Ecstasy and Depression: Risk Factor or Potential Cure

Ecstasy Popularity

After several years of falling popularity, ecstasy use has
once again been increasing in clubs and on college campuses. As this
recreational drug first appeared on the arena, it gained popularity fast among
adolescents and young adults in the nightclub scene or dance parties known as
“raves.” However, the profile of the typical ecstasy user has been changing now.
The drug is widely used by all demographic groups because so many young people
believe that ecstasy is a safe drug. A person may experience feelings of mental
stimulation, emotional warmth, empathy towards others, a general sense of
well-being and decreased anxiety.

The reason
ecstasy popularity has increased might be lying under its main traits, outlined
above. The research made on the reasons of sudden increase in Ecstasy
Popularity show that some people turn to it as a temporary means of escaping
the problem. It is also been observed that young people have started taking the
MDMA as a part of their lifestyle. Ecstasy popularity studies also shows that
recently people have tendency to take ecstasy more than other drugs because, it
has very few direct effects, almost all the effects are indirect and hence it
is considered as harmless by many users.

Young adults are not aware that ecstasy can produce a
variety of adverse health effects, including nausea, chills, sweating,
involuntary teeth clenching, muscle cramping, blurred vision and, in some
cases, death due to overdose. Ecstasy can affect the brain by altering the
activity of chemical messengers, or neurotransmitters with symptoms such as
high blood pressure, faintness, panic attacks, and in severe cases, a loss of
consciousness and seizures.

In this publication, we will not review in details all
negative effects on health and wellbeing, which ecstasy may cause to its
consumers, but we will focus on the scientifically proven facts, that its use
can lead to the severe consequences to the mental health, causing clinical depression.

What is Ecstasy?

Ecstasy is a slang or street name for Methylenedioxymethamphetamines
(MDMA) It is a synthetic, psychoactive mind-altering drug with hallucinogenic
and amphetamine (stimulant) like effects. It alters perception of time and
distance.  MDMA was first developed in 1914 as an appetite suppressant or
diet drug. It was a legal substance up until 1985. 

As Ecstasy was
considered as a natural antidepressant, doctors used to prescribe it to the
patients until it was banned by UN and USA. Prior to this ban, the MDMA was one
of the main tools against depression, the doctors had. It was also widely used for
treating post traumatic stress disorder.

MDMA/Ecstasy is produced in clandestine laboratories, and is
seldom pure.  The amount in a capsule or tablet is likely to vary
considerably, which could lead to overdoses.  Now, MDMA is under a Federal
Drug Enforcement Administration (DEA) -- Schedule I Substance -- meaning that
it has no medical use and high abuse potential. The Federal penalty for
manufacturing or selling can lead to fines up to four million dollars.  A
ringleader or head manufacturer could receive life in prison. 

What does ecstasy do to the brain?

                    

Ecstasy works by stimulating the production of a brain
chemical called serotonin, key in the regulation of mood and emotion. The rush
you get comes from the release of much higher levels of serotonin than normal.
But by artificially messing with this production process, some scientists
believe users are diminishing their brain's ability to produce serotonin in the
future.

Mid-week Hangover

Ecstasy works by changing the way the brain produces and
handles the neurotransmitter serotonin that, among other things, regulates your
mood. 

"Experts agree that once the initial serotonin rush
produced by the drug (the 'high') has passed, levels of serotonin in the brain
will fall," says Ruth Goldsmith from the independent drug information and
expertise centre DrugScope. "This seems to account for the 'mid-week
hangover' or 'Tuesday blues'; the short period of depression experienced by
many ecstasy users in the days following their use of the drug." 

There are several possible reasons why ecstasy my cause the
short-term depression. MDMA works by
releasing from certain brain cells large amounts of the brain chemical,
serotonin. This release of serotonin is what causes Ecstasy’s mood elevation
effect, as well as the feelings of empathy, self-acceptance, and emotional
closeness with others that so many people find valuable and rewarding about the
drug. But in releasing large amounts of serotonin, MDMA also depletes the
brain’s supply. It then takes some time for the brain to replenish what was
released. How long does it take for serotonin levels to be fully restored after
someone takes Ecstasy? This depends on the individual’s diet, general heath,
genetic make-up, how much ecstasy the person took, and other random factors.
There’s no way to tell for sure, but based on animal studies, scientists say
that it could take anywhere from 48 hours to an entire week. The mild
depression some people feel after taking Ecstasy could be related to this
temporary depletion of serotonin.

Somehow similar theory states, that the release of serotonin also causes serotonin
receptors in the brain to down-regulate, which basically means turn themselves
off for a while. The up-and-down regulation of receptors is one of the primary
ways the brain tries to achieve homeostasis, or balance. These receptors work
in conjunction with the amount of serotonin around and are just as important in
the regulation of mood as serotonin itself. In trying to maintain a balanced
mood, these receptors respond to the amount of serotonin around by turning
themselves on and off (up-regulation and down-regulation). When they are
flooded with serotonin as a result of taking Ecstasy, many of them
down-regulate.

The majority of
these receptors will up-regulate again as soon as the excess serotonin is
metabolized away. However, some of these receptors may stay down-regulated
longer, perhaps days, weeks, or even months. The depression some people feel
after taking ecstasy may be a result of these serotonin receptors staying
down-regulated too long. Whether, how much, or how often this happens may
largely be a genetic factor unique to the individual.

Some people may
simply be genetically pre-disposed towards Ecstasy-related depression. Some
ecstasy users who experience depression might have been depressed before they
started using ecstasy. Depression is a common illness that often goes
undiagnosed and untreated. This is particularly true for teenagers and young
adults who suffer from mild to moderate depression. It is likely that many
compulsive ecstasy users are unconsciously trying to self-medicate their
depression. However, ecstasy use may play unfavorable role
in depression treatment, since by directly affecting serotonin, it may trigger
getting your neurotransmitters out of balance, especially if they already were in the
borderline condition.

 Ecstasy
and Clinical Depression

While danger of
short-term mild depressive episodes has somewhat limited effect on mental
wellbeing, the long-term consequences might be far more dangerous, and even
disastrous.

Based on the
study 2003 results in Britain, experts warned that the changes to the brain
brought about by the drug leave a legacy of long-term mental health problems,
including memory loss and lack of concentration. Psychologists have found that
even those who gave up taking the drug several years ago scored higher on a
depression rating than people who had never taken it.

A 2005 Cambridge University study discovered that people
with a certain genetic make-up showed greater signs of depression after using
the drug. The Cambridge team looked at the gene which controls serotonin
transporters in the brain. Everybody has two copies of each gene, and there are
two possible versions which people can carry, so they can either be classed as
ll, ls or ss. They found that 60% of people who had the ss version were
assessed as having at least mild depression after taking ecstasy, while
non-drug users with the ss type displayed no such problems.

Similar results were received in 2006 during the three-year
study conducted at the PET Center at Arhus Hospital in Denmark, showed the
recreational drug caused depression in laboratory pigs. The scientists injected
pigs with varying doses of Ecstasy to study the effect the drug has on the
pigs' brains. The study has significant importance for humans as well, as pigs'
brains are quite similar to human brains in many perspectives.

Controversial Studies

Recently, the
Ecstasy positive and negative therapeutic effects came in light of the general
community due to several researches, producing controversial results of weather
ecstasy may cause the long-term brain damage or not.

There is no
evidence that ecstasy causes brain damage, according to one of the largest
studies into the effects of the drug. Too many previous studies made
over-arching conclusions from insufficient data, say the scientists responsible
for the research, and the drug's dangers have been greatly exaggerated. It was
concluded that ecstasy has not been linked to damage to the central nervous
system and no long-term changes to emotional states and behavior have been
triggered by consumption of the drug.

