The Fruit of my contemplations

by Adrian Newington. © 1990

Written in a style of literature common to mystical India. It is a book rich in metaphor and parable, and is designed to deliver spiritual insights for people who live the modern western lifestyle whilst grappling with many of life's mysterious complexities. This takes the form of a spiritually uplifting dialog between a 'Troubled Mind' and the 'Heart'.

The Mind, (which deals with life rationally and analytically), converses with the 'Heart' after it has come forth from its silent abode out of compassion.

The heart, (source of wisdom & love), points out how the Mind is a continual seeker of contentment, yet how it never comes to realize that the peace it seeks through ongoing; unsatisfying worldly activities, is the permanent peace that naturally resides in every human heart

Download a free copy in Adobe PDF format for yourself

or... READ THE BOOK NOW ONLINE!

Also, check out the companion Meditation Course for I Am the Heart © click here

The Philosophy of the book is discussed to enable the seeker on the Inner Journey, to impliment a series of practical mediation techniques for the expansion of awareness. This is one of the many roads that lead to Self Knowledge and the all empowering Self Love.

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Home Study

Let's face it. Everybody worries some of the time. Some are quite helpful. But many worries are repetitious, unproductive thoughts that make you feel anxious or upset. They show up against your will, and you seem to have little control over them. Once you start worrying, it's hard to stop. Often you'll worry over things that others consider small or insignificant. And sometimes the more you try to argue against the worry, the stronger it becomes.

Whenever you have worries, your task is to handle them, one way or another. And that is just what this section will teach you.

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Sometimes a medication may cause unwanted side effects along with its needed effects. If these occur, you should check with your doctor. In addition to other possible side effects, each of the medications listed below may produce panic-like symptoms. (All medications are listed by their generic names.)

Aminophylline relieves shortness of breath and wheezing in acute bronchial asthma and to reduce asthma-like symptoms in chronic bronchitis and emphysema. Side effects can include nervousness, rapid heart rate and dizziness.

Heterocyclic antidepressants are used to treat depression and, more recently, panic attacks. Possible side effects are dizziness and irregular or rapid heartbeat.

Antidyskinetics are used in the treatment of Parkinson's disease. Side effects may include dizziness, irregular heartbeat, and anxiety.

Atropine is a medication used to dilate the pupil of the eye. It can produce an unusually fast heartbeat. (A number of drugs are atropinelike in their effects. These are usually called anticholinergic medications.)

Inhaler forms of beta-Z adrenergic agents, such as isoproterenol and metaproterenol (Alupent) relieve acute bronchial asthma and bronchospasms associated with chronic bronchitis and emphysema. Side effects can include general anxiety, dizziness, rapid strong heartbeat, and shaky hands.

Cycloserine is an antibiotic medication. Side effects may include anxiety, irritability, confusion, dizziness and restlessness.

Digitalis is a medication used to improve the strength and efficiency of the heart, or to control the rate of the heartbeat. It can produce an unusually slow or uneven pulse.

Ephedrine is a medication used for lung problems. Side effects can be nervousness, restlessness, dizziness, difficulty breathing, palpitations, and rapid heartbeat.

Epinephrine is a medication used in treatment of the eyes, the lungs, and allergies. Side effects can include faintness, trembling, rapid heartbeat, palpitations, nervousness, and difficulty breathing.

Insulin helps control diabetes. Increasing the dose of insulin can occasionally trigger a hypoglycemic reaction, which includes sweating, cold clammy hands, dizziness, palpitations and trembling.

Isoniazid, an antiinfection medication, may produce rapid heartbeat and lightheadedness.

Monoamine oxidase (MAO) inhibitors belong within the antidepressant family. Along with reducing symptoms of depression, physicians use them in the treatment of panic attacks (see Chapter 19). Possible side effects are dizziness or lightheadedness, especially when getting up from a lying or sitting position, and rapid or pounding heartbeat.

Nitrates are used to improve the blood flow to the heart and to relieve angina attacks. Possible side effects are dizziness, lightheadedness, and rapid heartbeat.

Prednisone is the most commonly used of the corticosteroids and is prescribed to relieve inflammation. Its side effects can include irregular heartbeat, nervousness, muscle weakness, and mood swings. Other corticosteroid medications may cause similar problems.

Reserpine is used to treat high blood pressure and certain emotional conditions, as well as a few other problems. Side effects may include dizziness, faintness, anxiety, and palpitations. Some individuals have even developed phobic reactions while taking reserpine.

Synthetic thyroid hormones are used for treating hypothyroidism. Excessive levels of these hormones can cause rapid heartbeat, palpitations, shortness of breath, nervousness, unusual sweating, and anxiety.

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Many physical illnesses can produce nervousness in individuals who are not emotionally troubled. Certain other physical disorders -- those discussed in this section -- can cause a cluster of symptoms that resemble those of panic.

