Originally Posted by yeah_yeah_yeah
On the topic of biological disposition
Correct - you can have a lower baseline tolerance to stress from birth. This is not genetic - it has to do with shortcomings in early attachment between parent and child. A depressed or anxious mother will not be as empathic and attentive as a non-depressed / anxious mother and so is less able to adequately soothe a new born. This has been shown through the work of Bowlby et al in his application of Attachment theory. You can read numerous peer reviewed papers on the topic. No 'gene' for anxiety has been uncovered - but this non genetic link of nurturance has been shown to predminate in families.
Because of this, it is possible to change DRAMATICALLY what you are capable of via therapy. Yes some people may take longer than others.
The thing that worries me here is that people say "oh but I have a biological disposition / chemical imbalance (which is STILL AN UNPROVEN THEORY - we still do not know how anti-depressants work, if at all - see recent posts on placebo effect)" then this hugely reduces any motivation to seek therapy. As it is typical for an anxious or depressed person to feel that they are "hopeless", or the "one true irredeemable case", anything that adds to that hopelessness is fatal to recovery.
Even if you suspect a biological cause - do not write off therapy just because it FEELS POINTLESS. EVERYTHING feels pointless when you are depressed and anxious - dont give yourself even more reasons to stay stuck.
I believe that what you approach to tackling SAD has a profound importance in understanding how SAD develops and in getting rid of it. A major problem with researchers biased towards a more biological basis or a more environmental basis for SAD is trying to work out which came first, the chicken or the egg ? Did these things come about because of a certain biological trait or disposition or did the trait develop because of learning. But any ideas which help to understand social anxiety is good. Because to the extent that a phenomenon is understood to the extent constructive therapeutic and preventive methods can be developed and put in place. I also have some things to add which may be of at least some importance (and maybe in need of some serious updating) in the development of SAD.
When trying to understand the underpinnings of avoidant personality disorder, shyness and social anxieties and how a significant minority of the population come to develop certain social phobias and intractable forms of shyness that debilitates one's life, one should never belittle or trash the biological and physiological perspective and vis-versa--never underestimate the environmental perspective either. One should definetely go in with an open mind.
If there is any reason to doubt that biology and genes play any sot of role in the development of social anxiety and shyness then consider the following.
People are not all born alike in terms of behavioural tendencies and personality. Take a new born baby for example, some new born babies are noisy whereas others are more quiet, some move around more than others whereas other remain rather still etc. In the animal kingdom temperamental differences are apparant with animals of the same kind; some are friendly whereas others are more secluse, some are passive whereas others are more assertive and sociable. Even lab animals can be raised for certain behavioural traits like high or low aggression and activity level. These behavioural patterns and tendencies have become known as temperament and represent the elements of personality that are innate or not learned through environmental interaction. The term "personality" normally refers to the elements of a person's stable behavioural patterns that are learned.
If you look at the dimensions of personality found in avoidant personality disorder you will discover "low extraversion" or "high introversion" and "high neuroticism". The work of Hans Eysenck seems to suggest that introversion is a natural outcome of higher levels of arousal in the cerebral cortex, caused by an ascending reticular activation system (believed to be the primary arousal centre of the brain) that is more active than people who are more extroverted. This higher arousal stimulates the higher brain and CNS to a quicker response activity when presented with stimuli (including social) that is threatening. Electroencephalograph studies have also shown differences between extroverts and introverts. High frequency alpha waves, indicating high arousal has been found in introverts, whereas lower frequency alpha waves have been found in extroverts, including infants, which indicate lower arousal. Being more easily aroused would seem to lead to the conclusion that introverts would be able to condition anxiety and neurotic behaviour patterns more quickly than an extrovert, or an ambivert for that matter. This may partially account for the large number of introverts who tend to be neurotic.
