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Amino acids for brain repair after addiction/how do they work?

Nov 09, 2008 - 4 comments

Amino Acids
Some amino acids have properties similar to neurotransmitters. This makes them useful in treating anxiety and depression.

Gamma-aminobutyric acid, or GABA, is a natural antianxiety chemical and is often found in low levels in depressed people. L-tryptophan is a precursor to the synthesis of serotonin, and so it too is vital for combating depression and maintaining emotional balance. Tyrosine is a precursor of norepinephrine and dopamine, two neurochemicals that are involved in mood. D-phenylalanine is another important amino acid that has been associated with depression.

DL-phenylalanine (DLPA)

DLPA, or phenylalanine, is an amino acid found to be effective for treating depression. It is a precursor (directly on the formative pathway) to nor- epinephrine, one of the main neurotransmitters that govern mood.

In one study, more than 75 percent of people with severe depression showed rapid improvement while taking supplements of phenylalanine and vitamin B6. Food sources for this are: sunflower seeds, black beans, watercress and soybeans.

Recommended dosage: Begin with 500 mg (one capsule) two times daily, on an empty stomach with juice. This can gradually be increased by 500 mg per day to two or three capsules, three times daily.

For maximum effect, it is best to take 50 mg of vitamin B-6 at the same time, as well as niacin, 500 mg per day, and one gram of vitamin C. Vitamin B-6 is particularly important in regulating the absorption, metabolism, and utilization of amino acids.

Caution: With both DLPA and L-tyrosine (described below.), you need to be watchful for increased blood pressure, headaches, or insomnia. These side effects are indications that an excessive stimulation of the nervous system has occurred. Do not take these amino acids if you are currently taking standard antidepressant medications. Do not take these amino acids if you are suffering from any of the following conditions: phenylketonuria (pKU), hepatic cirrhosis, or melanoma.

Melatonin

Melatonin is helpful for some cases of seasonal affective disorder. Some experts believe the body's melatonin mechanism is involved in this form of depression. Melatonin can also be helpful if you are having problems with insomnia.

Dosage: Take 3 milligrams each evening, between one-half hour and two hours before retiring for the night.

S-adenosyl- L-methionine (SAM or SAMe)

SAMe is an excellent supplement for depression. This amino-acid derivative is comparable to prescription antidepressants in their action, but without the side effects.

SAMe has been studied for decades internationally and is approved as a prescription drug in Spain, Italy, Russia and Germany. More than 1 million Europeans have used it, primarily for depression and arthritis. It is often touted as a depression remedy that is nontoxic, without side effects, and better and faster than traditional medications.

SAMe is produced in the body from methionine, a sulfur- containing amino acid, and the energy- producing compound adenosine triphosphate (ATP). SAM-e ranks with ATP as a pivotal molecule in living cells. It is distributed throughout the body; but it is most concentrated in the brain and liver.

SAM is involved in the methylation of monoamines, neurotransmitters, and phospholipids such as phosphatidylcholine and phosphatidylserine. Normally, the brain manufactures all the SAM it needs from the amino acid methionine. However, SAM synthesis is impaired in depressed patients.
Our diet yields insufficient quantities of SAM-e either for wellness or treatment of illness. Moreover, the form of SAMe found in food is not stable. It oxidizes too rapidly to absorb well. Our bodies can only generate a small amount of SAMe. Therefore, SAMe levels are to be increased through dietary supplementation, if that is necessary.

Supplementing the diet with SAMe in depressed patients results in increased levels of serotonin and dopamine and improved binding of neurotransmitters to receptor sites. This causes increased serotonin and dopamine activity and improved brain cell membrane fluidity, resulting in significant clinical improvement.

The results of a number of clinical studies suggest that SAMe is one of the most effective natural antidepressants. SAMe is also better tolerated and has a quicker onset of antidepressant action than tricyclic antidepressants.

