An Integrated Approach to Prevention and Treatment of Postpartum Depression (PPD) and Anxiety Disorder Postpartum (PPA)

Raffelock

Dean, DC, L. Ac, CCN DACBN, DIBAK

Cass

Hyla, MD

depressão

Postpartum (PPD) of postpartum anxiety (PPA) became a national epidemic in the United States, affecting 15% -20% of all new mothers, or about 600,000 to 800,000 women annually. (1) It is now estimated that more than 30 million Americans are on antidepressants or anti-anxiety medications. (2) Most 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 antidepressant SSRIs (selective inhibitors of serotonin reuptake). Anxiety Disorder Postpartum is most commonly treated by the family of drugs benzodiazepines like Valium, Ativan, Xanax, and Klonopin. Combining serotonin reuptake inhibitors and norepinephrine both (SNRIs) are also commonly used in postpartum depression. In the case of postpartum psychosis, antipsychotic medications are used and are immediately needed. Many women are now given samples of SSRIs as they are leaving motherhood. Most medical sources believe that PPD is caused by an imbalance of brain chemistry and pharmaceutical intervention is the treatment of choice. Although a certain percentage of women suffering from PPD need care, these are much less than they are actually receiving them. Recent meta-studies show that this is true. While it is clear that some women with PPD need and benefit of pharmaceutical intervention, it is our experience that an integrative approach produces the best results.

Transtorno Anxiety

Postpartum is mainly treated

The most common symptoms postpartum depression include the following:

1. Persistent feelings of hopelessness and / or anxiety;

32. The energy loss and low levels of daily functioning;

33. Eat and sleep;

34. Inability to focus, concentrate or make decisions;

35. Feelings of shame and guilt, worthlessness;

36. Feelings of indifference and / or resentment towards the baby;

37. Intrusive negative thoughts and / or obsessive preoccupations in more severe cases, this includes thoughts of harming oneself or the baby;

38. Reduced sexual desire;

39. Loss of joy and appreciation for life;

310. Irritability or anger.

excessiva

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

1. Postpartum Anxiety Disorder (PPA). Here, the main symptoms are excessive nervousness, hyper-vigilance, quick thinking and in some cases, total panic. Panic attacks are especially threatening, sufferers often believe they are dying, like shortness of breath, dizziness and a chest.

batendo

2. Postpartum Obsessive-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 worrying obsessive thoughts are those in which the mother provides harm your baby, somehow. These thoughts are unwanted, intrusive and frightening for the mother. Importantly, except in extremely rare case of psychosis (see below), these thoughts are not accompanied by any actions. However, the mother may be so frightened by his own thoughts that she keeps the baby and, consequently, neglects it. It’s awfully difficult for new mothers to acknowledge having such thoughts, and as a result, many suffer in isolation.

3. Post-traumatic stress. PTSD can occur in response to a real or perceived traumatic childbirth or due to past unresolved traumas, sometimes of a sexual nature unleashed during childbirth. A woman experiencing PTSD may have recurrent memories, dreams or even flashbacks of traumatic labor / birth. She will be hyper-vigilant and startle easily, and is likely to suffer from insomnia, irritability, poor concentration and lethargy. Women who have experienced a particularly traumatic birth often show symptoms of both PTSD and PPD.

4. Postpartum psychosis. This is the most extreme and rarest of all postpartum disorders. When this occurs, the mother loses touch with reality and its symptoms may include extreme disorientation (eg, not knowing who she is), delusional thinking or paranoia and visual or auditory hallucinations. The few, tragic cases in which mothers have harmed their children, while in a psychotic state has received huge media attention. As a result, many people wrongly associate with PPD psychotic symptoms and dangerous behavior. This is another reason why women can not get help, they want to avoid being labeled as a disorder.

estigmatizados

Article Premise: Fully Replenishing a new mother postpartum nutritional reserves has been largely ignored and should be an integral part of post-treatment Depression.