Physical Causes of Multiple Symptoms

• hypertension
• mitral valve prolapse
• menopause
• premenstrual syndrome
• hyperthyroidism
• hypoglycemia
• pheochromocytoma
• anemia
• iron deficiency anemia
• folic acid anemia
• B12 anemia
• sickle cell anemia
• heart attack
• hypoxia
• carcinoid syndrome
• compression neuropathies
• temporal lobe epilepsy
• caffeinism
• amphetamines
• cocaine
• phencyclidine (pcp)
• hallucinogens
• marijuana
• alcohol withdrawal
• pulmonary embolism
• withdrawal from antidepressants, narcotics, sedatives, barbiturates, benzodiazepines, or beta blockers

The predominant cardiovascular disorder that can produce multiple symptoms is hypertension, caused by a narrowing of the arteries. As your heart pumps blood through your body, it exerts a certain amount of pressure on the arterial walls. If these passageways become constricted for some reason, it requires greater force to maintain a steady flow of blood. The entire circulatory system is then under strain, and hypertension is the diagnosis. This, as mentioned earlier, is often a symptomless disease, but you might notice such symptoms as palpitations, nervousness, dizziness, and fatigue, as well as a general sense of ill health.

Mitral valve prolapse is a common condition found in approximately 5 to 15 percent of the adult population. In this disturbance a valve leaflet within the heart balloons into the left upper chamber (the left atrium) of the heart during contraction. About half of all people with mitral valve prolapse will complain of heart palpitation sometime in their life. Other possible symptoms are rapid heartbeat, shortness of breath, dizziness, and an increased awareness of the heart's action. This is a rather minor cardiac problem, but people can erroneously blame it as the sole cause of panic attacks. More often, though, it is the patient's fearful preoccupation with the action of his heart that produces panic. You will find a more extensive discussion of mitral valve prolapse in Chapter 6 of the self-help book Don't Panic.

Location of mitral valve and change in appearance after ballooning.

There is growing evidence that hormonal changes can dramatically affect a person's physical disposition and mood. For instance, approximately 50 percent of women experiencing menopause report some major physical and/or emotional changes. Another 25 percent have uncomfortable, even distressing, symptoms that can include intense moments of palpitations, sweating, hot flashes, and anxiety. Premenstrual syndrome identifies a complex of symptoms, including panic, occurring in the days just before menstruation. You will learn more about premenstrual syndrome in Chapter 5 of the self-help book Don't Panic.

A third hormonal problem is hyperthyroidism, the overactivity of the thyroid gland. This gland, located in the lower part of the neck, is controlled by a thyroidstimulating hormone produced in the pituitary gland. In hyperthyroidism, the normal control mechanisms are disrupted and the thyroid continues to produce an excessive amount of its own hormone, thyroxine. This overproduction causes a general speeding up of all chemical reactions in the body. The person may feel shaky and anxious, with heart palpitations, breathlessness, and increased perspiration -- feeling as though he or she is experiencing a constant anxiety attack. Additional symptoms make this disorder easier to diagnose: increased appetite, but with weight loss instead of gain; thinning hair; chronic tension and a sense of needing to keep moving despite fatigue and physical exhaustion. Instead of feeling cold, as the anxious person might, the person suffering from hyperthyroidism will feel hot, and his skin will be warm to the touch. Your doctor may order a thyroid screening test for you if you have several of these symptoms.

Physicians treat hyperthyroidism in one of three ways: through antithyroid medication, by surgically removing either a lump in the thyroid or all the thyroid, or, more commonly, by administration of a radioactive iodine fluid that controls the overactivity of the gland.

Hypoglycemia is the experience of several unpleasant symptoms while there is a lower than normal level of glucose in the bloodstream. This state of low blood sugar generally produces a feeling of being uncomfortable, with cold, clammy skin and profuse sweating. Other symptoms can be dizziness, weakness, trembling, tingling in the lips and hands, palpitations, and fainting. The condition is most often found in diabetics who take insulin. However, many individuals erroneously believe that hypoglycemia is the cause of their panic symptoms and therefore fail to explore other possible diagnoses. For further information on hypoglycemia and panic, see Chapter 5 of the self-help book Don't Panic..

The adrenal glands are located on top of each kidney. The adrenal medulla produces two hormones that play an important role in controlling your heart rate and blood pressure: epinephrine (adrenaline) develops within or near an adrenal gland and causes an increase in the production of this hormone. Tachycardia, sweating, anxiety, faintness, nausea and pallor -- all resembling panic -- can occur as a result of slight exercise, exposure to cold temperatures, or minor emotional upset. Typically the blood pressure will become extremely high, and the patient may have the frightening feeling of being about to die. This extremely rare disorder, called pheochromocytoma, is cured by surgically removing the tumor.