"Accumulated evidence indicates that SAM-e in higher doses is perhaps as effective for major depression as TCAS. SAM-e starts to work in approximately half the time needed for tricyclics. Studies show very few side effects, and SAM-e does not cause the sexual dysfunction or weight gain associated with other medications."
Richard P. Brown, M.D, author of "Stop Depression Now: SAM-E, the Breakthrough Supplement"




A recent study compared SAMe to the tricyclic desipramine. In addition to clinical response, the blood level of SAMe was determined in both groups. At the end of the four- week trial, sixty two percent of the patients treated with SAMe and fifty percent of the patients treated with desipramine had significantly improved. Regardless of the type of treatment, patients with a fifty-percent decrease in their Hamilton Rating Scale for Depression (HDS) score showed a significant increase in plasma SAMe concentration. These results suggest that one of the ways in which tricyclic drugs exert antidepressive effects is by raising SAMe levels.

Folate, B12 and B6 are necessary for efficient use of SAMe. SAMe has been effective for treating major depressive disorder in 13 trials comparing it to placebo and 19 trials comparing it to tricyclic antidepressants, with more than 1,400 patients studied.

No significant side effects have been reported from the use of oral SAMe.

Dosage: Because SAMe can cause nausea and vomiting in some people, it is recommended that it be started at a dosage of 200 mg twice daily for the first two days, increased to 400 mg twice daily on day three, then to 400 mg three times daily on day ten, and finally to the full dosage of 400 mg four times daily after twenty days.

Treatment for severe depression requires higher doses. Unipolar patients are given 800 mg or 1600 mg per day.

Caution: Do not take SAMe if you suffer from bipolar (manic) depression. Because of SAMe's antidepressant activity, individuals with bipolar depression are susceptible to experiencing hypomania or mania. This effect is exclusive to some individuals with bipolar depression.

More on SAMe- from Holisticonline.com

Trimethylglycine (TMG)

Research has found that TMG is converted into SAM in the body. TMG is less expensive than SAM.
Dosage: 3,000 milligrams a day, followed by a maintenance dose of 1,000 milligrams a day for up to three weeks.

Tyrosine

Tyrosine is an important amino acid that stimulates the production of norepinephrine, a hormone that is essential to the central nervous system. This nutrient is especially important for the depressed individual who is feeling excessive fatigue. The B-complex vitamins, particularly vitamin B6, allow the body to metabolize amino acids.

Foods containing tyrosine include eggs, green beans, lean meat, peas, seafood, aged natural cheese, seaweed, skim milk, tofu, whole wheat bread, and yogurt.

Dosage: 1,000 to 3,000 milligrams of the amino acid L-tyrosine first thing in the morning (on an empty stomach), followed by a B-complex vitamin supplement 30 minutes later, with breakfast.

Warning: If you are taking a monoamine oxidase (MAO) inhibitor drug or antidepressant, do not take supplemental tyrosine. A dangerous elevation in blood pressure may result when they are used in combination. Also do not take St. John's Wort with this amino acid.

Serotonin and Tryptophan

Serotonin is a very important brain biochemical and must be present at optimal levels to prevent depression.

Tryptophan supplementation increases the levels of serotonin and melatonin in the brain. Many depressed individuals have been found to have low tryptophan and serotonin levels. European studies have shown that L-tryptophan is of value in relieving depression. Unfortunately, other studies have given mixed results as to the effectiveness of tryptophan in depression.

Tryptophan is only modestly effective in the treatment of depression when used alone. In order to gain any real benefit from tryptophan, it must be used along with vitamin B6 and the niacinamide form of vitamin B3 to help block the kynurenine pathway to provide better results. Tryptophan manufacture is susceptible to contamination risk. The use of 5-HTP is more effective than the use of tryptophan for depression.

Tryptophan is found in certain foods, such as milk, turkey, chicken, fish, cooked dried beans and peas, brewer's yeast, peanut butter, nuts, and soybeans. Eat plenty of these foods together with a carbohydrate (potatoes, pasta, rice), which will ease the brain's uptake of tryptophan. Foods such as bananas, walnuts and pineapples are a good source of serotonin.

