Beware: Cholesterol Drugs Might Cause Depression

Multiple reports suggest strong association between cholesterol lowering statin drug use and affective disorders of all kinds, including depression and its most extreme form, suicide, and other affective manifestations include hostility, aggressiveness, rage, combativeness, accident proneness and special proneness for use of addictive substances.

"He or she is not the person I married," is a frequently recurring statement from spouses of statin users. And more ominously is the statement from surviving wives, "there was nothing wrong before his statin. "

The mechanism of action in explaining the association of these reactions to statins appears to be interference with the biochemistry of dolichols, one of the vital metabolic pathways collaterally affected by the use of statin drugs.

Dolichols are absolutely necessary for the formation of neuropeptides, known also as messenger molecules. These chains of peptides not only are the basis of every thought, emotion and sensation we have ever experienced; they are our every thought, emotion or sensation in a process we are only just beginning to understand.

In the tiny microtubular factories within each of our cells peptide segments are stacked one by one into the desired chain and passed on to the Golgi apparatus for packaging and delivery to other cells via the axons of nerves. This entire complex of activity is orchestrated by our dolichols and inevitably compromised by Statins. Need it be stated, the effects on human emotionality can be extremely varied.

Another reason for the potential danger of the excessive lowering the cholesterol levels might be related to drop it to the unacceptable low levels in the human body. Some doctors today are convinced that the lower one's cholesterol, the better. If your cholesterol is too low you have an increased risk of mood disorders, depression, stroke and violence. Artificially lowering cholesterol is dangerous because we need cholesterol to manufacture sex hormones, vitamin D, DHEA and cell membranes. Lowering cholesterol artificially affects mental acuity and severely disables the ability to cope with physical and mental stress.

Studies have shown a three to 13-fold rise in violent deaths among people taking cholesterol lowering drugs. This is not surprising when you realize that cholesterol is vital to the nervous system and too-low cholesterol triggers brain chemistry changes. Cholesterol levels directly affect the activity of serotonin, a brain neurotransmitter implicated in the control of violent behaviors. Indications are that lowered cholesterol levels lead to lowered brain serotonin activity and this can lead to increased violence.

While arranging the aggressive fight with cholesterol, remember that far from being a health destroyer, cholesterol is absolutely essential for life. According to PROTEIN POWER, by Michael and Mary Dan Eades:

"Although most people think of it as being "fat in the blood," only 7 percent of the body's cholesterol is found there. In fact, cholesterol is not really fat at all; it's a pearly-colored, waxy, solid alcohol that is soapy to the touch. The bulk of the cholesterol in your body, the other 93 percent, is located in every cell of the body, where its unique waxy, soapy consistency provides the cell membranes with their structural integrity and regulates the flow of nutrients into and waste products out of the cells.

"In addition, among its other diverse and essential functions are these: Cholesterol is the building block from which you body makes several important hormones: the adrenal hormones (aldosterone, which helps regulate blood pressure, and hydrocortisone, the body's natural steriod) and the sex hormones (estrogen and testosterone). If you don't have enough cholesterol, you won't make enough sex hormones.

• "Cholesterol is the main component of bile acids, which aid in the digestion of foods, particularly fatty foods. Without cholesterol we could not absorb the essential fat-soluble vitamins A, D, E and K from the food we eat.


• Cholesterol is necessary for normal growth and development of the brain and nervous system. Cholesterol coats the nerves and makes the transmission of nerve impulses possible.


• Cholesterol gives skin its ability to shed water.


• Cholesterol is a precursor of vitamin D in the skin. When exposed to sunlight, this precursor molecule is converted to is active form for use in the body.


• Cholesterol is important for normal growth and repair of tissues since every cell membrane and the organelles (the tiny structures inside the cells that carry out specific fundtions) within the cells are rich in cholesterol. For this reason newborn animals feed on milk or other cholesterol-rich foods, such as the yolks of eggs, which are there to provide food for the developing bird or chick embryos.


• Cholesterol plays a major role in the transportation of triglycerides -- blood fats -- through the circulatory system.

Official recommendations for several drugs already include disclaimer related to the possible depression related side effects. Recently, the Food and Drug Administration (FDA) has approved a product label change for the cholesterol-lowering drugs Zetia (ezetimibe) and Vytorin (ezetimibe/simvastatin), adding depression as a possible side-effect.

Letters to the drugs' co-marketers, Schering-Plough Corp. and Merck & Co., the FDA said depression will be added to the section of the drugs' package insert concerning adverse reactions in post-marketing experience. The new language also will be included in a section of the patient package inserts listing possible side effects of the drugs.

Vytorin is a combination of Zetia and simvastatin. Simvastatin is marketed by Merck under the brand Zocor.

Sources and Additional Information:

http://depression.about.com/b/2008/02/19/cholesterol-drug-may-cause-depression.htm

http://www.spacedoc.net/depression_statins.htm

http://www.thenhf.com/articles_08.htm

http://www.internetwks.com/owen/fear.htm

Link Acne Drug with Depression: True, False, Possible…

One of the most wide-known cases, when the medications was directly linked to the potential development of the depressive disorder is Accutane, drug used in treating severe forms of acne, in case other drugs have not been able to treat the condition. It is very effective as an acne-cure. However, the regular use of this drug has been associated with depression amongst the users. A number of suicide cases have been linked to the use of this drug.





The powerful drug manufactured by Roche Pharmaceuticals was first approved in the year 1982 as a medication to treat persistent acne problems, targeting the severe conditions associated with forward in the treatment of acne vulgaris, the most egregious and resistant form of the disease. But Accutane has been linked to serious health risks, including: strokes, suicide, depression, inflammatory bowel disease, Pancreatitis, and Crohn’s disease.

It is very potent and can cause severely birth defects if taken by women who are pregnant or of childbearing potential. Women using this drug must sign consent forms and promise to use at least two contraceptive procedures to prevent pregnancy during the course of using this drug. Accutane’s most common side effects are gastrointestinal. According to the Food and Drug Administration, the gastrointestinal adverse reactions include: "…inflammatory bowel disease, hepatitis, Pancreatitis, bleeding and inflammation of the gums, colitis, ileitis, nausea, other nonspecific gastrointestinal symptoms."

The long list of the possible side effects is provided at http://accutanesideeffects.net/.

People from different social strata have been long up in arms against the free availability of this particular drug. They are convinced that it creates suicidal tendencies among teenagers many of whom go to the extent of actually becoming suicidal.

In February of 1998 the manufacturer of Accutane, Roche Laboratories, issued a letter to physicians in which they added the following to the WARNINGS section of Prescribing Information for Accutane: Psychiatric disorders: Accutane may cause depression, psychosis and, rarely, suicidal ideation, suicide attempts and suicide. Discontinuation of Accutane therapy may be insufficient; further evaluation may be necessary.

A study published in Experimental Biology and Medicine offers a possible explanation for how the acne drug Accutane (isotretinoin) may cause depression. The authors speculate that it decreases the availability of serotonin, a neurotransmitter which is believed to be involved in the regulation of mood.