Anemia is the abnormal decrease of either hemoglobin or red blood cells. Red blood cells carry oxygen from the lungs to all parts of the body. Within each of these blood cells is the protein hemoglobin, which combines with the oxygen while in the lungs and then releases it into the tissues as the blood circulates through the body. Characteristic symptoms of anemia are lightheadedness, rapid heartbeat, difficulty breathing, and faintness. The anemic person may experience palpitations, because the heart is attempting to compensate for the lower levels of oxygen by pumping blood faster than normal. The diagnosis of iron deficiency anemia indicates that lower than normal levels of iron in the body limit the production of hemoglobin. Folic acid anemia and B12 anemia indicate that the body has insufficient amounts of these two essential vitamins, which are required for the production of healthy red blood cells. The inherited disease sickle cell anemia is found almost exclusively among people of African descent. In this condition, the red blood cells contain an abnormal hemoglobin, called hemoglobin S. This leads to deforming of the shape of each cell and thus impeding the smooth flow of blood into smaller vessels. Premature destruction of red blood cells, and anemia, results. A physician should diagnose and treat all forms of anemia.

Pulmonary embolism occurs when a blood clot detaches from the wall of a deep vein, moves through the bloodstream, and becomes lodged in the pulmonary artery close to or within the lungs. This reduces the volume of fresh blood returning to the left side of the heart and may produce sudden chest pain, rapid heart rate (tachycardia), rapid shallow breathing, and coughing up of bright red spit.

A heart attack often involves crushing chest pain as the predominant symptom, as mentioned earlier. Other symptoms can include dizziness, shortness of breath, sweating, chills, nausea and fainting.

Hypoxia means diminished availability of oxygen to the body tissues. It is a symptom of several possible underlying problems, such as altitude sickness or a pulmonary disorder. Symptoms can include difficulty breathing (dyspnea), rapid pulse, fainting and chest pain (angina pectoris).

A Carcinoid tumor, also called a argentaffinoma, is a small yellow growth occurring in the small intestine, appendix, stomach or colon. Carcinoid syndrome develops when a carcinoid tumor produces excess amounts of serotonin, a blood vessel constrictor. Exertion, intense emotion, or food or alcohol intake can trigger symptoms, which include one or more of the following: brief flushing of the neck and face, brief abdominal pain, diarrhea, racing heart (tachycardia), low blood pressure (hypotension), facial puffiness and difficulty breathing (caused by bronchoconstriction). Carcinoid tumors are rare.

Compression neuropathies, such as carpal tunnel syndrome, are disorders caused by some form of compression to localized nerves. Symptoms may include dysesthesia (a tingling or "pins and needles" feeling), similar to that which occurs during hyperventilation.

The symptoms of temporal lobe epilepsy (TLE) are highly variable, but in some cases sufferers experience them only as a sudden attack of immense fear or panic. In 60 percent of the cases, fear is the primary emotion. The patient may also have a feeling of unreality, as though he is far away from his surroundings (derealization), or may feel that his body is strange or dreamlike depersonalization). Highly charged emotional responses such as these can lead to a misdiagnosis of the problem as a psychologically based one. A distinguishing feature of TLE can be the presence of an aura, a sudden experience that often takes the form of a strange aroma or taste at the moment of fear.

Caffeinism refers to the uncomfortable side effects that can occur with high intake of caffeine from coffee, tea, cola drinks, chocolate, and overthecounter medication such as Excedrin and Anacin. Symptoms include anxiety, irritability, insomnia, headaches, stomach irritation, agitation, increased respiration, rapid heartbeat, and irregular heart rhythm. These side effects can occur with daily consumption between 250 mg to 500 milligrams. Between 20 and 30 percent of Americans consume more than 500 mg of caffeine a day (four to five cups of drip coffee contain a total of over 500 mg). Some panicprone persons are highly sensitive to caffeine, and symptoms can occur from less caffeine intake than the average person. If you experience any of these symptoms, you may wish to review your intake of all forms of caffeine. Use the following tables as a guide.

Caffeine in Medications*

• Vivarin 200 mg
• Fiorinal 40 mg
• Caffadrine 200 mg
• Medigesic 40 mg
• Cafergot 100 mg
• Triad 40 mg
• No Doz 100 mg
• Vanquish 33 mg
• Excedrin (Extra Strength) 65 mg
• Midol 32 mg
• Amaphen 40 mg
• Anacin 32 mg
• Esgic 40 mg
• Beta-Phed 32 mg
• Fiorecet 40 mg
• Empirin 32 mg
• *milligrams per each tablet/capsule

Caffeine in Beverages

(coffees, teas and cocoa (5-6 oz.)