Foundations delivery of a nutritional approach to PPD

3The human body is fully formed from nutrients. All muscles, organs, glands, bones, cells and fluid is composed entirely of nutrients (environmental toxins, however). All neurotransmitters, hormones, biochemical structures and pathways are formed from nutrients.

No normal physiological process and other uses is more vital nutrients and drains the body of a woman’s postnatal is that the process of pregnancy, childbirth, and caring for a newborn baby may include breastfeeding. The fact that the body of a mother donates all the nutrients needed to form the body of her baby is often overlooked when it comes to the medical treatment of PPD . Not only is the placenta literally rob the body of the mother of all essential nutrients needed for the body of a baby but the placenta is formed from nutrients taken from the mother’s body. This is the main reason many women after childbirth if this syndrome drained and nutritional depletion of nutrients can lead to postpartum depression and anxiety disorder.

fatores

Other that may contribute to the escape of the reserves of nutrients are a new mother’s blood loss during birth, sleep deprivation, breastfeeding, returning to work too early, and the enormous extra power needed to handle a new baby with severe needs. If a pregnant woman or new mother’s nutrient reserves are very low, it is much more vulnerable to experience PPD and PPA, because the whole body of normal metabolic processes are entirely dependent on nutrients. The preponderance of very poor quality pharmaceutical prenatal vitamins significantly contributes to the tendency of depletion.

nutrientes

Rarely is that there is no mention that the body’s production of neurotransmitters is completely dependent on its nutritional precursors. (4) Nor are the causes of these nutritional deficiencies precursor discussed. Moreover, the interdependent relationship between hormones and neurotransmitters is rarely taken into account by most physicians when considering treatment for PPD and PPA. The nutritional needs of mitochondrial function, the important function of the liver of Western and Eastern perspectives, and some individual nutrients such as Omega 3 fish oils, pharmaGABA, L-theanine, even, magnesium, inositol, and the herb St. John’s wort may also be helpful in the treatment of PPD and PPA. These will be briefly discussed.

An integrated approach to treat PPD may include nutritional therapy, bio-identical hormone replacement, moderate exercise, a diet rich in nutrients, adequate rest, psychological counseling / support, stress reduction techniques, the elimination caffeine, alcohol and other drugs, and if necessary, and intervention.

farmacêutica

Neurotransmitter Precursors

Nutricional

Serotonin Tryptophan

The amino acid L-Tryptophan is necessary for the body to produce serotonin. Ninety-five percent of serotonin in the human body is produced in the intestinal tract. About five percent is produced in the brain. The serotonin produced in the intestinal tract is not available to the brain of serotonin, because it can not pass through the blood-brain barrier. L-Tryptophan also not easily pass the blood-brain barrier and requires a protein carrier to ferry them to the brain. Consumption of simple sugars changes in the brain neuron selectivity of amino acids in the cell membrane, allowing entry of tryptophan into the brain more easily. Hence, the desire for sweets is often a sign of serotonin deficiency.

Serotonin has been referred to as the mood elevating brain chemicals and tranquilizing. inadequate levels of serotonin are associated 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:

-inhibition of glutamate excitability various regions of the CNS

3-stimulate their own receptors on neurons GABA GABA requesting compliance of its inhibitory function

3-inhibiting the release of catecholamines: dopamine, noradrenaline and Epinephrine.