Using cell cultures, scientists from the University of Bath (UK) and University of Texas at Austin (USA) were able to observe the effect of the drug on serotonin-producing cells. They found that the cells significantly increased production of proteins and cell metabolites that are known to reduce the availability of serotonin. A reduction in serotonin, say the scientists, could be a cause of depression in patients using the drug.

However, there is not enough evidence to prove that Accutane is the reason behind such occurrences. Recently, a study was conducted to establish a link between the drug and teenage suicides. The study confirmed to an extent that there was nothing like accutane depression. The teenagers on the drug did not show any significant mood swing compared to others treated with different drugs.





These findings were far from conclusive. According to a scientist, the sample group was rather small. The sample group should not have been less than 1000 if a relation were to be established comprehensively. A more recent research found that Accutane induces some changes in the frontal lobe region of the brain, which is identified as the centre of our emotions. Therefore, there is the possibility of a causative link between Accutane use and depression.

A different Canadian study has also found no association between the acne medication isotretinoin, which is sold in the U.S. under the brand name Accutane, and depression.

This study, which was conducted in a community dermatology clinic, looked at acne patients who were beginning treatment with isotretinoin. The control group were treated with either oral antibiotics or medication applied to the skin. The Center for Epidemiologic Studies Depression scale and the Zung Depression Status Inventory were used to assess depression both at the beginning of treatment and at the end of two months.

At the end of the two month period, the researchers found that neither depression assessment indicated any association between treatment with isotretinoin and depression.

The authors conclude that denying patients with significant acne treatment with isotretinoin, which is a very effective treatment, may not be warranted at this time as it does not appear to be associated with depression.

Why the Controversy?

While countless case reports suggest a relationship between Accutane use and depression, proving this connection has been difficult. Some studies suggest acne itself is more likely to cause depression in sufferers than Accutane use. Others have found no definitive link between Accutane use and an increased risk of depression.

Many acne sufferers find they are depressed because of their acne, and isotretinoin helps to clear their skin, making them feel less depressed and more confident.

Accutane is a miracle cure for acne treatment, a claim that most users will uphold. However, it is advisable to use the drug with caution, at least until the drug is proven innocuous beyond reasonable doubt.

Sources and Additional Information:

http://www.aboutstressmanagement.com/stressrelief/stress-management/causes-of-stress/does-accutane-cause-depression-and-suicide.htm

http://depression.about.com/od/secondary/f/accutane.htm

http://depression.about.com/b/2007/11/20/possible-mechanism-found-for-depression-accutane-link.htm

http://depression.about.com/b/2007/06/25/study-finds-no-link-between-acne-drug-and-depression.htm

http://acne.about.com/od/acnetreatments/a/sideeffectsaccu.htm

Can your Medicines Cause Depression?

There are multiple scientific studies, more or less substantial, providing data that certain medicine might trigger or influence in certain way the depression.

Some medications prescribed for various medical conditions do cause such feelings as sadness, despair, and discouragement. And those are feelings that are often associated with depression. Other medicines prescribed for medical problems can trigger mania (excessive elation and joy). That's usually associated with bipolar disorder. There are also many psychiatric medications which paradoxically might actually make depression, patient suffers from, worse. These include highly sedating medications such as antianxiety medications or antipsychotic medications and certain mood stabilizers, which not only are sedating, but can slow down thinking processes and lead people to feel more withdrawn and less motivated to go about their daily activities.

Medications that cause mania or depression appear to alter brain chemicals in some way. And even though the medications may be necessary to treat the condition, the side effect appearance might be unacceptable for the patents.

There are just examples of certain medications that can cause symptoms of depression Note that for some medications the various researches might present different, sometimes completely opposite results, but nevertheless you should be aware on the potential negative effects to be sensitive to your mental condition changes, while you take them. You should understand that every individual reaction might be completely different on the taken drugs, and in some cases not an individual medication make the difference, but combination of various prescribed medications causing the cumulative effect on your well-being.

So, be aware on the following drugs to be considered as might be causing the depression in adults:

• Accutane, which is prescribed for the treatment of acne, has been suspected to cause depression.


• Antihypertensives, such as clonidine (Catapres).

• Barbiturates, such as phenobarbital, pentobarbital (Nembutal), and secobarbital (Seconal).


• Benzodiazepines, such as diazepam (Valium), alprazolam (Xanax), or lorazepam (Ativan).


• Calcium channel blockers, such as verapamil (Calan).


• Corticosteroids, such as prednisone.


• Hormonal medications, such as birth control pills (oral contraceptives) and hormone therapy used to treat the symptoms of menopause.


• Medications used to treat Parkinson's disease or other neurological disorders, such as restless legs syndrome.


• Medications used to treat seizures, such as phenytoin (Dilantin).


• Pain medications, such as meperidine (Demerol) or codeine.

Symptoms of depression can also be caused by the use of or withdrawal from alcohol and illegal drugs, such as cocaine, amphetamines (methamphetamines, crystal meth, or crack), heroin, and cannabis (marijuana).

Sources and Additional Information:

http://www.webmd.com/depression/guide/medicines-cause-depression

http://www.wrongdiagnosis.com/d/depression/medic.htm

http://www.medicinenet.com/script/main/art.asp?articlekey=55169

http://vitaminlady.com/articles/depresmeds.asp

http://www.alternativementalhealth.com/articles/drugdepression.htm

http://www.emedexpert.com/side-effects/depression.shtml

http://health.msn.com/health-topics/articlepage.aspx?cp-documentid=100057030

http://abcnews.go.com/Health/DepressionScreening/story?id=4355948

Individual Personality and Depression

Individuals with certain personality styles - those who are aggressive and those who have low dependency on other people - are at higher risk for recurrent bouts of major depression, according to a new University of Washington study.

The study comes from the laboratory of UW psychology professor Neil Jacobson, who found that people at risk for relapsing reported lower levels of satisfaction or pleasure from their activities than did people who remained well. The study also indicated that a patient's level of negative or dysfunctional thinking at the end of treatment was not predictive of relapse.

"Depression is a recurrent disease for a lot of people just like cancer," said Gollan, professor assistant, "People who receive cognitive behavioral psychotherapy for depression tend to feel less depressed when they complete it. However, other factors in their lives beyond their mood need to be identified if we are to help them stay well. We need to consider who people are and how they interact with others to understand how patients remain nondepressed."

Researchers are anxious to identify risk factors for recurrent depression because relapse rates among patients who respond to treatment are alarmingly high. Studies have shown that between 50 percent and 80 percent of patients successfully treated with cognitive behavioral therapy suffer a relapse, often within two years of remission. Cognitive behavioral therapy is the standard treatment for depression, often in conjunction with anti-depressant medication.

Depression is the most common mental health problem in the United States, affecting an estimated 17 million people. Individuals with clinical or major depression, the most serious form of the disorder, often can't function, perform at work, need to be hospitalized and may attempt suicide.

In the new study, Gollan and Jacobson followed 78 patients who had recovered from major depression for two years to monitor changes. The patients all received 20 sessions of cognitive behavioral therapy for their depression and were considered symptom-free for at least two months before being accepted into the study. The researchers utilized a variety of interview questionnaires and self-report forms to measure depression, dysfunctional attitudes and pleasant activities at the beginning and end of treatment and every six months during the two-year follow-up. Personality styles were measured before and after treatment.

