In the last fifteen years in the field of endocrinology great deal of evidence that the loss of estrogen is generally occurring during the menstrual cycle is bringing about changes for women at increased risk for mood, anxiety and greed that has produced disease. Given the prevalence of these diseases in women, we are fortunate to have a better understanding of them.

Women are more than twice as oftenbecome depressed. Research shows that they also suffer more from fear. To develop more phobias. It ‘the same relationship of agoraphobia: almost 8% of women are agoraphobic, compared to only 3% of men. Most succumb to traumatic stress syndrome. Seventy percent of people with social phobia are women. What could be happening here?

The cyclical nature of the secretion of estrogen may represent for the women of “particular vulnerability to mood disorders and anxiety, Dr.Mary Seeman reported in the Journal of the American Psychiatric Association’s influence in an analysis of dozens of studies on female hormones psychopathology in men and women.

The theory of “deprivation of estrogen applicants” suggests that a low estrogen state is the beginning or the worsening of mood symptoms in women who are predisposed to drive – because of the already low levels of serotonin – the mood disorders and d ‘ anxiety. In 1996, researchers at the University of Edinburghpublished a report, the discussion of the molecular level that are experiencing these changes. Affected by estrogen is “a profound impact on mood, mental state and memory” in the hormone psychoprotectant as “natural.” There must be sufficient estrogen in the brain, that is, when receiving the mental stability. Estrogen, the importance of cognitive processes and memory is not an easy thing. It ‘was in fact discovered that neurons in the brain buffer againstDegeneration.

Until the late nineties, the test assembly had begun to show a unique and persistent hormone after almost all mental disorders in women. For example, the binging behavior in bulimics and diarrhea during premenstruum, when estrogen levels get worse . Sun has panic attacks in women with panic disorder. Impulse interference seemed even worse this week or ten days before the deadline – kleptomaniacs escapades continued to steal moretrichotillomaniacs more hair, leather cutters to cut the skin stretched .. All these diseases are linked to serotonin dysfunction, and, as we have seen, serotonin and estrogen are inextricably linked.

In the nineties, a Canadian psychologist, Barbara Sherwin, it was very interesting to carry out studies on the loss of estrogen affects the knowledge and memory. I went to Toronto to spend a day with Dr. Sherwin in his office at McGill University. I needed a mini-course of estrogen and she was willing toGive it to me.

Since the beginning of fetal life hormone receptors in the hypothalamus of the brain first. It is here that the organization of brain circuits, the requirements for puberty, regulating subsequent adult sexual behavior and control the frequency and intensity of emotional disturbances. Research in neuroendocrinology has to tell us a lot about the hardship of pre-menopausal women, who used to think that the result of women’s pain over the loss of fertility. NowE ‘known that the mood and cognitive changes are experts in physical origin.

Estrogen affects mood. What I had not known until the conversation with Dr. Sherwin is that to produce serotonin in the brain needs estrogen. I have not even announced that the estrogen in the brain. “There are estrogen receptors in various organs throughout the body, including the brain,” he said. “Consequently, the loss of estrogen makes many different physical symptoms – loss of elasticity of the skin, bonesConstriction, mood and cognitive decline. “

When estrogen levels increase, on the other hand, as in the first week after menstruation, increasing their overall impact on the amount of serotonin in the spaces between nerve cells in the brain cells. The mood improved. Within the brain, estrogen may act in fact as a natural antidepressant and mood stabilizer.

Dr. Sherwin has led me to the work of researchers, the important research base, including Bruce McEwen of RockefellerInstitute in New York, and Joseph LeDoux at New York University, the discovery of the molecular changes that support the view that estrogen had a profound impact on the mind and its capabilities.

It was not long after my visit to Dr. Sherwin, I learned an important contribution to the value of ten years from studies book, estrogens, serotonin and affective disorders: Where is the therapeutic bridge? Two researchers from the Perinatal and Reproductive Psychiatry Program at the Harvard Medical Schoolwas essentially the same question I had: What is the link hormone to the mental health of women? was motivated Joffe and Cohen one hundred twenty five studies examined the relationship between women’s reproductive hormonal changes, and their mental state. in study after study, they found that women with histories of depression seem more prone to recurrent episodes during periods of “significant reproductive endocrinologyChange.

Correlation does not prove causality. The fact that someone is morbidly depressed for the day of ovulation begins and remains so until the day that does not begin to try the bleeding drops of estrogen that premenstrual mood swings, but damn well raise suspicions. According to information provided by new imaging methods has been added to the mix was the case for a spiritual connection to the hormone’s weakness for women ‘as close as possible to an open and shut caseIt is likely that you get. Neuro-imaging has greatly improved our understanding shows the flashing light, when the activity in different parts of the brain, what was called the dark “that time of the month.”

