It appears that the man who created the theory of natural selection and inherited traits may have had a familial genetic predisposition for mental illness. The world of gene testing is exploding. Today, there are dozens of companies that can detect genetic predispositions to illness. As a result, new treatments are emerging which can alter gene expression. This is the world of genomics. All health practitioners need to have a working knowledge of this breakthrough. The mapping of the human genome has revealed a multitude of genes which are highly correlated with the presence of mental illnesses.
DNA is a series of molecules linked together in a microscopic spiral called a chromosome. Humans have 23 chromosomes, and every cell in our body has two versions of each of the 23 chromosomes — one from each parent. This combination is called a diploid genome. The human genome contains a total of 30, genes.
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Females have two X chromosomes, while males have one X and one Y chromosome. We inherit half of our genetic profile from each parent. Both males and females retain one of their mother's X chromosomes, but females retain their second X chromosome from their father. Since the father retains his X chromosome from his mother, human females have one X chromosome from their paternal grandmother and one X chromosome from their mother.
It is for this reason that many of us resemble our parents, not only in appearance, but in personality, demeanor, social skills, and coping skills. In addition, we also may inherit genes that can cause or increase the risk of medical disorders. The interplay between fraternal and maternal genes has consequences for mental illnesses as well.
It has long been established that most people with mental disorders have a genetic predisposition to their woes. We know this because mental disorders run in families. However, it is now evident that the predispositions to certain medical disorders are predictors of mental disorders in family members, and that family genetics contribute to mood, behavior, and mental well-being. These discoveries have revealed that a fundamental cause of many human maladies is how these two sets of genes interact. Ninety-nine percent of all human DNA is identical, but that one-percent difference is often the root cause of mental disorders.
The complete mapping the human genome has allowed researchers to scan DNA for genes that may cause, contribute to, or even prevent mental disorders. At the time of this writing, despite the explosion of genetic research, only a small number of these genes have been identified. But even though gene research in mental illness is still in its infancy, a person can still gather some information about their genetic risk of physical and mental illness simply by looking at his family tree.
Moreover, looking at the family history of certain maladies can predict other problems in family members. These familial problems can be said to be family fallout. It has long been known that mental problems run in families. What is not well known is that the children and relatives of people who have mental or medical illnesses are also prone to other illnesses.
The people you work with will tell you about their mental symptoms, but they will seldom disclose their physical maladies. Furthermore, without prompting, they will not discuss the medical problems of their family. Genetic penetrance is the likelihood that a certain gene will result in a specific disease.
In , researcher Roger Webb, at the University of Manchester in England, showed that the risk of fatal birth defects is higher in the children of parents who have been hospitalized for mood disorders. There is even more risk is associated with maternal schizophrenia. Moreover, children of mothers who had previously been admitted to a hospital for any type of psychiatric diagnosis had significantly higher risk of death from birth through early adulthood.
The risk of infant death among children with two mentally ill parents was significantly higher than that associated with having only one affected parent. Families with fathers or mothers who have a history of psychiatric hospitalizations also double the risk of sudden infant death syndrome SIDS compared with the general population.
If both parents were hospitalized, the risk of SIDS was increased by almost seven-fold. There is evidence that SIDS may be in part caused by abnormalities of serotonin in the brainstem. There is strong evidence of a genetic transmission of recurrent major depression. In fact, having a family member with major depression increases a person's risk eight-fold. Heritability is considered to be about percent. A history of depression in a parent is the strongest risk factor for depression in a child.
Researcher Myrna Weissman at New York State Psychiatric Institute found high rates of psychiatric disorders — particularly anxiety disorders — in the grandchildren of families with two generations of major depression. Fifty-nine percent of these grandchildren, with a mean age of twelve years, were suffering from a psychiatric disorder. A twin study found a 46 percent concordance of depression in identical twins and 20 percent in fraternal twins.
Interestingly, in this study, shared family environment had no impact on depression. This high level of mortality in families with depression may be linked to heart disease. A significant number of studies show a relationship between depression and cardiovascular problems. Studies report the prevalence of major depression in cardiac patients as between 17 percent and 27 percent in hospitalized patients. Serotonin may play a part in depression, but is also contributes to cardiovascular disorders.
