rough notes for my education group. People were into the presentation even non-Meth users. I was surprised by how many had tried it. Next week we take on crack.

Wikipedia: Methamphetamine is a potent central nervous system stimulant that affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and responses associated with alertness or alarm conditions. The acute physical effects of the drug closely resemble the physiological and psychological effects of an epinepherine-provoked fight, flight or freeze, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Users experience an increase in focus, increased mental alertness, and the elimination of fatigue, as well as a decrease in appetite.

Methamphetamine is a potent neurotoxin, shown to cause dopaminergic degeneration. High doses of methamphetamine produce losses in several markers of brain dopamine and serotonin neurons. Dopamine and serotonin concentrations, dopamine and 5HT uptake sites, and tyrosine and tryptophan hydroxylase activities are reduced after the administration of methamphetamine. It has been proposed that dopamine plays a role in methamphetamine-induced neurotoxicity because experiments that reduce dopamine production or block the release of dopamine decrease the toxic effects of methamphetamine administration. When dopamine breaks down it produces reactive oxygen species such as hydrogen peroxide.

Physical effects can include anorexia, hyperactivity, dilated pupils, flushing, restlessness, dry mouth, headache, tachycardia, bradycardia, tachypnia, hypertension, hypotension, hyperthermia, diaphoreses, diarrhea, constipation, blurred vision, dizziness, twitching, insomnia, numbness, palpitations, arrhythmias, tremors, dry and/or itchy skin,acne,pallor, and with chronic and/or high doses, convulsions, heart attack, stroke, and death can occur^.

Psychological effects

Psychological effects can include euphoria, anxiety, increased libido, alertness, concentration, energy, self-esteem, self-confidence, sociability, irritability, aggression, psychosomatic disorders, psychomotor agitation, hubris, excessive feelings of power and invincibility, repetitive and obsessive behaviors, paranoia, and with chronic and/or high doses, amphetamine psychosis can occur.

Withdrawal effects

Withdrawal is characterized by excessive sleeping, increased appetite and depression, often accompanied by anxiety and drug-craving.

Short-term tolerance can be caused by depleted levels of neurotransmitters within the synaptic vesicles available for release into the synaptic cleft following subsequent reuse (tachyphylaxis). Short-term tolerance typically lasts until neurotransmitter levels are fully replenished; because of the toxic effects on dopaminergic neurons, this can be greater than 2–3 days. Prolonged overstimulation of dopamine receptors caused by methamphetamine may eventually cause the receptors to downregulate in order to compensate for increased levels of dopamine within the synaptic cleft. To compensate, larger quantities of the drug are needed in order to achieve the same level of effects.

Methamphetamine is addictive^. While not dangerous, withdrawal symptoms are common with heavy use and relapse is common. Methamphetamine use causes hyperstimulation of pleasure pathways which leads to anhedonia. It is possible that daily administration of the amino acids L-Tyrosine and L-5HTP/Tryptophan can aid in the recovery process by making it easier for the body to reverse the depletion of dopamine, norepinephrine, and serotonin. The mental depression associated with methamphetamine withdrawal is longer lasting and more severe than that of  cocaine withdrawal.

ScienceDaily (Mar. 28, 2000) —In an article published in the March 28 issue of Neurology, scientists at the Harbor-UCLA Medical Center in Torrance, California, used magnetic resonance spectroscopy to take measurements of three parts of the brains of 26 participants who had used methamphetamine and then compared them with measurements of the same regions in the brains of 24 people who had no history of drug abuse.

“the meth users in this study hadn’t used the drug for some time–anywhere from two weeks to 21 months, this research strongly suggests that methamphetamine abuse causes harmful physical changes in the brain that can last for many months and perhaps longer after drug use has stopped,” In their study, Dr. Linda Chang and Dr. Thomas Ernst measured levels of brain chemicals that indicate whether brain cells are healthy or are diseased or damaged.

“We found abnormal brain chemistry in the methamphetamine users in all three brain regions we studied. In one of the regions, the amount of damage is also related to the history of drug use–those who had used the most methamphetamine had the strongest indications of cell damage,” Dr. Chang said.