The study was
carried out by a team led by Professor John Halpern of Harvard Medical School
and published in the journal Addiction February 2011. Many experts who
have argued that the drug is relatively safe welcomed the new paper. "I
always assumed that, when properly designed studies were carried out, we would
find ecstasy does not cause brain damage," said Professor David Nutt, who
was fired as chair of the Advisory Council on the Misuse of Drugs by Alan
Johnson, then home secretary, for publicly stating alcohol and tobacco were
more harmful than ecstasy.

Ronald Cowan, M.D., Ph.D., associate professor of Psychiatry
in his report in the May 2011 issue of Neuropsychopharmacology opposes
this viewpoint, insisting that recreational Ecstasy use is indeed associated
with a chronic change in brain function. Cowan and his colleagues examined
brain activation during visual stimulation, using functional magnetic resonance
imaging (fMRI), in subjects who had previously used Ecstasy (but not in the two
weeks prior to imaging) and in subjects who had not previously used Ecstasy. They
found increased brain activation in three brain areas associated with visual
processing in Ecstasy users with the highest lifetime exposure to the drug. The
findings were consistent with the investigators' predictions based on results
from animal models: that Ecstasy use is associated with a loss of serotonin
signaling, which leads to hyper-excitability (increased activation) in the
brain. The hyper-excitability suggests a loss in brain efficiency, Cowan said,
"meaning that it takes more brain area to process information or perform a
task." The investigators found that this shift in brain excitability did
not return to normal in subjects who had not used Ecstasy in more than a year.

Summary

While I am not expert on the topic, based on the various
resources, available on the Web, I can conclude that both proponents and
opponents of Ecstasy have their valid points, but research results are still
inconclusive to choose side. There are multiple studies and clinical ongoing
trials, trying to bring the positive effects of the drug to the safe medicine
(for PTSD, depression, and cancer treatment) in Europe, Israel, and USA, but there
is still a long way to go, and the resulting drugs might be substantially
modified by the scientists from the state as you may take it now.

For those, who use ecstasy as recreational drug on regular
basis, I have one question to ask: Are you ready to jeopardize your health for
short-term positive emotional effect, if there is a chance that it may cause
your mental destabilization on long run? Think about that, before you take next
pill.

In any case, there are safer alternatives, as marijuana,
for example...  

Sources and Additional
Information:

http://www.thedowneypatriot.com/bookmark/12393685-Ecstasy-growing-in-popularity-among-teens

http://vraelcontentblogs.wordpress.com/2011/06/21/why-did-ecstasy-increase-in-popularity/

http://www.taadas.org/factsheets/ecstasyFacts.htm

http://www.thesite.org/drinkanddrugs/drugsafety/drugsandyourbody/ecstasyanddepression

http://dancesafe.org/drug-information/ecstasy-and-depression

http://www.guardian.co.uk/society/2003/mar/16/drugsandalcohol.science

http://www.guardian.co.uk/society/2011/feb/19/ecstasy-harm-brain-new-study

Tryptophan - promising remedy against depression

Overview

Considering the depression as disease caused by chemical imbalance in the brain, we can search for natural supplements taken with food to neutralize the negative impact in our body. One way to increase amount of the useful components is consuming food that contain tryptophan. Tryptophan is a precursor to serotonin, which helps you relax and can generally improve your mood and treat your insomnia. Tryptophan is an essential amino acid, what means it cannot be produced in the body and needs to be taken  as a part of the diet or as a dietary supplement.

Tryptophan and Serotonin

Tryptophan is an essential amino acid that must be consumed with food, rather than any nonessential amino acid the human body might be able to generate with no relation to the diet. Obtained tryptophan is converted by our body into the chemical 5-hydroxytryptophan, or 5-HTP, which is then converted into melatonin, serotonin, and, very inefficiently, niacin. Serotonin is a neurotransmitter that facilitates the relay of signals between brain cells. Eating foods containing tryptophan is a way to increase serotonin in your brain naturally, which may have a positive effect not only on your mood and anxiety, but on your sleep, appetite and pain sensation as well.

Tryptophan and Depression

While regular antidepressant drugs help relieve depression by increasing the availability of serotonin in the brain and preventing its depletion, tryptophan allows to increase serotonin levels naturally. Research by Linda Booij and colleagues, reported in 2005 in "The British Journal of Psychiatry," found that acute tryptophan depletion causes a relapse into depression and depressive symptoms, such as lethargy and loss of appetite, in people with remitted depression, highlighting the importance of tryptophan for protection against depressed moods. Women need more tryptophan than men. Research in 1997 from McGill University found that men produce 52 percent more serotonin in their brains than women, with the result that women are more likely than men to suffer from depression unless their tryptophan levels are high.

What is Tryptophan used for (other than depression)?

Tryptophan is used as a natural cure for a variety of conditions, besides depression, such as anxiety, stress, low moods, poor mental health, migraine headaches, insomnia, nervousness, carbohydrate craving and other eating disorders, premenstrual tension, fibromyalgia, excessive alcohol use, other addictive states, aggression, irritability, attention deficit-hyperactivity disorder (ADHD), Tourette's syndrome and some psychiatric disorders.

Foods Containing Tryptophan

Foods that contain tryptophan include milk, turkey, beef, cottage cheese, oats, soy, bananas, cheese, nuts, sesame seeds and peanut butter. Nuts, in particular almonds, and sesame seeds, can be sprinkled on casseroles, breakfast cereals and salads.

Tryptophan Supplements

One disadvantage of tryptophan is that our bodies do not always absorb it efficiently, even when foods high in tryptophan, such as almonds and peanut butter, are eaten. Supplements of tryptophan are available at doses that can be readily absorbed by the brain. These supplements must be taken together with vitamin C and B-complex vitamins to support the transformation of tryptophan into serotonin. Like all supplements, tryptophan should be taken only on the recommendation of your doctor.

5HTP (5-hydroxy tryptophan) is considered by many to be more effective than tryptophan for depression. L-Tryptophan (which is the desired form) is converted to 5HTP before becoming serotonin; taking 5HTP bypasses this first step of the process. The effectiveness of 5HTP may be increased with gingko biloba, St. John's Wort, B-complex vitamins with magnesium, tyrosine, flax seed oil, and ginger. Vitamin B6 and folic acid may assist in the conversion to serotonin. An equivalent dose of 5HTP (compared to 1gm of tryptophan) is about 100 mg. Doses of 100mg tid have been used, but it may be best to start at a lower dose and slowly increase as the side-effect of nausea can occur at higher doses. Starting at a lower dose reduces the likelihood of nausea, which usually disappears in less than 2 weeks.

Side effects and precautions

Tryptophan is generally well tolerated, but there is a risk of several side effects (these are usually mild, occurring mostly at the higher doses and fading away by themselves after discontinuing Tryptophan supplementation).

Among possible side effects of Tryptophan are dryness of the mouth, nausea, stomach disturbances and drowsiness.

Make sure you know well your reaction to tryptophan before driving or any other activity demanding high alertness.

Do not take L-tryptophan in combination with other serotonin increasing drugs, such as SSRIs, MAOIs and sedatives, for abnormally high levels of serotonin are no better than its deficiency.

As with any other nutritional supplement, it is advisable to seek medical advice before taking tryptophan, as it may interact with other medications or cause adverse effects.

Sources and Additional Information:

http://www.livestrong.com/article/385527-tryptophan-depression-anxiety/

http://depressioncure4u.com/tryptophan.html

http://www.digitalnaturopath.com/treat/T138417.html

http://www.xomba.com/foods_fight_depression

Could Eating A Vegan Diet Cause Depression?

