Health And Dental Helper

Raffelock Dean, DC, L. Ac, NCC, DACBN, DIBAK

Hyla Cass, MD

Post-partum depression after the birth of fear

(PPD) (PPP) have become a national epidemic in the United States and affects 15% -20% of all new mothers, about 600000-800000 women per year. (1) It is now estimated that more than 30 million Americans take antidepressants or anxiolytics. (2) Most of these 30 million are women who have one or more children. The chance of suffering from PPD increases with each additional child. (3)

The most common medical treatment for postpartum depression are SSRIs (selective serotonin reuptake inhibitor) antidepressants. Anxiety disorder is frequently treated after birth with the benzodiazepine family of drugs such as Valium, Ativan, Xanax and Klonopin. Combination reuptake inhibitor of serotonin and norepinephrine (SNRIs) are also used frequently in postpartum depression. In the case of postpartum psychosis, antipsychotics are used and are needed immediately. Many women are now given samples of SSRIs, as they leave the maternity ward. Most medical sources estimate that the PPD is caused by an imbalance of brain chemistry and pharmaceutical intervention is the treatment of choice. Although a certain percentage of women with PPD need help pharmaceutical, it is to have a lot less than actually worked. Recent meta-studies show that this is true. While it is clear that some women with PPD do not need and benefit of a pharmaceutical intervention, it is our experience that an integrative approach that gives the best results.

anxiety disorder, post-partum is mostly treated

The most common symptoms of postpartum depression:

1. Persistent feelings of hopelessness and / or anxiety
2 Loss of energy and the low level of daily functioning;
3 Sleeping and eating disorders;
4 Inability to concentrate, 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 concern in severe cases, including thoughts about hurting yourself or the baby
8 Decreased sexual desire;
9th Loss of joy and gratitude for life
10 Irritability or excessive anger.

The literature generally describes its different types of postpartum disorders

, the special characteristics of the typical symptoms of depression. These include:

1. . Here are the main symptoms of excessive anxiety, hyper-vigilance, racing thoughts, and in some cases panic. Panic attacks are very frightening to think many times, she died when she shortness of breath, dizziness and chest beating experience.

2 Compulsive. They usually take the form of obsessive thoughts or worries about the baby and may be accompanied by compulsive behaviors such as constant supervision, if the baby is breathing, constantly washed to protect the baby from germs, etc. The way The most disturbing obsessive thoughts, in which the mother, given her baby is hurt in a way. These thoughts are unwanted, intrusive and frightening for the mother. It is important to note that, will not, except in rare cases of psychosis (see below), these thoughts are accompanied by actions. However, the mother so terrified of his own thought is that it avoids the baby and therefore it is not. It is terribly difficult for young mothers, those thoughts have to admit, and that is why many suffer from isolation. 3 . PTSD can occur in response to real or perceived traumatic birth or due to a past trauma, unresolved, sometimes sexually initiated during the birth. A woman who experiences PTSD, recurrent memories, dreams or memories of the traumatic labor / birth. It will be hyper-vigilant and fearless and will probably suffer from insomnia, irritability, poor concentration, and apathy. Women who have experienced a particularly traumatic birth, often show symptoms of PTSD and two PPD.4 . This is the most extreme and rarest of all postpartum disorders. If it happens, the mother loses touch with reality and its symptoms may include extreme disorientation (eg, not knowing who she is), delusions or paranoia and auditory and visual hallucinations. The few tragic cases in which mothers have harmed their children, have received while in a psychotic state of considerable media attention. As a result, many people mistakenly associate the PPD with psychotic symptoms, and risky behavior. This is another reason why women do not get to help, they want to prevent such a disease characterized by stigma.

The human body is composed entirely of nutrients. Every muscle, organ, gland, bone, cells, and the liquid completely (different environmental toxins) of nutrients together. All neurotransmitters, hormones, biochemical and metabolic structures are formed from nutrients.