The researchers found that levels of one chemical marker, N-acetyl-aspartate, were reduced by at least five percent in the methamphetamine abusers. “Many diseases associated with brain cell loss or damage, such as Alzheimer’s disease, stroke, and epilepsy, are also associated with reduced N-acetyl-aspartate,” said Dr. Ernst. “Reduced concentrations of N-acetyl-aspartate in the drug users’ brains suggest that long-term methamphetamine abuse results in loss or damage to neurons, the cells we use in thinking.” Two other chemical markers, myo-inositol and choline-containing compounds, are associated with glial cells, which act to support neurons. “Methamphetamine abusers showed increases of 11 percent and 13 percent in levels of these markers compared with normal individuals,” Dr. Ernst said. “This suggests an increased number or size of glial cells as a reaction to the injurious effects of methamphetamine.”

Abstinence Can Reverse Some Brain Damage

From JAMA News Release

Updated April 08, 2005

Adaptive changes in chemical activity in certain regions of the brain of former methamphetamine users who have not used the drug for a year or more suggest some recovery of neuronal structure and function, according to an article in the April 2005 issue of Archives of General Psychiatry, one of the JAMA Archives journals.

Methamphetamine use has been shown to cause abnormalities in brain regions associated with selective attention and regions associated with memory, according to background information in the article. Recent animal and human studies suggest that neuronal changes associated with long-term methamphetamine use may not be permanent but may partially recover with prolonged abstinence.

Thomas E. Nordahl, M.D., Ph.D., of the University of California, Davis, and colleagues compared eight methamphetamine users who had not used methamphetamine for one to five years and 16 recently abstinent methamphetamine users who had not used the drug for one to six months with 13 healthy, non-substance-using controls using a method of brain imaging, proton magnetic resonance spectroscopy (MRS), that allows the visualization of biochemical markers that are linked with damage and recovery to the neurons in the brain.

The researchers measured biomarkers in the anterior cingulum cortex, a region of the brain associated with selective attention. Levels of N-acetylaspartate (NAA), which is present only in neurons, were measured as a marker of the amount of damage (neuronal loss). Choline (Cho), which is generated by the creation of new membranes and, the authors write, “may be an ideal marker to track changes consistent with neuronal recovery associated with drug abstinence,” was measured as a biomarker of recovery.

Levels of NAA were abnormally low in all the methamphetamine users, the authors found. Levels were lower relative to the length of methamphetamine use, but did not change relative to the amount of time that the methamphetamine users had been abstinent. The researchers found elevated Cho levels in the methamphetamine users who had not used the drug in one to six months, but normalized levels in the longer abstainers.

Normalization of Function

“In the early periods following methamphetamine exposure, the brain may undergo several processes leading to increased membrane turnover. The relative Cho normalization across periods of abstinence suggests that when drug exposure is terminated, adaptive changes occur, which may contribute to some degree of normalization of neuronal structure and function,”

I put together some facts on the topic for a radio interview on KFRU. It went pretty well, the hosts (simon and renee) were engaging and funny, and we talked for about 45 minutes and got out a lot of good information. The four pages of notes made me feel a lot more comfortable and i think it came across in the interview. A couple of things really struck me. One was the idea of neurogenesis. I had always read that you had all the brain cells you would ever have and alcohol kills them. In fact it says that on the info web site but i am going to edit that out because its not true. What really happens is the brain makes more brain cells all the time unless you are chronically drinking large amounts of alcohol. The good news is after a week of abstinence brain cell production booms. The fact that hit on the radio was brain shrinkage. Renee Hulshoff seemed aghast to learn your brain shrinks as you age and she referenced it on another story i caught on the drive back to the salt mines. I think I will do my next education group on the same topic, my as well learn the rap. On a practical note i will be promoting thiamine,. exercise and antidepressants for chronic alcoholics.

(lifted from NIAAA’s alcohol alert)

Equal numbers of men and women reported experiencing blackouts, despite the fact that the men drank significantly more often and more heavily than the women. This outcome suggests that regardless of the amount of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts.

