the observation that the mortality of amphetamine may be reduced by depletion of catecholamines or by receptor blockade.



CLINICAL USES OF STIMULANTS

Perspectives on Clinical Indications

Since amphetamine-like stimulants have high abuse potential and other adverse toxic consequences, why do we continue to use them? In the US, there are only two Food and Drug Administration (FDA) approved indications for dextroamphetamine and methylphenidate: 1) narcolepsy and 2) attention deficit hyperactivity disorder (ADHD). In Europe, some countries have prohibited any use of stimulants. However, most experts agree that in ADHD and narcolepsy, stimulants have an definitive and uncontroversial therapeutic role when used judiciously. Because of this agreement on specific therapeutic applications for these drugs, their use will not be reviewed here. Rather, we will discuss the use of stimulants for other problems, those for which stimulant administration may be somewhat more controversial.


If you are just taking these medications for a high and to not to help your ADD ....U are just making it worse on you.....YOU ARE NO LONGER IN CONTROL.....THE DRUG CONTROLS YOU! Think about that!
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Old 11-09-04, 10:23 AM
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Sorry Dragon Lady I'm still not getting it. That quote is about meth right? (Methamphetamine) But were talking about Ritalin (Methylphenidate)
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Old 11-09-04, 03:46 PM
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Ritalin is similar in a lot of ways to amphetamine - which the previous posts refer to. All of the amphetamines get lumped together because I gather they pretty much all work in the same way - the slight differences in the shape of the molecule and the way it's metabolized accounting for the slight differences in relative strength and half-life, etc. Methylphenidate is similarly shaped to amphetamines but the differences mean that it works in a slightly different way - in a very similar way to cocaine, actually. Ritalin overdose can certainly kill you, just like amphetamine overdose can. Commonly it will induce a heart attack or a fatal arrythmia in those who are susceptable - just like people drop dead from the recreational use of cocaine. Ritalin is safer in that it's LD50 is higher, compared to it's theraputic dosage range, than amphetamine (in other words, if you took say, 20 days worth of pills all at once, you'd be in more danger from Adderall than Ritalin - so the risk of accidental OD is less with ritalin).
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Old 11-09-04, 04:16 PM
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My Point???? Ok no med jargon crapolla....I know that taking too much stimulant increases heart rate and it could have killed me if I didn't stop myself before too late...We talking 60 pills in a week and I am telling myself I am not going to take anymore but a few minutes later I am talking another one after another...I could literally see My heart Pumping THROUGH my chest and it felt like my brain and forhead turned numb....Can You say Wake up call????????

My family has history of heart problems....Maybe that could have played a part in that...I wonder what was the family history of those who have died from REPORTED & RECORDED O.D. on stimulants.

I'm Sowwy, but the high generated from Stimulants is just not worth what my body was going through and maybe some have not experienced the same but body chem is different....and I did not even realize or that would have such an effect on me...So, think about it....does that 2 or 3 hours of omph that ya get really worth the possible long term Damage?

I need my meds to help me cope with ADD, not to get that high that turns me into Speedy Gonzales Meets the Road Runner....I'm taking dexadrine now...and I admit it is Hard, sometimes, to not want to take just one more...and fight it as hard as I can..

Can You stop yourself if you really wanted to..if not...U aint in control anymore..and U need help. END UV STORY!
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Last edited by Draga; 11-09-04 at 04:31 PM..
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