Question by Mrs. Rucker: DEpression?
does anybody know a way to get rid of it?

Best answer:

Answer by girly_koda
Get medication

What do you think? Answer below!

 Mail this post

Technorati Tags: Depression

Fort Lauderdale, FL (PRWEB) December 27, 2011

The holiday season leading up to Christmas and New Years is typically a high demand borrowing season as consumers search out money to meet Holiday shopping demands. With the current economic troubles, consumers are having trouble coming up with cash to pay for gifts, groceries, or holiday trips to spend time with their loved ones, according to ReallyBadCreditOffers.com. According to the site, the run-up to New Years is busy, but consumer’s really feel the pinch after Jan 1, as borrowers scramble to find emergency loans for bad credit following Holiday spending.

The loan comparison site specializes in connecting consumers with a bad credit history to services and offers with flexible qualification standards. Providing recommendations as to the top credit cards, credit repair, consolidation loans as well as bankruptcy help, the site has helped 10′s of thousands since it’s creation in 2008.

The holiday spending brings with it a rude awakening when the bills come due in January, 2012. With average rates on credit cards ranging between about 17% up to as high as 29%, according to the site, bills can quickly become unmanageable.

“One of the quickest ways to get financial relief is by using debt consolidation to lower monthly payments, putting money directly in the borrowers pocket,” said Ariel Pryor, offer comparison expert.

The site works to empower visitors by showing what help is available at a glance so that each person can choose what offer is most appropriate for their situation. “Everybody deserves another chance, a helping hand at this point is often when it is needed most,” said Pryor.

?There is nothing more depressing than entering a brand new year with added debt that a consumer is not prepared for, because one missed, or late, payment can send the interest rates skyrocketing. The new year is a time to rebuild one’s financial future on firmer ground,? added Pryor.

ReallyBadCreditOffers.com was built to provide consumers with the facts regarding bad credit loan offers, bankruptcy, credit repair, bad credit car loans and other financial challenges. The financial products available include personal loans, secured personal loans, payday loans, debt consolidation loans credit cards and counseling services.

The options are varied, but they all have one factor in common, they are relatively easy to get because they are designed for people with bad credit scores.

The rates can vary widely between the lenders, and ReallyBadCreditOffers.com allows the consumer to comparison shop before applying.

About ReallyBadCreditOffers.com

Serving the bad credit loan market since 2007, the staff has helped thousands find the information necessary for the bad credit loan consumer to get the best possible interest rate available with the least amount of paper work in the shortest amount of time.

Contact:

Ariel Pryor, Loan Researcher

http://www.reallybadcreditoffers.com

(520) 344-2001

# # #

Find More Depression Press Releases

 Mail this post

Technorati Tags: 2012, Best, Credit, Loan, Made, Offers, Post, Ready, Year

Question by Mrs. Rucker: DEpression?
does anybody know a way to get rid of it?

Best answer:

Answer by girly_koda
Get medication

Know better? Leave your own answer in the comments!

 Mail this post

Technorati Tags: Depression

Question by Mrs. Rucker: DEpression?
does anybody know a way to get rid of it?

Best answer:

Answer by girly_koda
Get medication

Give your answer to this question below!

 Mail this post

Technorati Tags: Depression

Question by muh-muh-muh-muh: DEPRESSION!!!!!!!………………….?
normally, is depression a continuation of a certain bad event that happened in your life? does it continue especially if you over analyze or think things and you just kept it all to yourself? depression is normal to appear, right?

Best answer:

Answer by Mark
“Depression is normal to appear” You don’t like a whole lot of people has well as some doctors who don’t understand depression. Depression is caused by a lack of Serotonin just like a diabetic who doesn’t who doesn’t have he ability to produce its’ own insullin. Depresion is being sad empty and alone even if your surrounded by familly members during a special fest.

Add your own answer in the comments!

 Mail this post

Technorati Tags: Depression

Question by RastaMan: depression?
i have depression …my question is if it’s normal to obsess about existential thoughts when u have depression? and how to overcome it? thnx

Best answer:

Answer by plusenergy
what did your therapist say?

Give your answer to this question below!

 Mail this post

Technorati Tags: Depression

Dean Raffelock, D.C., L. Ac, CCN, DACBN, DIBAK

Hyla Cass, M.D.

Postpartum depression (PPD) Postpartum Anxiety (PPA) have become a national epidemic in the United States, affecting 15%-20% of all new mothers, or about 600,000-800,000 women annually. (1) It is now estimated that over 30 million Americans are on antidepressant or anti-anxiety medications. (2) The majority of this 30 million are women who have one or more children. The chance of suffering from PPD increases with each successive child. (3)

The most common medical treatment for postpartum depression is SSRI (selective serotonin reuptake inhibitors) antidepressant drugs. Postpartum Anxiety Disorder is most commonly treated by the benzodiazepine family of drugs like Valium, Ativan, Xanax, and Klonopin. Combination reuptake inhibitors for both serotonin and norepinephrine (SNRIs) are also commonly used in postpartum depression. In the case of postpartum psychosis, antipsychotic drugs are used and are immediately necessary. Many women are now given samples of SSRIs as they are leaving the maternity ward. Most medical sources believe that PPD is caused by an imbalance of brain chemistry and that pharmaceutical intervention is the treatment of choice. While a certain percentage of women suffering from PPD do need pharmaceutical assistance, these are far fewer than are actually receiving them. Recent Meta-studies show this to be true.  While it is clear that some women with PPD do need and benefit from pharmaceutical intervention, it is our experience that an integrative approach yields the best results.

 

Postpartum Anxiety Disorder is mostly treated

The most common Postpartum Depression symptoms  include the following:

1. Persistent feelings of despair and/or anxiety;
2. Loss of energy and low levels of daily functioning;
3. Sleep and eating disturbances;
4. Inability to focus, concentrate or make decisions;
5. Feelings of worthlessness, shame and guilt;
6. Feelings of indifference and/or resentment towards the baby;
7. Intrusive negative thoughts and/or obsessive worries–in the most serious cases, this includes thoughts of harming oneself or the baby;
8. Reduced sex drive;
9. Loss of joy and appreciation for life;
10. Irritability or excessive anger.

The literature generally outlines several types of postpartum disorders that have special features beyond the typical symptoms of depression. These include:

1. . Here, the primary symptoms are excessive nervousness, hyper-vigilance, racing thoughts and in some cases outright panic. Panic attacks are especially frightening–sufferers often believe they are dying, as they experience shortness of breath, dizziness and a pounding chest.

2. -Compulsive Disorder. Most often, this takes the form of obsessive thoughts or worries about the baby and may be accompanied by compulsive behaviors such as constantly checking if the baby is breathing, constantly washing to protect the baby from germs, etc. The most disturbing type of obsessive thoughts are those in which the mother envisions harming her baby in some way. These thoughts are unwanted, intrusive and terrifying to the mother. It is important to emphasize that, except in extremely rare instance of psychosis (see below), these thoughts are not accompanied by any actions. Nonetheless, the mother may be so frightened by her own thoughts that she avoids the baby and consequently neglects her. It is terribly difficult for new mothers to acknowledge having such thoughts, and as a result, many suffer in isolation.

3. . PTSD can occur in response to a real or perceived traumatic childbirth or because of unresolved past trauma–sometimes sexual in nature–triggered during childbirth. A woman who experiences PTSD is likely to have recurring, memories, dreams or even flashbacks of the traumatic labor/birth. She will be hyper-vigilant and startle easily, and will likely suffer from sleeplessness, irritability, poor concentration and apathy. Women who have experienced a particularly traumatic childbirth often show symptoms of both PTSD and PPD.

4. . This is the most extreme and rarest of all postpartum disorders. When it occurs, the mother loses touch with reality and her symptoms may include extreme disorientation (e.g., not knowing who she is), delusional or paranoid thinking, and visual or auditory hallucinations. The few, tragic cases where mothers have harmed their children while in a psychotic state have received enormous media attention. As a result, many people inaccurately associate PPD with psychotic symptoms and dangerous behavior. This constitutes yet another reason why women fail to get help–they want to avoid being labeled with such a stigmatized disorder.

The human body is entirely formed from nutrients. Every muscle, organ, gland, bone, cell, and fluid is composed entirely of nutrients (environmental toxins notwithstanding). All of the neurotransmitters, hormones, biochemical structures, and metabolic pathways are formed from nutrients.

No other normal physiological process uses up and drains more vital nutrients from a postnatal woman’s body than the process of being pregnant, giving birth, and caring for a new infant which may include breastfeeding. The fact that a mother’s body donates all the nutrients required to form her baby’s body is too often overlooked when it comes to the medical treatment of PPD. Not only does the placenta literally rob the mother’s body of all the key nutrients required to make a baby’s body, but the placenta itself is formed from nutrients taken from the mother’s body. This is the main reason that many postpartum women become nutritional drained and this nutrient depletion syndrome can lead to postpartum depression and anxiety disorder.

Other factors that may contribute to a drain of a new mother’s nutrient reserves are loss of blood during the birth process, sleep deprivation, breastfeeding, returning to work too soon, and the immense extra energy required to take care of a new infant with intense needs. If a pregnant woman’s or new mother’s nutrient reserves are too low, she is much more vulnerable to experiencing PPD and PPA because all of the body’s normal metabolic processes are entirely dependent upon nutrients. The preponderance of extremely poor quality pharmaceutical prenatal vitamins significantly adds to the tendency of nutrient depletion.

