Beer lift your spirits up
The taste of beer alone is enough to raise one’s spirits. The taste is linked with the release of dopamine, a neurotransmitter that controls the brain’s distribution of pleasure, according to a news study published in Neuropsychopharmacology.
“This is the first human demonstration that a stimulus that is reliably associated with alcohol association – that flavor alone, without any significant amount of alcohol – is able to induce a dopamine response,” said study author David Kareken.
The results were discovered by giving men a small gulp of their favorite beer and then scanning their brains. A scan revealed activity in the area of dopamine production. The amount of beer doled out was not large enough to change the subject’s blood-alcohol content level.
“This paper demonstrates that taste alone impacts on the brain functions associated with desire,” Peter Anderson, a professor of substance use, policy and practice at Newcastle University, U.K., said in a statement.
According to researchers, the study demonstrates that the smell of alcohol can cause relapses for addicts.
by RTT Staff Writer
• Fruits like apples and bananas are excellent foods that trigger the release of dopamine. Bananas contain an amino acid called tyrosine which is the most important stimulant for the brain to produce dopamine. The brown spots on the banana contain the highest amount of dopamine. NaturalBuy.com explains that adding bananas to a diet may helps treat symptoms of depression. Apples contain an antioxidant called quercetin. Quercetin works to preserve dopamine levels in the body by protecting the dopamine cells from getting destroyed. Other fruits trigger the release of dopamine are blueberries, cranberries, prunes, and strawberries.
Protein rich foods
Eating foods high in amino acids will trigger the release of dopamine. Proteins hold an amino acid called tyrosine which triggers the release of dopamine after entering the body. Dopamine is found in foods such as almonds, cheese, chicken, fish, and any other protein containing Omega 3 fatty acids. Dairy products such as cheese, milk, and yogurt contain protein. Black beans, chick peas, lima beans, and fava beans are all sources of rich protein foods that will help trigger dopamine. Eggs are a source of protein and contain choline, which is a vitamin that helps improve concentration and memory. Almonds are nuts loaded with protein but should be eaten in moderation because they can cause weight gain and headaches.
Chocolate contains phenylalanine, which is an essential amino acid that turns into tyrosine. The University of Maryland explains that tyrosine is a building block for the neurotransmitter that triggers dopamine. The stimulant in chocolate is in the cocoa and greater amounts of tyrosine are found in dark chocolate. In chocolate, the fat from the milk will also trigger dopamine because it’s a dairy product. Dark chocolate contains many antioxidants , however too much could harm the liver and cause weight gain. According to Chocolate.org, chocolate contains phenylalanine which is related to amino acids. Phenylalanine increases activity and has been proven to relieve depression in 60 percent of depressed patients.
Foods high in sugar, cholesterol and saturated fats can lower your levels of dopamine. While these foods may produce a temporary feeling of satisfaction, they interfere with proper brain function and so the production of dopamine. Your eating habits closely correlate with your mood, so picking fresh fruits and vegetables and other foods with high nutritional value will not only keep you slimmer, it’ll keep your mood more balanced and you feeling better.
Dopamine and MAO
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.
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.
Foods To Avoid When Taking Monoamine Oxidase Inhibitors
Q. Please review the dietary restrictions that should be observed when a patient is receiving monoamine oxidase inhibitor (MAOI) therapy?
R. Tyramine is an amino acid which is found in various foods, and is an indirect sympathomimetic that can cause a hypertensive reaction in patients receiving MAOI therapy.
Monoamine oxidase is found in the gastrointestinal tract and inactivates tyramine; when drugs prevent the catabolism of exogenous tyramine, this amino acid is absorbed and displaces norepinephrine from sympathetic nerve ending and epinephrine from the adrenal glands. If a sufficient amount of pressor amines are released, a patient may experience a severe occipital or temporal headache, diaphoresis, mydriasis, nuchal rigidity, palpitations, and the elevation of both diastolic and systolic blood pressure may ensue (Anon, 1989; Da Prada et al, 1988; Brown & Bryant, 1988).
On rare occasions, cardiac arrhythmias, cardiac failure, and intracerebral hemorrhage have developed in patients receiving MAOI therapy that did not observe dietary restrictions (Brown & Bryant, 1988).
Therefore, dietary restrictions are required for patients receiving MAOIs. Extensive dietary restrictions previously published were collected over a decade ago and due to changes in food processing and more reliable analytical methods, new recommendations have been published (Anon, 1989; McCabe, 1986).
The tyramine content of foods varies greatly due to the differences in processing, fermentation, ripening, degradation, or incidental contamination. Many foods contain small amounts of tyramine and the formation of large quantities of tyramine have been reported if products were aged, fermented, or left to spoil. Because the sequela from tyramine and MAOIs is dose-related, reactions can be minimized without total abstinence from tyramine-containing foods. Approximately 10 to 25 mg of tyramine is required for a severe reaction compared to 6 to 10 mg for a mild reaction. Foods that normally contain low amounts of tyramine may become a risk if unusually large quantities are consumed or if spoilage has occurred (McCabe, 1986).