And ‘the dance between the two types of hormones, ovarian hormones and hormones of the brain that ultimately determined, as is symptomatic of a particular woman has during her menstrual cycle, and in other parts of the reproductive risk. For example, if a woman is geneticallyencoded at a low or borderline levels of serotonin in the brain of estrogen drops occurs menstruation everything you need to send a spiral of serotonin below the optimal level of functioning, from a mental condition disturbing that for all their symptoms disappear mysteriously as soon as he began his estrogen levels and to trace

Why is it so? Since the serotonin it needs for its metabolism of estrogen in the brain. The two hormones are a dynamic duo, the operationArm. Falls, as the levels of estrogen, this serotonin. When estrogen increases (as, for example, begins as soon as menstruation), the levels of serotonin immediately return with him, and calm was restored. The ebb and flow of menstruation is orchestrated moods of woman ‘, not by the moon, but by secretions in his brain and ovaries. What we know is that sometimes the negative results of these changes in the secretion is not inevitable. Just as science has learned to changes in insulin and changes in the thyroid, the changemay change now, changes in the ovaries. If you do not want your mood on your ovaries blame the blame on the brain. Blame it on what you like, do not resign themselves to suffer the view that women are born.

For me it is fascinating that the pieces of this puzzle were not important to us twenty years ago. And the effect of dynamite that has the pieces together, occurred only in the last ten years. Based on previous knowledge and assemblyImage step by step, an endocrinologist at places such as the Neuropsychiatric Institute in California, and sexual organs Mood Disorder Program at the University of Texas Medical Center have understood that women not only at risk during premenstruum are vulnerable to all reproductive risk points. Furthermore, a woman who suffers from one of these points is subject to danger is always a symptom of another. If it is a genetic low serotonin in the brain,Estrogen drops going to affect them, simple.

Things have taken place since then in turn, enlightened, thank God, but we are only now beginning to understand what is really happening, women, mental well-being during times of stress hormones. Especially the scientists, including psychiatrists and reproductive endocrinologists like Barbara Sherwin, a unique and important contribution to the wave of research, which currently designing a whole newParadigm for understanding the role of hormonal changes in the female creates well-being and mental state.

http://www.womenhealth.pannipa.com/2010/03/hormones-after-the-womens-mental-health/

It is a very vital timing for women when she appears at the age of 40. Various health problems switch on at this age. Heart diseases, breast cancer, osteoporosis, osteoarthritis, depression, insomnia, fatigue, obesity, diabetes, various types of mental and physical diseases are very common at this age. The main cause of these diseases is decline ofestrogen hormone in body. This female hormone regulates almost all part and organs of a woman’s body.Various health problems switch on at this age. Heart diseases, breast cancer, osteoporosis, osteoarthritis, depression, insomnia, fatigue, obesity, diabetes, various types of mental and physical diseases are very common at this age. The main cause of these diseases is decline of estrogen hormone in body. This female hormone regulates almost all part and organs of a woman’s body.

The greatest risk of a woman who has approached 40 is heart related ailments. The hormoneestrogen protects from risks related to heart disease. From the 40′s the secretion of estrogendecreases and women comes under great risk. The risk declines by the age of 60. Chest pain, nausea, vomiting, shoulder ache, shortness of breath are few symptoms of heart disease. Excessive smoking and addiction to alcohol, heredity, diabetes, obesity, blood pressure, high cholesterol, and physical inactiveness are reasons behind the illness. A well balanced low fat diet and regular exercise is essential to remain fit.

OSTEOPOROSIS:Osteoporosis is one of the vital problems that come with age as Calcium level and the calcium absorption power of body go down. As a result the bone density decreases making bone structure brittle. This results in back pain, rheumatism, joint pain etc. Calcium rich food like leafy vegetables, milk, and curd, etc. together with regular intake of calcium and vitamin D may prevent the disease. Another way to fight such ailments is through regular exercise.

BREAST CANCER IN WOMAN:Breast cancer is another health risk that lurks around this age. It is the commonest type of cancer among women. Increasing age, gene, personal history , heredity, early onset of menstruation (before 12) and late menopause (after 55), not having children and not breast feeding, addiction to alcohol , continuous use of oral pills , wrong medication etc. are the main causes of breast cancer. Conduct regular medical check up for the early detection of the disease.

Hormonal changes trigger problems like mood swing, excessive sweat, insomnia, depression are other problems related to the age. Causes range from family history, stressful life as well as idle life, different types of chronic diseases etc. a disciplined life with regular exercise, yoga and meditation and a balanced diet helps a lot to stay healthy.

Women’s Health Problems Diet Treatment Foods to Avoid Disorders in Women: Diet for Women’s Health Care:

They say your health is determined by what you eat. When it comes to one’s health, your diet tells it all. The food that we eat regularly is important. What it seems is that the food that we take in every day is always short of what is required by our body. A healthy diet is always in demand to maintain and address all health issues.