Eat healthy – that is the slogan you hear everywhere, and if you follow-up this popular appeal, it might definitely help you with multiple physical and mental health issues. But what is healthy? Some specialists consider healthy diet as well balanced diet, other recommend strictly vegetarian or vegan diets. But that is just the beginning of the healthy diets definition list. You may find completely well-rounded scientific explanations on the usefulness of high-protein and other special diets. Who is right, and who is wrong? I guess, one size does not fit all. What may be a good idea for one individual, might be absolutely bad idea for another.

In this post we will review the concept that vegan diet might lead to the clinical depression due to the lack of certain food-related components, which are not received by the strictly restricted food consumption.

In general, a vegan diet might or might not cause depression, depending on the individual characteristics of the person and how it is applied. It is, however, well known that transitioning to a vegan diet most likely will cause all sorts of physical and emotional symptoms while your body gets used to it, just like transitioning to any new diet or even a new altitude or lifestyle can. These symptoms generally pass after a few weeks. While that is understandable and acceptable, a vegan diet can put you at risk for certain nutritional deficits if you are not careful about meeting your nutritional needs, specifically protein, iron and B12, with B12 being the most worrisome.

There is increasing evidence that diet may play a causative role in some cases of depression. The food production in industrialized societies uses intensive farming and processing techniques. This can contribute to depleted levels of omega 3 fatty acids, certain amino acids and other essential nutrients in the food we eat. Also over time our food choices and preferences have changed, which has led to a skewed ratio of fats in out diet.

Omega 3 is an important essential fats for the body. Its deficiency has been linked to depression, anxiety, aggressiveness and even insomnia. In some studies it was observed that patients suffering from depression have lower levels of omega-3 fatty acids in their cell membranes. More startlingly, its deficiency worsens the conditions of ADHD children considerably. Research has shown that patients with bipolar depression who increased their consumption of foods containing omega 3 showed remarkable improvement in mood, which supports the role of omega 3 fatty acids in the treatment of depression .

Omega 3 is required in the diet and cannot be made within the body. Foods rich in omega 3 include oily fish such as salmon and mackerel, flaxseeds walnuts, olive oil, pumpkin seeds. Ensuring 2-3 portions of oily fish per week should provide adequate omega 3 in your diet.

Amino acids are also not produced within the human body. Tryptophan is an amino acid which is converted into serotonin in the body and is a natural relaxant. This can be used in the treatment of depression to assist with a good night’s sleep, treat migraines and even boost the immune system. Deficiency in the essential amino acid Lysine may cause fatigue, irritability and a lack of concentration. Good sources of lysine include meat, chicken, and eggs and legumes.

Carbohydrates are important in the fight against depression. They help to release the chemical monoamine serotonin. This chemical is found in the brain and is a mood-enhancer. It induces sleep and brings on relaxation. Depression seems to stem from reduced serotonin in the brain. Hence the feeling of satisfaction as soon as a person eats a meal with carbohydrates. Increasing complex carbohydrates that are absorbed slowly such as brown rice, whole grain wheat, bran, fruits and vegetables may be important in the treatment of depression, as this will help ensure a steady supply of serotonin.

Depression can also be intensified or even caused by deficiencies of vitamins and minerals, like folate, B12 and vitamin C and magnesium. In a major study, a direct link between low folate levels and neuropsychiatry disorder was established. It has also been suggested that an increased intake of folate can help reduce the high levels of homocysteine often present during depression. Foods rich in folate and vitamin c include spinach, broccoli, tomato juice, kidney beans, lentils and asparagus and increasing amounts of these foods in the diet could be useful in the treatment of depression.

Vitamin B12 is found in animal products such as milk, meat, cheese and yogurt. Vegans and strict Vegetarians who do not drink milk products can be lacking in Vitamin B12. Elderly people often suffer from malabsorption of this vitamin due to a lack of acidity in the stomach (which assists in its digestion) and this can lead to mood disorders or even depression. Vitamin B12 is therefore a key vitamin to consider in supplementing for the treatment of depression. It takes a long time for B12 deficiency to show up, because your requirements are quite low and it stays in the body for a long time, so someone could be vegan for years before they have problems. The best vegan source for this nutrient is nutritional yeast. Many vegetarians/vegans make the mistake of eating refined carbohydrates. Avoid these as much as you can; they deplete the body of B vitamins, which can make you feel depressed/anxious. Make sure you get enough protein, too–the brain needs it!

A deficiency of magnesium is sometimes associated with forms of depression. A diet rich in magnesium such as nuts and grains, spinach, and meat may be beneficial in alleviating the symptoms of depression.

The most common mineral deficiencies in vegetarians are related to poor iron intake. Iron is a mineral that comprises hemoglobin, necessary for oxygenating the blood. A diet that does not include animal products requires higher percentages of daily intake from alternative sources. If you are not getting enough iron through dried beans and dark leafy green vegetables every day, you can develop an iron deficiency, which results in fatigue, depressive symptoms and anemia. These generally go away as soon as your iron is back on track. You can definitely prevent this by eating lots of beans, leafy greens and whole grains.

Protein deficiencies can also cause depression. For example, long term veganism leads to a lack of Tryptophan in the diet. Tryptophan is an amino acid found only in animal protein, and is the precursor to the neurotransmitter Seratonin, which is directly responsible for happiness.

 Too many simple carbohydrates can also cause depression, especially when protein is low. Try leafy greens such as collards (calcium and magnesium are essential).

While vegans generally report good overall health, some staples in their diet are common allergens. For example, peanuts, tree nuts, soybeans and wheat are repeat offenders that cause an array of symptoms from leaky gut syndrome to mental disturbances such as depression. When the body suspects a foreign antigen is present, it quickly responds via the immune system. Over an extended period of being exposed to an allergy, the body remains in attack mode, depleting many other resources and increasing the likelihood of autoimmune disease. Autoimmune disease is both a cause and effect of depression.

Candida, or candida overgrowth, is common in the vegetarian diet. This is due to the high consumption of fruit and fruit juice, pasta, breads, honey and similar products laden with parasites, bacteria or yeasts. The National Candida Center reports that a single yeast cell produces over 75 known toxins that act like poison in the human body and result in a weakened immune system. They impair the brain and central nervous system. Depressive symptoms are not uncommon, as the body simply cannot stave off multiple attacks.

Diet and depression may well have a cyclical relationship. Depression may be exacerbated by dietary deficiency in the first place and can go onto lead to a loss of appetite or apathy towards food and wellbeing. A dietary approach to the treatment of depression is by no means the whole answer but it could play an important role.

And most important, no matter what you eat, do not forget that health diet is only a part of the healthy lifestyle. You also need sun, exercise, friendship, therapy, and a spiritual practice such as meditation for best results.

Sources and Additional Information:

http://www.vegetarianvitaminsguide.com/vitamins-supplements/could-eating-a-vegan-diet-cause-a-chemical-imbalance-in-your-brain/

http://www.artificialgrassmasters.com/can-a-vegan-diet-cause-depression.html

http://rekindlingthereformation.com/H-deception_Nedley_depression_nutrition_food.html

http://www.livestrong.com/article/364101-depression-as-a-vegetarian/

Neuroreasons for Clinical Depression by Charles Nemeroff

Charles Nemeroff, a writer for Scientific America, states both decreased activity of a neurotransmitter, as well as overactivity of a hormonal system, can lead to severe depression and, concurrently, suicide. Neurotransmitters travel between neurons, or nerve cells, in order to perform functions vital to life. Nemeroff states norepinephrine and serotonin, both monoamine type neurotransmitters, are natural anti-depressants. In order to understand the way these monoamines affect human biological make-up, it is necessary to have a brief understanding of the way neurotransmitters work.