Serotonin plays a role in platelet aggregation, and platelet serotonin levels correlate negatively with severity of depression. In a clinical study University of Pittsburgh, blood platelet serotonin levels were 39 percent lower in patients who had made a suicide attempt.
Recently, scientists have discovered a gene that contributes to depression, called the serotonin transporter gene. Two forms of the gene have been discovered, described as the short and long gene form.
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Some studies suggest that inheriting the short form of the gene doubles the risk of depression, but recent studies found no correlation. Those who carry two copies of the short version of the gene are also more prone to alcohol abuse. It has long been known that bipolar disorders also have a high genetic predisposition. The genetic penetrance of bipolar disorder is about 70 percent.
What is not as well known is that bipolar disorder has also been genetically linked to cystic kidney disease , a disorder in which cysts growing in the center of each kidney cause them to malfunction. In one study, out of seven members with medullary cystic kidney disease, five had bipolar I disorder, one had unipolar depression, and one had a hyperthymic phenotype. Two known genetic loci of cystic kidney disease are found in regions of chromosomes 1 and 16 — areas that have been previously linked to bipolar disorder and schizophrenia.
The children of parents diagnosed with bipolar disorder are more likely to exhibit disruptive behavior disorders, separation anxiety disorder, generalized anxiety disorder, social phobias, or depression. These problems usually emerge in early or middle childhood. Hagop Souren Akiskal, the director of the International Mood Center in San Diego, has found temperament dysregulation as an important familial genetic factor in the vulnerability for manic- depressive episodes.
He believes that a trait known as hyperthymic temperament is a state often found in families with full-blown bipolar disorder. This temperament is characterized by upbeat, highly energetic, and overconfidence. People with these traits do not seek help for mental problems and, therefore, are rarely seen by mental health professionals. They often, however, will seek help for marital problems, job instability, or problems with impulse control.
According to the National Institute of Mental Health, more than two million Americans are affected by some form of schizophrenia. This array of illnesses can severely impair a person's ability to manage emotions, interact with others, and think clearly. Symptoms include hallucinations, delusions, disordered thinking, and social withdrawal. Although there are several treatments available today, the majority of people suffering from these maladies will suffer chronically or episodically throughout their lives. Even with treatment, one of every ten people with schizophrenia eventually commits suicide.
There seem to be genetic and epigenetic contributors to schizophrenia. The heritability of schizophrenia is about 70 percent. Several studies suggest that there is an increased risk of schizophrenia in people with older fathers. The risk of schizophrenia is increased for both males and female with fathers 55 years or older.
The seasonal peak in schizophrenic births increases the further north a person resides. There is evidence that lack of UV light and low vitamin D may contribute to schizophrenia. In , scientists at Columbia University asserted that up to one fifth of all schizophrenia cases are caused by prenatal infections. Interestingly, Cox 2 inhibitors, which are powerful anti-inflammatory drugs, are an effective treatment for schizophrenia.
Patrick McCann, at the University of Oklahoma, has developed a diagnostic breath test that uses lasers to measure the amount of carbon disulphide in breath of children. Carbon disulphide is known to be at higher levels of in the breath of people with schizophrenia — even in infants. This allows him to make diagnoses decades before symptoms occur. Family members of schizophrenics but without the disorders are at higher risk for other problems.
For example, idiosyncratic use of language a trait similar to the thought disorder observed in schizophrenia occurs in 37 percent of clinically unaffected first-degree relatives of individuals with schizophrenia, a rate almost six times higher than the presence of schizophrenia in the same families. Other researchers have noted that family members of a person diagnosed with schizophrenia have a higher incidence of seizure disorders. When the rates for thought disorder, schizophrenia, and related clinical conditions are combined, the proportion of potential gene-carrying relatives is close to 50 percent, consistent with a dominant gene, and much higher than the 6.
Family members also have difficulty following a slow-moving target with one's eyes, syntax errors, or idiosyncratic use of language. Physically, they often have subtle anomalies in the midline of the face, and have difficulty filtering out noises and other irrelevant stimuli, a condition known as sensory gating. Although methamphetamine does not cause schizophrenia, the greater familial incidence for schizophrenia, the more likely an amphetamine user in that family would develop psychosis and the longer that psychosis is likely to last.