A compare the effects of levels serotonin ideal for low levels of serotonin, which reveals the following contrasts:

1) Hopeful/optimistic——Depressed

32) Calm ——— Anxious

33) humorous ——- Irritable

34 ) Patient ——— Impatient

35) Reflective / thoughtful—–Impulsive/Reactive

36) Loving / Caring Capable ——- Abusive

37) to focus attention —— Short span

3Creative / focused——Blocked/scattered

39) — moderate carbohydrate intake too much carbohydrate intake

310) Good sleep and remembering dreams — insomnia and bad dreams recall

Tryptophan is converted to its metabolite, 5 – hydroxy-tryptophan (5-HTP), which is then converted into serotonin. Niacin, iron and folic acid are required for L-tryptophan to be converted into 5-HTP. The body also requires pyridoxal-5-phosphate, together with 5-HTP to produce serotonin. Magnesium and riboflavin (B2) are required for the conversion of pyridoxine (B6) in 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 medications with fewer side effects and more lighter and often better tolerated. (5-11)

From Martin Hintz, MD-Neuro Research

A number of factors contributed significantly to the low levels of L-Tryptophan in many people, especially women after childbirth, whose bodies are providing the necessary proteins to form another body human, these include excessive levels of cortisol, epinephrine, norepinephrine and dopamine. The proportion of L-tryptophan to other amino acids available in most foods is very low.

An excess cortisol, the hormone of the adrenal gland (a very common occurrence in the states of psychological and physiological stress) affects negatively the production of serotonin and sensitivity four different ways:

1. Excess cortisol levels significantly reduces the number of serotonin (5-HT1A) receptor sites. (12)

32. Excess cortisol suppresses serotonin receptors. (13, 14)

33. Excess cortisol increases serotonin reuptake. (15)

34. Excess cortisol causes tryptophan oxygenase (TO) to metabolize tryptophan to kynurenine, leaving less tryptophan to become serotonin. (15.16)

If cortisol levels are very low in the amygdala, serotonin has an inhibitory effect on glutamatergic activity, suggesting that cortisol plays a key role in maintaining the serotonin-mediated modulation. (16,17) This may be another factor involving insomnia PPD.

Added to why the deficiencies of serotonin are increasingly common and contributes to PPD is an overabundance of stress related catecholamines. Epinephrine, norepinephrine, serotonin and dopamine also deplete because serotonin, monoamine neurotransmitter is supposed to balance these three monoamine neurotransmitters excitatory. The more stress a person has, the more the body increases production of catecholamines in an attempt to respond to this stress. This requires a postpartum body to produce more serotonin – although the shortcomings of precursors of nutrients can interfere with your production.

The use of 5-HTP as a precursor of serotonin nutrition has significant advantages over tryptophan. 5-HTP easily passes directly through the blood-brain barrier without the need for a carrier protein, allowing an easy conversion into serotonin in the brain. Sublingual forms of 5-HTP faster. The dosage ranges from 25 mg daily to 300 mg per day or more.

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

Some controversy exists regarding the concurrent use of SSRIs and serotonin precursors nutrition. Pharmaceutical companies seem adamant about how to avoid this and often mention the possibility of serotonin syndrome, a dangerous condition, usually caused by a combination of drugs increasing serotonin, especially MAO inhibitors, with medicines, herbs, or nutritional precursors that also increase serotonin activity. Symptoms of serotonin syndrome may include nausea, headache, agitation, sweating, hypertension, tachycardia and hyperthermia, which can go over 104 F. This seems a remote possibility at best, while only using 5-HTP or 5-HTP use in combination with an SSRI medication. (20)

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

Dr. Dean Raffelock-catacholamine chart

catecolaminas

The are predominantly energizing and mood elevation, when produced at adequate levels. Synthesis of catecholamines occurs in the central nervous system, adrenal medulla and peripheral sympathetic neurons. Norepinephrine and dopamine act mainly as a neurotransmitter in the central nervous system. Epinephrine acts primarily as an adrenal hormone mobilize catecholamines energy.

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

Dopamine: Dopamine is the precursor of catecholamines norepinephrine and is found in both CNS and adrenal medulla. His duties include posture and motor function, cognitive function (attention, attention, working memory and problem solving), and feelings of pleasure. Dopamine can act as an excitatory or inhibitory neurotransmitter in response to input signals.

aferentes

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

3 (21.22)

Epinephrine (adrenaline): synthesis of epinephrine is dependent noradrenaline in adrenaline that is being converted by methylation.