Rarely is there is any mention that the body’s production of neurotransmitters is completely dependent upon their nutritional precursors. (4) Nor are the causes of these nutritional precursor deficiencies discussed. Additionally, the interdependent relationship between hormones and neurotransmitters is rarely taken into consideration by most physicians when considering treatment for PPD and PPA. The nutritional requirements of mitochondrial function, the importance of liver function from Western and Eastern perspectives, and some individual nutrients like Omega 3 fish oils, pharmaGABA, L-theanine, SAMe, inositol, magnesium, and the herb St. John’s Wort can also be of great assistance in treating PPD and PPA. These will be briefly discussed.

An integrative approach to treating PPD may include nutritional therapies, bio-identical hormone replacement, moderate exercise, a nutrient dense diet, proper rest, psychological counseling/support, stress reduction techniques, elimination of caffeine, alcohol and other addictive drugs, and if needed, pharmaceutical intervention.

Serotonin and Tryptophan

The amino acid L-Tryptophan is required for the body to produce serotonin. Ninety-five percent of the serotonin in the human body is produced in the intestinal tract. Approximately five percent is produced in the brain. The serotonin produced in the intestinal tract is unavailable to the brain because serotonin cannot pass through the blood- brain barrier. L-Tryptophan also does not easily pass through the blood-brain barrier and requires a carrier protein to ferry it into the brain. The consumption of simple sugars changes brain neuron cell membrane amino acid selectivity, allowing tryptophan to enter the brain more easily. Hence, the craving of sweets is often a sign of serotonin deficiency.

Serotonin has been referred to as the brain’s mood elevating and tranquilizing chemical. Inadequate serotonin levels are linked with depression, anxiety, insomnia, irritability, and weight gain. Serotonin mediated depression usually contains an element of anxiety. Serotonin is considered an inhibitory neurotransmitter. Its functions include:

- Inhibiting Glutamate excitability over diverse regions of the CNS
-Stimulating its own receptors on GABA neurons prompting GABA to perform its inhibitory function
- Inhibiting the release of the Catecholamines: Dopamine, Norepinephrine, and Epinephrine.

A comparison of the effects of optimal serotonin levels to low serotonin levels to reveals the following contrasts:

1) Hopeful/optimistic—————-Depressed
2) Calm—————————Anxious
3) Good-natured——————–Irritable
4) Patient————————–Impatient
5) Reflective/ thoughtful————–Impulsive/Reactive
6) Loving /Caring——————–Abusive
7) Able to concentrate—————-Short attention span
Creative/focused——————Blocked/scattered
9) Moderate carbohydrate intake——–Excessive carbohydrate intake
10) Good sleep and dream recall——–Insomnia and poor dream recall

Tryptophan is converted to its metabolite, 5- Hydroxy-Tryptophan (5-HTP) which is then converted to serotonin. Niacin, iron, and folic acid are required for L-Tryptophan to be converted into 5-HTP. The body also requires pyridoxal-5-phosphate along with 5-HTP in order to produce serotonin. Magnesium and riboflavin (B2) are required for the conversion of pyridoxine (B6) into pyridoxal-5-phosphate. Deficiencies in any of these nutrients can limit the production of serotonin. Numerous double-blind studies have shown 5-HTP to be as effective as antidepressant drugs with fewer and milder side effects and most times better tolerated. (5-11)

 

    

 A number of significant factors contribute to low L-Tryptophan levels in many people, especially postpartum women whose bodies are providing the proteins needed to form another human body, these include excessive levels of cortisol, epinephrine, norepinephrine, and dopamine. The ratio of L-tryptophan to other amino acids available in most foods is quite low.

An overabundance of the adrenal gland hormone cortisol (a very common occurrence in stressful psychological and physiologic states) adversely affects serotonin production and sensitivity in four different ways:

1. Excess cortisol significantly decreases the number of serotonin (5-HT1A) receptor sites. (12)
2. Excess cortisol suppresses serotonin receptors. (13, 14)
3. Excess cortisol increases serotonin reuptake. (15)
4. Excess cortisol, causes tryptophan oxygenase (TO) to metabolize tryptophan into kynurenine, leaving less tryptophan to become serotonin. (15,16)

If cortisol levels are too low in the amygdala, serotonin no longer has an Inhibitory effect on Glutamatergic activity, suggesting that cortisol plays a key role in maintaining Serotonergic-mediated modulation. (16,17) This may be another factor involving insomnia in PPD.

Added to the reasons that serotonin deficiencies are growing more common and contributing to PPD is a stress-related overabundance of the catecholamines. Epinephrine, norepinephrine, and dopamine also deplete serotonin because the inhibitory monoamine neurotransmitter serotonin is supposed to balance these three excitatory monoamine neurotransmitters. The more stress a person experiences, the more the body increases the production of the catecholamines in an attempt to respond to this stress. This requires a postpartum body to produce even more serotonin – though deficiencies in nutrient precursors may interfere with its production.

The use of 5-HTP as a nutritional precursor to serotonin has significant advantages over tryptophan. 5-HTP easily passes directly through the blood-brain barrier without the need for a carrier protein, allowing for an easier conversion into serotonin in the brain. Sublingual forms of 5-HTP work more quickly. Dosage varies from 25 mg per day to 300 mg per day or more.

A deficiency of vitamin B6 (pyridoxine), which is required for serotonin synthesis, is often found in premenopausal female patients with depression. (18) Replacing B6 in cases of deficiency is an important aspect of PPD treatment that may enhance serotonin production in the brain. (19) The use of the vitamin B6 metabolite, pyridoxal-5-phosphate, instead of B6 is suggested especially when magnesium and/or riboflavin deficiencies are suspected or confirmed. There is some controversy whether it is best to supplement 5-HTP and pyridoxal-5-phosphate together or take them separately, adhering to a two-hour wait period. Our clinical experience indicates that it fine to supplement them together. Many products including a combination of 5-HTP and P-5-P are available.

Some controversy exists regarding the simultaneous use of SSRIs and serotonin nutritional precursors. The pharmaceutical companies seem adamant about avoiding this and often mention the possibility of Serotonin Syndrome, a dangerous condition generally brought about by combining serotonin enhancing medications, especially MAO inhibitors, with medications, herbs, or nutritional precursors that also enhance serotonin activity. Symptoms of serotonin syndrome may include nausea, headache, agitation, diaphoresis, hypertension, tachycardia, and hyperthermia that can go over 104 F. This appears a remote possibility at best when just using 5-HTP or using 5-HTP in combination with one SSRI medication. (20)

SSRIs appear to not only keep serotonin in the neuron synapses longer by inhibiting reuptake, but also by pulling the nutritional precursors for serotonin from the storage vesicles and reuptake ports. In fact, in our clinical experience, many women with PPD do better when taking 5-HTP and P-5-P along with their SSRIs than taking SSRIs alone. Serotonin precursor deficiencies may be the reason that SSRIs don’t work for some, work and then stop working for others, and why it is not unusual for a woman with PPD to have been prescribed two or more different SSRIs over time. The SSRIs do not give a net increase of serotonin so they need enough available serotonin in order to have enough to re-uptake.

 

The catecholamines are predominantly energizing and mood elevating when produced at appropriate levels. Synthesis of the catecholamines occurs in the CNS, adrenal medulla, and peripheral sympathetic neurons. Norepinephrine and dopamine act primarily as neurotransmitters in the CNS. Epinephrine acts primarily as an adrenal hormone to mobilize energy.

The catecholamines influence most organ systems. When levels are excessive they are catabolic and can lead to the body metabolizing its own nerve, muscle and bone tissue. Low levels can lead to depression, fatigue, and weight gain.

Dopamine: Dopamine is the catecholamine precursor for norepinephrine and is found both in the CNS and adrenal medulla. Its functions include motor function and posture, cognitive function (attention, focus, working memory and problem solving), and pleasure sensations. Dopamine can act either as an inhibitory or excitatory neurotransmitter in response to incoming afferent signals.

Norepinephrine (noradrenaline): CNS norepinephrine mediates mood regulation, drive, ambition, learning and memory, alertness, arousal and focus. Clinically, there is often an inverse relationship between norepinephrine (excitatory) and serotonin (inhibitory). When serotonin is low, norephinephrine may be over-upregulated, resulting in “fight or flight” responses leading to anxiety and/or panic attacks. Over-expression of CNS norepinephrine is clinically associated with anxiety, aggression, irritability, mania or bipolar disease, immune suppression, and hypertension; low norepinephrine is associated with atypical depression, with symptoms of fatigue, hypersomnia, hyperphagia, lethargy and apathy.
(21,22)

Epinephrine (adrenaline): Epinephrine synthesis is dependent upon norepinephrine being converted into epinephrine by methylation.
Hans Selye (1974) described the three phase s of the “General Adaptation Syndrome” to stress (23):

Phase I: Alarm reaction: high epinephrine/high cortisol

Phase II: Resistance: high cortisol/low DHEA, variable epinephrine

Phase III: Exhaustion: depletion of cortisol, epinephrine and DHEA
Adrenal exhaustion is a major factor in depression related to chronic or severe stress.