Prenatal influenza virus infection has been associated with an increased risk of schizophrenia. Mental symptoms of Wolfram Syndrome. Physical symptoms of Wolfram Syndrome. Wolfram Syndrome was first described in as a familial disorder usually presenting with Type 1 juvenile-onset diabetes and vision loss. The syndrome is an autosomal recessive disorder meaning that it only occurs in individuals who have received one copy of the gene from each parent.
It is caused by a gene on the short arm of chromosome 4. The frequency of carrying the recessive genetic trait in the US population is approximately one percent. The syndrome is also characterized by the presence of neurogenic bladder frequent urination , hearing deficits, and other neurological problems.
A majority of individuals who have two mutant Wolfram Syndrome genes have these distinctive symptoms. Despite the array of symptoms, most people will have the disorder for several years before an accurate diagnosis is made. Wolfram Syndrome may also present with psychological symptoms, such as depression, violent and assaultive behavior, chronic anxiety, panic attacks, and hallucinations. Many attempt suicide.
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Most people with the disorder die prematurely with progressive, widespread atrophic changes throughout the brain. Unfortunately, 60 percent of those with the syndrome die by age While it takes two aberrant genes to manifest the full-blown syndrome, those who carry a single mutation, a condition called Wolfram Syndrome Heterozygotes , have no distinguishing physical characteristics but constitute approximately one percent of the population.
Family members who carry a single mutation in the Wolfram Syndrome gene are 26 times more likely to require hospitalization for depression and suicide attempts than people who do not have the gene. Researchers Ronnie and Michael Swift at New York Medical College estimate that even though only one percent of the general population carries the gene — about 25 percent of the patients hospitalized for psychiatric difficulties may be carrying the gene.
Mental symptoms of hemochromatosis. Physical symptoms of hemochromatosis. Hemochromatosis is a genetic disorder that causes iron accumulation in the body. People of Western European descent — with ancestors from Ireland, Wales, Scotland, or Great Britain — have a percent probability of carrying a gene for hemochromatosis.
According to the Centers for Disease Control, Type 1 hemochromatosis is the most common genetic disease in the United States. Like Wolfram Syndrome, hereditary hemochromatosis is an autosomal recessive condition. The person must inherit two mutated genes called HFE one from each parent. This type of the disorder is deemed responsible for sexual dysfunction in percent of men.
They exhibit loss of libido and potency, and have high iron and low plasma levels of testosterone. However, in some cases, inheritance of only one mutated gene may eventually lead to significant iron accumulation. Although the majority of these people will never know that they carry the gene, some will begin to feel aches and pains and changes in energy and mood. This condition is also thought to contribute to what is called treatment resistant mental disorders. A study by researchers David Feifel and Corinna Young Casey at the University of California in San Diego showed that 80 percent of people with treatment resistant bipolar disorder carried one gene and lacked a family history for this disorder.
They estimated that one percent of psychiatric patients were likely candidates for iron overload. Common symptoms of hemochromatosis are fatigue, aches and pains, disorientation, confusion, and memory problems. In these cases, the diagnosis is often missed for several years, as symptoms are mistaken for depression or dementia. Signs of the illness usually appear between ages 40 to 60, but some people show symptoms as early as Patients suffering from idiopathic hemochromatosis exhibit low plasma levels of testosterone with loss of libido and potency.
It was Eugene Weinberg that was the first to look at the effect of iron in our bodies. He found that the presence of high iron could cause chronic inflammation. Hemochromatosis causes inflammation in the liver, joints, heart, lungs, pancreas, and the brain, especially in the basal ganglia. This part of the brain is rich in dopamine, and in these cases, iron may cause damage to the dopamine system contributing to many neurological disorders, including Parkinson's and Alzheimer's disease.
The gene is thought to accelerate the onset of Alzheimer's disease by five years. In the past, people with hemochromatosis usually did not survive past their forties or fifties. But as a result of better recognition and treatment, most people with the disorder now have normal life spans. This has resulted in another problem, iron overload in the central nervous system. Bloodletting has been a treatment for this illness for centuries and is still the treatment of choice. Another treatment is chelation therapy. We now know that lowering iron is not only useful for hemochromatosis, but may actually be beneficial to the immune system.
