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  • Questions and Answers Page for the 2007 NAMI Family-to-Family Class

    There are often questions asked that require the instructors to do some out-of-class research.

    This page lists those questions posed by our 2007 Family-to-Family Education class, and our best try at answering those questions. We hope that this will serve as a resource for other families seeking similar information.

    Answers to March 7th Class Questions:

  •  Is post-partum depression included in the overall numbers for major depression?

  • The average number of (depression)  recurrences is 7 in a lifetime (see class handout #5  (p 2.24) ).    Is this true even when they are on medications?
  • Answers to March 21st Class Questions:

  • What is the percentage risk of someone, over their lifetime, "getting" a mental illness when there is no prior family history of mental illness?

  • What is the percentage risk of someone, over their lifetime, "getting" a mental illness when there IS a family history of mental illness?

  • Regarding page 4.34, Handout #9: Concordance Rates in Mental Illness - Why is there was no listing for depression if both parents were had that diagnoses?
  • Are there charts that list other types of concordance rates(for example - the risk of developing one type of mental illness when your parents have another type)?
  • Answers to April 4 Class Questions (Medications):

  • Is Thorazine still used for medication for consumers?
  • What exactly does dopamine/serotonin/noipenephrine/gAmino-butyric acid do in a normal brain?
  • Any extra information you can provide about Repetitive Transcranial Magnetic Stimulation (rTMS)?
  • Are transdermal patches approved by the FDA for Major Depressive Disorder?
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    Answers to March 7th Family-to-Family Class Questions

    Question #1:  Is post-partum depression included in the overall numbers for major depression?

    We couldn't find references that specifically discussed whether post-partum depression was included in the overall statistics for major depression.

    However, we guess that post-partum depression is implicitly included in the overall numbers, because the following references indicate that a subset of women that develop post-partum depression have a prior history of clinical depression.

    "Studies suggest that women who experience major depression after childbirth very often have had prior depressive episodes even though they may not have been diagnosed.

    This page mentions that that clinically depressed pregnant women who discontinue their meds before conception or during the pregnancy are at considerable risk of relapsing.

    And this article quotes data from an article in the  Journal of the American Medical Association article  (Feb 1 2006).

    Stopping Antidepressant Use While Pregnant May Pose Risks - Contrary to the belief that hormonal changes shield pregnant women from depression, this study demonstrates that pregnancy itself is not protective. Among the pregnant women who stopped taking antidepressants, 68 percent relapsed during pregnancy compared to 26 percent who relapsed despite continuing their antidepressants. Among the women who discontinued use and relapsed, 50 percent experienced a relapse during the first trimester and 90 percent did so by the end of the second trimester."

    Question #2:   The average number of (depression)  recurrences is 7 in a lifetime (see class handout #5  (p 2.24) ).    Is this true even when they are on medications?

    We couldn't find a reference that said whether staying on the meds reduced the # of lifetime incidences below 7.   However, the following reference mentions the meds "substantially prevent recurrent episodes of unipolar depression".  Note that the follow-up period of these studies only went out to three years, so we don't know if the lifetime incidence was decreased or not.   

    Mood Disorders: Pharmacologic Prevention Of Recurrences - Unipolar Disorder - Many controlled studies have shown that preventive treatment with lithium or antidepressants (imipramine and amitriptyline) can substantially prevent recurrent episodes of unipolar depression. In most patients, lithium and tricyclics decrease the frequency and/or intensity of recurrences. In six studies with follow-up periods ranging from 5 months to 3 years, the percentages of patients who relapsed or had a recurrence on placebo were significantly greater than the percentages of patients who relapsed or had a recurrence on lithium. In a similar manner, a significant difference between tricyclic however, find lithium and tricyclics to be equally effective or lithium to be somewhat superior.

    Individual patients may respond better to either lithium or tricyclics. One multicenter study suggests that patients whose last episode was severe have a better response to imipramine and that patients whose last episode was of only moderate intensity respond equally well to lithium and tricyclics. Research to date has not produced clear-cut guidelines for choosing one over the other when all other factors are equal, nor has it supported the combination of the two as superior to either alone.