At the end of the study, 34 people, or 44 percent, had relapsed. Gollan said there seems to be different subsets of people who are at-risk for recurrent bouts of depression. One of those groups is made up of individuals who have a low dependency on other people. People with low dependency are usually independent people who may have little or no social support system, she said.

"Low dependency increases risk for relapse while moderate dependency encourages recovered patients to seek out social relationships that may function, over time, to reduce relapse risk," she said.

People who exhibited aggressive, hostile styles at the end of treatment also were more likely to relapse, "perhaps because they don't make good friends and turn off people," Gollan explained. "In their professional careers they have channeled aggression in productive, socially acceptable ways to their advantage and use people to their advantage. They also are pathologically independent and independence may be a risk factor if you have depression."

She added that clinicians working with depressed patients need to pay more attention to the enjoyment and satisfaction people get from activities rather than on the type and number of activities they engage in.

"We need to focus on how the activities feel," Gollan said. "We don't know why, but it is becoming clear that people are less at risk for relapse when they do things they enjoy rather than working on overcoming their negative thinking patterns. The treatment should be tailor-made to the depressed patient."

Depression

Other studies extend the personality factor influence on the potential development of the depressive disorder. It was found that people with the following types are in greater risk of developing depression than others:

1. People with high levels of anxiety.


2. Extremely shy people, when it is expressed in forms of “social avoidance” and “personal reserve”.


3. People with high levels of self-criticism and low self-esteem.


4. People with high interpersonal sensitivity.


5. Perfectionists.


6. People, who are extremely self-focused.

Researches show that people who fit the first four factors description are in substantially greater risk to depression, especially non-melancholic depression. Perfectionists are protected to certain degree from the depression, however, if the depressive disorder episodes occurs, they will be significantly longer than for non-perfectionists. Self-focused individuals are likely to be in greater risk for brief depressive episodes. While melancholic depression development was not found to be in any correlation with patients’ temperament or personality.

Another study reviewed the possible personality changes after depression is over, and concluded that personality traits of people who suffer a period of major depression remain unchanged.

"Our findings do not support the scar hypothesis," says Dr. M. Tracie Shea, associate professor of psychiatry and human behavior at Brown University, Providence, Rhode Island. "Essentially, our findings were that when people get better, they look fine. There aren't changes in the personality traits from prior to the onset of major depression."

In their report, Shea and her colleagues point to numerous studies in which people with a history of depression were characterized by having high levels of certain personality traits, including dependency on others, lack of social self-confidence, submissiveness, irritability, and social introversion.

"Our findings suggest these traits might represent a vulnerability to becoming depressed, rather than being an outcome of depression. Personality changes that might be present during an episode of major depression will resolve following full recovery -- they will not be lasting," she asserts.

Causes of Gender Differences in Depression

Moods: they are the modulating tone, the ambient pitch and temper of our lives. It would seem that our moods are a matter of mind, part of self awareness and self control; but if the intricate checks and balances of the brain are disturbed, moods, like every part of our being, can become diseased. Psychiatrists call these diseases of mood depression. And they are not rare. It has been estimated that fifteen percent of all Americans will suffer from at least one serious depressive episode, and approximately three million will commit suicide. Beyond the repeatedly confirmed finding that women diagnosed with mood disorders greatly outnumber men lies a widely varying set of hypotheses that attempt to explain the suspected causes, incidence, symptoms, and comorbidities from various perspectives.

Depression is a loss of an important life goal without anyone to blame. Such a loss affects our behavior, our moods, our subjective feelings, our skills, our attitudes and motivations, and our physical functioning and health. This psychiatric disorder features dysphoric mood or pervasive loss of interest or pleasure, which are associated with many somatic symptoms. The explanation of depression and its symptoms are found in the Diagnostic and Statistical Manual of Mental Disorders, 4^thed. (DSM-IV,1994) under Axis I, below the classification of mood disorders. The clinical syndrome of depression is assessed most often by clinical interview, based on the DSM-IV criteria. Depression can either be reactive, which is precipitated by some event, or endogenous meaning that it is biological in nature or that one is predisposed to being depressed. Some researchers say there is not a strong relationship between how happy you were as a child or an adolescent and how happy you are as an adult. Yet, keeping in mind that happiness and depression are independent, several childhood experiences have been related to adult depression: feeling guilty as a child and a strained relationship with the same-sexed parent, especially if a divorce is involved, a mother depressed enough that she needs help caring for the children, and dominant, over-protective parents using poor child-rearing practices, especially if fathers gave poor child care. Depressed adolescents usually involved symptoms of low self-esteem, anti-social behavior, over-involvement with peer group, and little with parents. Younger people (<40) are three times more likely to get depressed than older people (yet suicide goes up with age). Going through a divorce doubles the chance of getting depressed, especially for women.

In adulthood, some studies have found that depression is most likely to occur in unmarried women who are poor and have little education. They are disadvantaged and have little control over their lives so depression is not surprising. What is surprising is the overwhelming preponderance of depressed females compared to males. Women’s increased risk is approximately twice as high as men’s for depressive disorders. The risk that a woman will experience an affective episode associated with her female gender may be surpassed only by the high risk associated with a family history of affective disorders. Despite the clear association between gender and affective disorders, the causes are decidedly unclear.

A great deal of literature has been published on the causes of depression. Researchers have examined factors inherent to the individual, including: genetics, neurochemical, and neuropsychological traits. Attention has also been given to environmental factors, such as: extreme loss, socialization processes that foster helplessness, and severe trauma. In general, it seems most likely that a complex interaction between biologic vulnerability and environmental stress predisposes some people to depression. In an attempt to explain gender differences in depression, many researchers have focused on differing neurobiological tasks that must be carried out by the brain of a woman as compared to that of a man. Some researchers have argued that the neurochemical messenger systems in a woman’s brain are more finely tuned and therefore more likely to be chronically disrupted when normal development processes are interrupted or modified. Another neurobiological phenomenon that has been identified in depression has to do with the relative activity of the two hemispheres of the brain. The goal of this paper is to examine the noted causes of depression, focusing on those that are exclusive to gender differences. Many psychological and medical studies are included to provide evidence for the theories of gender differences in depression.

Gender-related Socialization

A ratio of two to one typically is found in both community survey populations and diagnosed and treated cases of depression. Weissman and Klerman reached the conclusions that the male-female difference in rates of depression is real and not merely an artifact of corresponding sex differences in rate of help-seeking behavior. To be thorough, a brief examination of social and environmental causes of depression is necessary.





Despite the emergence of clear gender differences in mood disorders only after adolescence and reports of slight male preponderance prepubertally, developmental perspectives have placed the origins of women's later vulnerability to mood disorders in childhood socialization. Traditionally, psychoanalytic theory emphasized the extent to which biological sex was a significant determinant of personality differences between men and women, but it had relatively less to say about sex differences in loss experiences hypothesized to predispose to depression. Notman, incorporating gender socialization experiences into a psychoanalytic model, has provided a further explanation of women’s vulnerability to depression. Others have hypothesized that early childhood sexual abuse is a relatively common occurrence in the early development of girls and constitutes a major risk for later mood disorders. Notman sights that an estimated 37 % of all females will experience sexual abuse by the age of 21. The significance and specificity of early abuse in accounting for women’s increased population rates of depression remain largely unassessed.