Recommended dosage: For depressive symptoms, take 2 grams (2,000 mg) of tryptophan two or three times daily. It should be taken between meals, with fruit or juice (simple sugars) to improve its utilization. It should not be taken with a protein meal, because tryptophan competes poorly with other amino acids for absorption. To convert tryptophan to serotonin, the body must have adequate levels of folic acid, vitamin B-6, magnesium, niacin, and glutamine.

5-Hydroxytryptophan (5-HTP)

5-HTP is one step closer to serotonin lineage than tryptophan. Hence, it is preferred for the treatment of depression (versus tryptophan).

Advantages of 5-HTP over Tryptophan

5-HTP is extracted from the seed of an African plant (Griffonia simplicifolia). Tryptophan is synthesized with the help of bacteria. Tryptophan has greater chance of contamination during manufacture. 5-HTP is safer for use.

Unlike tryptophan, 5-HTP cannot be converted to kynurenine; so it can easily cross the blood brain barrier. While only three percent of an oral dose of tryptophan is converted to serotonin, over seventy percent of an oral dose of 5- HTP is converted to serotonin.

5-HTP causes an increase in levels of endorphin and other neurotransmitters that are often decreased in cases of depression. 5-HTP also increases serotonin levels. Thus, it is much more effective for depression.

Numerous double-blind studies have shown that 5- HTP has equal effectiveness compared to drugs like Prozac, Paxil, and Zoloft (SSRIs) and tricyclic antidepressant drugs like imipramine and desipramine in terms of effectiveness.

Advantages of 5-HTP over antidepressants

5-HTP is less expensive

5-HTP is better tolerated

5-HTP has fewer and much milder side effects than antidepressants.


Dosage: 100 to 200 mg twice daily between meals.



Omega-3 Fatty Acids

An insufficiency of omega-3 oils in the diet has been linked to depression. Scientists believe that a lack of essential fatty acids (particularly the omega-3 oils) combined with an excess of saturated fats and animal fatty acids can lead to the formation of cell membranes that are much less fluid than normal. This will disrupt the cell's ability to control its internal environment.

Studies have shown that the physical properties of brain cell membranes, including their fluidity, directly influence:

Neurotransmitter synthesis

Signal transmission

Uptake of serotonin and other neurotransmitters

Neurotransmitter binding

The activity of monoamine oxidase-the enzyme that breaks down serotonin and other monoamine neurotransmitters such as epinephrine, dopamine, and norepinephrine.


All of these factors have been implicated in depression and other psychological disturbances.
Researchers have found several reasons why omega-3 fatty acids may reduce the development of depression. These are:

Recent studies have suggested that lowering plasma cholesterol levels by diet and medications increases suicide, homicide, and depression.

The quantity and type of dietary fats consumed influence serum lipid levels and alter the biophysical and biochemical properties of cell membranes.

Dietary advice to lower cholesterol levels tends to increase the ratio of omega-6 to omega-3 and decreases the level of the essential omega-3 fatty acid, docosahexanoic acid.

Population-based studies in various countries and the United States have indicated that decreased consumption of omega- 3 fatty acids correlates with increased rates of depression.

There is a consistent association between depression and coronary artery disease.

Evening primrose oil

The essential fatty acids in evening primrose oil provide additional nutrients to cope with depression. Evening primrose oil lifts the spirits because it produces Prostaglandins, hormone- like substances which are key to many chemical processes, including those responsible for depression.

Dosage: 1,000 mg three times daily.

Other effective nutritional antidepressants include lithium, rubidium, phenylalanine, and tryptophan.

Hypoglycemia and Depression

Depression can result from hypoglycemia (low blood sugar), a condition characterized by fluctuating emotions from extreme highs to extreme lows. Hypoglycemia is caused by too much sugar in the diet. To balance this extreme surge of blood sugar the pancreas overproduces insulin. This drastically lowers the blood sugar level, causing fatigue, depression, and anxiety .

If you suffer from hypoglycemia, avoid sugar, alcohol, coffee, and fruits with a high sugar content. Fresh vegetables, whole grains, miso soup, sprouts, and seaweed are excellent foods that balance the above substances.