A woman suffering from PPD should be closely questioned about her symptoms; SSRIs are routinely given to women who have functional hypoadrenia involving the adrenal cortex and/or medulla, or low thyroid function (discussed below). Low glucocorticoid and/or catecholamine levels can cause the symptoms of fatigue, malaise, and depression. (24,25)

Many women with PPD require pharmaceuticals and/or nutriceuticals that address deficiencies in both serotonin and the catecholamines. Nutritional therapies for catecholamine balance include:

]]>

§ DL-phenylalanine and L-tyrosine, the amino acid precursors for epinephrine, norepinephrine, and dopamine. DL-phenylalanine also helps to increase endorphins, which are mood-elevating. Many PP women diagnosed with bipolar disorder will respond well to high dose DL-phenylalanine therapy (26), along with serotonin precursors and high-dose (6 grams per day) omega-3 fatty acids in the form of fish oils. (27)

§ L-cysteine, sulfur, iron, and folate, required for conversion of L-tyrosine into L-dopa.

§ Pyridoxal-5-phosphate, required for the conversion of L-dopa into dopamine. Copper and vitamin C are required to convert dopamine into norepinephrine. Pridoxal-5-phosphate, B12, and folic acid are required to convert norepinephrine into epinephrine.

Gamma-Aminobutyric Acid (GABA)

GABA is the most important and widespread inhibitory neurotransmitter in the brain. Low levels of GABA are particularly important to look for when anxiety and insomnia are included in the symptom display of PPD/PPA. GABA is essential for balancing excitatory neurotransmitters and hormones such as cortisol, epinephrine, norepinephrine, and glutamate. Too much excitation without adequate GABA inhibition can lead to: (28)

- Insomnia
- Restlessness
- Irritability
- Anxiety
- Panic Attacks
- Seizures

GABA’s job clinically is to induce relaxation, calmness and aid sleep. Where there are glutamate receptors (powerful excitatory neurons), there will be GABA receptors nearby. GABA allows only the most important excitatory signals to pass by and dampens or quenches extraneous excitatory signals when GABA levels are adequate.

Benzodiazapines (Valium, Klonopin, Zanax, Ativan, etc.) and sleep pharmaceuticals like Ambien and Sonata work on GABA receptors, as does moderate alcohol consumption. L-theanine, lactium (milk peptides), L- glutamine, taurine, and bio-identical progesterone can act as nutraceutical/hormonal GABA agonists. The drug Gabatril is a GABA re-uptake inhibitor as is Valerian extract. A newer nutriceutical product called pharmaGABA seems to yield more effective results than synthetic GABA.

From a Chinese Medicine perspective, serotonin and GABA would be Yin (relaxing, harmonizing, cooling, nurturing, moisturizing, inhibitory) and the catecholamines would be Yang (energizing, mobilizing, warming, excitatory, drying). From both Eastern and Western perspectives, it is important to balance these opposing groups of brain chemicals to obtain balance. A woman with PPD who now has more energy but can’t sleep is just as unhappy as a woman who now can sleep but who is even more lethargic than before treatment.

Balancing neurotransmitters is key. Balancing neurotransmitters and hormones is clinically even more effective.

The relationship between neurotransmitters and hormones in PPD is often overlooked. Neurotransmitters and neuropeptides are required in order to mediate hypothalamic production of releasing hormones, enabling the pituitary gland to properly conduct the hormonal orchestra. The hypothalamus is considered a key part of the mid-brain, the “emotional brain,” so there is little wonder why imbalances in neurotransmitters and hormones can adversely affect emotional states.

. The catecholamines and thyroid hormones are closely related in many of their functions. L-tyrosine, along with iodine, is the precursor for thyroglobulin and thyroid hormones T-3 and T-4. A depression with no anxiety, with the predominant symptoms of exhaustion and difficulty stringing multiple positive thoughts together, is most often associated with low adrenal (29) and/or thyroid function (30-32) and generally doesn’t respond well to SSRIs or serotonin nutritional precursor therapy.

It is well known that low thyroid function can cause physiologic depression and fatigue. Giving T3 induces a rise in serotonin, and in animals with hypothyroidism, serotonin synthesis is reduced. (33) T3 appears to desensitize presynaptic Serotonin autoreceptors. (34) Conversely, the diurnal peak of TSH, observed during the physiological circadian rhythm, is serotoninergic dependent. (35)

Thyroid function and serotonin function are interdependent both clinically and bio-chemically. Optimal thyroid function is dependent on optimal serotonin levels. Optimal serotonin balance is dependent on optimal thyroid function. TSH increase is dependent on adequate serotonin stimulation of hypothalamic TRH, allowing TSH to rise. (36) Suppressed TSH currently may more appropriately represent low serotonin states than any real assessment of true thyroid function. The thyroid hormone triiodothyronine (T3) augments and accelerates the effects of antidepressant drugs. Fluoxetine + T3 are better at desensitizing 5-HT hypothalamic autoreceptors than either alone. (37-39)

A growing body of evidence points to estrogen’s importance in serotonergic function. (40) Estrogen inhibits serotonin reuptake. (41,42) Estrogen treatment is shown to selectively enhance serotonin (5-HT1A-mediated) responses in the hippocampus (43,44) Estrogen increased the firing activity of 5-HT (serotonin) neurons in both male and female rats. (45,46) In short, estrogen appears to be nature’s SSRI.

Presently, there is a great deal of controversy regarding estrogen HRT. The HERS study and WHI studies have stirred the controversy without making the important distinction between bio-identical and pharmaceutically altered estrogens; neither is any distinction made between progesterone and progestins. The clinician is encouraged to become very well versed in this area regarding risks versus benefits of HRT. Many women with PPD can benefit from low-dose bio-identical estrogen HRT if indicated and potential benefits outweigh risks.

: Bio-identical progesterone has a known anti-depressant/anti-anxiety effect. Throughout pregnancy, the placenta produces copious amounts of progesterone, increasing blood levels to many times pre-pregnancy levels. Post-partum, this supply is suddenly gone, along with its soothing effects on the mother’s nervous system.
Allopregnanolone is synthesized by the reduction of progesterone via the enzymes 5-reductase and 3-hydroxysteroid dehydrogenase (3-HSD). Allopregnanolone is one of the most potent known modulators of GABA receptors. (47,48) Allopregnanolone has behavioral and biochemical characteristics similar to ethanol, barbiturates, and benzodiazepines. (49,50)

Bio-identical progesterone can be very helpful for women with PPD with anxiety and insomnia. Using the  PharmaGABA and bio-identical progesterone simultaneously is often very helpful to relieve anxiety and sleep issues.

: DHEA increases the firing activity of serotonin neurons. (51) DHEA also increases dopamine and norepinephrine synthesis via mRNA for tyrosine hydroxylase. (52) Because of this, DHEA can be helpful in some forms of PPD. DHEA also inhibits GABA and is therefore a GABA antagonist. (53) Clinically, if the use of DHEA causes insomnia and irritability, most likely the patient is GABA deficient and this should be addressed before continuing to supplement DHEA.

: increases serotonergic neuron firing in the raphe area, increasing mood. (54)

      

 

from Metametrix Lab- Ion Panel Booklet

 

Inefficient mitochondrial function can limit ATP production, lower energy and contribute to or cause physiological depression. More than 90% of all cellular oxygen consumption is used to fuel mitochondrial metabolism. Mitochondria must transfer huge numbers of electrons to produce energy. Mitochondrial dysfunction can affect all organ systems, including neurons and glands.

Dietary fats, carbohydrates , and proteins all need to be converted into acetyl-coenzyme A (acetyl CoA) before entering the Krebs cycle and electron transport chain. The nutritional precursors required for fatty acids, glycerol, and cholesterol to enter the Krebs cycle and generate ATP are riboflavin (B2), L-carnitine, niacin, and biotin. Thiamin (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), biotin, and alpha-lipoic acid are required for carbohydrates and proteins to enter the Krebs cycle in the mitochondria.

Within the Krebs cycle, cysteine and iron are needed to convert cis-aconitate to isocitrate. Niacin, magnesium, and manganese are required to convert isocitrate into alpha-ketoglutarate. The amino acids glutamine, histidine, arginine, proline and glycine are needed to form alpha-ketoglutarate. Thiamin, riboflavin, niacin, pantothenic acid, and alpha lipoic acid, are needed to convert alpha-ketoglutarate into succinyl-CoA. The amino acids isoleucine, valine, and methionine are needed to form succinyl-CoA. Magnesium is required to convert succinyl-CoA into succinate. Riboflavin is required to convert succinate into fumarate. The amino acids tyrosine and phenylalanine are needed to form fumarate. Niacin is required to convert malate into oxaloacetate.

All these nutrients are required to produce 36 units of ATP per molecule of acetyl CoA in the Krebs cycle. A significant deficiency of any of these key nutrients can cause mitochondrial dysfunction and contribute to fatigue and depression.

Niacin and coenzyme Q10 are required for oxidative phosphorylation (electron transport chain, or ETC). Normally, the ETC produces another 3 units of ATP in the mitochondria in addition to the Krebs cycle’s 36. A significant deficiency in either of these can also reduce ATP production and contribute to a physiologic depression.

Mitochondrial dysfunction is often overlooked in the treatment of PPD. A study done with postpartum women showed that a comprehensive postnatal nutrient program, including many of the Krebs cycle/oxidative phosphorylation nutrients, relieved many postpartum symptoms including mild to moderate PPD.

 

For many centuries, Chinese medicine has correlated liver meridian dysfunction with anger, irritability, and depression. From this perspective, suppressed anger often leads to depression. Concepts such as rising liver heat and stagnant liver Qi are used to depict how faulty liver meridian function could dramatically affect emotional states. When the flow of electrons within a meridian is up or down-regulated, the organ dependant upon that meridian will become dis-eased. Many practitioners of Chinese medicine are taught to consider the liver the “seat of the emotional body” because of this strong correlation of liver dysfunction with negative emotions.