Developmental psychology uses learning principles in theories of socialization that account for gender differences to vulnerability to depression. Sex-stereotypical socialization practices by caregivers are hypothesized to lead to gender differences in self-concept and depressive vulnerability in boys and girls. For instance, Ruble and colleagues argued that the research base supports the hypothesis that parents have different expectations for girls and boys, including belief that girls will be more nurturing and concerned with social evaluations of others and that boys will be more independent. According to this theory, stereotypical gender socialization leads to a lower sense of mastery and control and a higher concern for external evaluation in girls than in boys. Their analysis of a large body of published literature on childhood self-evaluation for success and failure in physical, school-related, and social achievement domains found support for such differences. Differences are seen as forming a stable basis in the self-concept of depressive vulnerability.

Theories that stress early developmental socialization processes as the basis for depressive vulnerability generally are not integrated with most current adult psychopathology research. Relatively little is known about continuities and discontinuities between child and adult behavior. Nor is much known about the relationship between childhood socialization and abnormal adult development as defined by specific diagnostic categories in psychiatry. Developmental learning theories view socialization agents as predominantly influencing the child’s behavior and gender differences as the outcome of primarily unidirectional processes. Elsewhere, however, there is evidence of the inheritance of stable temperamental traits that influence caregiver/child interaction and also predispose to characteristic responses. In this regard, more research on the influence of sex steroids on the developing brain and on observed gender differences in child’s behavior is needed to provide a more complete and integrated picture of reciprocal influences on sex differences in caregiver/child interaction, child behavior, personality, and psychopathology.

Nolen-Hoeksema has developed a theory of women’s increased vulnerability to depression based on the identification of a self-focused coping style in response to depressed mood. In her research, she found relatively weak support for overall gender differences in personality characteristics of passivity and assertiveness, but she noted that differences occur in women’s response to depression; they focus on negative emotions while men use distracting responses to cope with depression. Their Aruminative style is seen as providing a general link to women’s tendency to have longer and more severe depressive episodes, specifically, rapid cycling and mixed-state bipolar forms. According to this theory, higher rates of depression in girls at adolescence are triggered by their greater exposure at this time to concerns with personal appearance, safety, and self-worth. Nolan-Hoeksema found that men are more likely to engage themselves in distracting activity, especially sports and athletic activities. Physical activity has been found to enhance the self concept of women who are depressed. These findings may be related to research that has shown exercise to produce a shift in cerebral activation such that the left frontal region becomes more active relative to the right.

Some researchers suggest that aerobic exercises are as effective as other forms of psychotherapy, and that the exercises have an antidepressant effect on patients with mild to moderate forms of depression. There is also evidence that women experience more life events than men. Karp and Frank report more life events six months before the onset of a depressive episode in women than men in a treated sample and raise the possibility that women experience higher rates of reactive depression than men. Such research may provide a link between epidemiologic risk findings and specific vulnerability factors in a large percentage of women. The generality of cognitive risk factor findings needs study in representative samples of depressed women but it has clearly testable gender-related hypothesis and treatment implications.

Genetics

The role of genetic factors in increased occurrences of depression has been shown to be the most significant. Linkage analysis studies aimed at the disclosure of the location of a gene on a particular chromosome used biological characteristics as genetic markers, linking their occurrence to patients with mental disorder. The hope was that knowledge of the genetic locus of such a physical characteristic would eventually lead to the identification of the genetic locus for the disorder under study. In fact, through DNA analysis, a gene on chromosome eleven of patients with major depression has been identified as a marker for depressive illness.





In linkage studies of the Old Order Amish of Lancaster County, Pennsylvania, Medical Anthropologist Janice A. Egeland PhD suggested that the tyrosine hydroxylase gene, which maps to chromosome 11, should be considered as a candidate gene for depressive illness because this enzyme catalyzes an important step in the dopamine synthesis pathway. This gene is merely a marker, and has not been shown to positively indicate depression in all of its inheritors.

Genetic imprinting with different phenotypes based on transmitting parent and clinical evidence of mitochondrial inheritance in mood disorders provide genetic models of sex effects on depression. An epidemiologic twin study that modeled sources of variance in rates of mood disorders in a sample of women found evidence for direct and indirect genetic factors as well as proximate (current life events) and distal (childhood loss) environmental influences. There may be gender differences in the inheritance of a number of predisposing susceptibility traits, with environmental influences modifying the specific clinical results differently for the two sexes.

Female Reproductive Cycle

Biological explanations for the female excess of mood disorders have tended to focus on intervals of well-defined hormonal changes such as those experienced at menarche, menstruation, postpartum, and menopause, The implicit or explicit assumptions of such research are that changes in levels of female reproductive hormones provide a general model for women's increased vulnerability to depression. In preadolescent samples, depression in girls is relatively rare: in fact, a slight male preponderance is typically found. Once girls enter puberty, rates of mood disorders begin to rise. Girls’ risk relative to boys increases dramatically. Problematic, however, is the identification of casual factors operating at this time. The few studies that have examined mood changes in relation to hormonal changes in adolescence do not generally indicate direct relationships between hormone levels and mood in girls. In a prospective study of adolescent depression female gender failed to explain increased risk for depressive episode once psychosocial and life-event variables were included in a predictive model. Angold and Worthman proposed a model of adolescent psychopathology in which girls’ increased susceptibility to mood disorders results from a complex interplay of biological, social, and developmental factors as they are interpreted by the adolescent in relationship to peers.

Human male and female bodies are distinctly different in numerous ways besides relative size and reproductive structure and function. Basic biological principles underlie these hormonal based sex differences. Hormonal influences on sex differentiation may be categorized as organizational or operational. Organizational sex differences occur during embryonic and fetal differentiation. They affect primary sex characteristics and brain development. Numerous sex-specific anatomic differences have been identified in the hypothalamus, the region of the brain that mediates gonadotropin production, including four discrete nuclei that vary in size and cell number between females and males. Sexual orientation and preference have also been linked to sex-specific anatomic differences in other hypothalamic nuclei. Numbers of callosal fibers and lateralization of specific cognitive functions like language and spatial reasoning relate to the prenatal influence of sex steroid hormones.

A significant proportion of women report moderate mood changes in relation to their menstrual cycle, with dysphoric mood, peaking in the late luteal phase of the cycle. In fact, approximately four percent of all women report changes of sufficient severity to meet DSM-IV criteria for late luteal phase dysphoric disorder. Some researchers have proposed that late luteal phase changes may serve as a model for women's general vulnerability to depression. Parry has proposed that chronological changes in the late luteal phase lead to alteration in circadian rhythms, and there is evidence from animal studies that gonadal steroids affect circadian rhythms and activity level. Parry also found some preliminary evidence of variable phase and amplitude of melatonin rhythms in women with late luteal phase disorder, but direct evidence of cycling variability in melatonin in normal women over the menstrual cycle is lacking. The hormonal triggers for ovulation are the pituitary hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH). But the more psychoactive hormones seem to be estrogen and progesterone. Estrogen peaks before the woman ovulates, and there is a smaller peak afterward. Progesterone peaks after ovulation, but before menses. These are big changes. Some women are very vulnerable to the emotional effects of hormonal changes, increasing vulnerability to depression. Leibenluft examined the menstrual cycle variability in a number of biological measures commonly assessed in psychiatric research on depression. Findings indicated the potential for significant confounding in biological research that fails to take menstrual status into account, depending on the specific measure. For example, there is little evidence of significant menstrual cycle variability in such traditionally prominent biological assessments as cortisol, but there may be considerable variability in others such as serotonin-binding parameters which is examined later in this paper.