• Drip Coffee, automatic 137 mg/cup
• Drip coffee, non-automatic 124 mg/cup
• Percolated Coffee 110 mg/cup
• Instant Coffee 60 mg/cup
• Decaffeinated Coffee 3 mg/cup
• Tea, brewed 40-65 mg/cup
• Instant tea 33 mg/cup
• Decaffeinated tea 1 mg/cup
• Hot Cocoa 5-13 mg/cup

Cola Beverages (12 oz)

• Coca Cola 45 mg
• Dr. Pepper 61 mg
• Mountain Dew 55 mg
• Diet Mountain Dew 54 mg
• Tab 49 mg
• Pepsi Cola 38 mg
• 7-up, Sprite, Fresca, Hire's Root Beer 0 mg

Chocolate

• Baker's baking chocolate (1 oz) 25 mg
• Milk chocolate candy (1 oz) 6 mg
• Sweet dark chocolate candy (1 oz) 20 mg
• Chocolate milk (8 oz) 5 mg

Amphetamines, whether taken for treatment of depression, for weight control, or illicitly for recreation, can cause severe anxiety to the point of panic. This extreme reaction is also possible with illicit drugs such as cocaine, phencyclidine (PCP), and the hallucinogens (LSD, mescaline). It is possible that these drugs stimulate brain receptors associated with anxiety, making panic attacks more likely. Marijuana causes increased heart rate that can lead to a severe anxiety reaction.

Alcohol withdrawal can produce nervousness, rapid heartbeat, confusion, high blood pressure, and panic as well as other symptoms. Too rapid withdrawal from antidepressants, narcotics, sedatives, barbiturates, benzodiazepines (Valium, Librium, etc.), or beta blockers can cause symptoms such as anxiety, rapid heartbeat, high blood pressure, and panic, especially after longterm use.

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Anybody who thinks that society pressures women to live up to our image should think of what we have to go though to maintain that image. - Supermodel Carol Alt

With the recent hospitalization of Mary-Kate Olsen for symptoms of anorexia nervosa, the public is starting to examine this widespread phenomenon. Why would someone who seems to have the world at her fingertips stop eating? Why are eating disorders such a problem? Are young performers at more of a risk for body image issues than adult performers?

The Link Between Performers and Eating Disorders

The world has lost many talented women to eating disorders including Boston Ballet dancer Heidi Guenther, Olympic gymnast Christy Henrich and singer Karen Carpenter. In addition, many high profile performers have spoken publicly about the suffering they endured as a result of these disorders: actress Tracey Gold, singer Paula Abdul, talk show host Oprah Winfrey, actress Ally Sheedy, '60s teen idol Sandra Dee and actress Courtney Thorne-Smith, to name a few.

Psychological experts have found that many of the personality traits which make children great athletes or performers are the very same characteristics which make them more susceptible to eating disorders; the most common being: perfectionism; the desire to please; the ability to ignore pain and exhaustion; obsessiveness and the burning desire to reach their goals. When you add into the mix the difficult physical expectations in television, movies, and professional athletics to be dangerously thin, you have a recipe for disaster. Studies have shown that the rate of anorexia nervosa in this group is ten times that of the general population and due largely to these professions in which thinness is a prerequisite for success.

What's normal?

According to Eating Disorder Awareness and prevention (EDAP), there are three red flags parents should look out for which can help indicate future eating disordered behavior: body dissatisfaction, dieting behavior, and a drive for thinness.

During the normal adolescent growth spurt, a young woman's body fat increases by 125%, compared to her lean body mass, which only increases by 42%. This kind of normal change in physiology can panic adolescents as well as their parents, agents, managers, and coaches. Often, it is at this crucial age when girls are likely to try their first diet. Be aware - this is often a precursor to an eating disorder.

The Problems with Diets

Studies have shown that the risk of developing an eating disorder is 8 times higher in dieting than non-dieting 15-year-old girls. Even though diets have been estimated to have a 95% failure rate, it has been estimated that half of all American women are on a diet at any given time. So commonplace are diets in our society that one San Francisco study reported that 50% of 8-year-old girls are on diets. While it was once believed that this was a problem that predominantly affected white, teenage girls, it has been shown that the unhealthy eating attitudes and practices which contribute to this problem affect nearly all ethnicities, genders and classes, irrespective of age or location.

There have been many theories explaining why dieting leads to a loss of control with food and binge eating. Many theorists believe that it is the dieter's inability to manage powerful surges of hunger which leaves her vulnerable to erratic eating behavior and binges. Researchers have found the greater the degree of dietary restraint, the more severe the eating pathology.

In addition to lowering the dieter's metabolic level, or in other words - slowing down her ability to burn calories, research has revealed that the metabolic changes have a profound impact on the brain. For the 4% of the population which has the biological pre-disposition to develop an eating disorder, this is the beginning of a serious eating disorder

Media Images

Today's teens are at higher risk than those of previous generations. They are bombarded by images of unrealistic standards of beauty on television, the internet, in magazines, and in movies. The message which teens today are being fed is that beauty and thinness can change your life. Tune into any episode of a show like "The Swan" and you will start to believe it, too.

Studies have shown there is a direct correlation between how much exposure a woman has to contemporary media and the frequency of eating disordered symptoms she experiences. One study in which women viewed slides of overweight, average, and thin models found exposure to thin models resulted in lower self-esteem and decreased weight satisfaction.