Three lists were compiled (foods to avoid, foods that may used in small quantities, and foods with insufficient evidence to restrict) to minimized the strict dietary restrictions that were previously used and improve compliance and safety of MAOI therapy. The foods to avoid list consists of foods with sufficient tyramine (in small or usual serving sizes) that would create a dangerous elevation in blood pressure and therefore should be avoided (McCabe, 1986).
ALCOHOLIC BEVERAGES – avoid Chianti wine and vermouth. Consumption of red, white, and port WINE in quantities less than 120 mL present little risk (Anon, 1989; Da Prada et al, 1988; McCabe, 1986). BEER and ALE should also be avoided (McCabe, 1986), however other investigators feel major domestic (US) brands of beer is safe in small quantities (1/2 cup or less than 120 mL) (Anon, 1989; Da Prada, 1988),
but imported beer should not be consumed unless a specific brand is known to be safe. WHISKEY and LIQUEURS such as Drambuie(R) and Chartreuse(R) have caused reactions. NONALCOHOLIC BEVERAGES (alcohol- free beer and wines) may contain tyramine and should be avoided (Anon, 1989; Stockley, 1993).
BANANA PEELS – a single case report implicates a BANANA as the causative agent, which involved the consumption of whole stewed green banana, including the peel. Ripe banana pulp contains 7 mcg/gram of tyramine compared to a peel which contains 65 mcg/gram and 700 mcg of tyramine and dopamine, respectively (McCabe, 1986).
BEAN CURD – fermented bean curd, fermented soya bean, soya bean pastes contain a significant amount of tyramine (Anon, 1989).
BROAD (FAVA) BEAN PODS – these beans contain dopa, not tyramine, which is metabolized to dopamine and may cause a pressor reaction and therefore should not be eaten particularly if overripe (McCabe, 1986; Anon, 1989; Brown & Bryant, 1988).
CHEESE – tyramine content cannot be predicted based on appearance, flavor, or variety and therefore should be avoided. CREAM CHEESE and COTTAGE CHEESE have no detectable level of tyramine (McCabe, 1986; Anon, 1989, Brown & Bryant, 1988).
FISH – fresh fish (Anon, 1989; McCabe, 1986) and vacuum- packed pickled fish or CAVIAR contain only small amounts of tyramine and are safe if consumed promptly or refrigerated for short periods; longer storage may be dangerous (Anon, 1989). Smoked, fermented, pickled (Herring) and otherwise aged fish, meat, or any spoiled food may contain high levels of tyramine and should be avoided (Anon, 1989; Brown & Bryant, 1988).
GINSENG – some preparations have resulted in a headache, tremulousness, and manic-like symptoms (Anon, 1989).
PROTEIN EXTRACTS – three brands of meat extract contained 95, 206, and 304 mcg/gram of tyramine and therefore meat extracts should be avoided (McCabe, 1986). Avoid liquid and powdered PROTEIN DIETARY SUPPLEMENTS (Anon, 1989).
MEAT, nonfresh or liver – no detectable levels identified in fresh chicken livers; high tyramine content found in spoiled or unfresh livers (McCabe, 1986). Fresh meat is safe, caution suggested in restaurants (Anon, 1989; Da Prada et al, 1988).
SAUSAGE, BOLOGNA, PEPPERONI and SALAMI contain large amounts of tyramine (Anon, 1989; Da Prada et al, 1988; McCabe, 1986). No detectable tyramine levels were identified in country CURED HAM (McCabe, 1986).
SAUERKRAUT – tyramine content has varied from 20 to 95 mcg/gram and should be avoided (McCabe, 1986).
SHRIMP PASTE – contain a large amount of tyramine (Anon, 1989).
SOUPS – should be avoided as protein extracts may be present; miso soup is prepared from fermented bean curd and contain tyramine in large amounts and should not be consumed (Anon, 1989).
YEAST, Brewer’s or extracts – yeast extracts (Marmite) which are spread on bread or mixed with water, Brewer’s yeast, or yeast vitamin supplements should not be consumed. Yeast used in baking is safe (Anon, 1989; Da Prada et al, 1988; McCabe, 1986).
The foods to use with caution list categorizes foods that have been reported to cause a hypertensive crisis if foods were consumed in large quantities, stored for prolong periods, or if contamination occurred. Small servings (1/2 cup, or less than 120 mL) of the following foods are not expected to pose a risk for patients on MAOI therapy (McCabe, 1986).
FOODS TO USE WITH CAUTION
(1/2 cup or less than 120 mL)
Alcoholic beverages – see under foods to avoid.
AVOCADOS – contain tyramine, particularly overripe (Anon, 1989) but may be used in small amounts if not overripened (McCabe, 1986).
CAFFEINE – contains a weak pressor agent, large amounts may cause a reaction (Anon, 1989).
CHOCOLATE – is safe to ingest for most patients, unless consumed in large amounts (Anon, 1989; McCabe, 1986).
DAIRY PRODUCTS – CREAM, SOUR CREAM, cottage cheese, cream cheese, YOGURT, or MILK should pose little risk unless prolonged storage or lack of sanitation standards exists (Anon, 1989; McCabe, 1986). Products should not be used if close to the expiration date (McCabe, 1986).