Despite the seriousness of postpartum psychosis, it does not contribute greatly to increased prevalence of major mood disorders in women. While hospitalizations rise in the postpartum period, they account for only a small portion of all mood episodes in women. Hormonal changes that occur in the puerperium are dramatic and massive. During the course of a full-term pregnancy, the levels of hormones secreted by the corpus luteum and the placenta rise dramatically. For example, from eight to thirty-eight weeks, progesterone rises up to seven times, estradiol up to 130 times, and prolactin up to nineteen times. A major reason why these hormone levels are so high is that the placenta is an endocrine organ that produces hormones, many of which are psychoactive. When the baby and placenta are delivered, estrogen and progesterone drop dramatically. Some people are more vulnerable to hormonal changes, and thus are more vulnerable to depressed or sometimes hypomanic. The people who are most vulnerable are the ones who have a history of affective illness either independent or related to reproductive events.

Despite earlier clinical beliefs that menopause was associated with increased depression, the preponderance of evidence now indicates that the climactic stage in a female’s reproductive cycle is not associated with increased risk for affective episodes. Incident or recurrent rates of mood disorders in fact decline in women after menopause and rise in men in later years, so that gender difference in mood disorders narrow with age. Such trends are more consistent with psychiatric models that link depression to psychosocial vulnerability factors than they are with simple biological models linking estrogen deprivation to depression. Reports of diminished anxiety and depressive symptoms in women receiving estrogen-replacement therapy after menopause do offer validity to the linkage between the risk of depression in women, estrogens, and female biology. Menopausal women treated with hormone replacement levels of estrogen or estrogen/androgen combination experienced more positive moods. Estrogen treatment was also associated with better performance on verbal memory tasks, while the women receiving androgens alone or in combination with estrogens had higher levels of sexual desire and arousal. Nonetheless, estrogen has generally not been shown to be antidepressant for women during the menopausal transition. The evidence for the antidepressant role of estrogens in clinical mood disorders is ambiguous. There is some indication of their effectiveness in alleviating the mood and somatic symptoms of menopause.

Young indicated that postmenopausal women with recurrent depression have higher cortisol levels than premenopausal depressed women. She hypothesized that estrogens buffer depressed women premenopausally against cognitive or affective changes resulting from hippocampal neuronal loss. With the loss of such protection at menopause, special clinical and treatment issues may arise. Young also reported evidence of gender differences in normal samples of older men and women on biological parameters such as MHPG which may indicate dysregulation of the norepinephrine system. She found lower levels of serotonin and cortisol in women than in men.

Emotional factors have been shown to influence the pituitary-ovarian axis at the level of the hypothalamus. Relatively little work has been focused on the interacting effects of the ovarian hormones on the hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axes or neurotransmitter systems in relation to depression. Young hypothesized that estrogens buffer the HPA axis in premenopausal women, but that depressed postmenopausal women fail to suppress cortisol production, leading to mean cortisol concentrations higher than those found in postmenopausal women. The significance of this finding is somewhat tempered, however, since the depressed men in the sample did not exhibit significant evidence of HPA axis activation.

Neurotransmitter Model

The difference in the rates of depression in women versus men are similar using the serotonin model. Lepage and Steiner hypothesized that serotonergic insufficiency causes depression more in women and violence more in men. Impulsive eating and mood disorders are also suspected results of an insufficiency. Men with depression are more likely than women to make lethal suicide attempts; and a link between suicide and serotonin deficiency has been established. In a healthy male brain, serotonin is synthesized at a much higher rate than in a female brain. When deprived of tryptophan, a precursor to serotonin, serotonin synthesis drops four times more in women than in men. ALower brain serotonin levels or function have been implicated in various types of psychopathology, including depression, suicide, aggression, anxiety, and bulimia, reported Dr. Diksic. He hypothesized that the female brain has a harder time adjusting to the newer levels of tryptophan. If men and women have similar stores of brain serotonin, then a lower rate of synthesis in women may be insufficient in maintaining adequate stores during stressful moments. Tryptophan depletion can also reverse the effects of selective serotonin reuptake inhibitors (SSRI) in depression. During stressful situations, increased levels of the neurotransmitter may be utilized. This might explain why emotional insults may affect women more than men.

As we continue to learn more about serotonin and other neurotransmitters involved in depression, it is apparent how deficiencies in neurotransmitter precursor molecules such as folate might contribute to psychopathologic states. Under experimental conditions, clinical depression can arise or worsen as a result of lowering the CNS availability of building blocks for serotonin and possibly other neurotransmitters. Yet it remains unknown to what extent deficiencies of neurotransmitter precursors such as folic acid or tryptophan are responsible for depression that arises under non-experimental conditions. Albert and Fava site several studies suggesting that RBC folic acid concentrations are abnormally low in up to thirty-eight percent of depressed patients. A negative correlation has been reported between serum folate and duration of a current episode of depression in a sample of 44 depressed patients whose folate levels fell within the normal range. These findings seem to indicate that folate deficiency is associated with the emergence and severity of depressive illness. Lower folate concentrations may be linked to greater persistence of depressive symptoms. In response to antidepressant treatment, the individuals who had low serum folate levels prior to receiving treatment were less likely to respond to eight weeks of treatment with SSRI’s than were patients with normal folate levels.

The association between low folate levels and depression has suggested a potential role for folate in the treatment of depressive disorders. Psychiatric surveys report that patients treated with folic acid spent less time in the hospital and exhibited mood improvement and better social functioning than those with low folate levels who did not receive supplemental folate. Although the relationship between low folate levels and depression is well supported, as is the importance of correcting folate deficiency in the treatment of depression, the potential neuropsychiatric morbidity associated with increased folate levels among depressed patients remains unclear. The evaluation of folate level, however, and the supplementation with folate is still considered valuable in effective antidepressant treatment.

Conclusions

If we return to the fact that the female gender is nearly equivalent to family history in accounting for risk for mood disorders, certain conclusions are inevitable. One is that future research on mood disorders must explicitly incorporate study of gender in relation to genetic contributions, environmental and psychological factors, and biological factors in depression. Of these approaches, muck work has been done in the area of genetics, with an uncertain yield and very little information to address women’s differential vulnerability. The biological factors remain the weakest in terms of what research can tell us about gender and depression. Many studies have provided evidence to support various hypotheses of why the gender gap in depression is so large. Based on models of differences in socialization, genetics, hormonal variations throughout a woman’s reproductive cycle, and neurotransmitter deficits, researchers attempt to explain the enigma of gender differences in depression. Depressed patients of the future are likely to be referred to a radiologist to determine his or her structural and functional brain characteristics, including the localization of brain activity, the status of the neuroreceptors, neuronal cell structure, and neurotransmitter distribution. Genetic testing of the patient and his or her close family will also play a key role in diagnosis and treatment, whether pharmacological or psychotherapeutic.