Healthy food in the right amount should be considered. Drinking plenty of water, more than what is required, is always good. Lots of fruits and vegetables with the right amount of protein are required for a balanced diet.
Whole-grain foods and high-fiber foods are also required. Choose bread made from whole grains. Try to have fat-free food and low-dairy products. Choose low fat milk, fish, poultry, legumes, and lean meat. Avoid food that has saturated fat, high in cholesterol and trans fat.

When preparing food, try to avoid putting in so much salt. Too much sugar should likewise be prevented. Food and beverages that have added sugars should likewise be minimized. Alcohol should be prevented. If it cannot be helped, one drink per day will do.

Women’s health care costs keep soaring:Females experiencing physical abuse from intimate partners spend 42% more on health care per year than nonabused women, according to a study at Ohio State University, Columbus, and the costs do not end when the abuse does.

“Along with all the physical and emotional pain it causes, domestic violence also comes with a substantial financial price,” underscores Amy Bonomi, associate professor of human development and family science.Women were surveyed about whether they have experienced any physical or emotional abuse from intimate partners and, if so, when it occurred. Researchers then studied patterns of health care use and costs by the women over an 11-year period.

Those experiencing ongoing physical abuse had the highest health care costs. “It’s likely that these women need more health care because they are seeking care for immediate injuries and associated health problems,” Bonomi surmises. Those who had been physically abused within the last live years, but not currently, have 24% higher yearly health costs. Abuse that occurred more than five years ago results in 19% higher costs.Another striking finding was that all abused women, whether they experienced physical or psychological abuse, used significantly more mental health services than nonabused individuals. Those suffering ongoing physical abuse were about 2.5 times more likely to have visited a mental health provider in the past year than were nonabused females, The rate for psychologically abused women was two times higher.

Women’s Health & Neonatal Medicine: Our expertise spans the whole spectrum of women’s health & neonatal medicine – from laboratory science to clinical skills to social and behavioural sciences – with the objective of making a major contribution to the health of women, both in the UK and internationally, by pioneering research, education programmes and clinical initiatives. The UCL Elizabeth Garrett Anderson Institute for Women’s Health was established in 2004 to lead and coordinate these developments and is established as one of the leading european centres in clinical care, research and education in women’s health. We aim, for the first time, to address women’s health & neonatal medicine in its broadest sense, taking into account the social, psychological, economic, ethical and legal dimensions of health care, and working with models of health, illness and health care that move beyond the traditional.Amongst the areas of research strength are: Screening and diagnosis of cancer of the ovary; Genetic and epigenetic basis of gynaecological cancer; Preimplantation genetic diagnosis; Aetiology, prevention, management and outcomes of perinatal brain injury; Fetal and maternal medicine; and prevention and screening for sexually transmitted disease.

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 [Continued from John Langdon Down's Autism: A Stealth Disease - Part 1 at: articlesbase.com ]]> http://www.pregnancydepression.org/john-langdon-downs-autism-a-stealth-disease-part-2.html/feed 0 http://www.pregnancydepression.org/the-health-benefits-of-vitamin-d.html http://www.pregnancydepression.org/the-health-benefits-of-vitamin-d.html#comments Sat, 02 Apr 2011 14:34:20 +0000 admin http://www.pregnancydepression.org/the-health-benefits-of-vitamin-d.html  

The Vitamin D Conference just finished in Victoria was nothing short of spectacular. On the bus into Victoria, I met a representative from the National Cancer Institute whose job was simple: her bosses at the NIH wanted to know if they should fund the flood of grant requests about vitamin D. Given the quality of the papers presented, I can’t imagine her answer was anything but yes.

Dr. Tony Norman and Dr. Roger Bouillon, the conference organizers, had to choose from over 300 submissions from scientists around the world. The venerable Dr. Bouillon did not try to back off his recent widely quoted warning that more than a billion people in the world are vitamin D deficient. Both men did a great job balancing presentations on vitamin D nutrition, vitamin D basic science, and the patentable vitamin D analogs sought by drug companies. Of course, I thought more time should have been devoted to vitamin D nutrition but Dr. Norman pointed out that more time was devoted to vitamin D nutrition than ever before. Like Dr. Norman, I am unable to comment on all the presentations that merited it, or this newsletter would be 50 pages long.

Dr. Barbara Gilchrest, who fired Dr. Michael Holick from one of his professorships several years ago after Holick wrote a book saying God knew what she was doing when she created sunlight, gave the Plenary Lecture. Wisely, Dr. Gilchrest overwhelmed the audience with graphic pictures of invasive skin cancer to support her argument that sunlight is evil. Of course, it’s harder to show pictures of invasive colon cancer, breast cancer, prostate cancer, and the 15 other internal cancers caused by sunlight deprivation.