Using imaging with computerized tomography, two studies compared brain shrinkage, a common indicator of brain damage, in alcoholic men and women and reported that male and female alcoholics both showed significantly greater brain shrinkage than control subjects. Studies also showed that both men and women have similar learning and memory problems as a result of heavy drinking.

Wernicke–Korsakoff Syndrome

Up to 80 percent of alcoholics, however, have a deficiency in thiamine, and some of these people will go on to develop serious brain disorders such as Wernicke–Korsakoff syndrome (WKS)). WKS is a disease that consists of two separate syndromes, a short–lived and severe condition called Wernicke’s encephalopathy and a long–lasting and debilitating condition known as Korsakoff’s psychosis.

The symptoms of Wernicke’s encephalopathy include mental confusion, paralysis of the nerves that move the eyes (i.e., oculomotor disturbances), and difficulty with muscle coordination. For example, patients with Wernicke’s encephalopathy may be too confused to find their way out of a room or may not even be able to walk. Many Wernicke’s encephalopathy patients, however, do not exhibit all three of these signs and symptoms, and clinicians working with alcoholics must be aware that this disorder may be present even if the patient shows only one or two of them. In fact, studies performed after death indicate that many cases of thiamine deficiency–related encephalopathy may not be diagnosed in life because not all the “classic” signs and symptoms were present or recognized.

Approximately 80 to 90 percent of alcoholics with Wernicke’s encephalopathy also develop Korsakoff’s psychosis, a chronic and debilitating syndrome characterized by persistent learning and memory problems. Patients with Korsakoff’s psychosis are forgetful and quickly frustrated and have difficulty with walking and coordination). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is their difficulty in “laying down” new information (i.e., anterograde amnesia) that is the most striking. For example, these patients can discuss in detail an event in their lives, but an hour later might not remember ever having the conversation

Prolonged liver dysfunction, such as liver cirrhosis resulting from excessive alcohol consumption, can harm the brain, leading to a serious and potentially fatal brain disorder known as hepatic encephalopathy ammonia and manganese, have a role in the development of hepatic encephalopathy. Alcohol–damaged liver cells allow excess amounts of these harmful byproducts to enter the brain, thus harming brain cells.

Hepatic encephalopathy can cause changes in sleep patterns, mood, and personality; psychiatric conditions such as anxiety and depression; severe cognitive effects such as shortened attention span; and problems with coordination such as a flapping or shaking of the hands (called asterixis). In the most serious cases, patients may slip into a coma (i.e., hepatic coma), which can be fatal.

More facts from: www.bloodalcohol.info

Alcohol can affect several parts of the brain, but in general, alcohol contracts brain tissue and depresses the central nervous system. Excessive drinking over a prolonged period of time can cause serious problems with cognition and memory.

When alcohol reaches the brain, it interferes with communication between nerve cells, by interacting with the receptors on some cells. The alcohol suppresses excitatory nerve pathway activity and increases inhibitory nerve pathway activity. Among other actions, alcohol enhances the effects of the inhibitory neurotransmitter GABA. Enhancing an inhibitor has the effect of making a person sluggish. Also, alcohol weakens the excitatory neurotransmitter glutamine, which enhances the sluggishness even farther.

The cerebral cortex processes information from your senses, processes thoughts, initiates the majority of voluntary muscle movements and has some control over lower-order brain centers. In the cerebral cortex, alcohol can:

• Affect thought processes, leading to potentially poor judgement.
• Depresses inhibition, leading one to become more talkative and more confident.
• Blunts the senses and increases the threshold for pain.

The limbic system, which consists of the hippocampus and septal area of the brain, controls memory and emotions. The affect of alcohol on this sytem is that the person may experience some memory loss and may have exaggerated states of emotion.

The cerebellum coordinates muscle movement. The cerebral cortex initiates the muscular movement by sending a signal through the medulla and spinal cord to the muscles. As the nerve signals pass through the medulla, they are influenced by nerve impulses from the cerebellum, which controls the fine movements, including those necessary for balance. When alcohol affects the cerebellum, muscle movements become uncoordinated.