In other cultures, the rate of eating disorders has risen in direct correlation with the influx of American exports, such as television programs and feature films, which bring with them new concepts of beauty and femininity as well as Western clothing, which is geared towards the slimmer figures. . For example, in Fiji after being exposed to American television for only three years, Fijian teens who had never before been exposed to Western culture experienced significant changes in their attitudes and behaviors towards food and body image. In this culture where a comment like "you look fat today" was once considered to be a compliment, the standard of attractiveness changed. As a result the teen risk for eating disorders doubled to 29%, 15% of high school girls started vomiting for weight control (a five fold increase), 74% of Fijian teens said they felt ``too big or too fat'' at least some of the time, and 62% said they had dieted in the past month.

What You Can Do

There is a lot you can do as a parent. To begin with, every parent needs to look out for the warning signs of an eating disorder: dramatic changes in weight, rituals surrounding eating, food avoidance, frequent trips to the bathroom after meals, wearing baggy clothes, a constant, low body temperature, and dramatic mood shifts. It is important that you encourage body acceptance and discourage dieting behavior. Teaching your child how to listen to her body's signs like hunger, thirst and satiety are important lessons. It is especially important that you work through your own food and body image issues so that you can be a model of healthy behavior for your children, which is ultimately one of the greatest tools you can give them.

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Learn how taking hallucinogens, opioids, amphetamines, or marijuana during pregnancy can affect you or your baby.

Use of illicit drugs (particularly opioids) during pregnancy can cause complications during pregnancy and serious problems in the developing fetus and the newborn. For pregnant women, injecting illicit drugs increases the risk of infections that can affect or be transmitted to the fetus. These infections include hepatitis and sexually transmitted diseases (including AIDS). Also, when pregnant women take illicit drugs, the growth of the fetus is more likely to be inadequate, and premature births are more common.

Babies born to mothers who use cocaine often have problems, but whether cocaine is the cause of those problems is unclear. For example, the cause may be cigarette smoking, use of other illicit drugs, deficient prenatal care, or poverty.

Hallucinogens, such as methylenedioxymethamphetamine (MDMA, or Ecstasy), rohypnol, ketamine, methamphetamine (DESOXYN), and LSD (lysergic acid diethylamide) may, depending on the drug, lead to an increased incidence of spontaneous miscarriage, premature delivery, or fetal/neonatal withdrawal syndrome.

Opioids: Opioids, such as heroin, methadone (DOLOPHINE), and morphine (MS CONTIN, ORAMORPH), readily cross the placenta. Consequently, the fetus may become addicted to them and may have withdrawal symptoms 6 hours to 8 days after birth. However, use of opioids rarely results in birth defects. Use of opioids during pregnancy increases the risk of complications during pregnancy, such as miscarriage, abnormal presentation of the baby, and preterm delivery. Babies of heroin users are more likely to be small.

Amphetamines: Use of amphetamines during pregnancy may result in birth defects, especially of the heart.

Marijuana: Whether use of marijuana during pregnancy can harm the fetus is unclear. The main component of marijuana, tetrahydrocannabinol, can cross the placenta and thus may affect the fetus. However, marijuana does not appear to increase the risk of birth defects or to slow the growth of the fetus. Marijuana does not cause behavioral problems in the newborn unless it is used heavily during pregnancy.

Source:

• Merck Manual (last reviewed May 2007)

Results of recent studies on antidepressant use during pregnancy are a bit confusing, but do show it's important to consider the mental health of the mother.

In-Utero Antidepressant Exposure

Data on the risk of fetal malformations and adverse peripartum events associated with in-utero exposure to antidepressants are reassuring, especially with regard to the tricyclics and some of the selective serotonin reuptake inhibitors (SSRIs). Prospective data on the longer-term neurobehavioral sequelae associated with such exposure are much more limited, however.

In the last several years, some studies have been published in which researchers tracked neurobehavioral function over a period of months to years in children exposed to SSRIs in-utero. While it's exciting to have some new information in this previously uncharted area, some of the data are inconsistent and have led to confusion among patients and health care providers.

A recent study conducted by investigators at the Motherisk Program at the University of Toronto prospectively evaluated the neurodevelopment of 86 children aged 15-71 months who were exposed to fluoxetine (Prozac) or a tricyclic antidepressant throughout pregnancy.

The study showed no differences in well-established neurobehavioral indices between these children and 36 unexposed children of non-depressed women (Am. J. Psychiatry 159[11]:1889-95, 2002). This study was a follow-up to an earlier study that looked at neurobehavioral function in children exposed to these medications only during the first trimester, and the results were consistent.

Of note, the duration of maternal depression was a significant negative predictor of cognitive function in children; for example, the number of depressive episodes after delivery was negatively associated with language scores. These data support the now well-established finding that an uncontrolled postpartum mood disorder can have adverse effects on the baby's neurocognitive development.