Infections need iron to survive. The human body contains many natural chelators. Mental symptoms of Wilson's disease. Wilson's Disease affects approximately 1 in 30, people worldwide, making it a rare disorder. However, it is estimated that at least half of the people with Wilson's Disease are never diagnosed, and therefore will suffer, and sometimes die, from the disease. Wilson's is a genetic disorder that causes the body to retain copper.
The liver of a person who has the disease cannot release copper into bile as it should. Over time, the copper reaches a toxic level and injures liver tissue. Eventually, this damage will result in high levels of copper in the bloodstream, which leads to damage in the kidneys, brain, and eyes. Untreated, high copper will eventually cause liver failure and brain damage. Wilson's Disease occurs equally in men and women. Although some cases of Wilson's Disease can occur due to spontaneous genetic mutation, most cases are transmitted from generation-to-generation.
The responsible gene is called ATP7B and is located on chromosome In order to inherit the disease, both parents must carry the gene. Siblings of Wilson's Disease patients have a one-in-four chance of having the disease. Since both of a siblings' parents are carriers, one-fourth of the siblings' children have the disease, one-half are carriers, and one-fourth are disease-free and carry no Wilson's Disease gene.
A child of a Wilson's Disease patient has a percent chance of getting one abnormal gene. The patient's spouse has a one-in-one-hundred chance of carrying the abnormal Wilson's Disease gene, and half the time, he or she will pass it on. For this reason, all siblings and children of Wilson's Disease patients should be tested for Wilson's Disease. Other relatives who have had symptoms or laboratory tests that indicate liver or neurological disease also should also be tested. Because Wilson's Disease is often mistaken for other maladies such as multiple sclerosis, Parkinson's disease, or psychiatric problems, medical specialists estimate that only about one thousand cases per year are ever diagnosed.
In the early stages of the disease, especially when psychological symptoms occur, the diagnosis is often missed. The delay between symptoms and diagnosis ranged from one to five years. Depression sometimes leading to suicidal ideation and suicide attempts is common. Deteriorating academic and work performance is present in almost all patients.
Interestingly, many Wilson's Disease patients exhibit increased sexual preoccupation and reduced sexual inhibition. It is also linked with pedophilia. A barrier to the diagnosis of Wilson's Disease is that most patients have no family history of it. Because both parents must carry the gene to manifest the disorder, people with only one abnormal gene usually have no symptoms, or may have mild, but medically insignificant, abnormalities of copper metabolism, and do not become ill. People with Wilson's Disease may not have any outward signs, symptoms, or evidence of illness.
However, people with mild or non-apparent Wilson's Disease will become seriously ill and eventually die if they are not treated. Diagnoses are usually made by blood and liver tests. Chelation therapy is commonly used as treatment. Doctors will also recommend avoiding foods high in copper such as liver, shellfish, mushrooms, nuts, chocolate, dried fruit, dried peas, beans and lentils, avocados, and bran.
Scientists believe the XXY condition is one of the most common chromosome abnormalities in humans. About one of every five hundred males has an extra X chromosome, but many have no symptoms. It is likely that about 60 percent of the cases are undiagnosed. Symptoms depend on how many XXY cells a man has, how much testosterone is in his body, and his age when the condition is diagnosed. Children with this condition will often exhibit attention deficit disorder.
The syndrome is normally diagnosed during puberty. At this age, those with Klinefelter's Syndrome often have less facial and body hair and may be less muscular than other boys. They are often shy and have trouble fitting in with peers. Mature men with this syndrome have several distinguishing characteristics, such as tall stature, long arms and legs, lanky build, feminized physique, little chest hair, female-patterned pubic hair, testicular atrophy, hypogonadism, osteoporosis, breast development, and low levels of testosterone.
The low testosterone accounts for the lack of development of male secondary sex characteristics. They may be infertile and are more likely to have certain health problems, such as autoimmune disorders, breast cancer, vein diseases, osteoporosis, and tooth decay. Behaviorally, they exhibit reduced aggression and lack of exploratory behavior. They also have trouble using language to express their thoughts and needs, but experience increased levels of emotional arousal.