Next Topic: Suggested Daily Supplements

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Seemed like this slide show just summed it all up

Nov 07, 2008 - 0 comments

http://www.thejoymovie.com

Just wanted to share

Does everything "FUN" have a potential for addicion?

Oct 26, 2008 - 1 comments

Addiction to Fun
Blake Ellison
The word “addiction” is used all too loosely in modern America. From its
traditional applications conjuring up images of chemically dependent social
delinquents, to 5-year-olds refusing to put down a PlayStation controller, addiction is
now a term that encompasses countless habits and behaviors. Despite its perhaps
overly broad use as a word, scientists have actually come to agree with laymen:
addiction today is a very broad concept that collectivizes people from all walks of life.
Today, classical addiction to mood-altering drugs is merely one type of addiction
which is explained by the same mechanisms as addictions to shopping, sex, or
gambling. Thanks to sensationalized media, Americans are also quickly becoming
aware of the newest hook for their youth: video games. Video gaming, like the above
activities, can become an addiction and it has already become necessary to educate the
public on its realities.
Despite their apparent differences, all of the above addictions have their root in
the brain. All brain activity, from the regulation of involuntary motions to the
sensation of pain to the abstract pondering of relativity, is conducted by neurons, which
are the individual cells of the brain. Moreover, neurons have to communicate in a style
not unlike “playing telephone” in order to accomplish anything. The method of
communication, or the telephone line, is via neurotransmitters, which are molecules
that jump from one neuron to the next. This activity occurs all over the brain billions
of times per day.
There is an ability to modify the communication among neurons.
Neuromodulators are substances which change the efficacy of the neurotransmitters.
They can be excitatory or inhibitory, which means that neuromodulators can make
neurons “talk” more or less. Many are naturally occurring in the brain, such as
endorphines. Endorphines are inhibitory because they limit the transmission of the
neurotransmitter for the sensation of pain. One of the triumphs of modern medicine
has been to artificially introduce neuromodulators. Anti-depression medications, for
example, specifically inhibit the neurotransmitter for depression.
This possibility has been known, if not scientifically explained, for centuries.
Cocaine, for instance, is an excitatory neuromodulator which causes a massive release
of dopamine, the neurotransmitter for the sensation of pleasure and reward. Dopamine
is naturally released in any rewarding event: eating after extended hunger and sexual
climax are two of the most common of such events. More importantly, dopamine is
the key neurotransmitter in addictions.
Traditionally addiction was split into two types, chemical and behavioral.
Chemical dependency referred to alcoholism and hard drug addictions, while
behavioral addictions were the label given to destructive habits in activities like
shopping or gambling. Today, due to their numerous common qualities, the two are
collectively labeled as addiction. To this end, psychologist Iain Brown has developed
what he calls a “hedonic management model” which accounts for addictions of all
varieties. This theory unites all forms of addictions into one model which explains
addiction as a warping of cognitive processes. In Brown's model, addiction is defined
as the mismanagement of the pursuit of pleasure.1 Physiologically, the key feature of
addiction is arousal, which is measured by heart rate.2 Therefore, activities which raise
arousal can potentially become addictive. Common to all addictions, in Brown's view,
are twelve key features:
1. Everyone learns to pursue “good hedonic tone,” or pleasurable experiences, in
the normal pursuit of happiness.
2. Individuals have varying predispositions to addiction due to psychological and
socioeconomic factors.
3. Addictions are initiated when the addict discovers they can exploit the activity
to maintain pleasurable sensations.
4. Addicts choose their activity based on availability and social support for the
activity, as well as the unique factors that also determine predispositions.
5. Addictions develop through events which create the desire for the modified
“hedonic tone.” As the activity continues, salience (the sense of “control” the
activity has over the individual) makes the addict believe that the activity is the
only rewarding one. As salience increases, so does tolerance.
6. Addictions evolve into cycles in which classical conditioning reinforces the
activity, and cognitive distortions eliminate barriers to the activity. That is,
Pavlovian cues begin to have similar effects to the activity and produce
cravings. Additionally, people will change their belief systems to account for
their need for the activity.
7. When addiction is fully established, salience is so great that the activity
becomes “virtually the sole source of reward” and begins to be used to avoid
withdrawals.9
8. Recovery requires “a radical change in the policy and style of management of
hedonic tone.”10 This change is two-fold: the addict's decision-making must
suddenly change for the better, and the addictive activity must be replaced with
a number of other rewarding activities, or else the addict must suffer short-term
dysphoria by quitting the activity entirely.11
9. As recovery progresses, the risks of reversion (the return to full addiction) and
of cross-addiction (developing a different addiction from the previous one)
decrease over time.12
10. After any addiction, despite how successful the recovery or how long the addict
has gone without, “there always remains a residual vulnerability. Unusual cues
... can trigger a flashback ... with a full and rapid reinstatement” of the
activity.13
11. “Addictions are not habits, obsessions, compulsions, or attachments and can be
12. No addiction is fully good nor fully bad. “Even the most destructive have some
secondary beneficial effects. ... [Also,] some positive addictions may be very
constructive for individuals and societies