Between two neurons lies a small gap called the synapse. Neurotransmitters cross the synapse, being “fired” from one neuron and attaching to the next. Sometimes the receiving neuron will send out a message instructing the sending neuron to slow its rate of firing neurotransmitters. The sending neuron then has to pull the neurotransmitters back into itself, a process known as “reuptake”. Nemeroff points out that, due to overactive reuptake, reduced levels of norepinephrine have been noted in the brain of many depressed patients. Similarly, the study points out that in many patients who have committed suicide increased norepinephrine receptors were located in the brain’s cortex. Often receptors in the brain expand in number in order to compensate for low levels of transmitter molecules.

Due to these findings, reports Nemeroff, some drugs are now available that block norepinephrine reuptake and increase norepinephrine in the synapse, allowing it to act as an antidepressant. Serotonin is also a natural antidepressant and relates to drugs such as Prozac, which blocks serotonin reuptake. Nemeroff details how cells which produce serotonin often extend into many areas of the brain thought to contribute to depression, such as the hypothalamus. The drugs which prohibit serotonin reuptake are some of the most effective antidepressants ever made. Effexor is an especially effective drug because it blocks reuptake of serotonin and norepinephrine. Neurotransmitters are not the only biological elements which contribute to depression. Much research has been done that seems to show correlation between hormones and depression.

The hypothalamus regulates the hormonal system in the human body. As Nemeroff observed, the system that manages the body’s stress response is often singled out for causing severe depression. When there exists a physical or psychological threat to the body, the HPA-axis (hypothalamus-pituitary-adrenal) increases production of cortisol and, in effect, initiates the “fight or flight” function of the body. Nemeroff reports numerous studies show over-activation of the HPA-system may lead to depression. Because this system reacts to stress, however, it is unlikely that it will initiate itself without some type of anxiety-causing event. External sociological forces, coupled with increasingly negative psychological conflict, can cause the stress necessary to activate the HPA-system.

Biochemical functions, though extremely powerful and relevant to human behavior, rarely act alone. Simply because one may have a hyperactive HPA-axis or low levels of serotonin or norepinephrine monoamines, it is not definite a person will suffer from extreme depression or attempt suicide. Obviously emotions, though they may exist in chemical form, result from the ways people internalize and perceive external events as well as the ways in which people view themselves. The fact of the matter is people are strongly influenced by society, on conscious and subconscious levels. Society exists inside and outside of people, intermixing with the mind and with the psyche. The entire idea of consciousness is so complex and enigmatic, it is severely limiting to relate any aspect of it to only one particular school of science.

Nemeroff, 59, a psychiatrist at Emory University, is an internationally recognized expert on depression whose résumé spans 215 pages.

He has treated some of Atlanta’s top business leaders, including Ted Turner, retired CNN head Tom Johnson and the late J.B. Fuqua, whose family has given $10 million to Emory to study and treat depression. Under Nemeroff’s leadership, Emory’s psychiatry department pulled in more than $22 million in National Institutes of Health grants just

last year.



From 2000 through 2006, Nemeroff received just over $960,000 from GlaxoSmithKline (GSK), but only disclosed no more than $35,000 to Emory. Between 2000 and 2007, he earned more than $2.8 million from various drug makers but failed to report at least $1.2 million. He signed a letter in 2004 promising Emory administrators that he would earn less than $10,000 a year from GSK but on the same day he was at a hotel earning $3,000 of what would become $170,000 in income from the company—17 times greater than the figure he agreed upon. He was the principal investigator for a five-year $3.9 billion grant financed by the NIMH for which GSK provided the drugs, during which he received more than the annual $10,000 threshold allowed from the company. In 2006, he stepped down as editor of Neuropsychopharmacology after publishing a favorable review of the vagus nerve stimulation (VNS) device, manufactured by Cyberonics, for which he was a paid consultant.  In 2003, he coauthored a favorable review of three therapies in Nature Neuroscience failing to mention his significant financial interests in these, including owning the patent for one of the treatments—a lithium patch.  Nemeroff has consulted for 21 drug and device companies simultaneously.  In 1991 Nemeroff testified before the FDA on behalf of Eli Lilly in hearings into Prozac, saying that the drug did not cause suicidal acts of ideation—yet 13 years later, the FDA concluded the opposite and issued a black box warning about suicide risks. Nemeroff resigned his position at Emory in 2008.



Now he’s a primary target of a U.S. Senate Finance Committee investigation into whether pharmaceutical money compromises the integrity of medical research and scholarship, an ethics controversy that has set the international world of academic medicine abuzz. Studies, speeches and articles can influence which drugs are prescribed for patients (2008).

Sources and Additional Information:

http://newsgroups.derkeiler.com/Archive/Sci/sci.med.psychobiology/2008-10/msg00131.html

http://thebrain.mcgill.ca/flash/capsules/pdf_articles/neurobiology_depression02.pdf

http://www.cchrint.org/cchr-issues/the-corrupt-alliance-of-the-psychiatric-pharmaceutical-industry/

Tricyclic Antidepressants (TCA) Overview

About Tricyclic Antidepressants

Tricyclic antidepressants (TCAs) are an old class of antidepressive drugs, much older than Prozac and other SSRIs. The first TCA imipramine was discovered back in the 1950s, when psychopharmacology was still a new science. The name "tricyclic" comes from their molecular structure which contains three rings of atoms.

The TCAs are effective antidepressants, but because they tend to cause more side effects than newer drugs, they are rarely used to treat depression any more. They are, however, still commonly used in the treatment of chronic pain, sleep disorders and some other conditions, usually in doses much smaller than would be used for depression.

The SSRIs are fairly selective for serotonin, as their name, selective serotonin reuptake inhibitors, implies. TCAs on the other hand are far from selective. They increase brain levels of serotonin, but also norepinephrine (noradrenaline). In addition they block histamine receptors, muscarinic acetylcholine receptors and alpha adrenergic receptors and have some other actions.

How TCAs work

Tricyclic antidepressants (TCAs) inhibit the reabsorption (reuptake) of serotonin and norepinephrine by brain cells. To a lesser extent, TCAs also inhibit reabsorption of dopamine. These antidepressants also block other cell receptors, which accounts for many of their side effects. TCAs are called tricyclic because of their chemical structure. They were among the earliest antidepressants developed and remained the first line of treatment for depression before newer antidepressants arrived.

Antidepressants, in general, may also work by playing a neuroprotective role in how they relieve anxiety and depression. It's thought that antidepressants may increase the effects of brain receptors that help nerve cells keep sensitivity to glutamate — an organic compound of a nonessential amino acid — in check. This increased support of nerve cells lowers glutamate sensitivity, providing protection against the glutamate overwhelming and exciting key brain areas related to anxiety and depression.

Therapeutic effects of antidepressants may vary in people, due in part to each person's genetic makeup. It's thought that people's sensitivity to antidepressant effects, especially selective serotonin reuptake inhibitor effects, can vary depending on:

• How each person's serotonin reuptake receptor function works


• His or her alleles — the parts of chromosomes that determine inherited characteristics, such as height and hair color, which combine to make each person unique

Antidepressant medications are often the first treatment choice for adults with moderate or severe depression, sometimes along with psychotherapy. Although antidepressants may not cure depression, they can help you achieve remission — the disappearance or nearly complete reduction of depression symptoms.