The degree or level of neuroticism is another result of differences in physiology mainly in the autonomic nervous system and lymbic system. The visceral brain regulates emotional reactions and therein lies the central aspect of this dimension of personality. Emotionality, the physiological expression of anxiety represents a number of reactions of the body like increased rate of breathing, increased heart rate, and other various reactions involved in the fight/flight mechanism. The higher the neuroticism, the more unstable these reactions tend to be. These reactions tend to occur faster, more intensely, and for longer periods in those who are high on neuroticism or the emotionality dimension. Studies involving vigilence, degree and pace of conditioning, sensory thresholds, reactions to emotion-producing stimuli have revealed differences between those who are high on neuroticism and those low on it. People who are high on neuroticism experience anxiety more quickly, more intensely, and hence more painfully, whenever exposed to stimuli (including social) that is associated with anxiety or is seen as threatening. If the level of neuroticism is high a person will very rapidly and all too easily condition anxiety and avoidance behaviour patterns.
A percentage of children become distressed in social situations that are unfamiliar such as being placed in the company of an unfamiliar child or adult. These inhibited children become anxiety-ridden, withdraw, become very quiet and behave in a highly reserved fashion in new social situations. Infants with this trait, called behavioural inhibition by J. Kagan, will typically react to an unfamiliar event by stopping whatever they are doing in an attempt to understand what had occured. Those without this trait simply take note of the event but quickly move on. Studies have shown that the heart rate of those who are behaviourally inhibited stabalizes when exposed to an unfamilar or strange event. The best explaination for this stable heart rate pattern has to do with the balance between the sympathetic and parasympathetic nervous system. When you inhale the action of the sympathetic nervous system increases the heart rate, and when you exhale the parasympathetic nervous system decreases it. Action on part of the sympathetic nervous system blocking the vagus nerve would stop the heart rate decreasing on the exhale, therefore making it become more stable. It could be that those who are behaviourally inhibited (including adults) have a certain biologically-based tendency to become aroused in situations and events (including social) that are unfamiliar, novel, unexpected, ambiguous and unstructred and hence unpredictable.
Seven male children were noted for being excessively inhibited and exceedingly fearful during their first three years. They were followed up until they became adults and they were found to have temperaments notably different from others in the study. They were all still very inhibited and "shy", especially in the sort of ambiguous situations that would occur during chit-chat or small-talk at a party for example. All these men were particularly vulnerable to having panic attacks and suffered from a host of internal conflicts.
Pregnant mothers who are chronically nervous and irritable or those who suffer from stress during their pregnancy tend to give birth to shy, passive children (if the children are male). If enzymes that allow the testosterone to do its job on the male fetus' brain are crippled or neutralized for one reason or another (such as stress in the pregnant mother) then the brain will not masculinze properly and will therefore be in some ways a female brain. If the area of a male's brain that relates to "masculine" assertiveness and competitiveness isn't properly developed (from a result of hormal deficiency or enzyme neutralization) then that male will likely be born passive, shy, and tends to be conspicuously unaggressive and non-competitive. And if an adult or teenager suffers from a lot of stress and anxiety, these feelings in the person can also act to cripple enzyme activity. Having healthy, well-functioning enzymes may help a person deal more effectively with stress in the environment. Defective enzymes could lower a person's resistance to stress, thereby creating more stress, in a kind of vicious cycle.
Looking at depression, a lot of cases are most likely the result of biochemical imbalances rather than a purely environmental-caused disorder. During the 1950s, Iproniazid, a chemical initially designed to treat tuberculosis patients was unexpectedly found to have strong antidepressant effects. Research has shown depressed paitents to have abnormalities in brain chemicals, and that these abnormalities can be corrected with certain drugs. Antidepressant drugs can correct the irregular flow and amount of neurotransmitters in depressed paitents. Paitents who are depressed show hormonal abnormalities in their blood and abnormal levels of brain chemicals in their urine. Depression doesn't discriminate when it comes to age. Toddlers, children and adults can be affected. Young people who are depressed tend to sleep too much, whereas older depressed people cannot fall asleep and/or wake up a lot in the morning.
The large majority of suicides are believed to be the result of biologically-based depression. However, people can be depressed but may not be suicidal. People who are depressed and have a low amount of a chemical known as "5-hiaa" (the end product of serotonin) are at a significantly higher risk of suicide than those with higher amounts of this chemical. Tests can be carried out on depressed paitents to indicate who is at more of a risk of suicide and who is not.