    Tricyclic antidepressants and lithium prevent recurrences of unipolar depression in both men and women of all ages from early adulthood to old age; however, few data are available for children and adolescents and for the elderly.

    Successful prevention of recurrence may involve other important gains, including increased stability of mood during intervals between episodes, regained self-esteem, renewed hope for the future, improved social relations, enhanced vocational abilities, and increased enjoyment of recreational activities.

    Because the preventive treatment of recurrent mood disorders is clearly effective for large numbers of persons suffering from these conditions, and because a substantial proportion do not now seek treatment or are not accurately diagnosed, systematic efforts should be made to bring about a greater awareness and understanding by both health professionals and the public of the nature and effective treatment of these illnesses.

    Note that people can relapse into depression even when on meds - this article claims that the meds will stop working in 20% of patients (for various reasons:)

    Depression: Skirmish or Siege? - Still, it's not as simple as just putting everyone who is depressed on long-term drug therapy. Some patients will run into so-called "Poop-out"; the medications simply stop working after a while. There are no official data on the antidepressant poop-out rate, but experts estimate it at about 20%. According to Klein, poop-out is highly unlikely to occur before three or four months of treatment; after that, there is no saying whether or when it wilt. "Poop-out is not uncommon, but it's not the expectation" says Goodwin. "It is possible to keep taking these drugs indefinitely at the same dose and maintain the same level of relief."

    Another unknown is what's behind poop-out--whether it is true pharmacologic failure or a worsening of the disease, a relapse that overrides medication. Other factors that can dent a medication's apparent effectiveness are aging (which tends to worsen or change depressive symptoms), substance abuse, a co-existing medical illness and noncompliance, a big problem.

    "So why not just stop the medication after one episode is cured and wait until the next one hits before resuming treatment? Kramer points to a phenomenon known as kindling: the more episodes you have, the worse they get--and the less stress it takes to trigger them. Anecdotal evidence also suggests that going on and off medications may increase the dose needed next time to achieve the same benefit as last time. In the long run, stopping and starting doesn't reduce overall drug exposure.

    Finally, this recent study indicates that relapses are less likely when the treatment completely eliminates symptoms: The National Institute of Mental Health just completed a major study on depression treatment - results were published in the American Journal of Psychiatry, November 1st, 2006.  Am J Psychiatry.2006 Nov;163(11):1905-17,  Acute and longer-term outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. 

    Also see:

    Questions and Answers about the NIMH Sequenced Treatment Alternatives to Relieve Depression (STAR*D) Study — All Medication Levels - The analysis also found two important indicators of treatment success. Those who become symptom-free have a better chance of remaining well, as measured in the follow-up period, than those who experience only symptom improvement. Those who need to undergo several treatment steps before they become symptom-free are more likely to experience a relapse during the one-year follow-up phase, reminding clinicians that even if a patient overcomes the depression, he or she still needs attention. These results underscore both the need for a better understanding of how different people respond to different depression treatments, and the challenges in finding broadly effective, short- and long-term depression treatments.

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    Answers to March 21st

    #1: What is the percentage risk of someone, over their lifetime, "getting" a mental illness when there is no prior family history of mental illness?

    The classical numbers are the same as in your handouts (See page 4.34, Class 4: Class Handout #9: Concordance Rates in Mental Illness):

    Mental Illness

    Risk of Developing Mental Illness when there is no Genetic Relationship.



    Bipolar Disorder


    Panic Disorder



    2 to 3%

    Major Depression


    However, often there may actually be a Genetic Relationship even if the family swears that no one else has ever had this problem.


    Many families "hide" mentally ill relatives in the family tree. Think about your extended family - if there was someone whose name occasionally comes up - but no one ever talks about them - then there is a good chance that they suffered from a mental illness.

    Also suspect mental illness when there is a family history of alcohol and/or drug abuse, and when relatives have attempted or committed suicide. (According to the Ithaca's Suicide Prevention Hotline staff, half their calls come from people suffering from mental illness).