TCA and Clinical Depression

For many years the TCAs were the first choice for pharmacological treatment of clinical depression. Although they are still considered to be highly effective, they have been increasingly replaced by the SSRIs and other newer antidepressants. Notably, however, a recent Cochrane review of the efficacy of the SSRIs concluded that they were only slightly more effective than placebo for the treatment of people with depression. Other indications of SSRIs were not tested. Newer antidepressants are thought to have fewer and less intense side effects and are also thought to be less likely to result in injury or death if used in a suicide attempt, as the doses required for clinical treatment and potentially lethal overdose are far wider in comparison.

Nonetheless, the TCAs are still occasionally used for treatment-resistant depression that has failed to respond to therapy with newer antidepressants. They are not considered addictive and are somewhat preferable to the monoamine oxidase inhibitors (MAOIs). The side effects of the TCAs usually come to prominence before the therapeutic benefits against depression and/or anxiety do, and for this reason, they may potentially be somewhat dangerous, as volition can be increased, possibly giving the patient a greater desire to attempt or commit suicide.

TCAs approved to treat depression

Here are the TCAs approved by the Food and Drug Administration specifically to treat depression, with their generic, or chemical, names followed by available brand names in parentheses:

• Amitriptyline


• Amoxapine


• Desipramine (Norpramin)


• Doxepin (Sinequan)


• Imipramine (Tofranil, Tofranil-PM)


• Nortriptyline (Pamelor)


• Protriptyline (Vivactil)


• Trimipramine (Surmontil)

Some of these medications come in forms that must be injected or as oral solutions that must be mixed with liquids, such as water or juice.

Some of these medications may also be used to treat conditions other than depression.

Side effects of TCA

The most common side effects of tricyclic antidepressants, and ways to deal with them are as follows:

• Dry mouth -it is helpful to drink sips of water; chew sugarless gum; brush teeth daily. Or use saliva substitutes, which come in liquid and tablet forms and are available without a prescription.


• Constipation -bran cereals, prunes, fruit, and vegetables should be in the diet.


• Bladder problems -emptying the bladder completely may be difficult, and the urine stream may not be as strong as usual. Older men with enlarged prostate conditions may be at particular risk for this problem. The doctor should be notified if there is any pain.


• Sexual problems -sexual functioning may be impaired; if this is worrisome, it should be discussed with the doctor.


• Blurred vision -this is usually temporary and will not necessitate new glasses. Glaucoma patients should report any change in vision to the doctor.


• Dizziness -rising from the bed or chair slowly is helpful.


• Drowsiness as a daytime problem - this usually passes soon. A person who feels drowsy or sedated should not drive or operate heavy equipment. The more sedating antidepressants are generally taken at bedtime to help sleep and to minimize daytime drowsiness.


• Increased heart rate -pulse rate is often elevated. Older patients should have an electrocardiogram (EKG) before beginning tricyclic treatment.


• Increased sensitivity to sunlight. Even brief exposure to sun can cause severe sunburn or a rash. While being treated with this tricyclic antidepressants, avoid being in direct sunlight, especially between 10A.M. and 3 P.M.; wear a hat and tightly woven clothing that covers the arms and legs; use a sunscreen with a skin protection factor (SPF) of at least 15; protect the lips with a sun block lipstick; and do not use tanning beds, tanning booths, or sunlamps.

Special conditions

People with certain medical conditions or who are taking certain other medicines can have problems if they take tricyclic antidepressants. Before taking these drugs, be sure to let the physician know about any of these conditions:

-        ALLERGIES. Anyone who has had unusual reactions to tricyclic antidepressants or to carbamazepine (Tegretol), maprotiline (Ludiomil), ortrazodone (Desyrel) in the past should let his or her physician know before taking tricyclic antidepressants. The physician should also be told about anyallergies to foods, dyes, preservatives, or other substances.

-        PREGNANCY. Problems have been reported in babies whose mothers took tricyclic antidepressants just before delivery. Women who are pregnant or who may become pregnant should check with their physicians about the safety of using tricyclic antidepressants.

-        BREASTFEEDING. Tricyclic antidepressants pass into breast milk and may cause drowsiness in nursing babies whose mothers take the drugs. Women who are breastfeeding should check with their physicians before using tricyclic antidepressants.

-        DIABETES. Tricyclic antidepressants may affect blood sugar levels. Diabetic patients who notice changes in blood or urine test results while taking this medicine should check with their physicians

Suicidal feelings and TCAs

In some cases, antidepressants may be associated with worsening symptoms of depression or suicidal thoughts or behavior in those ages 18 to 24. These symptoms likely occur in the first one to two months of treatment or when you change your dosage. Be sure to talk to your doctor about any changes in your symptoms. You may need more careful monitoring when beginning treatment or changing dosage, or you may need to stop the medication if your symptoms worsen. Adults age 65 and older taking antidepressants have a decreased risk of suicidal thoughts.

Work with your doctor or a mental health provider to nix your irritability, sadness or guilt and boost your mood with tricyclics. Feel good again.

Recommended dosage

The recommended dosage depends on many factors, including the patient's age, weight, general health and symptoms. The type of tricyclic antidepressant and its strength also must be considered. Check with the physician who prescribed the drug or the pharmacist who filled the prescription for the correct dosage.

Always take tricyclic antidepressants exactly as directed. Never take larger or more frequent doses, and do not take the drug for longer than directed. Do not stop taking the medicine just because it does not seem to be working. Several weeks may be needed for its effects to be felt. Visit the physician as often as recommended so that the physician can check to see if the drug is working and to note for side effects.

Do not stop taking this medicine suddenly after taking it for several weeks or more. Gradually tapering the dose may be necessary to reduce the chance of withdrawal symptoms.

Taking this medicine with food may prevent upset stomach.

Sources and Additional Information:

http://chronic-illness-treatments.suite101.com/article.cfm/tricyclic_antidepressants

http://en.wikipedia.org/wiki/Tricyclic_antidepressant

http://www.mayoclinic.com/health/antidepressants/MH00071

http://www.depression-guide.com/tricyclic-antidepressant.htm

http://www.healthline.com/galecontent/antidepressants-tricyclic

Antidepressants for Major Depression - Selective Serotonin and Norepinephrine Reuptake Inhibitors (SNRI)

In one of our previous articles we discussed on why and how serotonin impacts our mood and mental stability. The three main neurotransmitters involved in depression are dopamine, norepinephrine, and serotonin (also known as 5-HT). When brain levels of one or more neurotransmitter are low or unbalanced, depression and other conditions can result. Generally, antidepressant drugs work by increasing the production or decreasing the breakdown of one or more neurotransmitter.



The new type of antidepressants (known as selective serotonin and norepinephrine reuptake inhibitors, or serotonin-norepinephrine reuptake inhibitors, or SNRIs for short) affect serotonin, as well as as norepinephrine and other neurotransmitter systems such as dopamine. SNRIs work like SSRIs in that they inhibit the reuptake of neurotransmitters at the synaptic junction. While low levels of both neurotransmitters are associated with depression, norepinephrine is thought to be involved more with alertness and energy, while serotonin influences mood. By increasing levels of both, SNRIs work on different aspects of depression.



Antidepressants, in general, may also work by playing a neuroprotective role in how they relieve anxiety and depression. It's thought that antidepressants may increase the effects of brain receptors that help nerve cells keep sensitivity to glutamate — an organic compound of a nonessential amino acid — in check. This increased support of nerve cells lowers glutamate sensitivity, providing protection against the glutamate overwhelming and exciting key brain areas related to anxiety and depression.