In the Orient the term “hot liver” is used to depict someone who has anger issues. The English use the “liverish” to describe one who is irritable. From a Western medicine point of view, most clinicians are aware how an alcoholic’s liver cirrhosis can first cause irritability and eventually depression.

In the past two decades much more information has come to light regarding phase one and phase two liver detoxification pathways. These pathways greatly contribute to the body’s ability to excrete exogenous and endogenous toxic chemicals. Environmental toxin levels (xenobiotics) are ever on the rise and require that the liver play a very important role in their excretion.

Added to this burden of detoxification are the internal production of increased stress hormones and other body chemicals that require excretion. All of these chemicals require that the liver have adequate nutrients to facilitate their excretion.

Phase one liver detoxification consists of oxidation, reduction, or hydrolysis. The cytochrome P450 system mixed function oxidases perform the most important beginning function of detoxifying these exogenous and endogenous toxins. Phase I liver detoxification requires an adequate supply of nutrients, enzymes, and antioxidants. This list includes riboflavin, niacin, pyridoxine, folic acid, cobalamin, glutathione, phospholipids, carotenes, vitamin C, bioflavonoids, flavonoids, vitamin E, selenium, copper, zinc, manganese, CoQ10, and nutrients contained in thiols, pycnogenol, and silymarin.

Phase II liver detoxification consists of conjugation pathways in the hepatocytes. Amino acid conjugation (binding) of toxins requires glycine, taurine, glutamine, ornithine, and arginine. Sulfation requires sulfur-bearing amino acids or elemental sulfur. Sulfation is required to break down and package estrogens, DHEA, thyroxine, cortisol, catecholamines, melatonin, ethyl alcohol, bile acids, tyramine, cholecystekinin, cerebrosides and others. Glucuronidation requires magnesium and B6 to break down estrogens, other steroids, melatonin, and many xenobiotics.

Methylation requires B12, B6, and folic acid to break down and eliminate catecholamines, histamine, and many drugs and xenobiotics. Glutathione conjugation helps to detoxify heavy metals and numerous xenobiotics. Glutathione requires glutamate, glycine, and cysteine or N-acetyl-cysteine plus selenium and vitamin C for its formation. Acetylation, another detoxification pathway, requires B2, B5, molybdenum, and vitamin C in order to do its function.Sulfoxidation transforms toxic sulfite molecules into usable sulfates.

Mothers in the U.S have a high toxic burden that is evidenced by the levels of toxins in mother’s milk. (55) If the liver is too burdened and unable to perform its many tasks of detoxification, this may contribute to PPD.

Omega-3 Fatty Acid Deficiencies and PPD

A deficiency of omega-3 fatty acids has been linked with depression. (56-59) Numerous studies have demonstrated the efficacy of fish oil supplementation in depression. (60,61)

The human brain is 60% fat. The quality of fats that compose neurons significantly influence brain function including moods. A relative deficiency of flexible omega-3 fatty acids compared to the more rigid omega-6, saturated, and cis-trans fatty acids impairs the function of cell membranes and their ability to selectively allow passage of molecules in and out of neurons. The brain is composed of and uses more fatty acids than any other body structure. DHA – referred to by Allport as the “queen of fats” (62) – is responsible for the fastest cellular movements. As the primary structural and cognitive fat of the brain, DHA also affects moods.

A developing fetus’ brain, nerves, eyes, skin, and cellular membranes all require omega-3 oils, especially DHA. The placenta selectively removes omega-3 oils from the mother’s blood stream via the placenta often leaving the mother significantly deficient in these essential oils. (63,64). The recommended dose for omega-3 fish oils when treating PPD is 6-12 grams per day.

Hypericum perforatum (St. John’s Wort):

Over twenty-five double-blind studies have shown the herb St. John’s Wort to produce as good or better results compared to SSRI drugs with significantly fewer side effects. (65-71) In Germany, where hypericum is a prescription drug and covered by insurance, over 20,000,000 take this herb for depression. One of the benefits of taking St. John’s Wort is an increase of serotonin. (72)

SAMe (S-adenosylmethione):

SAMe is a methyl donor in the production of monamines, neurotransmitters, and phospholipids such as phosphatidylserine and phosphatidylcholine. SAMe serves as a precursor for glutathione, coenzyme A, cysteine, taurine, and other essential compounds. SAMe is involved in converting methionine into sulfur and is important in homocysteine metabolism.

When compared with other antidepressants, SAMe tend to work faster and more effectively with virtually no negative side effects. In fact, SAMe has beneficial side effects including improved cognition, slowing of the aging process, improved joint function and less pain, and liver protection. (73)

Normally the brain synthesizes adequate SAMe from the amino acid methionine. Supplementing SAMe in depressed patients increases serotonin and dopamine levels, improves membrane fluidity, and improves the binding of neurotransmitters to receptor sites (74,75). Numerous double-blind studies demonstrate the efficacy of SAMe for depression. (76-78) The suggested dose of SAMe to treat depression ranges from 400-1600 mg a day.

Depressed patients have lower brain levels of inositol. (79) Inositol is useful in maintaining healthy serotonin metabolism, and by doing so helps treat many conditions like depression, agoraphobia, panic disorder (80-82), and obsessive compulsive disorder (83).
Research shows that taking 6-12 grams of inositol per day for 4 weeks significantly improves mood and reduces the severity of depression. (84-86) Inositol can be safely used with antidepressant medications. (87)

L-theanine is known to increase levels of GABA and has an anti-anxiety effect as well as improving cognitive function. (88) L-theanine may also normalize dopamine levels which are often depleted by various stresses. (89) L-theanine significantly reverses glutamate-induced toxicity. (90)

 

 

Clinically it is imperative that higher quality, higher potency, more comprehensive prenatal an postnatal nutrient systems be utilized in the treatment and prevention of postpartum depression. It is common knowledge in many 3rd world countries that the postpartum recovery period is 24 months because this is the amount of time women are told to wait between pregnancies to replenish their bodies and avoid many postnatal health problems. These women have more community and extended family support too which significantly reduces the incidence of PPD.

Most prenatal vitamin supplements are inadequate to fully supply developing baby and mother with the potency and quality of nutrients required to fuel pregnancy and the postpartum periods. These are highly nutrient dependent process.
A randomized, double-blind, placebo-controlled clinical trial done on a comprehensive postnatal nutrient program called After Baby Boost showed excellent results, improving 14 common postpartum symptoms including postpartum depression, anxiety, insomnia and mood swings. Parameters measured were breast tenderness, concentration, cramping, depression, dizziness, fatigue, headaches, insomnia, irritability, joint inflammation and pain, mood swings, nervousness, palpitations, sweating, temperature changes (hot or cold), vaginal dryness, and water retention.

After Baby Boost contains high-potency vitamins and minerals including CoQ10, alpha lipoic acid, 2 grams of fish oils with 3 antioxidants to prevent rancidity, and nighttime minerals (calcium and magnesium citrate). The placebo used was a leading prenatal vitamin.

After Baby Boost significantly outperformed the prenatal vitamin in all 14 symptom categories, indicating that most postpartum women require more comprehensive, higher potency nutrient replenishment than prenatal vitamins provide. (91)

Obstetricians rarely stress the importance of a high-quality, nutrient dense diet. Nor do they prescribe high quality prenatal vitamins.  Women are often told, “you are eating for two now, so eat whatever you want.” In actuality, only 300 extra calories are needed per day during pregnancy. It is important that these be nutrient-dense calories. Unrestricted eating of carbohydrates contributes to obesity and can contribute to metabolic diseases including physiologic depression and even, diabetes of pregnancy.

It is hoped that the reader becomes more aware of this simple concept: A baby’s body is entirely composed of the nutrients donated by its mother’s body. Because all physiologic processes and chemicals (neurotransmitters, hormones, metabolic pathways, etc.) are nutrient dependent, nutritional deficiencies can often be the fundamental cause of PPD. While antidepressant drugs are necessary for some, the longer-term solution often requires a well-thought-out integrative approach that includes (1) replenishing nutritional reserves through dietary supplements,(2) psychotherapy and/or  childbirth/PTSD therapies such as EMDR, (3)adequate sleep (often very difficult with a new infant), (4) moderate exercise, (5) deep belly breathing/meditation, (6) community support, (6) a nutrient dense diet, and (7) drug therapy when necessary

1. Gaynes BN, Gavin N, Meltzer-Brady S, et al. “Perinatal depression: prevalence, screening accuracy, and screening outcomes,” Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services, Rockville, MD: AHRQ Publication #05-E006-2, February 2005.

2. No authors listed. “Medication Therapy in Ambulatory Care: United States, 2003-2004,” Centers for Disease Control Vital and Health Statistics, posted at http://www.cdc.gov/nchs/data/series/sr_13/sr13_163.pdf.

3. Willen JM, Mounts KO. “Women with depression: ‘You can’t tell by looking,’” Matern Child Health J 2006 September; 10(Suppl 7): 183-187.

4. Wurtman RJ, Fernstrom JD. “Control of brain neurotransmitter synthesis by precursor availability and nutritional state,” Biochem Pharmacol 1976 Aug 1;25(15):1691-6.

5. Birdsall TC. “5-Hydroxytryptophan: a clinically-effective serotonin precursor,” Alternative Medicine Review 1998 Aug; 3(4):271-80.

6. Byerley WF et al. 5-Hydroxytryptophan: A review of its antidepressant efficacy and adverse effects. J Clin Psychopharmacol 1987;7:127-137.