Author: Jesup C. Szatkowski

Source: http://journalofscience.wlu.edu/archive/winter1999/articles/psych/depression.htm

Genetic Causes of Depression

It has long been known that depressive illnesses can run in families, but until fairly recently it was not fully known whether people inherited a susceptibility to these illnesses or if something else such as the environment was the true culprit. Those who research depression have been able to determine that to some extent depressive illnesses can be inherited. What appears to be inherited is a vulnerability to depression. This means that if we have close relatives who have clinical depression, we may inherit a tendency to develop the illness. It does not mean that we are destined to become depressed.

Genes that we inherit from our parents determine many things about us such as our gender and the color of our eyes and hair. Our genes also determine which illnesses we may be vulnerable to at some point in our lives. Every cell in the human body contains somewhere between 50,000 and 100,000 genes. They are all made up of something called deoxyribonucleic acid, or DNA. Genes are located on chromosomes within the nucleus of each cell. All of the cells in the body, except sex cells, contain 46 chromosomes, and genes are typically located in a specific place on a particular chromosome. Except for identical twins, no two people in the world have the exact same genetic makeup.

Research on the heredity of depression within families shows that some individuals are more likely to develop the illness than others. If you have a parent or sibling that has had major depression, you may be 1.5 to 3 times more likely to develop the condition than those who do not have a close relative with the condition. You would also have a higher chance of developing bipolar disorder. Because close relatives of those with clinical depression have such a vulnerability to developing the condition themselves strongly suggests that it can be an inherited illness.

Bipolar disorder has a strong genetic influence. Of those with bipolar disorder, approximately 50% of them have a parent with a history of clinical depression. When a mother or father has bipolar disorder, their child will have a 25% chance of developing some type of clinical depression. If both parents have bipolar disorder, the chance of their child also developing bipolar disorder is between 50% and 75%. Brothers and sisters of those with bipolar disorder may be 8 to 18 times more likely to develop bipolar disorder, and 2 to 10 times more likely to develop major depressive disorder than others with no such siblings.

Twin Studies

Much of what we know about the genetic influence of clinical depression is based upon research that has been done with identical twins. Identical twins are very helpful to researchers since they both have the exact same genetic code. It has been found that when one identical twin becomes depressed the other will also develop clinical depression approximately 76% of the time. When identical twins are raised apart from each other, they will both become depressed about 67% of the time. Because both twins become depressed at such a high rate, the implication is that there is a strong genetic influence. If it happened that when one twin becomes clinically depressed the other always develops depression, then clinical depression would likely be entirely genetic.





However because the rate of both identical twins developing depression is not closer to 100% this tells us that there are other things that influence a person's vulnerability to depression. These may include environmental factors such as childhood experiences, current stressors, traumatic events, exposure to substances, medical illnesses, etc.

Research has also been done with fraternal twins. Unlike identical twins who have the same genetic code, these siblings share only about 50% of their genetic makeup and do not necessarily look alike. Studies have shown that when one fraternal twin becomes depressed, the other also develops depression about 19% of the time. This is still a higher rate of depression when compared to overall rates for the general public, again pointing towards a genetic influence in the development of clinical depression.

A Gene for Depression?

Research on the genetic causes of clinical depression has attempted to identify one or more specific genes that may lead to the development of a depressive illness. Although there have been a number of studies that appear to name a particular gene as the culprit there has been little consistency among their results. However, the outcome of some research has suggested that there may be specific genes that cause clinical depression to develop within certain families and not in others.

At this time there is much that we do not know about how genes may predispose a person to a depressive illness. Research has yet to identify a clear link between a specific gene and a vulnerability to depression in everyone. Rather than the possibility of only a single gene being responsible for the development of clinical depression, it appears to be more likely that a number of genes acting together may cause a person to become vulnerable to depression.

Just because a person inherits a gene that predisposes him or her to a depressive illness, it does not mean that he or she is destined to develop major depression or bipolar disorder. It is believed that a genetic influence is only partially responsible for causing depression. Other factors may also play a role.

Testing for Genetic Disposition to Depression

The team, based at the Neuroscience and Psychiatry Unit (NPU), in the Faculty of Medical and Human Sciences, has set up a website (www.newmood.co.uk) where would-be volunteers can see how prone they may be to depression by identifying the emotions on people's faces and taking a gambling test.

The team aims to recruit more than 1000 UK volunteers for further tests as part of the five-year, EU-funded project called NewMood - New Molecules in Mood Disorders. They have already discovered how anti-depressants such as Prozac can affect how the brain reacts to fearful faces and which parts of the brain react to fear.

Professor Bill Deakin explains: "Anxiety is a contagious emotion. When you see other people who are anxious, as a primate you feel anxious as well. Our brains are wired to see anxiety - it makes sure we are safe. This is a fascinating test and, during further testing, we will be able to see which parts of the brain light up, or work harder, when you see a fearful face. Depressed people are more likely to see sadness or fear in a neutral face.

"The gambling test, where volunteers choose from pairs of spinners to 'win' money, will show us which parts of the brain light up when you are working for a reward. Depressed people are less affected by reward and more likely to give up easily as the test goes on."

Volunteers for this research study will be asked to fill in a confidential questionnaire and provide a mouth swab for genetic analysis. The team will then compare the DNA with the questionnaire group data.

In the other EU NewMood centres, rats and mice are also being tested for their predisposition to depression using similar reward and anxiety measures. When offered sweet-tasting drinks, depressed animals show no preference, much as humans lose pleasure in eating and often lose weight when they are depressed. And when given the opportunity to explore a new location depressed animals are more wary and take longer to emerge from dark corners, much as depressed humans avoid social situations.

"All humans have the same genes and they are very similar to those in all mammals - we turn out differently from each other because we inherit different versions of the same genes which can vary in their activity" Professor Deakin says. "We can see what genetic traits towards depression these animals have, then compare them with the same genes in the human DNA.

"Depression is a common trait like height or body build and, just like those, we suspect there are lots of genes involved. By measuring the important possible factors that can lead to a tendency to depression across a large number of individual people, we hope to find which ones act together to cause depression. Ultimately, this will help us to develop new ways of preventing and treating this illness."

Recent Studies – Genetic Link Discovery (Chromosome 15)

Researchers announce progress has been made on discovering why some people appear to be genetically predisposed to developing severe depression. A region on one chromosome appears to offer significant promise.

The research is lead by Douglas Levinson, MD, professor of psychiatry and behavioral sciences at the Stanford University School of Medicine.

“This finding has a very good chance of leading to a discovery of a gene that could yield important information about why some people develop depression,” said Levinson.

If problematic genetic variations could be identified, it would open the door to a whole new world of investigation, and eventually, treatment possibilities.

The team’s results are reported in two papers that will be published in the February issue of the American Journal of Psychiatry.

Levinson’s group, comprising researchers from six universities, achieved this breakthrough by studying 650 families in which at least two members suffered from repeated bouts of severe depression that began in childhood or early adult life.