Therapeutic effects of antidepressants may vary in people, due in part to each person's genetic makeup. It's thought that people's sensitivity to antidepressant effects, especially selective serotonin reuptake inhibitor effects, can vary depending on:



- How each person's serotonin reuptake receptor function works

- His or her alleles — the parts of chromosomes that determine inherited characteristics, such as height and hair color, which combine to make each person unique

Are there differences among the SSRIs and SNRIs in achieving remission in patients with major depression?



Remission of depression in the patient is the doctor's main goal. According to Dr. Jeffrey Kelsey, Medical Director, Georgia Institute of Mood and Anxiety Disorders, all of the antidepressants that are available in the U.S. market today are equally effective when it comes to response rates. "However, when it comes to remission, the data shows that SNRIs, dual-acting antidepressants, will, in some patients, confer an advantage. And the tricky part is going into it, we don't know which patients will benefit from one approach to the other."



Kelsey says "SSRIs are very effective treatments but some patients are going to get more benefit from a dual-acting antidepressant."



SNRIs Anti-depressants



Trazodone (Desyrel) inhibits serotonin reuptake in addition to blocking certain types of serotonin, norepinephrine, and histamine receptors. Histamine is a both a biological chemical involved in immune responses as well as a neurotransmitter. In low doses, Trazodone can be used as a sleep aid, especially for people who experience insomnia as part of their depression. Side effects of Trazodone include: allergic reactions, irregular heartbeat, prolonged and painful erection, drowsiness, fatigue, lethargy (exhaustion), psychomotor retardation (slow movements), lightheadedness, dizziness, difficulty concentrating, confusion, impaired memory, disorientation, excitement, agitation, anxiety, tension, nervousness, restlessness, insomnia, nightmares, anger, hostility and, rarely, hypomania, visual distortions, hallucinations (sensing things that aren't really there), delusions (false, fixed beliefs), and paranoia (suspicious fear).



Buproprion (Wellbutrin) is often a first choice treatment for Major Depressive Disorder. This medication is just as effective as SSRIs in treating depressive symptoms, with less risk of weight gain and sexual side effects. In addition to serotonin and norepinephrine, buproprion also inhibits dopamine reuptake. The most common side effects of buproprion are dry mouth, constipation, headaches, and insomnia. Care must be taken when using buproprion at higher doses, as it has been known to cause seizures.



Venlafaxine (Effexor) is often used for the treatment of depressive illnesses, but large numbers of studies demonstrating treatment success are lacking. In addition to inhibiting serotonin reuptake, venlafaxine inhibits norepinephrine and dopamine reuptake. Venlafaxine does not interfere with other brain chemicals, which makes it less "messy" and more powerful than other antidepressants. Some evidence suggests that venlafaxine relieves depressive symptoms more quickly than other medications with fewer side effects, and that it can be combined safely with other medications. However, more research is necessary to substantiate these claims.



Nefazodone (Serzone) inhibits serotonin reuptake by blocking a particular type of serotonin receptor. Serzone is sedating, and is useful for relieving anxiety and severe insomnia. Furthermore, sexual side effects are mild, if any. Unfortunately however, nefazodone is a strong inhibitor of liver enzymes and should be used cautiously. Many medications are metabolized in the liver, and functional liver enzymes are essential to proper liver functioning and overall health.



Mirtazapine (Remeron) blocks serotonin and norepinephrine reuptake. Mirtazapine is sedating, and has the disagreeable side effect (for most) of weight gain in comparison with other SSRIs. Although few studies clearly demonstrate Mirtazapine's usefulness in treating unipolar depression, this medication may be a good option for people who have experienced significant weight loss during their depressive episodes.



Which SNRI Antidepressant is Best?



Two recent studies found Cymbalta (duloxetine) and Effexor XR (extended-release venlafaxine) comparable in effectiveness. In both studies, patients took either 60 mg per day of Cymbalta or 150 mg per day of Effexor XR for 6 weeks. For 6 more weeks, patients continued on whichever drug they had started, with doses adjusted to as high as 120 mg per day for Cymbalta and 225 mg per day for Effexor XR. Nearly 75% of patients taking Effexor XR finished 12 weeks of treatment as compared to about 65% of patients taking Cymbalta. Cymbalta was associated with more nausea, but a few patients taking Effexor XR experienced increases in blood pressure.



In other studies, Cymbalta produced general responses that were better than placebo (inactive sugar pills) and similar to those seen with drugs from another class of antidepressants known as selected serotonin reuptake inhibitors (SSRIs)—most commonly Prozac (fluoxetine) or Paxil (paroxetine). An analysis of separate studies done with Cymbalta and Prozac found little difference in effectiveness between the two drugs.



As for Effexor XR, an analysis of over 40 studies that involved about 4,000 patients found that taking this medication was associated with a higher success rate than other types of antidepressants. Success was defined as an improvement of 50% or more in the rating scales used to measure depression. In the analysis, 73.7% of patients taking Effexor XR were considered to be successful, as compared with 61.1% of those taking a selected serotonin reuptake inhibitor (SSRI) and 57.9% taking a tricyclic antidepressant (TCA). In addition, fewer patients taking Effexor XR stopped taking medication before their studies were scheduled to end.



Another study of 348 adults compared the effects and side effects of Effexor XR and the miscellaneous antidepressant, extended-release bupropion (Wellbutrin XL) for 12 weeks. While both antidepressants worked about equally, Effexor XR may have produced more sexual side effects, which caused more patients in the Effexor XR group to stop treatment.



Drugmaker, Wyeth says Pristiq also may be a treatment option for patients who are on multiple medications. The compound has a low risk of drug-drug interactions. This is important when considering that depression often is a co-morbid condition in medically ill patients and that these patients frequently are taking multiple medications.



Side effects of SNRIs



All SNRIs have the same general mechanism of action and side effects. However, individual SNRIs have some different pharmacological characteristics. That means you may respond differently to a certain SNRI or have different side effects with a different SNRI. For instance, you may have unpleasant side effects with one SNRI but not another.



Side effects of SNRIs include:



- Nausea

- Vomiting

- Dizziness

- Insomnia

- Sleepiness

- Trouble sleeping

- Abnormal dreams

- Constipation

- Sweating

- Dry mouth

- Yawning

- Tremor

- Gas

- Anxiety

- Agitation

- Abnormal vision, such as blurred vision or double vision

- Headache

- Sexual dysfunction



Nausea is less common with the extended-release form of SNRIs.



Before Taking These Drugs



Just as with other antidepressants, you've got to be sure to tell your doctor if you've ever had allergies to any antidepressants, foods, preservatives, or dyes, and if you have suffered from manic depression, convulsions, or seizures. Be sure to report liver disease, since this condition may raise blood levels of any antidepressant, which can increase the risk of side effects. And if you've had a recent heart attack, you may not be able to take antidepressant medication.



In the last few years, some study results and case reports suggested that taking antidepressants was linked with an increase in suicides, attempted suicides, and thinking about suicide—especially for children, teens, and young adults. Generally, the risk is higher in first month or so and then appears to decrease as the body adjusts to the medication. Depressed individuals may be more likely to attempt or commit suicide whether or not they are taking antidepressants. Nevertheless, in 2004, the FDA required the manufacturers of all antidepressants to include on their labels the following safety warning:



Antidepressants increase the risk of suicidal thinking and behavior (suicidality) in children and adolescents with major depressive disorder (MDD) and other psychiatric disorders.



Possible Important Adverse Interactions with SNRI Antidepressants



As with all antidepressants, you should talk to your doctor before taking any other drugs (even nonprescription medications).



Both Effexor XR and Cymbalta may raise blood pressure in some patients. Your blood pressure should be controlled before starting treatment and should be monitored regularly.