7. Byerley W, Judd L, Reimherr F, Grosser B. 5-hydroxytryptophan: a review of its antidepressant efficacy and adverse effects. J Clin Psychopharmacol. 1987;7:127-137.

8. D’Elia G, Hanson L, Raotma H. “L-tryptophan and 5-hydroxytryptophan in the treatment of depression: a review,” Acta Psychiatra Scand 1978;239-52.

9. Poldinger W, Calanchini B, Schwarz W. “A functional-dimensional approach to depression: serotonin deficiency as a target syndrome in a comparison of 5-hydroxytryptophan and fluvoxamine,” Psychopathology 1991;24:53-81.

10. Shaw K, Turner J, Del Mar C. “Tryptophan and 5-Hydroxytryptophan for depression (Cochrane Review),” The Cochrane Database of Systematic Reviews 2002, Issue 1. Art. No.: CD003198. DOI:10.1002/14651858.CD003198

11. Turner EH, Loftus JM, Blackwell AD. “Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan,” Pharmacol Therapeutics 2006;109(3):325-338.

12. Crayton JW, et al. “Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex,” Brain Res 1996 Jul 29;728(2):260-2.

13. Tafet GE, Toister-Achituv M, Shinitzky M. “Enhancement of serotonin uptake by cortisol: A possible link between stress and depression,” Cogn Affect Behav Neurosci 2001 Mar;1(1):96-104.

14. Thakore JH, Dinan TG. “Cortisol synthesis inhibition: A new treatment strategy for the clinical and endocrine manifestations of depression,” Biological Psychiatry 1995 Mar; 37(6): 364-368.

15. Altar C, et al. “Glucocorticoid induction of tryptophan oxygenase,” Biochem Pharmacol 1983;32:979-84.

16. Stutzmann GE, McEwen BS, LeDoux JE. “Serotonin Modulation of Sensory Inputs to the Lateral Amygdala: Dependency on Corticosterone,” J Neurosci 1998 Nov 15;18(22):9529-38.

17. Drevetz WC. “Neuroimaging Abnormalities in the Amygdala in Mood Disorders,” Annals of the New York Academy of Sciences 2003;985:420-444.

18. Williams AL, et al. “The role for vitamin B-6 as treatment for depression: a systematic review,” Family Practice 2005 22(5):532-537.

19. Hartvig K, et al. “Pyridoxine effect on synthesis rate of serotonin in the monkey brain measured with positron emission tomography,” Journal of Neural Transmission June 1995;102(2).

20. No authors listed. “Monograph: 5-Hydroxytryptophan,” Alternative Medicine Review 1998;3(3):224-6.

21. Gold PW, Chrousos GP. “Organization of the stress system and its dysregulation in melancholic and atypical depression: high vs low CRH/NE state,” Molecular Psychiatry 2002, Volume 7, Number 3, Pages 254-275.

22. Asnis GM, McGinn LK, Sanderson WC. “Atypical depression: clinical aspects and noradrenergic function,” Am J Psychiatry 1995; 152:31-36.

23. Selye H. Stress Without Distress. Philadelphia: J. B. Lippincott Co., c1974.

24. Sulman FG, Pfeifer Y, Superstine E. “The adrenal exhaustion syndrome: an adrenal deficiency,” Annals of the New York Academy of Sciences 1977;301(1): 918-930.

24. Tsigos C, Chrousos GP. “Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress,” J Psychosom Res 2002;53:865-71.

25. Tsigos C, Chrousos GP. “Physiology of the hypothalamic-pituitary-adrenal axis in health and dysregulation in psychiatric and autoimmune disorders,” Endocrinol Metab Clin North Am 1994;23:451-66.

26. Holford P. “Depression: the nutrition connection,” Primary Care Mental Health 2003;1:9-16.

27. Stoll AL, et al. “Omega-3 fatty acids and bipolar disorder: a review,” Prostaglandins Leukot Essent Fatty Acids 1999 May-Jun;60(5-6):329-37.

28. Bowery NG, et al. “International Union of Pharmacology. XXXIII. Mammalian gamma-aminobutyric acidB receptors: structure and function,” Pharmacological Reviews 2002 June;54(2): 247-264.

29. Carroll BJ, Curtis GC, Mendels J. “Cerebrospinal fluid and plasma free cortisol concentrations in depression,” Psychol Med 1976;6:235-44.

30. Joffe R, Roy-Byrne P, Udhe T. “Thyroid function and affective illness: a reappraisal,” Biol Psychiatry 1984;19:1685-91.

31. Gold M, Pottash A, Extein I. “Hypothyroidism and depression: evidence from complete thyroid function evaluation,” JAMA 1981;245:1919-22.

32. Banki C, Arato M, Papp Z. “Thyroid stimulation test in healthy subjects and psychiatric patients,” Acta Psychiatr Scand 1984;295-303.

33. Sintzel F, et al. “Potentializing of tricyclics and serotoninergics by thyroid hormones in resistant depressive disorders,” Encephale 2004 May-Jun;30(3):267-75.

34. Bauer M, et al. “Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain,” Mol Psychiatry 2002;7(2):140-56.

35. Jordan D, et al, “Participation of serotonin in thyrotropin release. II. Evidence for the action of serotonin on the phasic release of thyrotropin,” Endocrinology 1979;105: 975-979.

36. Karamouzis M, et al. “The response of thyroid hormones FT3, FT4, TSH, serotonin and histamine in young persons during maximal physical work,” Hell J Nucl Med 1999;2:125-30.

37. Abraham G, Milev R, Lawson JS. “T3 augmentation of SSRI resistant depression,” Journal of Affective Disorders 91(2-3):211-215.

38. Aronson R, Offman HJ, Joffe RT, Naylor D. “Triiodothyronine augmentation in the treatment of refractory depression: a meta-analysis,” Arch Gen Psychiatry 1996; 53: 842-848.

39. Lifschytz T, et al. “Basic Mechanisms of Augmentation of Antidepressant Effects with Thyroid Hormone,” Current Drug Targets 2006 Feb;7(2): 203-210.

40. Joffe H, Cohen LS. “Estrogen, serotonin, and mood disturbance: where is the therapeutic bridge?” Biological Psychiatry 1998;44(9): 798-811.

41. Archer JS, “Relationship between estrogen, serotonin, and depression,” Menopause 1999;6(1): 71-78.

42. Koldzic-Zivanovic N, et al. “Intracellular signaling involved in estrogen regulation of serotonin reuptake,” Mol Cell Endocrinol 2004 Oct 29;26(1-2):33-42.

43. Bethea CL. “Ovarian Steroid Regulation of 5-HT1A Receptor Binding and G protein Activation in Female Monkeys,” Neuropsychopharmacology 2002;27: 12-24.

44. Clarke WP, Maayani S. “Estrogen effects on 5-HT1A receptors in hippocampal membranes from ovariectomized rats: functional and binding studies,” Brain Res 1990 Jun 4;518(1-2):287-91.

45. Klink R, Robichaud M, Debonnel G. “Gender and gonadal status modulation of dorsal raphe nucleus serotonergic neurons. Part I: effects of gender and pregnancy,” Neuropharmacology 2002 Dec;43(7):1119-28.

46. Robichaud M, Debonnel G. “Oestrogen and testosterone modulate the firing activity of dorsal raphe nucleus serotonergic neurones in both male and female rats,” J Neuroendocrinol 2005 Mar;17(3):179-85.

47. Andréen L, et al. “Pharmacokinetics of progesterone and its metabolites allopregnanolone and pregnanolone after oral administration of low-dose progesterone,” Maturitas 2005, 54(3); 238-244.

48. Marx CE. “Neurosteroids and psychiatric disorders,” Psychiatric Times 2001 Oct; vol XVIII(10).

49. Kaura V, et al. “The progesterone metabolite allopregnanolone potentiates GABA(A) receptor-mediated inhibition of 5-HT neuronal activity,” Eur Neuropsychopharmacol 2007 Jan 15;17(2):108-15.

50. Sinnott RS, Mark GP, Finn DA. “Reinforcing effects of the neurosteroid allopregnanolone in rats,” Pharmacol Biochem Behav 2002 Jul;72(4):923-9.

51. Robichaud M, Debonnel G, “Modulation of the firing activity of female dorsal raphe nucleus serotonergic neurons by neuroactive steroids,” Journal of Endocrinology 2004;182:11-21.

52. Charalampopoulos I, et al, “Dehydroepiandrosterone sulfate and allopregnanolone directly stimulate catecholamine production via induction of tyrosine hydroxylase and secretion by affecting actin polymerization,” Endocrinology 2005 Aug;146(8): 3309-3318.

53. Shen W, et al. “Pregnenolone sulfate and dehydroepiandrosterone sulfate inhibit GABA-gated chloride currents in Xenopus oocytes expressing picrotoxin-insensitive GABA(A) receptors,” Neuropharmacology 1999 Feb;38(2):267-71.

54. Robichaud M, Debonnel G. “Oestrogen and testosterone modulate the firing activity of dorsal raphe nucleus serotonergic neurones in both male and female rats,” Journal of Neuroendocrinology 2005;17(3):179-185.

55. Landrigan PJ (ed.) “Chemical Contaminants in Breast Milk,” Environmental Health Perspectives 2002 June; 110(6):A313-A315.

56. Bruinsma KA, Taren DL. “Dieting, essential fatty acid intake, and depression,” Nutrition Rev 2000;58(4):98-108.

57. Hibbeln JR. “Fish consumption and major depression,” Lancet 1998;351(9110):1213.

58. Logan A. “Neurobehavioral aspects of omega-3 fatty acids: possible mechanisms and therapeutic value in major depression,” Altern Med Rev 2003;8(4):410-425.)