The first of the studies was a genome-wide scan that looked for evidence of genetic “linkage” within families between depression and DNA markers on the various chromosomes. The linkage study identified regions worthy of more intensive examination.

The second study was a more detailed look at the most suspicious of these regions, located on chromosome 15. Levinson said the team studied six DNA markers in this region in the first study, and an additional 88 in the second.

“We found highly significant evidence for linkage to depression in this particular part of chromosome 15,” he said. “This is one of the strongest genetic linkage findings for depression so far.”

“It’s an important paper,” said Peter McGuffin, MD, dean of the Institute of Psychiatry at King’s College in London, who was not involved in the study. McGuffin wrote a commentary on the research that appears in the same issue. “This is one of the first big linkage studies on the genetics of depression.”

Researchers learned that depression is influenced by genetics by studying patterns of depression in twins and families. No single gene is thought responsible for determining the risk for developing depression.

Instead, multiple genes are probably interacting to create what amounts to a genetic baseline level of risk. On top of that baseline, environmental factors are likely mixed in as well, things such as non-genetic physiological problems or psychological traumas.

Some 10 to 15 percent of people suffer from severe depression at some point in their lives, and 3 to 5 percent have it more than once. Women are twice as likely to develop depression as men, although the reason is not yet known.

“We don’t think depression is entirely genetic, by any means, but there are important genetic factors,” said Levinson.

“If we can succeed in finding one or more genes in which there are specific DNA sequence variations that affect one’s risk of depression, then we would be able to understand what type of gene is it, what it does in the brain and by what mechanism it could make one more or less predisposed to depression.”

Knowing more about which genes are the major factors causing a predisposition for depression would also help researchers sort out the environmental factors that contribute to depression, Levinson said.

And knowing more about either genetic or environmental factors could help in developing more effective therapies to treat depression. “The treatments we have now are lifesavers for some people, but there are others who have only a partial response or no response at all,” he said.

“Understanding the biology would help the search for better treatments.”

Recent Studies – Genetic Link Discovery (Chromosome 12)

 A mutant gene that starves the brain of serotonin, a mood-regulating chemical messenger, has been discovered and found to be 10 times more prevalent in depressed patients than in control subjects, report researchers funded by the National Institutes of Health’s National Institute of Mental Health (NIMH) and National Heart Lung and Blood Institute (NHLBI). Patients with the mutation failed to respond well to the most commonly prescribed class of antidepressant medications, which work via serotonin, suggesting that the mutation may underlie a treatment-resistant subtype of the illness.

The mutant gene codes for the brain enzyme, tryptophan hydroxylase-2, that makes serotonin, and results in 80 percent less of the neurotransmitter. It was carried by nine of 87 depressed patients, three of 219 healthy controls and none of 60 bipolar disorder patients. Drs. Marc Caron, Xiaodong Zhang and colleagues at Duke Unversity announced their findings in the January 2005 Neuron, published online in mid-December.

“If confirmed, this discovery could lead to a genetic test for vulnerability to depression and a way to predict which patients might respond best to serotonin-selective antidepressants,” noted NIMH Director Thomas Insel, M.D.

The Duke researchers had previously reported in the July 9, 2004 Science that some mice have a tiny, one-letter variation in the sequence of their tryptophan hydroxylase gene (Tph2) that results in 50-70 percent less serotonin. This suggested that such a variant gene might also exist in humans and might be involved in mood and anxiety disorders, which often respond to serotonin selective reuptake inhibitors (SSRIs) — antidepressants that block the re-absorption of serotonin, enhancing its availability to neurons.

In the current study, a similar variant culled from human subjects produced 80 percent less serotonin in cell cultures than the common version of the enzyme. More than 10 percent of the 87 patients with unipolar major depression carried the mutation, compared to only one percent of the 219 controls. Among the nine SSRI-resistant patient carriers, seven had a family history of mental illness or substance abuse, six had been suicidal and four had generalized anxiety.

Although they fell short of meeting criteria for major depression, the three control group carriers also had family histories of psychiatric problems and experienced mild depression and anxiety symptoms. This points up the complexity of these disorders, say the researchers. For example, major depression is thought to be 40-70 percent heritable, but likely involves an interaction of several genes with environmental events. Previous studies have linked depression with the same region of chromosome 12 where the tryptophan hydroxylase-2 gene is located. Whether the absence of the mutation among 60 patients with bipolar disorder proves to be evidence of a different underlying biology remains to be investigated in future studies.

Sources and Additional Information:

http://www.allaboutdepression.com/cau_03.html

http://psychcentral.com/lib/2006/the-causes-of-depression/

http://www.news-medical.net/news/2005/08/30/12813.aspx

http://psychcentral.com/news/2007/02/02/progress-on-depressions-genetic-link

Social Causes of Depression

Depression is one of the most prevalent psychological disorders. Depression can be caused by several factors, including interpersonal relationships. Interpersonal relationships are the relationship between individuals and the reactions and emotions of each individual expressed directly and discreetly to each other. Common interpersonal relationships include (a) within the family, such as between the parents and between parents and children; (b) the social environment where differences in ethnicity and social class come into play; and (c) interactions between genders across age groups for both females and males.

Many people suffer from depression at one point in their life. It is inevitable, the feeling of hopelessness, sorrow, or being alone. These are all common emotions associated with depression. For a select few, depression can be hard to overcome, and this is where depression becomes a disorder that requires active treatment. Those 'selected few' account for over 100 million people worldwide and result in 75% of all psychiatric hospitalizations. Yet the question remains, why did these people become depressed? How did they become depressed? One of the answers that lead to the cause of depression would be a person's interpersonal relationship with their surroundings and the people around them. There are many interpersonal instances that can have the ability to lead to the onset of depression, such as the family environment, the socialization setting, and the discrimination against gender in certain cultures and instances.

Family

One could argue that out of all the interpersonal cases that can contribute on the onset of a depressive disorder, the ambiance of a family has the most weight and impact on a depressed individual. In the case of spouses, the well being of one spouse will have a notable impact on the other spouse and on the welfare of their marriage. For example, in 30% of all marriage problems, there is one spouse that can be described as clinically depressed. The reason why a spouse might have a unipolar mood disorder could be due to their relationship being "characterized by friction, hostility, and a lack of affection".

Martial distress can also be caused by the impact of having a child. When a woman is pregnant, she can experience a whole range of emotions due to the changing of interpersonal relationship with husband and the building of a new relationship with the unborn child. For example, the building of a new interpersonal relationship with the child can be very tasking and become a major stressful life event that can cause a mood disorder to develop.

Aside from the martial distresses of spouses, the impact of depressed parents can have an effect on their children as well. In a study on the relation between depressed adolescences and depressed mothers, they found that the depressed children of depressed mothers had more negative interpersonal behavior as compared with depressed children of non-depressed mothers. This is reinforced when a study shows that the parents of depressed children are less warm and caring and more hostile than parents of non-depressed children. Because of this negative interpersonal relation between kids and their parents, children can develop a negative view of their family. This negative view can lead to the feeling of lack of control and having a high risk of conflict, rejection, and low self-esteem.