However, Dr. Gilchrest is changing her mind. George Bernard Shaw once said, “Progress is impossible without change; and those who cannot change their minds, cannot change anything.” Dr. Gilchrest is changing her mind – not about the evils of sunlight – about vitamin D. She is in the process of admitting that this miraculous substance has benefits beyond bone.

Two years ago, she dismissed any concerns about vitamin D with a “take a multivitamin if you are concerned.” Now she believes the Food and Nutrition Board needs to consider raising both the Adequate Intake recommendations (how much one should take every day) as well as the Upper Level (the amount one can take on your own, without being under a doctor’s care, and without fear of toxicity). My compliments to Dr. Gilchrest.

Dr. Heike Bischoff-Ferrari did a wonderful job, not just presenting her data that optimal vitamin D blood levels need to be at least 40 ng/ml, but for presenting Dr. Ed Giovannucci’s data (who had to cancel for personal reasons). Dr. Bischoff-Ferrari reminded us that periodontal disease in inversely related to vitamin D blood levels. She also reminded us that there is strong scientific evidence that vitamin D improves neuromuscular performance in older people.

Dr. Bischoff-Ferrari then presented Dr. Giovannucci’s data that one reduces your risk of all cancers about 17% for every 10 ng/ml of vitamin D in your blood. For cancer of the digestive system, the risk reduction is 43%. His data indicates all Americans should be taking about 2,000 IU per day and some Americans need even more to minimize cancer risk. No one know where the curve flattens out; that is, no one knows how much further cancer reduction one gets from 20, 30, or 40 ng/ml incremental increases in blood levels.

Dr. Robert Heaney presented by video hookup and made his quiet but powerful case that about 75% of American women are vitamin D deficient (levels less than 35 ng/ml), that about 3,000 units a day are needed to bring 95 % of the population out of the deficient range, and that 10,000 units a day is the safe upper limit. (This does not mean you should take 10,000 units per day, it means scientists should be able to study 10,000 unit daily doses without the bureaucratic difficulty they now encounter).

Dr. Kimball, working with Dr. Reinhold Vieth, presented data that children (age 10 -17) only increased their average blood level by 11 ng/ml when given 14,000 units per week for eight weeks and that such dosing was safe.

Dr. Hollis presented evidence in Victoria that levels of at least 40 ng/ml are required to normalize the enzyme kinetics of vitamin D. [When I say vitamin D blood levels, I'm referring to 25(OH)D levels; Bruce is studying actual vitamin D levels (cholecalciferol) as well as 25(OH)D levels]. Dr. Hollis continues giving pregnant and lactating South Carolina women about 4,000 to 6,000 units a day in an ongoing study. We predict easier pregnancies and less depression in the moms – lower prenatal and perinatal mortality, fewer birth defects, fewer infections, less diabetes, less psychiatric illness, less asthma, stronger bones, and higher IQs in the children.

Dr. Hathcock did a great job reviewing the evidence that doses below 10,000 units per day have never been shown to be toxic and that 10,000, not 2,000, units per day should be the Upper Limit. He, like so many others, urged the Food and Nutrition Board to revise their outdated recommendations. Moreover, I understand from knowledgeable people at the conference that the Food and Nutrition Board is planning to do just that!

Dr. Dixon presented fascinating evidence that high vitamin D blood levels prevent sunburn! Of course, it makes sense. When vitamin D levels are low, the skin stays as white as it can to make as much vitamin D as it can, just in case you ignore Dr. Gilchrest’s advice. When vitamin D levels are high, the skin rapidly tans to prevent excessive vitamin D skin production. A number of people have emailed me that observation: now that their levels are high, they tan very quickly. I’ve noticed the same thing.

Dr. Marie Demay presented her basic science research that vitamin D is involved in hair follicles. I loved her talk although she’s a scientist and I’m a psychiatrist so I didn’t understand much of what she said. However, I’ve always thought that vitamin D will really take off once science shows it’s involved in any of three things: sex, athletic performance, or hair growth. In Victoria, we saw evidence for neuromuscular (athletic) performance and hair growth.

Dr. Cedric Garland recounted how, 26 years ago, he and his brother Frank first thought about the relationship between vitamin D and colon cancer. The brothers, together with colleague Ed Gorham, were the first to provide epidemiological evidence that vitamin D deficiency is involved in numerous cancers. Their seminal 1980 paper is going to be reprinted, a well-deserved honour. (Int J Epidemiol. 1980 Sep;9(3):227-31).

Dr. Thadhani and his group from Harvard reviewed their recent discovery that calcitriol and similar drugs increase survival in patients with renal failure. He also presented evidence that renal failure patients have profound deficiencies of both calcitriol and vitamin D and their vitamin D deficiency is not corrected by giving calcitriol or its analogs, which is the current practice.