No other normal physiological process and sewers is more vital nutrients the body of a woman after the birth of the process of pregnancy, childbirth and care for a new baby can breastfeed. The fact that the body is a gift from the mother all the nutrients to the body of her baby form is required too often overlooked when it comes to medical treatment for PPD. Not only is the placenta literally steal the body of the mother of all essential nutrients needed by the body of a baby but the placenta is formed by making the nutrients from the mother’s body. This is the main reason that many women after childbirth are dehydrated food and nutrient depletion lead-syndrome, postpartum depression and anxiety disorders.Other factors that may contribute

, a drain reserves of nutrients are a new mother needed blood loss during delivery, lack of sleep, breastfeeding, back to work too early, and immense energy to care for a new baby needs intensive. If a pregnant woman or new mother’s reserves of nutrients is too low, it is much more prone to PPD and PPA experience, as the whole body’s normal metabolic processes depend entirely on nutrients. The preponderance of extremely poor quality pharmaceutical prenatal vitamins in addition to the known trend nutrient depletion.

There is rarely any evidence that the body’s production of neurotransmitters totally dependent on their dietary precursors. (4) the causes of these shortfalls in the nutritional precursors are discussed. Moreover, the reciprocal relationship between hormones and neurotransmitters rarely by most doctors for the treatment of PPD and PPA considered. The nutritional needs of mitochondrial function, the importance of liver function from Western and Eastern perspectives, and some nutrients such as omega-3 fish oils, pharmaGABA, L-theanine, SAMe, inositol, magnesium, and word of St. John the grass can also be a great help in the treatment of PPD and PPE. These will be discussed briefly.an integrative approach to treating PPD can nutritional therapy, hormone replacement bio-identical, moderate exercise, a diet rich in nutrients, adequate rest, counseling / support, technology include reduced stress, reduce caffeine, alcohol and other drugs and, if necessary, pharmaceutical intervention.

serotonin and tryptophan

The amino acid L-tryptophan is necessary for the body to produce serotonin. Ninety percent of serotonin in the human body is produced in the intestinal tract. About five percent is produced in the brain. Produces serotonin in the gut is not available for the brain, because serotonin can not cross the blood-brain barrier. L-tryptophan is not easily pass through the blood-brain barrier and requires a carrier protein for the ferry in the brain. The consumption of sugar changes in the brain neuron cell membrane selectivity simple amino acids, tryptophan can enter more easily into the brain. Thus the desire for sweets often a sign of lack of serotonin.

serotonin in the brain was the mood lifting chemicals called tranquilizers. Inadequate levels of serotonin to depression, anxiety, insomnia, irritability and weight gain associated. Serotonin mediates depression usually includes an element of fear. Serotonin is an inhibitory neurotransmitter in question. Features include:

- inhibiting glutamate excitability of different regions of the CNS stimulants
own GABA receptors on GABA neurons incentive to carry out its inhibitory function
- inhibiting the release of catecholamines: dopamine, norepinephrine and adrenaline.

A comparison of the effect of serotonin levels found in optimal concentration of serotonin in the following contrasts:

1) Hopeful / optimistic ——
Depressed 2) Calm Anxious — ——
3) Good-natured irritable ——-
4) patient ———
5) Reflective / thoughtful- —-Impulsive/Reactive /> 6) Love / maintenance ——- abusive
7) the ability to concentrate —— short duration of respect
Creative / released concentrate —— / Supply distributes
9) — excessive carbohydrate intake moderate carbohydrate
10) A good sleep and dream recall memories — insomnia and bad dreams

tryptophan its metabolite is converted 5 – hydroxy-tryptophan (5-HTP), which is then converted into serotonin. Niacin, iron and folic acid for the L-tryptophan needed to be converted into 5-HTP. The body also requires pyridoxal-5-phosphate with 5-HTP to produce serotonin. Magnesium and riboflavin (B2) for the conversion of pyridoxine (vitamin B6) is required in pyridoxal-5-phosphate. Defects in these nutrients limit the production of serotonin. Many double blind studies have shown 5-HTP to be as effective as antidepressants with fewer side effects and mild, and generally better tolerated. (5-11)

A number of important factors that are too low L-tryptophan in many people, especially women with postpartum body to the necessary proteins, to another human body form is available, these excessive levels of cortisol, adrenaline, noradrenaline and dopamine. The ratio of L-tryptophan to other amino acids in most foods is very low.