NUTS – large quantities of PEANUTS were implicated in a hypertensive reaction and headache. COCONUTS and BRAZIL NUTS have also been implicated, however no analysis of the tyramine content was performed (McCabe, 1986).
RASPBERRIES – contain tyramine and small amounts are expected to be safe (McCabe, 1986).
SOY SAUCE – has been reported to contain large amounts of tyramine and reactions have been reported with teriyaki (Anon, 1989), however analysis of soy sauce reveals a tyramine level of 1.76 mcg/mL and fermented meat may have contributed to the previously reported reactions (McCabe, 1986).
SPINACH, New Zealand prickly or hot weather – large amounts have resulted in a reaction (Anon, 1989; McCabe, 1986).
More than 200 foods contain tyramine in small quantities and have been implicated in reactions with MAOI therapy, however the majority of the previous reactions were due to the consumption of spoiled food. Evidence does not support the restriction of the following foods listed if the food is fresh (McCabe, 1986).
FOODS WITH INSUFFICIENT EVIDENCE FOR RESTRICTION (McCabe, 1986)
anchovies – cream cheese – raisins
beetroot – cucumbers – salad dressings
chips with vinegar – egg, boiled – snails
Coca Cola (R) – figs, canned – tomato juice
cockles – fish, canned – wild game
coffee – junket – worcestershire sauce
corn, sweet – mushrooms – yeast-leavened bread
cottage cheese – pineapple, fresh
Any protein FOOD, improperly stored or handled, can form pressor amines through protein breakdown. Chicken and beef liver, liver pate, and game generally contain high amine levels due to frequent mishandling. Game is often allowed to partially decompose as part of its preparation. Ayd (1986) reported that the freshness of the food is a key issue with MAOIs and that as long as foods are purchased from reputable shops and stored properly, the danger of a hypertensive crisis is minimal. Some foods should be avoided, the most dangerous being aged cheeses and yeast products used as food supplements (Gilman et al, 1985).
With appropriate dietary restrictions, the incidence of hypertensive crises has decreased to approximately 4% (Zisook, 1985). Treatment of a hypertensive reactions includes the=7F administration of phentolamine (Anon, 1989) 2.5 to 5 milligrams intravenously (slow) titrated against blood pressure (Zisook,=7F 1985; Lippman & Nash, 1990). One report has suggested that the use of sublingual nifedipine 10 milligrams was effective in treating 2 hypertensive reactions following the ingestion of a tyramine-containing food in a patient receiving MAOI therapy (Clary & Schweizerr, 1987). Chlorpromazine also has alpha-blocking properties and has been recommended as an agent for discretionary use (patient-initiated treatment) in the setting of dietary indiscretion (Lippman & Nash, 1990).
Dietary restrictions are required for individuals receiving monoamine oxidase inhibitor therapy to prevent a hypertensive crisis and other side effects.
The foods listed in the dietary restrictions have been categorized into those foods that must be avoided, foods that may be ingested in small quantities, and those foods that were previous implicated in reactions but upon analyses of fresh samples only a small tyramine content was identified and should be safe to consume if freshness is considered.
1. Anon: Foods interacting with MAOI inhibitors. Med. Lett. Drug Ther. 1989; 31:11-12.
2. Ayd FJ: Diet and monoamine oxidase inhibitors (MAOIs): an update. Int. Drug Ther. Newsletter 1986; 21:19-20.
3. Brown CS & Bryant SG: Monoamine oxidase inhibitors: safety and efficacy issues. Drug Intell. Clinical Pharmacy 1988; 22:232-235.
4. Clary C & Schweizer E: Treatment of MAOI hypertensive crisis with sublingual nifedipine. Journal Clinical Psychiatry 1987; 48:249-250.
5. Da Prada M, Zurcher G, Wuthrich I et al: On tyramine, food, beverages and the reversible MAO inhibitor moclobemide. J. Neural Transm. 1988; 26(Suppl):31-56.
6. Gilman AG, Goodman LS & Rall TW et al (Ed): Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 7th ed., Macmillan Publishing, New York, NY, 1985.
7. Lippman SB & Nash K: Monoamine oxidase inhibitor update. Potential adverse food and drug interactions. Drug Safety 1990; 5:195-204.
8. McCabe BJ: Dietary tyramine and other pressor amines in MAOI regimens: a review. J. Am. Diet Assoc. 1986; 86:1059-1064.
9. Stockley I: Alcohol-free beer not safe for MAOI patients. Pharm. J. 1993; 250:174. 10. Zisook S: A clinical overview of monoamine oxidase inhibitors. Psychosomatics 1985; 26:240-251.
Theodore G Tong, Pharm D/C Hansen
Assistant Clinical Professor of Pharmacy
University of California
San Franscisco, California 94143
Revised by DRUGDEX(R) Editorial Staff
Denver, Colorado 80204, 09/82
Revised by DRUGDEX(R) Editorial Staff, 09/83; 07/85;07/86; 09/89; 04/93; 01/94
Stephen R. Saklad, Pharm.D. – firstname.lastname@example.org
Psychiatric Pharmacy Program
The Univ Texas College of Pharmacy
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