Of course, Dr. Robert Modlin stole the show when he reported on his research just published in Science that vitamin D may be, in effect, a powerful antibiotic. For the first time, the UCLA group showed that when researchers add vitamin D to African American blood, their blood makes more of the natural antibiotics that humans rely on the fight infection. Dr. Adrian Martineau, from the Imperial College in London, followed Modlin and showed vitamin D helped fight tuberculosis, probably from increasing these same natural antibiotics. Science has discovered more than 200 of these naturally occurring antimicrobial peptides; they are especially prevalent in the upper and lower respiratory tract; at least one inactivates the influenza virus. Let’s not forget that two other groups have also recently shown the antibiotic potential of vitamin D. (Science. 2006 Mar 24;311(5768):1770-3, J Immunol. 2004 Sep 1;173(5):2909-12, FASEB J. 2005 Jul;19(9):1067-77, J Virol. 1986 Dec;60(3):1068-74).

Dr. Lu presented evidence that the vitamin D content of fish is much less than previously thought, including mackerel. Salmon is OK but the vitamin D almost disappears when the salmon is fried.

Dr. Hardin, from Columbia University, presented evidence that blood levels above 50 ng/ml should help patients with lupus. A group from the University of Manchester presented the mechanism by which vitamin D should reduce arteriosclerosis. A group from the University of Chicago presented evidence that vitamin D should not only prevent colon cancer, but help treat it as well. Dr. Robert Scragg of the University of Auckland presented evidence that ethnic differences in vitamin D levels explain a significant proportion of the reason African Americans are more hypertensive than whites. The group from San Diego presented evidence that vitamin D deficiency is intimately involved in breast, colon, and ovarian cancer.

A group from the University of Manitoba presented evidence that one-month-old infants tolerate 2,000 units of vitamin a day for three months quite well without any evidence of adverse effects. A group from Wake Forest University demonstrated that higher vitamin D levels were associated with better neuromuscular (athletic) performance in older Americans (should help younger Americans too). A group from the University of Amsterdam showed that the increased risk of falling from vitamin D deficiency is much worse in people with a common genetic variation of the vitamin D receptor. Dr. Chen presented evidence that plain old vitamin D should prevent prostate cancer.

Dr. Barsony, of Georgetown University, presented evidence that low blood sodium is a risk factor for vitamin D deficiency and that such deficiencies may not be able to be corrected until the low blood sodium is corrected. Dr. Barsony really thought outside the box to discover this potentially very important clinical finding. Dr. Godar presented evidence that young Americans, not just older Americans, are not getting much vitamin D from sunlight. Dr. Taylor showed evidence that a significant number of young children have a previously undetected form of vitamin D in their blood. (Sunlight triggers the creation of a number of different versions of vitamin D in the skin, that’s why it’s risky to avoid the sun and only depend on oral vitamin D.) Dr. Patel and a group from the University of Manchester announced evidence that vitamin D deficiency may be involved in inflammatory polyarthritis.

Dr. Grant was involved in six presentations; the most interesting was his replication of a 1937 finding that squamous cell skin cancer reduces one’s risk for a number of internal cancers. That’s why I used to be so happy when my dermatologist found a squamous cell cancer on my skin. However, now that I maintain my level at about 60 ng/ml, he hasn’t been able to find any new ones.

Dr. Bulmer and his group from the Royal Victoria Infirmatory produced evidence that vitamin D may play a role in allowing fertilized ova to implant in the uterus and thus enhance fertility. Dr. Reichrath presented evidence that transplant recipients are at a high risk for vitamin D deficiency and that 50,000 units once a month may be the most practical way of ensuring sufficiency. Dr. Selby from the University of Manchester found the same problem in patients with chronic pancreatitis. A group from the University of Tennessee found the same problem in African Americans with heart failure. A group from Norway confirmed that cancer patients do better if they are diagnosed when vitamin D levels are the highest.

Finally, the Australian group headed by Dr. Darryl Eyles and Dr. John McGrath continue to present their convincing evidence (confirmed at this meeting by Dr. Abreu and a group from France) that profound maternal vitamin D deficiency in mammals causes permanent brain damage in their offspring. The racial implication of their work is overwhelming because most of the women in the USA who are profoundly deficient are African American. Are African Americans more likely to be born brain damaged than whites? Would pennies worth of vitamin D improve the disparate prenatal, perinatal, and postnatal outcome in African Americans? The sad fact is that McGrath’s and Eyles’ work will continue to be ignored because our society has no way to rationally discuss, assimilate, or act on such racially charged scientific discoveries.

If this article is reproduced please ensure the link to my website is kept live. If you can’t see the links hover your mouse over the words in the bio box.

Kevin Flatt is a Freelance Journalist specialising in Alternative Medicine. He is the publisher of Natural Health Remedies. If you are searching for information on The Benefits of Vitamin D then this website is for you.