Problems with reading, trouble processing what they hear, emotional instability, and anorexia nervosa may occur. The main treatment is for this syndrome is testosterone. It has long been known that certain families show tendencies for hyperthyroidism and hypothyroidism. What is not usually known is that members of such families are also prone to other conditions including insulin-dependent diabetes, pernicious anemia lack of vitamin B12 , premature gray hair, vitiligo white spots on the skin , arthritis, and allergic conditions, including asthma, hives, and hay fever.
There is also an increased tendency for members of these families to have various types of perceptual learning problems and dyslexia. Researcher Lawrence Wood suspects this relationship is missed because women in the family tend to get thyroid problems, while predominantly the men in the family have learning problems, but are seldom seen by family physicians. See more on thyroid later in this document. DNA is found in every cell of the body. Another type is found in a part of the cell called mitochondria.
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DNA in the mitochondria, therefore, identifies maternal risk factors of medical and mental illnesses. Mitochondria are specialized organelles found in every cell of your body, except red blood cells. There are approximately 1, mitochondria in each human cell. They are vital to the production of cellular energy. In fact mitochondria are responsible for creating more than 90 percent of the energy needed by the body to sustain health.
Inside the mitochondria, ingested sugar is broken down in the body by a process known as glycolosis , which changes glucose to a compound called adenosine triphosphate ATP , which is then converted in to pyruvate. The pyruvate next delivered to tiny mitochondria. When this system fails, less and less energy is generated within the cell. Cell malfunction, and even cell death, may follow.
Diseases of the mitochondria appear to cause the most damage to cells of the brain. Mitochondria damage contributes to developmental delay, mental retardation, autism, dementia, seizures, atypical cerebral palsy, atypical migraines, stroke and stroke-like events, and other psychiatric disturbances. In early , researchers Kato Tadafumi and Kato Nobumasa at the University in Tokyo proposed a mitochondrial dysfunction hypothesis for bipolar disorder.
Postmortem tissue samples extracted from the hippocampi of the brains of nine individuals with bipolar disorder showed significant mitochondrial depletion.
A search for mutant mitochondrial DNA in the tissue samples revealed two suspect genes. A Cleveland Clinic survey of 38 outpatients with mitochondrial diseases found 70 percent met the criteria for major mental illness, including 54 percent with lifetime depression, 17 percent with lifetime bipolar, 11 percent with lifetime panic, and 11 percent with current generalized anxiety. On average, the mitochondrial disease was diagnosed about four years after the onset of psychiatric symptoms, and 14 years after a physician was seen for diagnoses.
Genetic testing has helped significantly in identifying mitochondrial risk factors. Out of our 30, genes, only two percent of deoxyribonucleic acid DNA codes for proteins. These genes were considered to be the byproduct of millions of years of evolution — genes were still inherited but were no longer used. Recently, however, scientists have discovered that some of this junk DNA actually switches on RNA that interacts with other genes. The field of research of these phenomena is epigenetics. Epigenetics is the science of turning genes on- and-off with nutrients and other chemicals, resulting in changes of expression of those genes.
The process of suppressing and enhancing genes is called methylation, a chemical process that, among other things, aids in the transcription of DNA to RNA and is believed to defend the genome against parasitic genetic elements called transposons. Transposons are spans of DNA that — through a process called transposition — can actually move to different positions within the genome of a cell. Transposition was first observed by researcher Barbara McClintock; this discovery earned her a Nobel Prize in More fascinating is the finding that these mutations may be inherited by children.
Environmental toxins have been shown to alter the activity of genes through at least four generations after exposure. For example, women who smoke while pregnant double the risk of asthma in their grandchildren. For this reason, no two brains are alike, including those of identical twins. It is thought that about 40 percent of our genes can be modified epigenetically. Although identical twins share the same DNA, their epigenetic material can be different.
Moreover, the older the twins become, the more discrepancies will occur in their DNA. Fifty-year-old twins have four times as many differentially expressed genes than three-year-old twins. Even more interesting is the discovery that genes are regulated by maternal care. Thus far, at least nine hundred genes can be altered by maternal care. For example, the presence of a variation in the monoamine oxidase A gene MAO-A combined with maltreatment predicts antisocial behavior. In mid, researcher Moshe Szyf at McGill University reported that commonly-used pharmaceutical drugs can cause such persistent epigenetic changes.