In a study published in April, Stanford University investigators compared the perinatal and neurobehavioral outcomes of 31 children exposed in utero to fluoxetine, sertraline (Zoloft), fluvoxamine (Luvox), or paroxetine (Paxil), with those of 13 children whose mothers had a major depressive disorder and received psychotherapy but did not take medication during their pregnancies.

When evaluated between ages 6 months and 40 months, the SSRI-exposed children had significantly lower scores on psychomotor indices and on neurobehavioral function (J. Pediatr. 142[4]:402-08, 2003).

On the surface, the results of these two studies are somewhat confusing: Among the possible explanations for the different findings are methodologic limitations of the Stanford study. The Motherisk study was a controlled study in which maternal mood during pregnancy and the postpartum period was assessed prospectively. But the mood of women in the Stanford study was not prospectively assessed; a significant number had already given birth when they were asked to recall what their mood was during pregnancy. As a result, the impact of antidepressant therapy on their mood is unknown. This is a major confounding factor because of the considerable data indicating that maternal mood disorders can adversely affect neurobehavioral function in children.

The results of the Stanford study are interesting, but given these methodologic limitations, it is particularly difficult to draw any conclusions from it or to use the findings to inform clinical care. There certainly is nothing in these findings to suggest that women should avoid taking antidepressants during pregnancy.

The Stanford authors, who acknowledged the difficulty in controlling for certain confounding variables and concluded that it should be viewed as a pilot study, should still be commended for their efforts to perform prospective neurobehavioral assessments and address the potential for behavioral teratogenicity--information that is profoundly lacking in the literature.

Multiple studies have shown the importance of keeping women euthymic during pregnancy, in light of the adverse effects of maternal depression on perinatal outcome and the extent to which maternal depression in pregnancy predicts postpartum depression.

In future studies, it will be important to include prospective assessments of both maternal mood and drug exposure, so the two variables can be teased apart in terms of their relative contribution to both perinatal outcome and long-term neurobehavioral outcome.

Dr. Lee Cohen is a psychiatrist and director of the perinatal psychiatry program at Massachusetts General Hospital, Boston. He is a consultant for and has received research support from manufacturers of several SSRIs. He is also a consultant to Astra Zeneca, Lilly and Jannsen - manufacturers of atypical antipsychotics. He originally wrote this article for ObGyn News.

While using SSRI antidepressants during pregnancy appears relatively safe, it appears there are some risks to the baby.

SSRIs and Neonatal Neurobehavior

With increasing recognition and treatment of depression in women during their childbearing years, more patients and their physicians are faced with the dilemma of whether to use antidepressants in pregnancy. The literature over the last decade has been relatively consistent regarding the absence of teratogenic effects associated with the use of selective serotonin reuptake inhibitors (SSRIs). The data have not been so straightforward regarding the potential risk for perinatal syndromes when these drugs are used during pregnancy.

An increasing number of studies have described syndromes occurring during the perinatal period in babies whose mothers used SSRIs. Symptoms ascribed to perinatal exposure to SSRIs have included tremulousness, increased motor activity, jitteriness, and heightened startle. One trial suggested that fluoxetine (Prozac, Sarafem) exposure during the latter part of pregnancy through labor and delivery was associated with higher rates of special care nursery admissions for what the authors called "poor neonatal adaption." But in another study, my colleagues and I found no evidence of neonatal toxicity in newborns exposed to fluoxetine at term that could be directly ascribed to exposure to this medicine.

Studies that have evaluated the effects of SSRIs on neonatal outcome have suffered from consistent methodologic limitations, the most notable being the failure to blind investigators evaluating the infants with regard to in-utero drug exposure and the failure to take into account the potential impact of maternal mood disorder on acute neonatal outcome.

In a study published last month, 34 healthy, full birthweight newborns were evaluated in a prospective trial; 17 mothers took SSRIs during pregnancy and 17 were unexposed. The investigators noted that exposed newborns exhibited significantly more tremors, heightened levels of motor activity and tremulousness, and fewer changes in behavioral state during an hour-long observation period, compared with unexposed newborns (Pediatrics 113[2]:368-75, 2004).

While this is an important study, in which the evaluators were blinded, it is limited by its small sample size. Though both groups were matched for maternal use of cigarettes, alcohol, and marijuana during pregnancy, alcohol use was not insignificant, and four women on SSRIs used marijuana while pregnant.

Most notably, the study failed to include an assessment of maternal mood during pregnancy and did not control for the impact of maternal depression on the outcome variables measured.

The authors acknowledge the negative impact that maternal depression can have on neonatal outcome, though they do not acknowledge adequately how the failure to measure maternal depression in their study could have confounded it greatly. They note that maternal depression, "through its action as a stressor, may have an impact on fetal development through its effect on the hypothalamic-pituitary-adrenal axis, adrenocorticotropic hormones, and b-endorphins," and that infants of depressed mothers are at risk for physical anomalies and birth complications, delayed habituation of fetal heart rates, higher neonatal cortisol levels, higher levels of indeterminate sleep, and elevated norepinephrine levels."