59. Mamalakis G, Tornaritis M, Kafatos A. “Depression and adipose essential polyunsaturated fatty acids,” Prostaglandins Leukot Essent Fatty Acids 2002;67:311-318.

60. Mischoulon D, Fava M, “Docosahexanoic acid and omega-3 fatty acids in depression,” Psychiatr Clin North Am 2000;23:785-794.

61. Puri BK, Counsell SJ, Hamilton G, et al. “Eicosapentaenoic acid in treatment-resistant depression associated with symptom remission, structural brain changes and reduced neuronal phospholipid turnover,” Int J Clin Pract 2001;55:560-563.

62. Allport S. The Queen of Fats: Why Omega-3s Were Removed From the Western Diet and What We Can Do To Replace Them, University of California Press, Berkeley, CA: 2006.

63. Kendall-Tackett K. “A new paradigm for depression in new mothers: the central role of inflammation and how breastfeeding and anti-inflammatory treatments protect maternal mental health,” Int Breastfeed J 2007;2.

64. Stoll A. The Omega-3 Connection, Free Press, New York, NY: 2002

65. Halama P. “Efficacy of the Hypericum extract LI 160 in the treatment of 50 patients of a psychiatrist,” Nervenheilkunde 1991;10:305-7.

66. Hansgren D, Vesper J, Ploch M. “Multicenter double-blind study examining the antidepressant effectiveness of the hypericum extract LI 160,” J Geriatr Psychiatry Neurol 1994 (7 Suppl 1):S15-8.

67. Harrer G, Hubner WD, Podzuweit H. “Effectiveness and tolerance of the hypericum extract LI 160 compared to maprotiline: a multicenter double-blind study,” J Geriatr Psychiatry Neurol 1994 (7 Suppl 1);S24-8.

69. Hubner WD, Lande S, Podzuweit H. “Hypericum treatment of mild/moderate depressions with somatic symptoms,” J Geriatr Psychiatry Neurol 1994 (7 Suppl 1):S12-4.

70. Kasper S, et al. “Superior efficacy of St John’s wort extract WS® 5570 compared to placebo in patients with major depression: a randomized, double-blind, placebo-controlled, multi-center trial,” BMC Med 2006.

71. Vorbach EU, Hubner WD, Arnoldt KH. “Effectiveness and tolerance of the Hypericum extract LI 160 in comparison with imipramine: randomized double-blind study with 135 outpatients,” J Geriatr Psychiatry Neurol 1994 (7 Suppl 1);S19-23.

72. Morrazzoni P, Bombardelli E. “Hypericum perforatum,” Fitoterapia 1995;66:43-68.

73. Baldessarini RJ. “Neuropharmacology of S-adenosyl-L-methionine,” Am J Med 1987 (Suppl 5A);83:95-103.

74. Bottiglieri T, et al. “Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine,” J Neurol Neurosurg Psychiatry 1990;53(12):1096-8.

75. Bottiglieri T. “Ademetionine (S-adenosylmethionine) neuropharmacology: implications for drug therapies in psychiatric and neurological disorders,” Expert Opin Investig Drugs 1997;6(4):417-26.

76. Kagan BL, et al. “Oral S-adenosylmethionine in depression: a randomized, double-blind, placebo-controlled trial,” Am J Psychiatry 1990;147:591-595.

77. Mischoulon D, Fava, M. “Role of S-adenosyl-L-methionine in the treatment of depression: a review of the evidence,” Am J Clin Nutr 2002 Nov;76(5): 1158S-1161S.

78. Rosenbaum JF, et al. “The antidepressant potential of oral S-adenosyl-l-methionine,”Acta Psychiatrica Scandinavica 1990 May;81(5):432-436.

79. Bersudsky Y, et al. “Epi-inositol and inositol depletion: two new treatment approaches in affective disorder,” Curr Psychiatry Rep 1999 Dec;1(2):141-147.

80. Belmaker, R. H. et al. “Manipulation of inositol-linked second messenger systems as a therapeutic strategy in psychiatry,” Adv Biochem Psychopharmacol 1995;49: 67-84

81. Benjamin J, et al. “Double-blind, placebo-controlled, crossover trial of inositol treatment for panic disorder,” Am J Psychiatry 1995;152 (7):1084-6.

82. Palatnik A, et al. “Double-blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder,” J Clin Psychopharmacol 2001;21(3): 335-339.

83. Fux M. “Inositol treatment of obsessive-compulsive disorder,” Am J Psychiatry 153(9): 1219-1221.

84. Colodny L, Hoffman RL. “Inositol-clinical applications for exogenous use,” Altern Med Rev 1998;3(6):432-47.

85. Levine J, et al. “Double-blind, controlled trial of inositol treatment of depression,” Am J Psychiatry 1995;152(5):792-794.

86. Levine J. “Controlled trials of inositol in psychiatry,” Eur  Neuropsychopharmacol 1997;7(2):147-55.

87. Levine J, et al. “Combination of inositol and serotonin reuptake inhibitors in the treatment of depression.” Biol Psychiatry 1999;45(3): 270-273.

88. Nathan PJ, et al. “The neuropharmacology of L-Theanine(N-Ethyl-L-Glutamine): a possible neuroprotective and cognitive enhancing Agent,” Journal of Herbal Pharmacotherapy: Innovations in Clinical and Applied Evidence-Based Herbal Medicinals 2006; 6(2).

89. Mason R. “200 mg of Zen; L-theanine boosts alpha waves, promotes alert relaxation,” Alternative & Complementary Therapies 2001 Apr 7:91-95.

90. Nagasawa K, et al. “Possible involvement of group I mGluRs in neuroprotective effect of theanine,” Biochem Biophys Res Commun. 2004 Jul 16;320(1):116-22.

91. Blum J et al., “A randomized double-blind clinical trial investigating fourteen postpartum symptoms comparing After Baby Boost comprehensive postnatal nutritional system vs. a leading prenatal vitamin as placebo.” 

 

Related Depression Articles

 Mail this post

Technorati Tags: Anxiety, Approach, Depression, Disorder, Integrative, Postpartum, prevention, Treatment

Question by maslyn_jl: Depression?
I have been suffering from Bipolar depression for several years now…somewhere around 10 years. The doctor has put me on several different medications that caused me more issues (weight gain, fatigue and other stuff like that) that I could not handle. I have not been on medicine since I had my son 2 years ago. Things seem to be getting worse lately with all the stress that has been added since my wedding in May. I have an appointment with my doctor today to try to get something to help me. It has gotten to the boilling point where I can see my condition hurting my family. Anyone have any suggestions on what medications worked good for you or someone you know? Or any other comments for me…please don’t be negative..that is not going to help me at all..it will only make it worse.
I agree with all of you. I appreciate soo much your suggestions or words of support for me. It helps.

Bill – you are right, I am lacking self-confidence but I have had that problem all of my life. It’s not something I can just snap out of by myself. I almost wonder if at times I need people around me that feel like I do so that we can support each other…I am too embarrased most the time to tell anyone about my problems.

Best answer:

Answer by jjthinstrips
Bravo! You are on the right course! It seems that you are probably too used to the same medicine, and you may need a change…Believe me, it will be worth it!

Add your own answer in the comments!

 Mail this post

Technorati Tags: Depression

By Alan Harper, MA, LLP

Many adults are surprised when told that children and adolescents can and do become clinically depressed. We often think only adults have the type and severity of life stressors that can result in depression. After all, we adults have to deal with careers, financial concerns, marital issues, parenting challenges, tax season, home repairs, health problems, and more. Children and adolescents have little to worry about in their relatively stress-free lives. Children simply have to do their best in their fun classes at school, play with their friends, enjoy all the toys they’ve accumulated, and put up with Mom and Dad when told it’s time to go to bed so they can rest up for another fun-filled, stress-free day.

Adolescent boys and girls have lives filled with Friday night football games, sleepovers at friends’ houses, weekends at the mall, movie dates with their exciting new boyfriend or girlfriend. They enjoy group outings at local fast food restaurants where talk is friendly and no one is teased or ostracized. Life is good as a child and adolescent. School is fun, home is stable, friends are true, and bodies are healthy. Depression can wait until the real stressors of adulthood. Right? Well…not exactly.

As much as we may want the above scenarios to be true, the fact is the time of our lives from childhood through adolescence can be an emotionally tumultuous time. It can be filled with uncertainty, insecurity and confusion caused by difficult peer-relational issues, heart-breaking dating experiences, academic stressors, health problems and conflictual home environments. This is a time of transition from the relative protection of young childhood to the significant challenges of adulthood. The demands placed on children and adolescents by society, parents, peers, and the girls and boys themselves can be staggering.

Depression can and does occur in children and adolescents and is more prevalent in our culture than previously thought. The U.S. Center for Mental Health Services (CMHS) reports as many as one in every 33 children and one in every eight adolescents may be experiencing depression at some level. Two-thirds of children with mental health problems do not get the help they need. CMHS also reports that once a young person has experienced a major depression, he or she is at risk for developing another depression within the next five years. Plus, children or adolescents who have a family history of depression are more likely to struggle with it. Depression can significantly impact the life of a child or adolescent (and their families) through the disruption of peer relationships, academic performance and development, self-image and selfesteem. Thoughts of suicide or other self-destructive behaviors can occur with depression, which places further stress on the child or adolescent and increases the risk of physical harm or even death.