An excess of cortisol, the hormone of the adrenal gland (very common in the psychological and physiological stress) has a negative effect on the production of serotonin and sensitivity in four different ways:

2 Excess cortisol suppresses serotonin receptor. (13, 14)
3 Excess cortisol increases serotonin. (15)
4 Excess cortisol causes of kynurenine to tryptophan oxygenase (TO) in the metabolism of tryptophan, so that less tryptophan into serotonin. (15.16)

When cortisol levels are too low in the amygdala, serotonin no longer has an inhibitory effect on glutamatergic activity, suggesting that cortisol plays an important role in maintaining the serotonin-mediated modulation. (16,17) This may be another factor in insomnia with PPD.

to the reasons that serotonin deficiency is becoming more common and contribute to the PPD is an excess of catecholamines added stress. The adrenaline, noradrenaline and dopamine and serotonin lead, because serotonin, a neurotransmitter monoamine to these three excitatory neurotransmitter monoamines balance. Experience more stress a person, the more the body increases production of catecholamines in an attempt to respond to this stress. This requires a post-partum body to produce more serotonin -. If nutrient deficiency may interfere with his predecessors in the production

Using 5-HTP as a precursor of serotonin, has significant advantages over dietary tryptophan. 5-HTP easily crosses directly through the blood-brain barrier without a carrier protein, allowing for easier conversion to serotonin in the brain. Sublingual forms of 5-HTP to work faster. The dose is 25 mg to 300 mg per day or more.

A deficiency of vitamin B6 (pyridoxine), which is responsible for the synthesis of serotonin, is frequently found in premenopausal patients with depression. (18) replacement for B6 deficiency is an important aspect of the treatment of PPD, which can improve the production of serotonin in the brain. (19) The use of vitamin B6 metabolite, pyridoxal-5-phosphate instead of B6 is recommended, especially if deficiencies in magnesium and / or riboflavin are suspected or confirmed. There is some controversy as to whether it is better to take 5-HTP and pyridoxal-5-phosphate together or completely separate, they shall by joining a waiting time of 2 hours. Our clinical experience shows that, in order, the complete set. Many products are available including a combination of 5-HTP-5-P and P.Some controversy about the concomitant use of SSRIs and serotonin precursors of nutrition. Pharmaceutical companies seem adamant about avoiding this and often talk about the possibility of serotonin syndrome, a condition usually improve by the dangerous combination of medications serotonin, especially MAO inhibitors with drugs, herbs, nutritional or precursors also enhance serotonergic activity. Symptoms of serotonin syndrome may include nausea, headache, restlessness, sweating, high blood pressure, tachycardia and hyperthermia, which can go over 104 F. This seems a remote possibility at best, if only with the 5-HTP or the 5-HTP in combination with an SSRI drug. (20)

SSRIs seem not only to keep serotonin in the synapses of nerve cells by inhibiting the reuptake more, but under nutritional precursors of serotonin by the vesicle storage and recovery ports. In fact, in our clinical experience many women with PPD do better when taking 5-HTP-5-P and P with SSRIs that SSRIs alone. Precursor of serotonin deficiencies of the reason that SSRIs do not work for some work and then stop working for others, and why it was not unusual for a woman with PPD two or more different prescribed SSRIs in the course of time. SSRIs do not give a net increase of serotonin, they need enough serotonin available to be enough to re-absorption.

catecholamines are usually stimulating and mood lift, if produced at the appropriate levels. Synthesis of catecholamines occurs in the CNS, adrenal medulla and peripheral sympathetic neurons. Norepinephrine and dopamine act primarily as a neurotransmitter in the CNS. Adrenaline acts mainly as adrenal hormones to mobilize energy.

