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Depression | An Integrative Appro ...An Integrative Approach to the Prevention and Treatment of Postpartum Depression (PPD) and Postpartum Anxiety Disorder (PPA)Total Word Count: 7196 Author Rating: NA  Rate this article
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Prevention and Treatment of Postpartum Depression (PPD) and Postpartum Anxiety Disorder (PPA).
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; The literature generally outlines several types of postpartum disorders that have special features beyond the typical symptoms of depression. These include: 1. Postpartum Anxiety Disorder (PPA). 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. 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 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. Post-traumatic Stress Disorder. 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. Postpartum Psychosis. 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. Article Premise: Fully Replenishing a New Mother’s Postpartum Nutritional Reserves Has Been Largely Ignored and Should be An Integral Part of Treating Postpartum Depression. Foundations of A Nutritional Approach to PPD 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.
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. Neurotransmitter Nutritional Precursors 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
1) Hopeful/optimistic—————-Depressed 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) From Martin Hintz, M.D. –Neuro Research 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) 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.
Dr. Dean Raffelock- catacholamine chart 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. Epinephrine (adrenaline): Epinephrine synthesis is dependent upon norepinephrine being converted into epinephrine by methylation. 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 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 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. Hormone-Neurotransmitter Interactions 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. Thyroid hormones. 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) Estrogen: 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. Progesterone: 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. 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: 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. Testosterone: increases serotonergic neuron firing in the raphe area, increasing mood. (54) Mitochondrial Function
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. Liver Detoxification
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):
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. Inositol 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). L-Theanine 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)
Integrating High Quality, High Potency Prenatal and Postnatal Nutrient Systems into Preventing and Treating Postpartum Depression and Anxiety
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. |