There is help for the depressed child or adolescent. Before help can be provided, however, the signs and symptoms of depression within the child and adolescent age range must be understood so parents and other caregivers can better determine when outside intervention is needed.

There are a number of signs and symptoms of childhood and adolescent depression, some of which are readily observable by others. Some others require questioning of the child or adolescent and/or deliberate monitoring of his or her moods and behaviors. Parents cannot count on their child or adolescent to openly state they are feeling depressed or are struggling in various areas of their lives. It is important that parents pay close attention to changes in their child or adolescent’s general level of functioning in areas such as academics, peer relations, physical appearance and grooming, and involvement in usual areas of recreation. Significant and lasting declines in one or more of these areas may be an indication of depression, and should prompt further investigation. Parents must also listen for words indicating feelings of low self-worth and watch for observable moods that suggest chronic sadness, irritability or discouragement.

Common signs and symptoms of depression among children and adolescents include:
• Frequent sadness, tearfulness, or crying
• Relationship problems
• Feelings of hopelessness or helplessness
• Threats or attempts to run away from home
• Frequent complaints of various physical ailments
• Frequent school absences and/or poor school performance
• Low energy or restlessness
• Alcohol and/or drug use
• Persistent boredom
• Decline in activity level or interest in previously enjoyed activities
• Communication difficulties
• Social isolation
• Excessive guilt or low self-esteem
• Significant changes in eating and/ or sleeping patterns
• Increased levels of anger, irritability, or hostility
• Increased sensitivity to rejection or failure
• Concentration problems
• Thoughts or threats of suicide or other self-destructive behaviors

Not all children or adolescents will share the same signs and symptoms of depression. Some may appear sad, while others may act angry or irritable. One child may sleep excessively while another may have difficulty falling or staying asleep. It is important to look for changes in the typical moods, behaviors or physical functioning to determine whether depression may be present.

Also, it is important to remember that each individual sign or symptom above is not necessarily an indication of depression (although suicidal thoughts, threats or attempts do require immediate intervention). It is the combination of the various signs and symptoms that determines whether a depression diagnosis is made.

It is important that parents pay close attention to changes in their child or adolescent’s general level of functioning… It is important to look for changes in typical moods, behaviors or physical functioning to determine whether depression may be present. It is also important to remember the above changes in moods, behaviors, physical symptoms and general functioning must be present on a fairly consistent basis for at least two weeks before a depression diagnosis should be considered. Children and adolescents will occasionally experience emotional turmoil that may mimic depression, but be resolved within a few days. This is not considered depression, but rather a temporary emotional upheaval that does not require the same type of intervention. This is not to say parents should wait two weeks to seek help if serious concerns exist. Rather, the depression diagnosis itself requires two consecutive weeks of impairment.

]]>

Unfortunately, there is a risk of suicide with depressed children and adolescents, especially when the depression is severe, stressors are significant, and social support is perceived by the child as minimal or non-existent. Suicide has been identified as the third leading cause of death within the 15 – 19 year-old age range and the sixth leading cause of death with 5 – 15 year olds. Parents should always take threats of suicide seriously. Seek immediate intervention to determine the level of risk and develop a plan of action to prevent the child from harming him or herself.

If it appears a risk of suicide exists, measures need to be taken to make the home as safe as possible by denying easy access to firearms, razor blades, potentially dangerous medications, etc. Studies show girls are more likely than boys to attempt suicide, but boys are more likely to succeed given the fact they often choose more lethal methods such as guns. Again though, all threats need to be taken seriously. Parents should seek immediate help if it appears their child is in imminent danger of self-harm. Options for getting assistance include calling 911, contacting suicide prevention hotlines, and reporting concerns through the crisis lines at inpatient facilities.

Medications

Treatment options for the depressed child or adolescent have improved dramatically over the past few decades. Much has been learned about the physiological and psychological nature of depression, which has prompted both medical and therapy advances. It is now known that clinical depression involves declines in neurotransmitter functioning within the brain, which can be alleviated through the use of a wide assortment of antidepressant medications. These medications can be prescribed through the child’s physician or psychiatrist following a thorough review of the history and nature of the specific evidence of depression. Side effects can occur with antidepressant medications and should be discussed with the prescribing physician prior to beginning the medication treatment. Intolerable or overly-concerning side effects may require a change in medication, however many side effects tend to be temporary and relatively mild. Any concerns need to be promptly addressed with the prescribing physician.

In most cases, therapy should be a part of the treatment plan when medication is prescribed, in order to determine whether underlying issues are contributing to the depression. If a child or adolescent relies entirely on an antidepressant medication to alleviate depression symptoms, the symptoms may return once medication treatment is completed. Working with a qualified therapist can help the child or adolescent identify and resolve the issues and problems that may have caused the depression. These issues may be social in nature, prompting a therapy focus on building and maintaining effective peer relationships.

Or perhaps they may be associated with specific family issues that can be addressed through family therapy with an emphasis on family dynamics, communication styles and individual roles. Specific trauma events can result in depression including emotional, physical and sexual abuse, loss of a loved one (pets included) through death or other means, or serious health concerns with the child or another family member. Significant transitions such as changing residences, schools or peer groups, changes in the family structure, or parental divorce can also contribute to the onset of depression.

Entering a new phase of life such as middle school or high school, enduring the challenges of puberty, or experiencing new responsibilities through employment or extracurricular school activities can create emotional turmoil as the child or adolescent struggles to establish and maintain a sense of confidence, competence, and control.

Whatever the underlying issue(s) may be, therapy can help alleviate contributing self-defeating thoughts, perspectives, and behaviors. Therapy can help the child or adolescent respond to his or her daily challenges and circumstances in ways that are both realistic and productive. Therapy that emphasizes proactive problem-solving, monitoring and modifying selfdefeating thoughts and behaviors, and building effective communication and relational skills can be very helpful in treating depression. This assumes therapy efforts take into account, and consistently honor, the individuality of the child or adolescent in treatment.

Sometimes intervention beyond medication and therapy is needed, especially when the risk of suicide or other self-destructive behaviors exist. Admission to a child and adolescent inpatient facility may be considered as a means to provide immediate safety and initiate medication treatment and therapy intervention. Admissions are typically brief (a few days), can help stabilize the child, and significantly lower the risk of self-harm behaviors. Partial program admissions are also available at some facilities. These programs are typically held from morning until late afternoon and provide more intense interventions than traditional outpatient therapy, while allowing the child to return home to his or her family until the program resumes the following morning. Continuation of schoolwork is encouraged, so that additional stressors are not placed on the child upon discharge from the program.

In cases of identified trauma or various issue-specific problems contributing to depression, support groups within the community may be available. The child’s therapist, physician, or psychiatrist may be able to assist in identifying some of these resources.

The issue of which intervention to seek can be a challenge. In cases when the child’s depression is strictly biological (although that’s difficult to determine), medication treatment may be sufficient. At other times, it may be best to forego medication treatment until a course of therapy has been tried. This is especially true in cases when the child or adolescent is struggling with grief/loss issues. In these types of cases, medication treatment may mask the issues causing the depression, resulting in the continuation of the contributing issues and the return of the child’s symptoms when termination of medication treatment is attempted. Parents may seek advice regarding the various treatment options from any of the above professionals.

What Can Parents Do To Help?

There are many things parents can do to help their child or adolescent recover from depression. Conversely, there are also many things parents sometimes do that can actually create more difficulties for the child and perhaps even worsen the depression. Below is a list of some of the ways parents may support and assist their child or adolescent, as well as a number of reactions to avoid.

• Seek help from a qualified mental health professional as soon as it appears the child or adolescent may be depressed. Do not hesitate to take emergency measures (crisis line, 911, etc.) if it appears the child is at immediate risk of self-harm.
• Stay involved throughout the course of the child’s treatment whether it involves medication, therapy, or both. Ask questions of the mental health professionals regarding treatment plans, medication issues, and ways you can assist with treatment through necessary changes in the home environment and/or ways you respond to the child.
• Proactively address any concerns or reasonable suspicions of drug or alcohol use. Drug and alcohol use can intensify the downward spiral of depression and can be a significant obstacle to effective treatment.
• Monitor the depressed child or adolescent’s moods and behaviors without “suffocating” him/her with outward concern or questions.
• Maintain home rules and expectations concerning the child as consistently as possible, except in cases when specific changes have been discussed and identified as part of the treatment plan. Parents sometimes become overaccommodating to a depressed child or adolescent, which can actually encourage the continuation of the depression due to the perceived “benefits” of being depressed.
• Monitor and encourage healthy nutrition and sleep habits with the depressed child. Clinical depression has a biological dimension that can be affected by the consistency and quality of physical self-care.
• Encourage the depressed child to maintain reasonable physical, recreational, and social activity levels. These activities will provide opportunities for emotional respite from the depression and help maintain much-needed social contacts.
• Make it clear that you are available to the child to assist in any reasonable way possible, but don’t be surprised if he or she rarely takes you up on your offer. Simply sensing you as an available quiet strength can sometimes be enough to help the child feel your support.
• Allow the depressed child some “space,” but discourage prolonged isolation.
• Do not be overly critical of your depressed child, or suggest they “snap out of it.” They probably would if they could and what they really need from you is nonjudgmental support, encouragement, and understanding. But remember, reasonable expectations should continue in most areas of the child’s life, including academics, behavior, and household responsibilities.