catecholamines affect most organ systems. If levels are too high are catabolic and can lead to metabolize the body’s own nerves, muscles and bones. Low levels can lead to depression, fatigue and weight gain. Dopamine: Dopamine is the precursor of the catecholamines norepinephrine and is both the CNS and adrenal medulla found. His responsibilities include motor skills and posture, cognitive functions (attention, concentration, working memory and problem solving), and the feeling of joy. Dopamine can act either excitatory or an inhibitory neurotransmitter in response to incoming afferent signals. noradrenaline (norepinephrine) noradrenaline mediated CNS mood control, drive, ambition, learning and memory, attention, concentration and voltage. Clinically there is often an inverse relationship between norepinephrine (excitatory) and serotonin (inhibitory). When serotonin is low, up-regulated over-norephinephrine, resulting in “fight or flight” reaction that leads to anxiety and / or panic. Overexpression of norepinephrine is clinically with CNS disorders anxiety, aggression, irritability, mania or bipolar disorder, hypertension and immunosuppression with lower norepinephrine atypical depression with symptoms of fatigue, hypersomnia, hyperphagia, lethargy and apathy,(21.22)

epinephrine (adrenaline) epinephrine-norepinephrine synthesis is dependent on methylation are converted by adrenaline in
Hans Selye (1974) describes the three phases of the s “general adaptation syndrome” to stress (23 )

Phase I:. Alarm reaction of the adrenaline high / high cortisol

Phase II: Resistance: High cortisol / DHEA down, adrenaline variable

Phase III: Fatigue: exhaustion of cortisol, adrenaline and exhaustion
adrenal DHEA is a important factor in depression-related chronic or severe stress

.

A woman with PPD should be placed precisely on the symptoms in question, SSRIs are often women who have hypoadrenia functional involvement of the adrenal cortex and / or bone marrow, or low thyroid function is given (see below). Low glucocorticoids, and / or catecholamines cause symptoms of fatigue, malaise and depression. (24.25)

Many women with PPD

require pharmaceutical and / or nutraceuticals that gaps in serotonin and catecholamines nutrition therapy for the rest of catecholamines include:. § DL-phenylalanine and L-tyrosine, precursor amino acids adrenaline , noradrenaline and dopamine. DL-phenylalanine also increases endorphins, which are euphoric. PP Many women are diagnosed with bipolar disorder respond well to high dose therapy of DL-phenylalanine (26), with precursors of serotonin and high dose (6 grams per day) omega-3 fatty acids than fish oil. (27)

§ L-cysteine, sulfur, iron and folic acid for the conversion of L-tyrosine to L-dopa. required

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

Gamma-aminobutyric acid (GABA)

neurotransmitter GABA is the most important and widespread inhibitory brain. Low levels of GABA are particularly important because if anxiety and insomnia are included in the display style symptoms of PPD / APP. GABA is essential for the balance of excitatory neurotransmitters and hormones such as cortisol, adrenaline, noradrenaline and glutamate. Too much excitement, without enough GABA inhibition may cause: (28)

-
Insomnia – Agitation
-
irritability – anxiety
- panic attacks
- induce seizures

jobs

GABA clinically to relax, rest and sleep aid. Where there are glutamate receptors (potent excitatory neurons), it is in the vicinity of GABA receptors. GABA passes only signals of the primary excitatory and absorbed or extinguished, when foreign excitatory GABA is appropriate.

Benzodiazepines (Valium, Klonopin, Zanax, Ativan, etc) and sleep, like Ambien and Sonata pharmaceutical products work on GABA receptors, as moderate alcohol consumption. L-theanine, Lactium (milk peptides), L-glutamine, taurine and bio-identical progesterone can be used as nutraceutical / hormone agonist GABA. Drug Law Gabatril GABA is a serotonin-reuptake inhibitors such as valerian extract. A new nutraceutical called pharmaGABA seems to work more effectively than synthetic GABA.

From the perspective of Chinese medicine, serotonin and GABA yin (relaxing, harmonizing, cooling, feeding, hydrate inhibitor) and catecholamines is yang (stimulating, mobilizing global, excitatory and drying). In Eastern and Western perspectives, it is important to balance these opposing groups of chemicals in the brain to achieve balance. A woman with PPD, the now more energy, can not sleep but is also unfortunate that the woman is sleeping now, but even more lethargic than prior to treatment.