Szyf and his co-author Antonei Csoka posit that drug-induced diseases, such as tardive dyskinesia and drug-induced lupus, are epigenetic in nature. More about Lupus below. They also propose that epigenetic changes from pharmaceuticals may be involved in heart disease, obesity, diabetes, infertility and sexual dysfunctions, as well as neurological and cognitive disorders. Smoking can cause changes in gene function. As stated earlier, there is compelling evidence that prenatal smoking increases the incidence and severity of ADHD.
The risk of a severe type of ADHD greatly increases in children whose mothers smoked during pregnancy and who also have variants of one or two genes associated with ADHD — one on chromosome 11 and the second on chromosome 5. Interestingly, even children of mothers who smoked during pregnancy who didn't fit all of the criteria for ADHD had more symptoms of the disorder. This was true if they had been exposed to cigarette use in utero or had genetic variations related to risk. The early human embryo consists of three cell layers: the mesoderm, endoderm, and ectoderm.
The mesoderm forms muscle and bone. The endoderm creates the cells lining the digestive and respiratory system. The ectoderm forms the skin, hair, fingernails, olfactory system, and neural cells, including the brain. This is intriguing, since people with hair, skin, nail, and olfactory problems seem to be more prone to mental disorders, which will be discussed later. The brain begins from a miniscule layer of tissue called the neural plate.
As the fetus continues to grow, there is neuronal migration up the plate to the head. The average human baby generates an astonishing 50, neurons per second during gestation. In the developed brain, there are two essential types of cells — neurons and glia. The word glia is derived from the Greek word for glue. Although we usually think of neuron problems when we look at mental disorders, 90 percent of brain cells are glial cells; only 10 percent are neurons. Unlike many neurons, glial cells are able to divide and reproduce rapidly.
Glial cells surround neurons and hold them in place, supply nutrients and oxygen to neurons, insulate one neuron from another, and remove dead neurons. University of California at Berkeley professor Marian Diamond has been one of the pioneers of the theory that an enriched environment increases brain function. Years ago, Dr. It had long been thought that glial cells were protectors of neurons. This suggests that that the environment in the early years sculpts the brain.
Astrocytes are a type of glial cell that surround the synapses between neurons. It appears that a dearth of these cells plays a part in mental illness. Postmortem studies on human brains of individuals with major depression or bipolar disorder have detected significantly lower than normal levels of glial cells. A reduction in the number of glial cells in the prefrontal cortex has been observed in people who are clinically depressed. There are alterations of glial cells in schizophrenia. The function of astrocytes is to supply neurons with energy, meaning a low astrocyte level would cause lower activity in the associated neurons.
Sodium valproate is a sodium salt of valproic acid used in the treatment of epilepsy, bipolar disorder, and a mood stabilizer. Valproic acid protects dopaminergic neurons in midbrain neuron and glia cultures by stimulating the release of neurotrophic factors from astrocytes. Researcher Serge Przedborski, the co-director of the Center for Motor Neuron Biology and Disease, has found that astrocytes with a mutated form of a gene, superoxide dismutase called SOD1 , kill neurons, which eventually is seen as amyotrophic lateral sclerosis. Research presented at the Second World Congress on the Fetal Origins of Adult Diseases suggests that osteoporosis may actually begin in the womb.
If a baby is undernourished, she will be small at birth, will be small at the first year, will often have low bone mass at 25, and will have a high probability of bone trauma at 70 and a high probability of hip fractures at Low bone mass is also linked to schizophrenia, depression, and other mental problems.
Scientists now believe that many disorders — including mental disorders — have their origins in the early stages of life. For example, low birth weight is correlated with depression after puberty. Low birth weight was not the only cause but increased the risk effects of other adversities, such as child abuse. The volume of the human brain increases more during the first year of life than at any other time; therefore, early physical health plays a part in brain development.
Researcher JWB Douglas found that children who had at least one admission to the hospital for more than a week's duration, or who had repeated hospital admissions before the age of five years, had significantly increased risk of behavior disturbance and poor reading in adolescence. The children were more troublesome in school and at home, and more likely to be delinquent in school. As adults, they were prone to show unstable job patterns than those who were not hospitalized in their first five years.