They do cite an important study from the Motherisk program in Toronto indicating that postpartum mood is one of the strongest predictors of neurocognitive function in children assessed up to 6 years of age.

The authors suggest that milder forms of tremulousness in the extremities during the neonate's first week may reflect "CNS depression and/or stress/withdrawal from prenatal drug exposure," and that these findings "may be a harbinger of the persisting tremors found in SSRI-exposed infants at 6-40 months of age," as observed in a study last year (J. Pediatr. 142[4]:402-08, 2003). But that study was also limited by a small sample size and the failure to prospectively assess maternal mood during pregnancy.

While data from the latest study are welcome, the recommendation to lower or discontinue antidepressants proximate to delivery is worrisome-not only because of the potential negative impact of depression during pregnancy on neonatal well-being, but because maternal depression also increases the risk for postpartum depression.

We remain at a point where the literature fails to take into account one of the strongest predictors of newborn neurobehavior, namely maternal mood during pregnancy. Pending better controlled studies that do consider these factors, it would be unwise to use small confounded studies for making clinical decisions, and best to make treatment decisions based on individual clinical situations and patients' wishes.

Dr. Lee Cohen is a psychiatrist and director of the perinatal psychiatry program at Massachusetts General Hospital, Boston. He is a consultant for and has received research support from manufacturers of several SSRIs. He is also a consultant to Astra Zeneca, Lilly and Jannsen - manufacturers of atypical antipsychotics. Dr. Cohen originally wrote the article for ObGyn News.

Some mood stabilizers (esp. Depakote) taken during pregnancy carry a significant risk of producing birth defects in the baby, but alternatives are available. Read more.

Two of the agents widely used to treat bipolar illness are established teratogens. Lithium is associated with a 0.05% risk of Ebstein's anomaly, a modest teratogenic effect. Sodium valproate is associated with a risk as high as 8% for major congenital malformations, most notably, neural tube defects and cardiac malformations, according to recent data from the North American Antiepileptic Drug (AED) Pregnancy Registry.

This increased risk for major organ malformations associated with first trimester exposure to these compounds raises concerns about the possible risk of longer term neurobehavioral sequelae associated with prenatal exposure.

Several studies published over the last few years have consistently shown an association between developmental delay and an increased risk for behavioral problems associated with in utero exposure to anticonvulsants, particularly sodium valproate (Depakote). This growing literature has suggested associations between in utero exposure and higher rates of problems ranging from mild behavioral disruption in school, attention-deficit disorder, and other behavioral problems characterized by hyperactivity, autistic-like behaviors, and problems with learning, speech delay, and gross motor delay.

One study of 52 children exposed to anticonvulsants in utero found that 77% had developmental delay or learning difficulties when followed up at a mean age of 6- ½ years; 80% had been exposed in utero to sodium valproate (J. Med. Genet. 2000;37:489-97).

In another prospective study, children born to women with epilepsy were assessed between ages 4 months and 10 years. The risk of adverse outcomes, including developmental delay, was higher among those exposed to sodium valproate than carbamazepine (Tegretol). Most of the cases were children born to women who received sodium valproate doses that were greater than 1,000 mg/day (Seizure 2002;11:512-8).

These studies were not ideally designed and have inherent methodologic limitations. Eventually, we will have long-term prospective data on children exposed in utero to anticonvulsants. These data will come from the North American AED Registry. Until then, however, the findings of these studies are consistent enough to indicate that in utero exposure to anticonvulsants may have neurotoxic effects; this appears to be the case particularly with sodium valproate monotherapy and polytherapy.

The potential for neurobehavioral sequelae is an issue that has not been adequately factored into the risk-benefit decision for treating women with epilepsy or bipolar disorder during pregnancy. For women with epilepsy, the situation is more difficult, since seizures during pregnancy are associated with particularly bad perinatal outcomes. But for bipolar disorder, we have a spectrum of treatment options.

Often women and their physicians choose to discontinue a psychotropic drug in the first trimester, and they assume that therapy can safely be reintroduced during the second trimester. Still, the data on potential behavioral toxicity, particularly with sodium valproate, should make one pause before reinstituting treatment with sodium valproate during the second and third trimester - and the data should raise the question of whether this is an appropriate medicine to be using at any point during pregnancy in women with bipolar illness.

There is no perfect answer. The goal is to keep women emotionally well during pregnancy and to avoid relapse during pregnancy. Prenatal exposure to a drug is sometimes necessary to sustain well-being of patients. Nevertheless, recent data have indicated that the risk of polycystic ovarian syndrome is increased in women treated with sodium valproate. When this finding is considered with the teratogenicity data for sodium valproate and its possible longer term neurobehavioral sequelae, one has to reconsider the wisdom of using this medication in reproductive-age women, particularly since some of the treatment alternatives for bipolar illness are either less teratogenic or appear to be nonteratogenic.