Effexor also tends to increase the heart rate, especially at higher doses. Use Effexor with caution if you've recently had a heart attack, suffer from heart failure, or have an overactive thyroid gland.



Effexor may also cause cholesterol levels to rise in some patients who take it for 3 months or longer. This effect is more common among patients taking higher doses of Effexor.



Mydriasis (prolonged dilation of the pupil of the eye) has been reported with EFFEXOR XR. You should notify your physician if you have a history of glaucoma or increased eye pressure.



You will not be able to use Cymbalta if it causes an allergic reaction. In addition, you should not take Cymbalta if you have uncontrolled narrow-angle glaucoma, a disease that causes increased pressure in the eyes.



Overdose



An overdose of Effexor, combined with other drugs or alcohol, can be fatal. If you suspect an overdose, seek medical attention immediately.



Published retrospective studies report that Effexor overdosage may be associated with an increased risk of fatal outcomes compared to that observed with SSRI antidepressant products, but lower than that for tricyclic antidepressants. Epidemiological studies have shown that Effexor-treated patients have a higher pre-existing burden of suicide risk factors than SSRI-treated patients. The extent to which the finding of an increased risk of fatal outcomes can be attributed to the toxicity of Effexor in overdosage as opposed to some characteristic(s) of Effexor-treated patients is not clear. Prescriptions for Effexor XR should be written for the smallest quantity of capsules consistent with good patient management, in order to reduce the risk of overdose.

Symptoms of Effexor overdose include: Sleepiness, vertigo, rapid or slow heartbeat, low blood pressure, seizures, coma.



There is limited clinical experience with Cymbalta overdose in humans. In premarketing clinical trials, cases of acute ingestions up to 1400 mg, alone or in combination with other drugs, were reported with none being fatal. Postmarketing experience includes reports of overdoses, alone or in combination with other drugs, with duloxetine doses of almost 2000 mg. Fatalities have been very rarely reported, primarily with mixed overdoses, but also with duloxetine alone at a dose of approximately 1000 mg.



Signs and symptoms of overdose (mostly with mixed drugs) included:



- serotonin syndrome,

- somnolence,

- vomiting, and

- seizures.



Serotonin syndrome and SNRIs



A rare but potentially life-threatening side effect of SNRIs is serotonin syndrome. This condition, characterized by dangerously high levels of serotonin in the brain, can occur when an SNRI interacts with antidepressants called monoamine oxidase inhibitors (MAOIs). Because of this, don't take any SNRIs while you're taking any MAOIs or within two weeks of each other. Serotonin syndrome can also occur when SNRIs are taken with other medications, including:



- Pain relief medication such as tramadol (Ultram)

- Migraine medications such as sumatriptan (Imitrex) and rizatriptan

- Supplements that affect serotonin levels, such as St. John's worth



Serotonin syndrome requires immediate medical treatment. Signs and symptoms include:



- Confusion

- Restlessness

- Hallucinations

- Extreme agitation

- Fluctuations in blood pressure

- Increased heart rate

- Nausea and vomiting

- Fever

- Seizures

- Coma



SNRIs and Pregnancy and Breast-Feeding



If you want to get pregnant while you're on an antidepressant, you're going to have to weigh the risks to your baby against the risks to you if you don't take the drug. As with most antidepressants, what we know about their activity in pregnant women is mostly obtained from animal studies, not from large-scale studies in humans.

The effects of Effexor XR and Cymbalta during pregnancy have not been adequately studied. If you are pregnant or are planning to become pregnant, tell your doctor immediately.



If Effexor or Cymbalta is taken shortly before delivery, the baby may suffer withdrawal symptoms. It's also known that Effexor and Cymbalta appears in breast milk and could cause serious side effects in a nursing infant. You'll need to choose between nursing your baby or continuing your treatment with these SNRIs.



If a woman needs to take an antidepressant during pregnancy, most of the time the doctor will recommend an SSRI like Zoloft or Lexapro.



You and your doctor should weigh the potential risks to the fetus and to you before you decide whether or not to take antidepressants during pregnancy.



There's always a potential for adverse reactions in nursing infants. If you're a new mom, you need to weigh the risks to you of not taking medication against the potential harm to your baby.





Sources and Additional Information:

http://www.healthyplace.com/depression/antidepressants/snri-serotonin-norepinephrine-reuptake-inhibitors/menu-id-68/

http://www.mayoclinic.com/health/antidepressants/MH00067

http://en.wikipedia.org/wiki/Serotonin-norepinephrine_reuptake_inhibitor

http://www.medicalnewstoday.com/articles/161927.php

Therapeutic Gardening against Clinical Depression

Getting dirty might help lift our spirits, according to a new study which reveals that common soil bacteria could act like antidepressant drugs.



Mycobacterium vaccae, a harmless bacteria normally found in dirt, has been found to stimulate the immune system of mice and boost the production of serotonin, a mood-regulating brain chemical.

The bacterium has already been successfully used in people as a vaccine against tuberculosis. It is also being tested as a treatment for cancer patients and in asthma sufferers, as a way to control the allergic reaction and help 'rebalance' the immune system.



Now, studies on mice led by neuroscientist Christopher Lowry at the University of Bristol in England, suggests that the bacteria may have other applications as a treatment for mood disorders like depression.



"These studies help us understand how the body communicates with the brain and why a healthy immune system is important for maintaining mental health. They also leave us wondering if we shouldn't all spend more time playing in the dirt," said Lowry.



Interest in the unusual antidepressant properties of M.vaccae arose by accident following an experimental treatment for human lung cancer led by cancer researcher Mary O'Brien at the Royal Marsden Hospital in London, England. Under that treatment, patients received heat-killed inoculations of the bacteria.



Following the tests, O'Brien's team observed not only fewer symptoms of cancer, but also improvements in their patients' vitality, emotional health and mental abilities.



Lowry and his colleagues speculated that the bacteria in these earlier experiments might have activated brain cells to release mood-lifting chemicals. To investigate the idea further, they injected heat-killed bacteria into a group of mice and found that they initiated an immune response, which activated serotonin-producing neurons in the brain.



Low levels of serotonin cause depression – an illness which afflicts around 1.3 million Australians. The most commonly prescribed antidepressant medications help treat depression by delaying the re-uptake of serotonin, thus raising levels in the brain.



According to Lowry, the strange effect of the bacteria may work by prompting the body's immune cells to release cytokines, chemicals known to activate sensory nerves that stimulate the brain. The findings are published in the journal Neuroscience.



"We believe that the brain then responds by activating serotonin neurons," he said. "These studies help us understand how the body communicates with the brain and why a healthy immune system is important for maintaining mental health."



They also raise the question of whether exposure to common bacteria from a young age, could make us less vulnerable to disease. "We believe that prolonged exposure to [M.vaccae] from childhood could have a beneficial effect," said Lowry.

Further studies are required to confirm the effect in people and to see if other types of bacteria might have a similar effect, he said.



The study lends further support the 'hygiene hypothesis' whereby exposure to bacteria and pathogens from an early age helps balance the immune system. The idea is that some experience of disease early in life prevents our immune systems from attacking our own bodies - leading to allergies, asthma and other so-called auto-immune diseases.



Gardening benefits in combating depression are not limited exclusively to the bacteria related weaponry. Dr Cosmo Hallstrom, a psychiatrist in Chelsea and member of the Royal College of Psychiatrists, said gardening provides also a distraction therapy, vital in helping deal with depression.