The hypothalamus controls and influences many automatic functions of the brain (through the medulla), and coordinates hormonal release (through the pituitary gland). Alcohol depresses nerve centers in the hypothalamus that control sexual arousal and performance. With increased alcohol consumption, sexual desire increases – but sexual performance declines.

By inhibiting the pituitary secretion of anti-diuretic hormone (ADH), alcohol also affects urine excretion. ADH acts on the kidney to reabsorb water, so when it is inhibitted, ADH levels drop, the kidneys don’t reabsorb as much water and the kidneys produce more urine.

The medulla (brain stem) influences or controls body functions that occur automatically, such as your heart rate, temperature and breathing. When alcohol affects the medulla, a person will start to feel sleepy. Increased consumption can lead to unconscious. Needless to say, alcohol’s effect on the medulla can be fatal if it is excessive.

More stuff:

Detoxified alcoholics often have visuospatial and visuoperceptual deficits, characterized by difficulties completing tasks such as putting pieces of a puzzle together or map reading. A new study has found that, even with prolonged sobriety, alcoholics show deficits in visuoperception and frontal executive functioning of the brain.

Furthermore, alcoholics utilize a more complex higher-order cognitive system, frontal executive functions, to perform the same tasks as individuals without a history of alcoholism. Results are published in the November 2004 issue of Alcoholism: Clinical & Experimental Research.

The UNC findings, from research at UNC’s Bowles Center for Alcohol Studies, were based on an animal model of chronic alcohol dependence, in which adult rats were given alcohol over four days in amounts that produced alcohol dependency. The study is in the Nov. 3 issue of the Journal of Neuroscience.

In 2002, Dr. Fulton T. Crews, Bowles Center director, and Bowles Center research associate Dr. Kim Nixon were the first to report that alcohol, during intoxication, has a detrimental effect on the formation of new neurons in the adult rat hippocampus. This brain region is important for learning and memory – in animals and humans – and is linked to psychiatric disorders, particularly depression.

“When used in excess, alcohol damages brain structure and function. Alcoholics have impairments in the ability to reason, plan or remember,” said Crews, also professor of pharmacology and psychiatry in UNC’s School of Medicine. “A variety of psychological tests show alcoholics have a difficulty in ability to understand negative consequences.”

In the new study, senior co-author Crews and co-author Nixon found inhibition of neurogenesis, or brain cell development, during alcohol dependency, followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence.

“And when they stop drinking, you can show in a period of weeks, months, years, the brain grows back, there’s a return of metabolic activity, and cognitive tests show a return of function,” Crews said.

“Pharmacological agents such as antidepressants and behaviors such as running, increased physical activity and learning experiences apparently help regulate the process of neurogenesis,” he added. “Our research suggests they could be considered in the treatment of chronic alcohol dependency.”

In their report, Nixon and Crews also said that their findings for the first time provide a neuronal regeneration mechanism that may underlie the return of normal cognitive function and brain volume associated with recovery from addiction during abstinence from alcohol.

“This is really the first biological measure of a major change in neuronal structure consistent with changes that are known to occur when individuals are able to stop drinking,” said Crews.

Number of Brain Cells Not Fixed

For decades, neuroscientists believed the number of new cells, or neurons, in the adult brain was fixed early in life. Adaptive processes such as learning, memory and mood were thought tied to changes in synapses, connections between neurons.

More recently, studies have shown that the adult human brain is capable of producing new brain cells throughout life, a neurogenesis resulting in formation of hundreds of thousands of new neurons each month. “Prior to our work, everyone merely assumed that glia, the supporting cells of the brain, regenerated or that existing brain cells altered their connections,” said Nixon. “We have shown a burst in new cell birth that may be part of the brain’s recovery after the cessation of alcohol.”

Chronic alcoholism, a disease affecting more than 8 percent of the adult U.S. population, or more than 17 million Americans, produces cognitive impairments and decreased brain volumes, both of which are partially reversed during abstinence.