Children and adolescents can, indeed, become depressed. Contributing factors vary among individuals, as do specific signs and symptoms. But risk factors apply to all, including the potential for social problems, academic impairment, family disruption, selfesteem problems, self-abuse, and even death through the act of suicide. Children and adolescents cannot be counted on to openly point out they are struggling with depression. Often they are not even aware they are depressed or that help is possible. Parents and other caregivers must be aware of the signs and symptoms of child and adolescent depression in order to determine when professional intervention may be needed. They also should be knowledgeable of area resources available for the diagnosis and treatment of depression for their children, or for addressing immediate crises. Traditional treatment for depression includes therapy and/or medication, as well as support groups and other options when deemed necessary and beneficial. The period of childhood through adolescence can be a time of excitement, happiness and growth. It can also be a time of uncertainty and despair as significant challenges and transitions are negotiated. If and when depression occurs, help is available. Parents should seek help through qualified mental health professionals and become knowledgeable about depression and the issues specific to their child’s struggles. They should remain involved in the treatment process and be willing to make reasonable changes in the home environment and in the ways they respond to their child. Finally, they should consistently provide support, encouragement and stability to the child.

 

 

 Mail this post

Technorati Tags: Adolescent, Childhood, Depression, Realities, Understanding

Getting depression is not a sign of weakness. There are no particular ‘personality types’ that are more at risk than others. However, some risk factors have been identified; these include inherited (genetic) factors, such as having parents or grandparents who have suffered from depression and non-genetic factors such as the death of a parent when you were young or suffering a trauma of some kind..

It is often impossible to identify a ’cause’ in many people, and this can be distressing for people who want to understand the reasons why they are ill. However depression, like any illness, can strike for no apparent reason. There are drugs on the market that can really help, but many people are reluctant to take these, as the side effects can almost be as unpleasant as the depression, but there are alternatives, and Hypnotherapy is one of them. 

Self-Hypnosis is designed to combat the most common symptoms of depression, and lift that dark shadow of misery, anguish, gloom, and despondency.
Only a qualified doctor or health practitioner can formally diagnose you with clinical depression. However, how they reach this diagnosis gives an incredibly important insight into how to treat depression.

Depression Screening and Tests for Depression
Screening for depression is becoming more common, as we begin to realize how much is left undiagnosed. So let’s look now at how clinical depression is normally diagnosed.

Common Signs of Depression
The 5 most common signs of depression, according to research published in The International Journal of Psychiatry in Medicine (1998) are as follows:

These five signs of depression were reported by at least 90% of those in the study.
Reduced enjoyment from usual activities
Disappointment with self
Hopelessness
Irritability
Difficulty sleeping

If you are experiencing some or all of these, it still doesn’t mean that you would necessarily be diagnosed with depression. There are of course many more symptoms of depression, both physical and mental.

Diagnosing Depression

According to the definitions of most medical, psychological, and psychiatric bodies, there is a commonality in the diagnosis of depression. Most depression tests have a very similar framework. Almost without exception, clinical depression will be diagnosed if a certain number of feelings, that are signs of depression, are present over a certain period of time.

Below is the ‘official’ guide for diagnosing clinical depression:

A person can be diagnosed as suffering from clinical depression if:

(A) Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.

(1) Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood.

(2) Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others)

(3) Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gains.

(4) Insomnia or hypersomnia nearly every day

(5) Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down)

(6) Fatigue or loss of energy nearly every day

(7) Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick)

(8) Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others)

(9) Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
 
(B) The symptoms do not meet criteria for a Mixed Episode.

]]>

(C) The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

(D) The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).

(E) The symptoms are not better accounted for by Bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

To even start to feel better, you have to muster up from the depths of despair, enough energy and motivation to take action, and once your subconscious mind starts this process for you,  there is no reason why you shouldn’t be able to make all those positive, life-changing, decisions you need to make to turn your life around.

The fact that you are reading this means you are ready…you’ve got this far…now just take the next step!

Depression – A Natural Response?

OK, so that’s what the doctors use but if we look at E), it raises some interesting questions.
It says that clinical depression can be diagnosed if the symptoms cannot be attributed to bereavement. So, since grieving is a natural response, we can see that depression is simply an out-of-place natural response. And of course it is. If it were not, we would have to take drugs to create it.

So what about the incredibly popular idea that depression is due to some unnatural chemical imbalance in the brain. That this ‘imbalance’ is the source and root cause of depression?

It’s possible, but it just doesn’t make sense for the majority of cases. And when we look at the increase in depression over the last 50 years or so, we will see that our brain chemistry just can’t change that quickly.  Understanding this is one of the keys to understanding depression itself.

Typical Symptoms of Depression

ALTHOUGH it is often classed as ‘mental illness’, clinical depression often has as many physical symptoms as mental. The feelings or emotions that are depression symptoms, actually begin to cause the physical effects. How this happens is a vital part of understanding depression and the symptoms that come with it.

If you are depressed at the moment some of the following symptoms may sound familiar:

You feel miserable and sad.

You feel exhausted a lot of the time with no energy.

You feel as if even the smallest tasks are sometimes impossible.

You seldom enjoy the things that you used to enjoy-you may be off sex or food or may ‘comfort eat’ to excess.

You feel very anxious sometimes.

You don’t want to see people or are scared to be left alone. Social activity may feel hard or impossible.

You find it difficult to think clearly.

You feel like a failure and/or feel guilty a lot of the time.

You feel a burden to others.

You sometimes feel that life isn’t worth living.

You can see no future.
 There is a loss of hope.
You feel all you’ve ever done is make mistakes and that’s all that you ever will do.

You feel irritable or angry more than usual.

You feel you have no confidence.

You spend a lot of time thinking about what has gone wrong, what will go wrong or what is wrong about yourself as a person.

You may also feel guilty sometimes about being critical of others (or even thinking critically about them).

You feel that life is unfair.

You have difficulty sleeping or wake up very early in the morning and can’t sleep again.
You seem to dream all night long and sometimes have disturbing dreams.

You feel that life has/is ‘passing you by.’

You may have physical aches and pains which appear to have no physical cause, such as back pain.

It’s this wealth of depression symptoms, and the broad scope that confuses many people as to what depression actually is. Explanations rarely cover all the symptoms, and everybody’s experience is different.

1) Know about your condition – what you know about your depression has been shown to have an effect on how well you respond to treatment. Start helping yourself.

2) Get deep rest – It may not feel like it, but depression is a form of exhaustion, where  over-dreaming caused by depressive thinking styles, doesn’t allow the body to recover properly. So it’s highly important to be able to relax properly and deeply. Getting back your energy and understanding how your body works are vitally important. Hypnotherapy is excellent for deep relaxation.

3) Find ways to lessen the impact of the outward emotions of depression, such as anxiety and anger. Along with getting proper rest, being able to relax is incredibly important. And a lot harder than it seems, and Self-Hypnosis can teach you have to establish a regular routine of relaxation both mentally and physically.

4) Find ways to assess and monitor your depressive episodes – The way depression makes us adopt all or nothing thinking, is a unique and crucial part of understanding depression. The way depression makes us generate seemingly hopeless outcomes to our situation, can make it almost impossible to see a way out of it.

5) Finding ways to gauge your depression can help to show the shades of grey that will ultimately defeat the black and white thinking on which depression thrives. This is often done in the form of a diary, where you grade how bad your days have been on a scale of 1 to 10, where 1 is the worst and 10 is the best. Then, after 2 weeks or so, you can look back and see how things have varied over that time.

6) Get exercise if you can. If you can increase the amount of physical exercise you get, it can be a great self-help for depression. The results of the physical exertion will lift your depression temporarily at least, in addition to the other benefits of exercise. (As always, consult your medical practitioner before starting any strenuous exercise regime.)

7) Cut down on rumination. Do whatever you can to decrease the amount of rumination you are doing. (Ruminating is ‘chewing over’ emotional issues in your mind without coming to any decision to act.)  If possible, decide to put off difficult decisions for 1 or 2 weeks while you get your energy back.

Ways to cut down rumination are to:

a) Read novels when you have nothing to do, to occupy your mind. (Make them exciting novels, not romance or self-help books!)

b) Do exercise (see 5 above)

c) Work if you can.

Basically, anything that keeps your mind active and of your problems for a while. This is not ‘avoidance’; it is simply giving you a chance to recover.

8. Do What You Enjoy.

Do what you used to enjoy doing, even if you don’t particularly feel like it. Even complete small tasks within the home if you don’t feel like meeting other people. Seemingly mundane tasks, if they have an end result, can result in a feeling of satisfaction, and actually increase your serotonin levels!

Relaxation therapies are effective in overcoming some of the other issues that can co-occur with depression. The effects of panic attacks, anxiety and anger, etc can be lessened and overcome with the ability to relax properly and deeply.

Remember, Self-Hypnosis is a powerful self-help tool for implementing change within your life. It is simple, effective, and non-invasive, produces long-term changes, and can be used by almost everyone.

Hypnotherapy sessions often include the benefit of soothing music at strategic points, helping you to relax even more, and absorb the information whilst the therapist guides you with gentle suggestions, positive language, and life changing imagery. You will always be in control at all times, able to awaken immediately should the need arise and attend to anything that you need to. Hypnotherapy cannot make you do anything or say anything that you would not normally say or do, and it will never coerce you to try to.

By using self-hypnosis pre-recorded material such as a CDs and mp3 download, you will have at the touch of button, a full Hypnotherapy session that can be used whenever you need to, as often as you need to. It’s as simple as that.

 Mail this post

Technorati Tags: Behind, Depression, Easily, Hypnotherapy, Leave, Quickly, SelfHypnosis