Depression is a complex of psychological and physical symptoms. Low mood level or sadness is often the most prominent symptom. The common property of these symptoms is a decreased activity level in parts of the brain.
THE SYMPTOMS OF DEPRESSION
Depression may give one or more of these symptoms:
-Low mood level or sadness.
-Lack of joy or interest in activities that were joyful before.
-Pessimism.
-Feel of guilt of something without any substantial reason to feel so.
-Inferiority thoughts.
-Irritability.
-Slowness in the thought process.
-Slowness in interpreting sensorial stimuli.
-Slowness of digestion or other internal physical processes, and symptoms caused by this slowness, for example inflated stomach, constipation or difficulties by urination.
-Slow physical reactions.
Depression can be a mild disease that only causes some annoyance in the daily life, but can also get very serious and make a person totally unable to work and unable to participate in social life. By depression of some severity, there is also a greater risk of suicide.
Depression can occur in all age classes. In teenagers lack of interest in school work, withdrawal from social life and difficult mood can be signs of depression.
THE PHYSIOLOGICAL CHANGES THAT PRODUCE THE SYMPTOMS
By depression there is a decreased amount of neurotransmitters in parts of the central nervous system, mainly deficiency of serotonin, but also to some extend of noradrenalin, acetylcholine, dopamine or gamma-amino-butyric acid (GABA), or the nerve cells do not react properly by stimulation from neurotransmitters. A neurotransmitter is a signal substance that transmits the nerve signal through the junctions between two nerve cells.
Serotonin and noradrenalin cause nerve cells to send impulses along to other nerve cells, and thus increase the activity in the brain. Deficiency of these substances causes slowness in parts of the brain, and that again causes the depressive symptoms.
The role of GABA is the opposite, namely to slow down some nerve impulses, mainly those causing anxiety and panic response. Lack of GABA causes higher anxiety and easier panic response. Yet, lack of this transmitter also seems to cause depressive symptoms. This is because a too high activity in some brain processes may slow down other processes.
There are many causes and subtypes of depression with different physiological mechanisms involved.
TYPES OF DEPRESSION
Depression is often divided into subtypes according to exhibited symptoms.
1. Mono-polar depression and dysthymic disorder
By mono-polar depression there are pure depressive symptoms. Mild cases of mono-polar disorder that do not affect a persons ability to work and to participate in social activities are often called dysthymic disorder.
2. Bipolar disorder (manic-depressive disease) and cyclothymic disorder
In this condition there are periods with symptoms of depression – the depressive phase, alternating with periods of elevated mood level with increased mental and physical activity – the manic phase. In the manic phase, the affected person also sleeps poorly and has concentration difficulties. A mild form of this disease is called cyclothymic disorder.
3. Manic disorder
This condition is characterized by abnormally elevated mood, by unrealistic optimism, by lack of sleep and by hyperactive behaviour. Many psychiatrists think that this disorder is simply the same disease as bipolar disorder where the depressive face has not yet occurred.
4. Depression with mainly physical symptoms
Sometimes the physical symptoms of depression are alone or dominant, as for example: Digestive problems, constipation, difficulties with urination, slow response to sensorial stimuli or slow physical reactions.
CAUSES OF DEPRESSION
Two or more factors can have an effect simultaneously to cause depression. Depression can be an independent disease, or a part of other disease. Depression is also divided into different subtypes according to cause.
1. Reactive depression
This disease is simply a result from psychological stress, physical struggle or mental straining without proper rest or sleep over a long time period. The straining will simply wear out the nervous system or deplete the organism from nutrient necessary for the nervous system to work properly.
2. Endogenous depression
When there has not been any period of stress, straining or lack of rest that can explain the condition, the condition is often called endogenous depression. Inheritance is thought to be a part of the cause.
3. Depression by physical disease
Depression or depressive symptoms may be a symptom of physical disease. This is perhaps the most common cause of depression. Generally there are three categories of diseases that give depression:
Diseases often associated with depression are: Heart disease, Parkinson’s disease, stroke, hypertension or Cushing’s syndrome.