Etiology

Schizophrenia is the core disorder in adult psychiatry. Much debate has raged about the nature of schizophrenia,

or even whether it is a valid clinical entity. It is probable that schizophrenia is not a single disease but a group of related conditions. Both genetic and environmental factors are important in the aetiology of schizophrenia. It is best seen as a developmental disorder of the brain to which genetic and perinatal factors (birth trauma or maternal viral infection) contribute, but manifesting itself in late adolescence when brain maturation is finally completed. Pathogenic environments contribute to relapse in schizophrenia, but their role in aetiology is uncertain. It is possible that abnormal brain development may result from unstimulating or traumatic environments.

• Twin and adoption studies have demonstrated the role of heredity in schizophrenia. The concordance rate for identical twins is about 50%, that for nonidentical twins around 15%.

• The efficacy of antipsychotic drugs such as chlorpromazine, with its inevitable parkinsonian side-effects, suggests a disturbance of midbrain dopaminergic pathways in schizophrenia (the ‘dopamine’ hypothesis). There is convincing evidence of increased D2 activity in patients with positive symptoms of schizophrenia. Dopamine abnormality may be the end result of other metabolic aberrations. It seems likely that serotonin (5HT) is also involved, perhaps by increasing D2 levels. Also glutamate, an excitatory neurotransmitter, may behave abnormally, leading to underactivity of Nmethyl- D-aspartate, which in turn may stimulate abnormal dopamine and 5HT activity.

• A subgroup of patients show ventricular abnormalities on CT scan. There is slight ventricular enlargement, a reduction in the normal asymmetry between the cerebral hemispheres and, particularly in males, a reduction in cortical grey matter, especially in the temporal lobes. It has been suggested that structural abnormalities are more common in patients who lack a family history of the illness, suggesting that non-genetic organic factors, perhaps associated with perinatal brain injury, may be important in some cases. Family and social factors have also been shown to be important, although not pathognomonic. In established schizophrenia the relapse rate is high when the patient is living in an over-involved family where there is a negatively charged emotional atmosphere (high ‘expressed emotion’, or ‘EE’)

• Schizophrenic patients have a high state of psychophysiological arousal, possibly related to family stress. This may reflect limbic system dysfunction and lead to a difficulty in processing sensory stimuli.

Clinical features

Schizophrenia usually starts in young adulthood (the exception being paraphrenia, a form of paranoid schizophrenia affecting the elderly). There is a slight preponderance of men. The features of the illness can be divided into two parts: the effects on mental processes, and the effects on social functioning.

Mental disturbance

There is a general disturbance of mental functioning in schizophrenia. The normal progression of logical thought is disrupted (‘thought disorder’). The privacy of the self is breached. Certain patterns of disorganization of thinking are characteristic of schizophrenia, and are known as Schneider’s first-rank symptoms.

Hallucinations

These are usually auditory. Characteristic of schizophrenia are ‘third-person’ hallucinations, in which more than one person is heard discussing the patient and referring to him as ‘he’, ‘she’ or ‘it’. Voices commenting on a person’s actions like a ‘running commentary’ are also characteristic, as are voices that echo the patient’s thoughts. Tactile or ‘kinaesthetic’ hallucinations, for example electric-shock feelings in the limbs, are rare but pathognomonic.

Delusions

In schizophrenia these include the feeling that one’s thoughts originate from outside (‘thought insertion’), that they are being interfered with, removed (‘thought block’ and ‘thought withdrawal’) or transmitted to outsiders as though on a loudspeaker (‘thought broadcasting’). ‘Passivity feelings’ are the feeling that one’s thoughts or actions are ‘made’ from outside.

Delusional perception

In delusional perception, a neutral stimulus (e.g. a car number plate or a traffic light) suddenly acquires special and often frightening significance for the patient.

Social deterioration

The second main feature of schizophrenia is social deterioration. This is known as a negative feature of the illness, as opposed to the positive features of thought disorder, delusions and hallucinations. The patient may withdraw from social contact, give up his job, shun his friends and family, and spend many hours in isolation.

Differential diagnosis

An important subtype of schizophrenia is paranoid schizophrenia, characterized by paranoid delusions. Here theonset is later (around 30-40 years of age), social deterioration is much less marked, and the personality is relativelywell preserved. Schizoaffective disorder has features of both schizophrenia and an affective illness, e.g. first-ranksymptoms plus considerable depression. Its diagnosis is intermediate between that of the two ‘parent’ disorders.Not all madness is schizophrenia. The differential diagnosis includes:

• Organic psychosis, such as acute confusional states and drug- and alcohol-related psychosis;

• Manic or depressive psychosis (in which auditory hallucinations occur but are more often ‘second-person’, in which voices speak directly to the patient);

• Hysteria;

• Stress-induced or ‘psychogenic’ psychosis;

• Severe personality disorder.