Brown's model also accounts for many of the individual characteristics of
virtually all behavioral addictions. Brown mentions the vast increase in heart rate seen
in blackjack players as an example of his mechanics of gambling addiction.
Although the language of Brown's model seems obtuse, his model also accounts for the
behavior of addicts. Brown accounts for the distortion of reality often documented as
addictions intensify. For example, an addict may continue using a drug under the
excuse that their addicted friend would be lonely if the former did not join their
friend.
Mark Griffiths, a British psychologist, uses a similar model. To him, all
addictions (chemical and behavioral alike) have the following properties: salience,
mood modification, tolerance, withdrawal, conflict and relapse.behavior of addicts, they only superficially cover the biological mechanics of
addiction: that is, what happens in the brain of an addict as his or her habit forms and
sustains itself. Recalling the earlier discussion of neurological biology, addictions
hinge on specific neurotransmitters. Modern scientists attribute virtually all addictive
activity to dopamine, though it is believed among some that serotonin (a different
neurotransmitter for pleasure) also has a part to play. Brown cites experiments which
found arousal in the autonomic and cortical nervous systems associated with
behavioral addictions. As a result, any activity seen as enjoyable could theoretically
become addictive. Naturally, activities that facilitate larger dopamine releases stand a
greater risk for becoming addictive.

For many years it has been observed that vulnerability to alcoholism is
heritable, but only recently have scientists begun to understand the mechanism causing
that vulnerability. Currently, scientists believe that mutation of the A1 and DRD2
genes reduce the number of neurological receptors for dopamine, which means that
people choose commonly addictive behaviors in seeking compensatory boosts of
dopamine. This also gives way to the theory that satiety and tolerance are caused by
the brain “rewiring” itself to have more dopamine receptors, which causes the brain to
no longer be overwhelmed with dopamine with a certain level of activity or chemical
dose. Moreover, since this genetic theory only affects dopamine, the A1 and D2
mutations allow for the facilitation of any form of addiction, not just chemical ones

Drug screens for employment

Oct 25, 2008 - 0 comments

There is no simple answer as to how long drugs will remain in your system, since the answer is influenced by the specific drug half-life, intensity of the usage, method of usage, length of usage, tolerance, fluid intake, body size, body fat, metabolism, andthe specific range which the drug testing lab uses to signify a “positive” for drug use. But the following table provides some general guidelines for the amount of time a drug can be detected by most standard drug tests:

Drug Detection Time
Alcohol 6–24 hours
Amphetamines 2–3 days
Barbituates 1 day to 3 weeks
Benzodiazepines 3–7 days
Cocaine 2–5 days
Codeine 3–5 days
Euphorics (MDMA, Ecstasy) 1–3 days
LSD 1-4 days
Marijuana (THC) 7–30 days
Methadone 3–5 days
Methaqualone 14 days
Opiates 1-4 days
Phencyclidine (PCP) 2–4 days
Steroids (anabolic) 14–30 days

Keep in mind that detection time listed above does not mean that the drug is fully expelled from your body within that amount of time—just that it has dissipated enough that it can no longer be accurately detected—or at least is not high enough to register a “positive” on a drug test. Most drugs are treated by the body as toxins which take time to eliminate. Rather than allow excess toxins to potentially affect vital organs, they are often stored in fat cells, making them typically difficult to release or detoxify from the body.