3Hans Selye (1974) described the three stages of the “General Adaptation Syndrome” to stress (23): I

Phase : alarm reaction: Adrenaline high / high cortisol

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

Phase III: Exhaustion: depletion of cortisol, adrenaline and exhaustion DHEA

3Adrenal is an important factor in depression associated with chronic or stress.

grave

A woman suffering from PPD should be carefully questioned about their symptoms, SSRIs are routinely given to women who have hypoadrenia functional involving the adrenal cortex and / or bone marrow, or low thyroid function (discussed below). Low glucocorticoid and / or catecholamine levels may cause symptoms of fatigue, malaise and depression. (24.25)

Many women with PPD require pharmaceutical and / or nutritional supplements that address the deficiencies of both serotonin and catecholamines. therapies for the nutritional balance of catecholamines include: §

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

iron L-cysteine, sulfur and folic acid, needed for the conversion of L-tyrosine into L-dopa.

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

Gamma acid-aminobutyric acid (GABA)

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

-Insomnia

3-Restlessness

3-Irritability

3-Anxiety

3-Panic-Attacks

3 Seizures

Emprego

GABA is clinically is to induce relaxation, calm and sleep aid. Where there are glutamate receptors (powerful excitatory neurons), GABA will be nearby. GABA allows only the most important signals to pass and dampens excitatory or excitatory signals strangers extinguished when the levels of GABA are adequate.

Benzodiazapines (Valium, Klonopin, Zanax, Ativan, etc.) and pharmaceutical products such as Ambien to sleep and work Sonata in GABA as well as moderate consumption of alcohol. L-theanine, Lactium (peptides from milk), L-glutamine, taurine, and bio-identical progesterone can act as nutraceuticals / hormone agonist GABA. The drug is an inhibitor Gabatril GABA re-uptake as valerian extract. A new product called nutriceutical pharmaGABA seems to have more effective results than GABA.

sintético

From a perspective of Chinese medicine, serotonin and GABA would Yin (rest, harmonize, cooling, stimulating, hydrating, inhibitory) and catecholamines was Yang (energizing, mobilizing , heat, excitement, drying). In both Eastern and Western perspectives, it is important to balance these opposing groups of chemicals in the brain for balance. A woman with PPD, which now has more energy, but can not sleep is as unhappy as a woman who can sleep now, but what is even more apathetic than before treatment.

Balancing neurotransmitters is critical. Balancing neurotransmitters and hormones is clinically more effective.

Hormone neurotransmitter-Interactions

The relationship between neurotransmitters and hormones in the PPD is often overlooked. Neurotransmitters and neuropeptides are required to mediate the production of hypothalamic releasing hormones, allowing the pituitary gland to properly conduct the orchestra of hormones. The hypothalamus is considered a key part of the midbrain, the “emotional brain”, so it’s no wonder why the imbalances in the neurotransmitters and hormones may adversely affect states.

emocional

Thyroid hormones. Catecholamines and thyroid hormones are intimately related in many of its functions. L-tyrosine with iodine, is the precursor of thyroglobulin and thyroid hormone T-3 and T-4. A depression without anxiety, with predominant symptoms of fatigue and difficulty stringing together several thoughts positive, it is most often associated with low adrenal (29) function and / or thyroid (30-32) and typically do not respond well to SSRIs or precursor Nutritional therapy.