Prognosis

The course of schizophrenia is very variable. About 30% of patients have only one episode. A good prognosis is more likely if the psychosis has an acute onset, a clear precipitant, florid symptoms, marked mood change in addition to disturbance of thinking, and good previous social adjustment and personality. At the other end of the scale, about 15% remain severely disabled and will still be in institutional care after a year. In these patients the negative features of schizophrenia (withdrawal and inertia) may predominate. In the middle group, representing the majority of patients, the illness has a fluctuating course but relapse and some residual disability are likely to occur.

Management of schizophrenia

• First attack: admit to hospital or day hospital for assessment, confirm diagnosis, establish contact and initiate treatment.

• Treat symptoms with neuroleptics. Chlorpromazine 100mgt.d.s. by mouth

Trifluoperazine 5mg t.d.s. by mouth

Risperidone 2-4 mg b.d. by mouth Examples of

Olanzapine 5-10 mg b.d. by mouth moderate doses

Flupentixol (‘Depixol’) 40 mg 2-weekly

Fluphenazine (‘Modecate’) 25 mg 2-weekly

Treat side-effects as necessary with antiparkinsonian agents,

e.g. Kemadrin 5 mg t.d.s.

• Assign ‘community key worker’ as part of community care programme who will offer supportive psychotherapy and coordinate care package.

• Assess family situation: offer psychoeducational programme to lower ‘EE’ if indicated.

• Rehabilitation: attend day hospital, day centre, sheltered workshop, live-in hostel, sheltered housing.

• Where resistant to medication consider newer neuroleptics: clozapine and risperidone.

Psychosocial treatment of schizophrenia

Exciting results have recently been claimed for cognitive- behavioural treatment in schizophrenia. Contraryto earlier views, it seems that patients can develop some control and mastery over their symptoms, especiallyabnormal beliefs and auditory hallucinations. Patients can, for example, distract themselves from voices byconcentrating on external tasks, by playing music on Walkman’ headphones, or even by ‘bargaining’ with thevoices so that they confine ‘their’ attentions to particular times of the day. With the help of a therapist, or evena self-help ‘voices’ group, patients can also be encouraged to test the validity of delusions, e.g. ‘if I go into thatshop I will be killed’, and on the basis of the ‘results’ of these ‘tests’, modify their beliefs. Early studies of  these approaches are encouraging in producing, for some patients at least, reduced symptoms, improved social functioning and compliance, and reduced drug dosages.

Postpartum depression was once thought of as a make believe disorder and was widely discriminated upon. It has only been since the extreme actions of some mother experiencing postpartum depression, that the international community even took serious notice of the issue. That is why programs like this one have been developed and will continue to be developed in the coming years.

Postpartum depression residential treatment training is a series of courses that were developed from a research study conducted at the University of Cambridge, Uk. This study pertaining to the postpartum depression residential treatment training studied the different types of psychological treatments and designed a program suited to best address these needs in new mothers.

There are three main courses of postpartum depression residential treatment training. They are predominantly aimed at doctors to provide them with a set of skills to identify depression and then to treat it. The treatment is centered on a structured, well thought out intervention using techniques and skills acquired from understanding cognitive behavioral theory.

The second phase to postpartum depression residential treatment training is a two-day course that covers the detection of depression and of intervention techniques. Following that is a one-day workshop that also helps in the aiding of detection and of perinatal mood disorders as well as raising general awareness of the issue.  This should have any practitioner ready to handle any postpartum depression case.

There is also a postpartum depression residential treatment for trainers. This is a three-day course that is in large part, designed for those in charge of training primary care workers. This course is an on campus course and is available to adhere to your independent needs.

This postpartum depression residential treatment training has an online presence and you can access their site for more detailed information on course availability. Their website is very informative and has a contact us option so that you may email them your particular needs.
It was once thought of as a make believe disorder and was widely discriminated upon. In recent years it has received international fame through extreme displays of postpartum depression.

DATELINE:  IRVINE, CA… According to Postpartum Support International, one in eight women suffer from a postpartum mood disorder.  New dads (and veteran dads) should know the difference between the Baby Blues and Postpartum Depression (PPD).  Oftentimes, these disorders go undiagnosed because a new mother’s support system, typically the husband/partner, does not know what to look for and where to go to get help.

Working with more than 200,000 new dads over the past 19 years, Boot Camp for New Dads (bcnd.org), a non-profit orientation program for fathers-to-be, operating in more than 260 hospitals, clinics, schools, fire stations and churches around North America and internationally, advises new fathers to watch for signs of PPD in mom and offers tips on how to recognize it.