Cummings (1995) stated that any changes in a family environment due to parental depression increase the risk of developing a mood disorder in children. The result of this can be found as early as preschoolers and infants, due to the insecure attachment they develop with their parents. The emotional distress of children can also have an effect on their parents, causing depression that in turn will also affect the children, theoretically creating a never-ending cycle unless they seek treatment. Sometimes It is not the depressed parents that lead to the onset of depression in their children, but rather it is the change in the family environment that stems from the parents' depression that causes the children to become depressed. Some studies suggest that martial troubles are a better predicator for the onset of depression than the depression of the parents or the children themselves.

Experiencing depression while as a child or an adolescent can also lead to reoccurring slips as an adult. Depressed persons often perform poorly in marriage and relationship with family members and they also might respond negatively to others, which have the ability to create stressful life events, which as a result might drive the person further into depression. Depressed people are dependant on other people and constantly seek reassurance in such a way that drives people away. Hammen and Brennan (2001) found that 13% of the sons and 23.6 % of the daughters who were depressed had depressed mothers as compared to 3.9% of the sons and 15.9% of the daughters who were depressed lacked a depressed mother.

Many people believe that children and parents suffer differently from depression, but not so. Depressed children can be like depressed parents, expressing sadness, anger, shame, and self-directed hostility. Just like adults, depressed children tend to blame themselves for bad events and accredit the environment for good events--they do not give themselves credit when due. This is why oftentimes, children will feel guilty if their parents get divorced and they believe that they were at fault but realistically, it was the parents' martial distress that was the cause of the divorce, not the children's depressive mood disorder.

Socialization

As in the family environment, socialization is key to maintaining healthy relationship and feeling well deserved and part of someone's life. Depression can have an adverse effect on the social capacity of depressed persons, affecting their social functioning and ability to react and deal with stressful situations. Gotlib and Hammen (1992) discussed the social functioning of people with depressive disorders and found that people with the symptoms of depression are found to test low in social activities, close relationships, quality close relationships, family actives, and network contact, yet they test high in family arguments.

One major part in the development of mood disorders in a social setting would be how well one could deal with stressful events. Normally, this is called coping strategies and it allows a person to manage their troubles and not be overwhelmed. Oftentimes, people can become depressed when unable to deal with "drama" from their friends-especially in children. Depressed children reported significantly higher level of hopelessness, lower general self-esteem, and lower coping skills than non-depressed children. Their ability to be unable to cope with stress can lead to fewer and less adaptive coping techniques.

Social settings can also include one-on-one interactions and the rejection that occurs. In a study performed by Joiner, Alfano, and Metalsky (1992), they tested whether a depressed individual would have an affect on other people in one-on-one interactions and they found that affected people did have such an influence on other people. This influence could be described as responding negatively to their constant searching of reassurance and rejecting them, which in turn will "confirm" the affected person's belief that he or she is unworthy as a person.

A depressed individual can impact their social settings by exhibiting a lack of self-esteem, becoming more sensitive to the opinions of others, and more importantly (and interestly), become less physically active. This means that they will not want to go out, that they do not want to exert themselves. A prime example of this would be an athletic in school that becomes depressed. He does not want to participate in athletic activities because he is depressed, but his coach forces him to. As a result, he performs poorly, and his teammates heckle him for his poor performance. As an affected person, the athletic becomes overly sensitive to his teammates' heckling and his self-esteem plummets and he drops out of sports and begins to withdraw and fight with everybody he knows.

The social class can also have a subtle effect on depression. Brown and Harris (1978) reported that the females with children in the working class were more prone to depression than females with children in the middle class. This can be attributed to the working class mother having to leave home to work, having to leave her child alone. This interpersonal relation can cause excessive worry and guilt that the women is not being a good mother as compared to the middle class mom, who can afford to stay at home and take care of the children/her family.

Okazaki (1997) found that Asian Americans are more depressed in a social and academic setting because they have to face more pressure than their white American peers due to the fact that they are part of a visible minority that has different culture values than others. This interpersonal relationship between the two "cultures" can be defined as competitive and stressful due to the fact that in America, white people "have it made" while as other ethnic groups have to work twice as hard to get their foot in the door. This extreme indicator of stress can lead to the dejection of many ethnic groups because they might have failed at succeeding in a competitive environment.

Gender

There are a lot of interpersonal relations when it comes to gender, such as the discrimination against gender in an academic setting. This is very prominent in females, where girls can face increased expectations to conform to the standards set forth by society, to pursue feminine type activities and occupations. It appears that parents tend to have "lower expectations" for girls when it comes to school. As a result of that lowered expectations, parents tend to not push their daughters toward a high-profile job, instead attempting to make their daughter conform to the stereotype of society, like become a teacher or a nurse. In fact, in 1986-1987, women only garnered 15% of the bachelor's degrees awarded in engineering as compared to 76% and 84% for education and nursing, respectively.

Breaking the social norm can also lead to depression; the more intelligent a girl is, the more likely she is to become depressed. This positive correlation could be attributed to the more intelligent girls being able to out-perform the boys yet get punished for doing so. Being depressed as a female adolescent can have consequences in the long run in terms of social functioning, career, and enjoyment of life. Theoretically, if one were to be depressed in high school, then their grades would suffer. If their grades were to suffer, then their chances of entering a good college would dwindle. If they cannot enter a top-notch college, then they might not be able to get the career they want, and with that they would not be able to enjoy their job and feel like they have missed out on life.

The different experiences of each gender can also be the cause of a mood disorder. The experience can vary by the age of the children, adolescences, or adults. For example, after the age of 15, females are twice as likely to become depressed as compared with men and in another study of 11-year olds, only 2.5% males met the criteria for major depression while only 0.5% females met the criteria, however in a study of 14-16 year olds, 13% of the females met the criteria while 3% of the boys did. This abrupt rise of depressive disorders in females during the mid-to-late adolescence years can be attributed to the more concerns a girl has as compared to boys. These concerns and worries can range from their achievements or lack of, body dissatisfaction, sexual abuse, and low self-esteem.

This is reinforced when another study found that between the ages of 15-18, the prevalence of depression in girls will increase to twice the prevalence of boys (20.69 to 9.58) but will taper off during 18-21 years of age for both genders (15.05 and 6.58).

Do not be mistaken that females are the only gender that that can become depressed; a good number of males can develop a unipolar mood disorder. In the average lifetime, 49% of all males will experience a depressive episode (as compared with 63% of all females). Males will become sad and dejected for different reasons, such as intimate relationships. When an intimate relationship ends, males are more likely to become depressed at the loss than females. This could be attributed to the male's primal desire to have a mate so he will be able to continue his family name.

Depression has been around for a long time, spanning over thousands of years, dating back to the time of Saul I, yet even though Depression is a disorder that is hard to understand. Even with all the studies conducted, there is still not much to regarding the causes of depression. There are so many ways one would be able to become depressed, but the most common and most prevalent way thus far would be the interpersonal relationships of a person and their family, social lives, and the relationship between their gender and the discrimination they suffer at the hands of others. Perhaps a better understanding of those relationships can open up new avenues where new options for treatment can be conceived and new ways of interacting to people to create a equality amongst people where they will not feel depressed.

Author: Gregory S. Beattie

Source: http://www.personalityresearch.org/papers/beattie.html