Although this type of historical data would be most helpful in making a diagnosis, it is rarely sought in an intake interview. Besides early illness, early nutrition also has lasting consequences. During the early years, nutrition is allocated in ways that give the child the best chance in early life, sometimes at the expense of later years. In the era of the Baby Boomers, formula was considered by many doctors as superior to breast milk. Most baby boomers were bottle fed babies. In one study, premature babies fed only standard-formula milk had noticeably lower IQs at school age than breast-fed infants, and they were particularly bad at mathematics.
A small area of their left parietal lobe was less active than expected. The developmental phenomenon called programming allows a fetus to adapt to sub-optimal conditions, such as malnutrition. In some cases, this can have an effect on brain development which could be the precursor to a mental disorder later in life. There are sensitive periods for growth; if not exposed to environment at the proper time, brain development is altered. For example, language is acquired in the first few years of life.
Neural Pruning is the deletion of cells. Over one-third of the neurons in the cerebral cortex are eliminated in the first three years. At six months, babies can differentiate human and non-human faces, such as monkey faces, but by nine months, they lose this ability to discriminate monkey faces. Since the monkey face discrimination is not needed, it is deleted. Some researchers believe that pruning is also responsible for dementia. The theory is that, late in life, the pruning system is turned on and cells begin to be deleted. Cortical migration and neuron proliferation are complete at five and twelve months of age, respectively, while myelination is only 50 percent complete at eighteen months after birth.
Seventy-five percent of human brain growth occurs during the first two years; the remaining 25 percent is not completed until adulthood. Brain size in the newborn is proportionately greater than in adults. The newborn brain weighs one-third of an adult brain, while the newborn weighs only four percent as much as the average adult. The blood-brain barrier, which restricts the penetration of toxins to the brain, is not fully developed in humans until about one year of age. It is not known when the barrier becomes fully functional. Connections in the visual system are not fully achieved until three or four years of age.
Brain development differs between boys and girls, with girls generally reaching peak gray matter thickness one to two years earlier than boys. Breastfeeding significantly decreases the risk of cognitive and behavioral problems. In full-term infants, increasing the duration of breastfeeding more than eight months is associated with consistent and statistically significant increases in IQ assessed at ages eight and nine reading comprehension, mathematical ability, and scholastic ability assessed at ages ten to thirteen.
While I am not suggesting that you measure the head of you clients, head size does correlate with mental function. So meditation for me is only a slight temporary relief. The most relief comes from reading a book. I just wonder if my bipolar brain is the reason my thoughts are constant. And by talking about it I will have some understanding, or gain an understanding about these constant thoughts and conversations I have with myself.
A few months ago, I started noticing things that were different about me that I had seemed to have for my entire life. Since I was homeschooled I thought that my social awkwardness was just a part of not having as much social interaction as other kids. I looked into bipolar disorders and every fact that I learned, I became more and more sure that I have a bipolar II disorder. I used to want to go into the military ROTC program, and my dad was very proud that I wanted to go that route.
Others would get confused or become upset that I started another tangent. Friends used to say it was hilarious listening to me, but I always thought.. I am awful at meditating, on a side-note. I meant to say that I sometimes think I might have bipolar 2 because of my frequent and mixed mania swings.. So maybe I am bipolar I know what rapid cycling is and mixed mania. Is that what it is? I find if I have several things going at once that it does a fairly good job at quieting the unceasing chatter in my head.
For instance, I just learned how to use a bead loom and I usually am working on a piece while binge-watching stuff on Netflix. Distractability can be a major challenge, but there are many things you can do to maintain focus throughout the day when you find your mind wandering. One thing we deal with a lot in the area of bipolar disorder is distractibility, which can be one of the symptoms of this condition.
Now, that may happen My entire face brightens in euphoric mania, so it makes sense I would open my eyes wider as well. The following picture captures the difference. Neither picture was taken with a flash. On the topic, I'm euphoric. A thought to ponder: People also report eye color changes when manic. I'm excited to announce this has now happened. The study is open for public participation. We are looking for 1, images of the eyes from people who have manic episodes.
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I often think of the scanners used on Star Trek: The Next Generation and imagine the possibilities this research holds for the future. Julie A. Help is needed when symptoms take away rational thought. The NRA theory that drugs cause mass shootings simply doesn't make sense.
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