Reproductive-age women who want to become pregnant or who are already pregnant should consult their physicians about alternative treatment strategies that can be continued throughout pregnancy. Such alternatives are lithium or lamotrigine (Lamictal), both of which may be used with or without one of the older typical antipsychotics, which do not appear to be teratogenic.

Our goal is to avoid exposure to a drug with known teratogenicity with respect to organs, and quite probably, with respect to behavior.

Dr. Lee Cohen is a psychiatrist and director of the perinatal psychiatry program at Massachusetts General Hospital, Boston. He is a consultant for and has received research support from manufacturers of several SSRIs. He is also a consultant to Astra Zeneca, Lilly and Jannsen - manufacturers of atypical antipsychotics. He originally wrote the article for ObGyn News.

Article on antidepressant withdrawal symptoms in babies whose mothers took SSRI antidepressant medications during pregnancy.

Multiple articles over the past several years have cited perinatal symptoms in newborns whose mothers were taking an antidepressant late in pregnancy, including transient restlessness, jitteriness, tremulousness, and difficulty feeding. There have now been enough reports to suggest certain vulnerable children or subgroups of newborns who were exposed in utero may be at a slightly increased risk for this syndrome.

Last year, the Food and Drug Administration required the addition of related information to the labels of selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs).

The results of a recent study of 93 cases worldwide (including 64 associated with paroxetine) from a World Health Organization adverse event reporting database do not represent new findings. The reports include descriptions of nervousness, agitation, abnormal crying, and tremors, which the authors consider a "signal" for perinatal or neonatal toxicity. The study also refers to 11 reports of neonatal convulsions and two grand mal seizures, with no further description of the cases (Lancet 2005;365:482-7).

Although the report of neonatal convulsions is relatively new, the study itself has several notable limitations. It is difficult to interpret these results because they are from a spontaneous adverse event reporting system, where typically adverse outcomes are over-reported and do not provide adequate information on when the drug was used, the duration of illness, or whether the woman was depressed during pregnancy. And the absence of a controlled sample makes it difficult to estimate the incidence, which likely is very low, considering the wide use of these medications among reproductive age women. Moreover, depression in the mother has been associated with many of the newborn symptoms reported.

The use of the term "withdrawal" syndrome is a dicey clinical call at best. Based on what we know about the kinetics and placental passage of these medications, certainly what we're seeing is not acute withdrawal, like we see with heroin or methadone use during pregnancy. The main metabolites of the drugs remain in the baby's circulation for at least days to weeks, so to see something so early and so transient, even for paroxetine (which has a shorter half-life than the other SSRIs), is not consistent with the pharmacokinetics of the compounds being described.

I don't disagree with these findings. Acknowledging the probable biases involved with collecting and reporting these cases, the report provides another data set that calls attention to the possibility of some type of perinatal syndrome associated with SSRI exposure later in pregnancy, which may not necessarily be a causal relationship. The authors suggest their findings are more of a "signal" that a problem may exist.

When considered with other case series, this study may indicate the potential risk for some type of perinatal syndrome associated with the use of these medications, particularly around the acute peripartum period.

What is of concern, however, is the impact this report may have on appropriate prescribing of these drugs to pregnant women, and that patients, as well as physicians, will uniformly and arbitrarily avoid these drugs during pregnancy.

The article falls profoundly short in terms of helping the clinician. While the results indicate that more vigilance is necessary during the peripartum period in cases of SSRI use, the data do not imply any particular SSRI should be avoided in women of reproductive age. The authors conclude that the signal is stronger for paroxetine, which they say should either not be used during pregnancy or used at the lowest effective dose. I certainly would not rule out using paroxetine in women of reproductive age on the basis of this report, with the possible exception of a woman with immediate plans to become pregnant or a woman with recurrent disease.

A reduction in the appropriate use of these drugs in depressed pregnant women would be a serious problem because relapse of recurrent depression during pregnancy is exceedingly common, and depression during pregnancy is the strongest predictor of risk for postpartum depression. Reducing the dose or discontinuing the antidepressant around the time of labor and delivery increases the risk of relapse, although some women may tolerate this approach, particularly if the drug is reinstituted immediately postpartum.

Physicians should remain vigilant and carefully plan their treatment approach in pregnant patients with depression. The data may, in fact, be a signal that a problem exists. But a signal should be a beacon that guides the clinician. In this case, we have more fog than we have clarification of an already complicated situation.

Dr. Lee Cohen is a psychiatrist and director of the perinatal psychiatry program at Massachusetts General Hospital, Boston. He is a consultant for and has received research support from manufacturers of several SSRIs. He is also a consultant to Astra Zeneca, Lilly and Jannsen - manufacturers of atypical antipsychotics. He originally wrote this article for ObGyn News.