Mononucleosis or flu may trigger depression that continues after the infection has gone.
By lack of thyroid hormones, hypothyroidism, the metabolism in the whole body is slowed down, including the production of neurotransmitters in the brain. Therefore depression is an important symptom of hypothyroidism.
4. Depressive symptoms as a consequence of unsound lifestyle
A general unsound lifestyle with too less exercise, too much of stimulants like alcohol, coffee or tea, too less of important nutrient and too much of sugar and fat may give depressive symptoms, as well as physical problems.
5. Postnatal depression
Women will often have a period of depression after pregnancy and berth of the baby Pregnancy and berth is physically and mentally exhausting, and may drain the body for nutrient. This in turn can cause depressive symptoms
.
6. Seasonal affective disorder
Depression can occur in cold and dark periods of the year and go away in warm and light periods. Light stimulates brain activity, and lack of light is a causative factor.
TREATMENT OF DEPRESSION
Serious or prolonged depression is often treated with anti-depressive medication. Medicines used against depression generally increase the level of neurotransmitters like serotonin in the central nervous system, or they mimic the neurotransmitters.
The medications mostly used today increase the serotonin concentration by decreasing the removal of serotonin from the space around nerve cells. Examples of this medication type are: Fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), escitalopram (Lexapro, Celexa), sentraline (zoloft).
By bipolar disorder in the manic face, heavy tranquilizers (neuroleptica) are used to stop the manic symptoms. By bipolar disorder, lithium salts are sometimes used to stabilize the condition, and prevent new outbreak of depressive or manic faces.
Psychotherapy is sometimes used by depression, usually in combination with medication.
Sometimes serious depression is treated by applying electric shock through the head, electroconvulsive therapy. The shock induces epileptic eruption of nerve signals through the brain and this gives cramps throughout the body. The cramps are alleviated or stopped by applying anaesthesia before the electroshock. This form of treatment is controversial, since it can cause memory loss and is suspected of causing brain damage. The possibility of brain damage is however denied by most psychiatrists.
By seasonal depression, light therapy maybe useful.
Adjustment of lifestyle should always be considered by depression or depressive symptoms. Lifestyle measures can sometimes be enough to cure depressive symptoms before a serious depression develop. Lifestyle adjustments can be:
– To slow down a stressful life with too much work or activities.
– Enough rest and sleep.
– A good diet with enough of necessary nutrients.
– Some physical exercise.
– Meditation.
– Supplement of vitamins, minerals, antioxidants, lecithin, amino acids and essential fatty acids.
– Stimulants like coffee or tea may help against depressive feelings in moderate amount. However, if you are a heavy user of these stimulants, you should cut down on your consumption.
There exist nutritional products in the marked to help against depressive symptoms. These contain ingredients that the brain uses as building blocks for neurotransmitters, for example amino acids and lecithin. They also often contain vitamins and minerals that the brain uses as tools to produce neurotransmitters, especially vitamin B6.
Supplements may further contain herbal extracts that trigger higher brain activity much like anti-depressive medications, but may have fewer side effects.
By: Knut Holt
Showing posts with label genome. Show all posts
Showing posts with label genome. Show all posts
Sunday, October 10, 2010
Monday, March 30, 2009
23andMe already testing for rare Parkinson's mutations?
23andMe already testing for rare Parkinson's mutations?
Posted on: March 23, 2009 9:15 AM, by Daniel MacArthur
This casual aside on a recent post on personal genomics company 23andMe's corporate blog caught my eye:
Mutations in several other genes have also been associated with Parkinson's disease, but these are extremely rare. Many have been found only in one or two families. While these mutations are so rare that they are not covered by 23andMe (to date we have found no customers with any of them), studying them could help scientists better understand the mechanisms of Parkinson's generally... [my emphasis]
In other words, the company already has probes on its custom chip targeting these variants, but it isn't yet reporting results back to customers.
Why isn't it reporting back? If you'd asked me a couple of months ago, I'd say the motivation was probably to avoid the regulatory hassles associated with testing overtly clinical markers - but the company's willingness to provide results for large-effect variants associated with breast cancer pretty much rules that out.