It serotonin is known that low thyroid function can cause depression and physiological fatigue. Giving T3 induces an increase in serotonin, and in animals with hypothyroidism, the synthesis of serotonin is reduced. (33) T3 seems autoreceptors desensitize presynaptic serotonin. (34) Moreover, the diurnal peak of TSH, observed during the physiological circadian rhythm, is serotonin dependent. (35) and serotonin function

Thyroid are interdependent, both clinical and bio-chemistry. Optimal thyroid function is dependent on optimal levels of serotonin. Great balance of serotonin is dependent on thyroid function ideal. increase of TSH is dependent on adequate stimulation of serotonin hypothalamic TRH, TSH letting up. (36) TSH may currently represent more adequately low serotonin states that any real evaluation of thyroid function truth. Thyroid hormones triiodothyronine (T3) increases and accelerates the effects of antidepressant drugs. Fluoxetine T3 + are better in desensitizing 5-HT autoreceptors hypothalamus alone. (37-39)

Estrogen: A growing body of evidence points to the importance of estrogen on serotonergic function. (40) Estrogen inhibits the reuptake of serotonin. (41.42) Estrogen treatment is shown to selectively increase serotonin (5-HT1A-mediated) responses in the hippocampus (43,44) with estrogen increased the firing activity of 5-HT (serotonin) neurons in male rats and females. (45,46) In conclusion, estrogen seems to be the nature SSRI.

Presently, there is great controversy about HRT estrogen. The WHI study and HERS studies have stirred controversy, without making the important distinction between bio-identical estrogens and pharmaceutically altered, nor any distinction between progesterone and progestins. The doctor is encouraged to become well versed in the story about the risks and benefits of HRT. Many women with PPD may benefit from low doses of estrogen bio-identical HRT if the potential benefits outweigh indicated and risks.

Progesterone: bio-identical progesterone has an effect anti-depressant/anti-anxiety known. During pregnancy, the placenta produces large amounts of progesterone, increased levels of blood to levels many times before becoming pregnant. Postpartum, this power is suddenly gone, along with its soothing effects on the nervous system.

3Allopregnanolone mother is synthesized by the reduction of progesterone by the enzymes 5-reductase and 3-hydroxysteroid dehydrogenase (3-HSD). Allopregnanolone is one of the most potent modulators of GABA receptors. (47.48) Allopregnanolone has similar biochemical and behavioral characteristics of alcohol, barbiturates and benzodiazepines. (49.50)

progesterona

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

DHEA: DHEA increases the activity of serotonin neurons firing. (51) DHEA also increases the synthesis of dopamine and norepinephrine, through mRNA for tyrosine hydroxylase. (52) Therefore, DHEA may be useful in some forms of PPD. DHEA also inhibits GABA and thus an antagonist of GABA. (53) Clinically, the use of DHEA causes insomnia and irritability, the more likely the patient has deficiency of GABA and that must be addressed before proceeding to complete DHEA.

Testosterone: increased firing of serotonergic neurons in the raphe area, increasing the state of mind. (54)

Mitochondrial Function

from Panel Lab-Ion Metametrix Booklet

Inefficient mitochondrial function may limit ATP production, energy and contribute or cause a physiological depression. Over 90% of total cellular oxygen consumption is used to fuel the mitochondrial metabolism. Mitochondria have a huge number of electron transfer to produce energy. Mitochondrial dysfunction can affect all organ systems, including neurons and glands.

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

Within cysteine and iron are needed to convert isocitrate to cis-aconitato. 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. Thiamine, riboflavin, niacin, pantothenic acid and alpha lipoic acid are required to convert alpha-ketoglutarate to succinyl-CoA. The amino acids isoleucine, valine and methionine are needed to form succinyl-CoA. Magnesium is needed to convert succinyl-CoA to succinate. Riboflavin is needed to convert succinate to fumarate. The amino acids tyrosine and phenylalanine are needed to form tenofovir. Niacin is needed to convert malate oxaloacetate.

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

Niacin and coenzyme Q10 are needed for oxidative phosphorylation (electron transport chain, or etc.). Normally, the ETC produces more than 3 units of ATP in mitochondria, and the Krebs cycle 36. A significant deficiency in any of these can also reduce the production of ATP and contribute to a physiological depression.

disfunção

Mitochondrial is often overlooked in the treatment of PPD.