"If I was seeing you in cognitive behavior therapy (CBT) I might say, 'Let's look at three things you enjoy doing,' and let's say you say one of them is gardening, I would then say, 'OK let's do one hour's gardening,' he said. "CBT is a modern form of psychological therapy dealing with the here and now as opposed to your past experiences looking at thinking and behavior and can include all manner of techniques.



"When you get depressed you stop doing things and get isolated which makes you more depressed. The theory is that if you do pleasurable things you will in time get better



"Gardening is a pleasurable activity and it focuses you away from thinking about your health problems.

"Why gardening and not running? Well I think at first it is a bit much doing things that are too physical. It is important to find something you enjoy."







Sources and Additional Information:

http://www.cosmosmagazine.com/news/1154/how-gardening-could-cure-depression

http://news.bbc.co.uk/2/hi/health/8027335.stm

http://www.epinions.com/content_3461390468

Is there a Link Between Adkins Diet and Clinical Depression?

Twice when I have done Atkins I see a huge change in my mental being. I get depressed. This usually starts around a month of doing Akins and basically lasted until I quit.

I talked to someone at The Akins Center and it was suggested I take vitamins especially B complex. I took the advice but saw no improvement. When I tried Atkins the 2nd time and added exercise to my plan the results were still the same, depression hit me like a ton on bricks. I do not take an antidepressant and will not take one. (which Dr. Atkins didn't like either).

P.S. I do want to mention I do not suffer from depression on a regular basis, it is when I low-carb that I get this way.

Post on LowCarbFriends Message Board

In one of our previous publications we provided an insight on the direct link between nutrition and depression. Here we will review the possible connection between Atkins Diet and Depression.

What is Atkins Diet?

Atkins style lower carbohydrate diet is one of the very popular diets that have helped people to lose weight. The most appealing aspect of the Atkins style lower carbohydrate diet, among other similar low carb diets, is that the foods you can eat are essentially the opposite of most other diets. With low carb diets, you eat a lot of protein and fats and very restricted carbohydrates.

The Atkins diet is a high protein and fat and very low-carbohydrate routine. It put emphasis on meat, cheese, and eggs, while recommending reduction in consumption of foods such as bread, pasta, fruit, and sugar. The key advantage of the diet is rapid and substantial weight loss.

By limiting carbohydrate intake, the body will burn more fat, stored in the body. Because there are no restrictions on the amount of calories or quantities of foods allowed on the diet, there is little hunger between meals. Uncontrollable hunger and food craving is the main cause of many dieting failures. It is in fact noted those who follow the Atkins style lower carbohydrate plan eventually find their effective individual range of carbohydrate intake, which is then considered as the tool that helps the dieters to maintain a healthy weight for the rest of their lives.

The primary reason that both men and women follow the Atkins style lower carbohydrate plan is to lose weight. With this principle, it is noted that many people who have followed the Atkins style lower carbohydrate procedure to weight loss readily take off inches and pounds.

The Atkins style lower carbohydrate plan has also worked for those people with strong metabolic resistance to weight loss. This diet provides many ways to surpass the barriers that obstruct a successful diet result. Those who have failed to lose weight with other diets, successfully do so with Atkins.

The Atkins style lower carbohydrate plan helps people to not only lose the weight, but to also keep it off. This fact makes the Atkins style lower carbohydrate nutritional approach more superior than other weight control programs.

Does Atkins cause depression?

In spite of the certain effectiveness in losing weight, the low-carb Atkins diet has prompted criticism from many doctors who fear it could increase the risk of long-term health problems such as kidney damage, high cholesterol and diabetes. For example, the group of prominent nutritionists, supported by The Physicians Committee for Responsible Medicine, has urged the hospitals to ban the Atkins diet completely. 



Latest researches have now suggested Atkins Diet could also affect mental health, leaving dieters feeling grumpy, tired, irritable, apathetic and restless.

A study of 100 men and women found that dieters on a protein-rich regime are far more prone to mood swings and depression than those on high- carbohydrate, low-protein diets.

The reason? Carbohydrates produce higher levels of serotonin, the body's "happy hormone" which is released by the brain to stabilize mood swings. Carbohydrates raise serotonin levels naturally, acting as a natural tranquillizer and antidepressant.

The team from the Massachusetts Institute of Technology in the U.S. found that eating sweet and starchy carbohydrates, such as potatoes, pasta and bread, increases the brain's production of serotonin when eaten with very small amounts of protein.

Serotonin is also the chemical which makes us feel full after eating.

'Emotional zombies'

Dr Judith Wurtmen, who led the study, concludes that dieters, who eat a lot of protein and fat, as recommended on the Atkins diet, are therefore in danger of becoming "emotional zombies".

Certain people, she says, are actually "carbohydrate cravers". They rely on carbohydrates to keep their moods steady, so cutting out this food group altogether is "like taking water away from someone hiking in the desert".

Dr Stuart Trager, chairman of The Atkins Physician Council, naturally disputes the claim that a low-carbohydrate diet can cause depression.

He says: "Mood and energy levels are related to many factors. Additionally, it is important to remember that serotonin is made within the body from ingested protein, rather than carbohydrates. Controlling carbohydrates helps people manage their weight, improve body image, and stabilizes blood sugar."

Protein lowers serotonin

But nutritionist Fiona Hunter says: "Although serotonin is made from the amino acid tryptophan which is found in protein-rich foods such as meat and cheese, eating a protein-rich meal actually lowers serotonin in the brain.

"This is because when you eat a protein-rich meal you flood the blood with other competing amino acids, as well as tryptophan, which all fight for entry into the brain. Only a small amount of tryptophan is able to get through, so serotonin levels do not rise greatly.

"In contrast, a carbohydrate-rich meal triggers the release of the hormone insulin which causes all amino acids, except tryptophan, to be absorbed into the cells. With the competition removed, tryptophan can freely enter the brain, causing serotonin levels to rise."

Dr Cecilia Tregear, who specializes in the effects that diet has on hormone levels, agrees: "In my experience people on the Atkins diet are prone to mood swings, anxiety and erratic behavior. Sugar is the main food for the brain and without it, the brain struggles.

"The thyroid gland needs to be activated by carbohydrates and without them it slows down, and a slow thyroid has been linked to depression.

"Overall, the Atkins diet is not a balanced diet, which will result in unbalanced hormones and therefore unbalanced moods."

Four years ago I went on the Atkins diet. It worked great; I lost over 60 pounds in about four months. I felt great and was on my way to being the best shape of my life.

However, as mentioned in the possible diet dangers it can affect the brain activity relying on carbohydrates, serotonin. In my case, I had a history of depression and with the Atkins diet after a couple months of the weight loss I went back into depression. So as mentioned be careful when thinking of going on this diet.

Comment on WeightLossandTraining Post

Summary

Based on the multiple sources, I have reviewed, there is hard to say, if the negative impact of Adkins Diet overweighs its positive results for the body weight loss.

However, the research materials and users feedback is sufficient to be extremely careful with using this diet in your nutrition program. The Atkins diet isn't for everyone. Some people need more carbohydrates than others. And many people don't need to go to the extreme of eating nothing but protein in order to lose weight.

If you notice any signs of depression, while on Atkins Diet, consult with your physician and therapist.

Sources and Additional Information:

http://www.dailymail.co.uk/health/article-299649/Does-Atkins-cause-depression.html

http://www.fitnesstipsforlife.com/facts-about-atkins.html

http://www.highbeam.com/doc/1P1-78815247.html

http://www.realpolice.net/forums/general-topics-ii-70/10370-atkins-diet-causes-mood-swings-depression.html

http://www.thehealthierlife.co.uk/natural-health-articles/weight-loss/atkins-diet-affect-mood-00993.html

http://www.network-admin.net/?p=359