Postpartum depression is not selective.  It can affect any woman who is pregnant, has had a baby or who has miscarried.  It’s important that when new mothers begin to experience such symptoms that they get help immediately.  A new mother’s mental health is very important to not only herself but her baby and family.  Get professional help for mom immediately.  Talk to an experienced counselor or your physician. 

Baby blues or postpartum?  Boot Camp for New Dads advises dads of several signs that indicate the more serious PPD:

Self-esteem issues – Mom may have very negative feelings about herself.  She may think she is worthless, unattractive or a bad mother.  If she does feel this way, a simple “pep talk” is not going to help. Constant fatigue – It’s a fact that when the baby arrives, mom probably won’t get as much sleep as she needs.  One of the signs to watch for is constant fatigue, even upon waking.  Fatigue is a symptom of depression. Weight loss or weight gain – Yes, while some moms lose a little of the pregnancy weight within the first few months after birth, other moms stay the same weight.  Significant weight loss from a lack of appetite or weight gain from overeating is sign that something is wrong. Crying often – Mom’s occasional crying is normal as her hormones fluctuate and she has difficulty getting that extra, much needed rest.  But, crying every day and/or more than once a day is a red flag. Disinterest — When mom is not interested in herself, her baby, family or other activities, it’s an indication that something is wrong. Mood swings – Similar to a roller coaster ride, mood swings are extreme changes in mood.  Mom’s joyfulness immediately followed by sadness and despair are not healthy moods.  Being afraid of hurting the baby or herself – If mom is afraid of hurting the baby or herself, get medical attention immediately.

According to Greg Bishop, founder of Boot Camp for New Dads and active Boot Camp coach, “Many new moms experience the baby blues, which can include symptoms of crying and mood swings, restlessness and fatigue that lasts for a few hours to a few weeks after delivery. PPD doesn’t always happen immediately after birth.  It can take hold months after the baby is born and moms usually experience exaggerated symptoms of the baby blues. PPD is a serious condition that can affect any mom – whether she’s just given birth to her first child or fifth.  PPD may be attributed to changes in hormone levels, the stress of a new baby, lack of sleep or a combination of things.  It’s important to know how to recognize the signs of the condition because moms with PPD will not get well without professional help.”

Katherine Stone Alliance

In an effort to reach and educate more men about PPD and what they can do; Boot Camp for New Dads is working with Katherine Stone, a nationally-recognized, award-winning advocate for women with perinatal mood and anxiety disorders, and author of postpartum progress. Boot Camp will be working with Stone in the development of a new section on the bcnd.org website that is dedicated to PPD, as well as collaborating with Postpartum Support International on their website.

Fatherhood Books Serve as a “Play by Play” Guides

Greg Bishop offers strategies from more than 200,000 new dads that have gone through the Boot Camp for New Dads program in both of his books, Crash Course for New Dads:  Tools, Checklists and Cheat Sheets and his first book, Hit the Ground Crawling, which covers work balance, being a dad, caring for a new mom and much more.  Both books are available online at www.DadsAdventure.com.

New Dads Learn What to Expect at Boot Camp Workshops

Dads-to-be will be better equipped to face the challenges and opportunities of fatherhood after attending a Boot Camp “hands on” educational workshop. Men attend the class when they are expecting their first baby, and are joined in the workshop by “veterans” who had previously attended and have returned with their two to four-month-old baby in tow.  They are able to give the dads-to-be a realistic idea of what to do and what to expect when their first baby comes.  For many men attending, it’s their first time holding a baby.

Boot Camp for New Dads        

Now celebrating their 19th year, Boot Camp for New Dads is nationally acclaimed as the “Best Practice” for preparing men to be fathers and has been named a U.S. Navy Model Program.  Boot Camp for New Dads has prepared more than 200,000 men for fatherhood over the years. 

With more than 4.1 million births (National Center for Health Statistics), and approximately 1.5 million men becoming new dads every year, it’s more important than ever for fathers to realize that being a “good provider” is only part of the very central role they have in their children’s lives. 

For more information about Boot Camp for New Dads, visit bcnd.org or to visit Dads Adventure, go to www.Dadsadventure.com.  To arrange an interview with Greg Bishop, please contact sdubin@prworkzone.com, (781) 582-1061.

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. 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
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.

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
-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)

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)
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.

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.
(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.

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.
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: 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

NUTRITION: A FUNCTIONAL APPROACH-Jeffrey Bland, Ph.D

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.

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).
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

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.
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.

Integrative PPD Treatment

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

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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.” 

Was your child a low birth weight baby?

Does small birth weight and other perinatal factors affect risk of suicide? It appears to show up stronger in males.

http://bjp.rcpsych.org/cgi/content/full/bjprcpsych;179/5/450

“Foetal under nutrition predisposes men to depression in late adult life. If replicated, these results would suggest a neurodevelopmental aetiology of depression, possibly mediated by programming of the hypothalamic—pituitary—adrenal axis.”

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