Certain types of depression can be distinguised from other types of depression. People can go from feeling quite normal too severely depressed for not apparant reason and then back to normal. Tests can be carried out to distinguish biological-based depression from other types. An artifical steriod called dexamethasone can be given to the sufferer. If the depression is not the particular biological-based type than the sufferer will stop producing the hormone cortisal. If the sufferer has biological-based depression than the artifical steriod will not shut off cortisol production. Blood tests will indicate this.
A person who isn't depressed but takes an antidepressant drug will not experience any feelings of pleasure. This is much like how aspirin taken will not lower body temperature in someone without a fever. Antidepressents do not normally need to be taken in increasingly larger doses. This may suggest that when they work they temporarily fix whatever it was that was malfunctioning. People with low self-esteem (particularly in cases where history doesn't seem to account for it) may be sufferering from a biologically-based depression. If medication is given that serves to sedates a normal person, increases self-esteem in the other, then maybe the low self-esteem is the result of faulty brain chemistry.
Seperation anxiety in children may be associated with biological rooted depression. A study by Donald Klien on paitents with agoraphobias revealed many had suffered from a strong phobia of attending school and homesickness. School phobia and overwhelming homesickness has traditionally been put down to unhealthy family dynamics and parent-child interaction. The discovery that agoraphobics who suffer from seperation-anxiety responded well to antidepressents lead to the hypothesis that homesick, school-phobic children involved in his study may respond well to drug treatment. Behaviour therapy alone did allow half of the children to return to school but the distress remained while they attended. Combined with antidepressants, the distress disappeared or reduced significantly. Advancing the explaination of underlying psychodynamics of such a problem does little to help the child or explain its basic biological cause.
Even obsessive-compulsive disorder has evidence backing it as a genetically and biochemically based disorder. Of course, the content of the obsession or compulsion is learned but the drive to own the obsessions and compulsion are not.
The point of discussing depression and OCD is to try to show those who insist that ALL aspects of personality and psychological problems are learned may not very well be entirely learned.
There is are a lot of strange circumstances cases involving identical twins seperated at birth and raised in totally different families. Quite by accident, bumping into their twin more than three decades later they discover that they have married someone of the same first name, physical description, career and education choice, they themselves have chosen the same education and career, they have the same type of dog and use the same name, they drive the same make and model of car, their children are of the same ages and same gender and have the same first names, their personality traits and behavioural dispositions all appear to be exactly the same. This obviously would have a significant bearing upon the genetics and physiology of shyness and social anxiety disorder.
Biogenic amines have a strong control over mood. Animals who were given drugs to reduce their brain's ability to produce them exhibted one of the primary symptoms of depression, ie, they became socially inactive. Low energy levels, irritability, strong feelings of anger, and a reduced ability to feel pleasure and emotion seem to be associated with biogenic amines deficiencies according to studies on animals and psychiatric patients. There may be a deficient production of the neurostransmitter, excessive breakdown of the neurotransmitter, decreased response sensitivity of the stimulated nerve cell, or inability to release the neurotransmitter.
According to David Sheehan, there 5% of all people in America are afflicted with a biologically-based problem he calls anxiety disease and that 9/10 victims can be cured via administration of a drug called nardil. Sufferer have different brain chemical activity than non-sufferers. Injection of a certain drug, can in less than 15 minutes set off an anxiety episode or a panic attack in a person with this type of brain chemical activity, whereas the injection of the same quantity of drug will have no affect on a non-sufferer.
People who have this problem experience anxiety or panic attacks for no apparant reason. If the anxiety attack occurs in a supermaket it will be attributed to agoraphobia, if it happens at night while asleep it may be attributed to having a nightmare. In all cases, remission cannot occur via behavioural therapy by itself. Neither can deep introspection, psychoanalysis or talking therapy cures be of much help. Administration of the appropriate drugs will be needed.