The basic drug test used by most corporate drug testing programs is called a “Five-Screen” (or “NIDA-5” or “SAMHSA-5”) which is testing for five types of drugs:

Cannabinoids (Marijuana, Hashish)
Cocaine (Cocaine, Crack, Benzoylecognine)
Opiates (Heroin, Opium, Codeine, Morphine)
Amphetamines (Amphetamines, Methamphetamines, Speed)
Phencyclidine (PCP, Angel Dust)
However, many drug testing firms now offer a “Ten-Screen” which expands to include five additional drugs:

Barbituates (Phenobarbital, Secobarbitol, Pentobarbital, Butalbital, Amobarbital)
Methaqualone (Qualuudes)
Benzodiazepines (Tranquilizers-Diazepam, Valium, Librium, Ativan, Xanax, Clonopin, Serax, Halcion, Rohypnol)
Methadone
Propoxyphene (Darvon compounds)
One major drug testing company is now offering the Ten-Screen for the same price as the Five-Screen. Result? Many employers end up testing for more, rather than less. Here is a list of other drugs that can be included in drug tests.

Ethanol (yes, that’s alcohol)
LSD
Hallucinogens (Psilocybin, Mescaline, MDMA, MDA, MDE)
Inhalents (Toluene, Xylene, Benzene)
If there is a drug out there, there is a drug test for it.

How about one more thing to worry about? Second-hand smoke from marijuana and crack cocaine can be absorbed into your hair. Problem? Some companies are now using hair testing to determine drug usage. Answer? Don’t even hang around others who are doing drugs. It can still be absorbed into your system and produce a positive test result. “I didn’t inhale . . .” is not a valid response. And sufficient second-hand smoke exposure can also cause failure of standard urine drug tests. You could fail both a primary and secondary test, with no recourse other than saying that it was someone else. It’s just not worth the risk.

So if you have been exposed to illegal drugs, your best insurance for a clean drug test is to stop using them immediately. And not just temporarily—permanently. Drug test or no drug test, using illegal drugs (and excesses of alcohol) will eventually catch up with you—sooner (if you are foolish enough to use them during work hours) or later (if you obliterate the rest of your life outside work).

Please note: this is not a lecture from Mom and Dad on the evils of drugs. This is a straightforward and honest warning from someone who has seen the negative effects that drugs can have in the workplace. Drugs have no place in work society today and never will.

If you are not a drug user and you fail the drug screening (it does happen), be as straightforward with the employer as possible, let them know that you are not a drug user and ask them if they would please do a confirmation test. Recent estimates from the Journal of Analytic Toxicology showed error rates of 5 to 14 percent on this initial test. The following is a list of over-the-counter medications which have been known to cause false positives in drug testing:

Ibuprofen (Advil, Motrin)
Midol
Nuprin
Sudafed
Vicks Nasal Spray
Neosynephren
Ephedra and Ephedrine-based products (often used in diet products)
Detromethorphan
Vicks 44
There are more, but suffice to say that not every drug test is accurate. That’s why almost all drug testing companies ask you in advance what medications you are presently taking or have taken in the last thirty days. Make sure you list them all, even over-the-counter medications. Some drug testing companies will either have a doctor (or other medical professional) personally interview those who fail a drug test to determine if there was a potential false positive.

If you do receive a failing grade (actually referred to as a “positive” on your drug test—this is one test you do NOT want a positive—you want all negatives) on your drug test, ask to be retested with a confirmation or secondary test. Many employers do not automatically perform the confirmation test since it is significantly more expensive than the initial test. However, if they are unwilling to offer retesting due to the expense, offer to pay the expense on your own and then use a different testing service—ideally a secondary testing provider recommended by the employer so that you won’t have a credibility problem with the second test. If you are turned down in your request or you have additional problems, you may want to seek the advice of a competent attorney for further counsel on your available options.