Instead, the most likely reason to hold back on giving results back to consumers is (perfectly reasonable) caution about the reliability of the test. Screening for extremely rare variants is tricky for two reasons: firstly, since there are very few individuals around who carry the mutation, obtaining positive controls is difficult; and secondly, screening accuracy needs to be extremely high to keep down the rate of false positives.
To illustrate that last point, let's say there was a genetic variant with a population frequency of just 0.1% (1 in every 1000 people carry it)*. Now, let's say you have a test with false positive and false negative rates of just 1 in every 1000 tests, and you run that test on one million people. Of the 1000 carriers in the population, the test will only miss one; but it will also give a positive result for 999 people who are non-carriers. In other words, even for this extremely accurate hypothetical test, only 50% of the people who test positive are actually carriers.
This means that testing for rare variants requires exceptionally high standards of accuracy, probably higher than could reasonably be expected from chip-based assays. Given the risks of reporting potentially unreliable results back to customers for serious risk variants it makes good sense for 23andMe to hold off until it has developed extra assays for quality control; and it's unlikely to do this until it has seen at least a few customers who actually do test positive for the variant in question.
As for obtaining samples from real carriers to enable the development of validation assays: what better way to do that than to recruit 10,000 customers suffering from Parkinson's? Targeted recruitment of customers with other diseases will no doubt follow.
It is now abundantly clear that 23andMe is intent on moving into the overtly clinical domain; Navigenics' purchase of its Affymetrix testing lab and deCODE's move into disease-specific genetic tests are other signs that this is a shift that will involve the entire personal genomics industry.
Personal genomics is getting serious.
Posted on: March 23, 2009 9:15 AM, by Daniel MacArthur
This casual aside on a recent post on personal genomics company 23andMe's corporate blog caught my eye:
Mutations in several other genes have also been associated with Parkinson's disease, but these are extremely rare. Many have been found only in one or two families. While these mutations are so rare that they are not covered by 23andMe (to date we have found no customers with any of them), studying them could help scientists better understand the mechanisms of Parkinson's generally... [my emphasis]
In other words, the company already has probes on its custom chip targeting these variants, but it isn't yet reporting results back to customers.
Why isn't it reporting back? If you'd asked me a couple of months ago, I'd say the motivation was probably to avoid the regulatory hassles associated with testing overtly clinical markers - but the company's willingness to provide results for large-effect variants associated with breast cancer pretty much rules that out.
Instead, the most likely reason to hold back on giving results back to consumers is (perfectly reasonable) caution about the reliability of the test. Screening for extremely rare variants is tricky for two reasons: firstly, since there are very few individuals around who carry the mutation, obtaining positive controls is difficult; and secondly, screening accuracy needs to be extremely high to keep down the rate of false positives.
To illustrate that last point, let's say there was a genetic variant with a population frequency of just 0.1% (1 in every 1000 people carry it)*. Now, let's say you have a test with false positive and false negative rates of just 1 in every 1000 tests, and you run that test on one million people. Of the 1000 carriers in the population, the test will only miss one; but it will also give a positive result for 999 people who are non-carriers. In other words, even for this extremely accurate hypothetical test, only 50% of the people who test positive are actually carriers.
This means that testing for rare variants requires exceptionally high standards of accuracy, probably higher than could reasonably be expected from chip-based assays. Given the risks of reporting potentially unreliable results back to customers for serious risk variants it makes good sense for 23andMe to hold off until it has developed extra assays for quality control; and it's unlikely to do this until it has seen at least a few customers who actually do test positive for the variant in question.
As for obtaining samples from real carriers to enable the development of validation assays: what better way to do that than to recruit 10,000 customers suffering from Parkinson's? Targeted recruitment of customers with other diseases will no doubt follow.
It is now abundantly clear that 23andMe is intent on moving into the overtly clinical domain; Navigenics' purchase of its Affymetrix testing lab and deCODE's move into disease-specific genetic tests are other signs that this is a shift that will involve the entire personal genomics industry.
Personal genomics is getting serious.
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