Frequently the sufferer having the anxiety attack will learn to associate the anxiety with the situation he/she is in at the time. An unprovoked panic attack in an enclosed space may turn into claustrophobia for example. A panic attack inside a crowded store may become agoraphobia. Or an anxiety episode in some kind of social situation may turn into a debilitating phobia of the particular situation or similiar situations. Normal feelings of stress arising from a simple lack of experience or potential risk-taking in any given situation may also quite easily set off an episode of anxiety in any suspectible person. It may very well be that some people with debilitating social phobias and shyness problems have a different brain chemical makeup than the rest of the population and that stress resulting from social inexperience due to habital social avoidance and non-participation may underly debilitating shyness and social phobias. Just to avoid a misunderstanding, many people with severe shyness problems and strong social phobias do not seem to have unprovoked panic attacks but may simply have a brain biochemistry makeup and activity all too similar to those who do experience such unprovoked attacks.
Anxiety can spring either from subjectively percieved stress from the environment, or from from some source inside the person. Anxiety provoked from completely outside the body has no biochemical or genetic base. Everyone sufferers from this type of response to stressful situations. Stress is subjective; what may be extremely stressful to one may be only mild to another. People suffering from unprovoked anxiety attacks would be a case of undiluted anxiety stemming from inside a person. Many cases of anxiety cannot be labelled as completely stemming completely from the outside or completely from the inside; there is a continuum. Interpreteing shyness-based social anxieties and social phobias as coming from either something completely on the outside (a stress) or completely from the inside (biochemical/genetic) will lead to an completely insufficient array of therapeutic methods created and put to use. I would think a reasonable explaination into why some people learn to see certain activites (like socializing) as extremely threatening in the first place is due to a high level of neuroticism.
Research has shown that panic-attack prone people and those without the tendecy to have panic attacks. Seven individuals were injected with lactate which in turn set off a panic response in them. Three of them had no lactate sensitivity and six of them did not have the anxiety disease discussed above. Blood flow was measured in areas of the brain that were throught to control anxiety and panic responses. One area, the parahippocampal gyrus, showed differences between lactate sensitive paitents and the non-sensitive paitents. In the sensitives, the blood flow on the right side of the gyrus was much higher than on the left. This abnormality clearly distinguishes lactate sensitive paitents and those who are not. This may reflect an exaggeration of the normal hemispheric specialization in part of the brain important to the expression of anxiety. Changes in blood flow reflect differences in the activity of nerve cells. Ferris Pitts (1966) administered sodium lactate to panic attack prone people which set off a panic episode. People sensitive to lactate can be given mao inhibitors and the tricylclics and given an injection of lactate and will not develop such anxiety feelings.
There is increasing evidence that dopamine activity in the brain is related to social phobia. Hence the drug of choice for treatment is the mao inhibitors.
Countless other research investigations could be cited.
In looking at shyness-based social inhibitions and anxieties which can be exceptionally strong, clinical psychologists there irrational fears are based on fear of rejection, of ridicule, of criticism, of negative evaluation, of shame, of humiliation, and such and such. And in many important respects they are absolutely correct. However, the fear of the pain of anxiety is perhaps the most powerful shyness-based fear. A person can "know" and can be told (and reassured) that he will not be rejected but the fear of a painful bout of anxiety or a panic attack will override under all circumstances any sort of rational, intellectual considerations. Strong pain caused by a large and sudden release of adrenaline in response to an anticipated, imagined or real social threat or anticipated social harm has been for the most part ignored when it comes to understanding many shyness-based inhibitions and fears. The fearful anticipation of this pain caused by an adrenic discharge and the resulting surge of painful anxiety can be compared to the fearful anticipation of experiencing a very sharp and painful electric shock and has been sorely underestimated as a very strong motivater for a number of shyness related behaviours such as lack of assertiveness, unable to initiate a conversation, communication anxiety (this includes selective mutism), and an unwillingness to self-disclose. This extreme fear of the excruciating pain caused by a sudden burst of adrenaline is far more potent than any fear of rejection or negative evaluation. These negative reactions by others simply serve to arouse the anticipated and much more feared painful anxiety response. And it is for this reason that people who are more neurotic will experience anxiety more quickly and more intensely, and so will feel and experience that anxiety as more painfully than others and quicky develop strong fears of experiencing it. But absolutely under no circumstance does biology and genes dicate what a person will fear. This must always be learned.