Balancing

neurotransmitters is the key. Balance of neurotransmitters and hormones is clinically effective.

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, so ask the pituitary gland, the endocrine orchestra. The hypothalamus viewed as a key center of the brain, the “emotional brain”, so it is little wonder why the imbalances in the neurotransmitters and hormones can influence the emotional states.

. Catecholamines and thyroid hormones are closely related to the number of their functions. L-tyrosine with iodine, is the precursor of thyroid hormones and thyroglobulin and T-3 T-4. Together without fear of depression, drawing out the dominant symptoms of fatigue and difficulties several positive thoughts, is usually associated with low adrenal (29) and / or thyroid function (30-32) and usually not good nutritional therapy to SSRIs or precursor of serotonin.It is known that low thyroid function can cause depression and physiological fatigue. Give T3 to an increase in serotonin, and animals with hypothyroidism, which is reduced synthesis of serotonin. (33) T3 seems to desensitize presynaptic serotonin autoreceptors. (34) In contrast, the TSH peak days is observed in circadian physiology, serotonin-dependent. (35)

thyroid function and the function of serotonin are dependent on each other, both clinically and biochemically. Thyroid function depends on the optimal concentration of serotonin optimally. Serotonin optimal balance depends on the optimal function of the thyroid. Elevated TSH is dependent on the stimulation of the hypothalamic TRH enough serotonin, so that increase in TSH (36). Deleted TSH can now be more adequately represented low serotonin states as a true assessment of the true function of the thyroid. The thyroid hormones triiodothyronine (T3) and accelerates the effect of antidepressants. Fluoxetine + T3 is the best in the desensitization of hypothalamic 5-HT autoreceptors than either alone. (37-39)

A growing body of evidence points to the importance of estrogens in serotonergic function (40). Estrogen inhibits the reuptake of serotonin. Treatment with estrogen (41,42) is given, the more selective serotonin (5-HT 1A-mediated) reaction of the hippocampus (43.44) estrogen increases to improve the activity of shooting 5-HT (serotonin) neurons in the male and female rats. (45.46) In short, estrogen appears to be natural SSRI.

Currently there is much controversy about estrogen HRT. HERS and WHI trials, studies of the controversy, without the distinction between bio-identical estrogen and pharmaceutically altered, nor a distinction between progesterone and progestins are prompted. The doctor is encouraged to be well versed in this area about the risks and benefits of HRT. Many women with PPD may benefit from low doses of estrogen bio-identical HRT, if specified, and the potential benefits outweigh the risks. : .. Bio-identical progesterone has a known asthma during pregnancy produces the placenta large amounts of progesterone, which increase the blood level of several levels of pre-pregnancy post partum, the power is suddenly gone, with its calming effect on the nervous system of the mother.
allopregnanolone is synthesized by the reduction of progesterone by the enzymes 5-reductase and 3-hydroxysteroid dehydrogenase (HSD-3). The allopregnanolone One of the strongest modulators of GABA receptors is known. (47.48), allopregnanolone has similar biochemical and behavioral characteristics of ethanol, barbiturates and benzodiazepines. (49.50)

bio-identical progesterone is very useful for women with PPD to anxiety and insomnia. Use of bio-identical progesterone and PharmaGABA is often both very helpful in relieving anxiety and sleep problems.

: .. DHEA increases the activity of serotonergic neurons (51) DHEA also increases the synthesis of dopamine and norepinephrine on tyrosine hydroxylase mRNA by (52) Thus, DHEA may be useful in some forms of PPD. DHEA also inhibits GABA is a GABA antagonist (53). Clinically, if the use of DHEA causes insomnia and irritability, the more likely the patient is deficient GABA .. Increases serotonin neurons firing in the raphe region, rising mood (54)

to be addressed / p>

Metametrix of lab- Ion Control Booklet

inefficient mitochondrial function, the ATP production to limit less energy and contribute to depression or physiological cause. About 90% of cellular oxygen consumption is used to power the mitochondrial metabolism. The mitochondria are required to transfer to a large number of electrons to produce energy. Mitochondrial dysfunction can affect all organ systems, including neurons and glands.

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