    Finally, if you discover such "hidden people", then it helps to talk about them with your ill relative. It lets them know that they aren't alone - and that developing the illness wasn't their fault. (At least that is the theory - ask your instructor about her "Genetic Counseling" conversation…;>)

    And here is some updated information from Dr. Fuller Torrey:

  • For Schizophrenia: "About 25% of people initially diagnosed with schizophrenia will only have one or two episodes in their life, and will recover completely. (See Torrey, Surviving Schizophrenia, edition, page 106)."
  • Unfortunately, when the first episode hits there is no way to know if your loved one falls into this category.

  • For Bipolar Disorder: "Beyond age 40, the onset of manic-depressive illness becomes increasingly unusual. Anyone presenting with the onset of mania over age 40 should be closely examined for underlying medical conditions that may be causing the symptoms." (excerpt from Torrey, Surviving Manic Depression, 1st Edition, page 96)
  • And I found" - (link is broken as of May 2014) - this chart on schizophrenia concordances - presentation by Roberta Palmour, PhD McGill University - no citation on the origin of this chart:  

    Note that this chart asks the question - if someone develops schizophrenia - what are the risks that another relative will develop schizophrenia?  The numbers seem to roughly match the numbers in the Class handout.  Unlike the handouts it provides some statistics for First Cousins, Nephews/Nieces, and Grandchildren.



    #2: What is the percentage risk of someone, over their lifetime, "getting" a mental illness when there IS a family history of mental illness?

    The concordance rates in your handouts are probably the best resource for now - but note that newer research is revising these numbers.

    For example, more recent studies produce different numbers for certain situations. In Torrey (Surviving Manic Depression, 1st edition, page 116), he mentions that more recent studies found that:

  • In identical twin has bipolar disorder, the chances of illness developing in the other twin are 44% (vs. the 74-80% figure listed in the chart).
  • Torrey (Surviving Schizophrenia, 5th Edition, page 367) also give some concordance numbers not listed in the handouts:

  • If my aunt or uncle has schizophrenia - my chances of developing it are 3%
  • If my grandfather or grandmother has schizophrenia - my chances of developing it are 4%
  • If both parents have schizophrenia, then my risk of developing it are 36% (vs. the 35-46% figure listed in the Handouts).
  • What if your family situation is more complicated - say having several ill relatives rather than just one? Unfortunately, we haven't found any studies that give updated statistics vs. the family pattern.

    About all that can be said is:

  • The more ill relatives - the higher the risk.
  • How much higher? No one knows how to estimate this higher risk.
  • Why can't they estimate this higher risk? Because no one truly knows how the illnesses develop…
  • #3: Regarding page 4.34, Handout #9: Concordance Rates in Mental Illness - Why is there was no listing for depression if both parents were had that diagnoses?

    We found the following paragraph in the article by Compton and Nemeroff:

    The strongest known risk factors for the development of depression are family history and previous episodes of depression. The risk of depressive disorders in first-degree relatives of patients with depression is two to three times that of the general population. If one parent has a mood disorder, a child's risk of a mood disorder is 10% to 25%; if both parents are affected, the risk roughly doubles. The importance of genetic factors in pathogenesis is also highlighted by the higher concordance rate of depression in monozygotic twins than in dizygotic twins.

    So according to this article - if having one parent with major depression boosts the risk to 10 to 25%, then having two parents with major depression implies a 20% to 50% risk of having a child that suffers from depression.

    If you believe the handout's statistic for having one depressed parent (15%), then having two depressed parents means a 30% risk.

    #4: Are there charts that list other types of concordance rates (for example - the risk of developing one type of mental illness when your parents have another type)?

         Yes - here and there.  We cite some examples below.

  • What is the risk of schizophrenia if there is a family history of other mental illnesses (such as depression and bipolar disorder)?
  • (Torrey, Surviving Manic Depression, 1st Edition, page 118) cites a study of 6,000 patients suffering from bipolar disorder, where:

  • 8% of their first degree relatives (parents, brothers, sisters) had bipolar disorder
  • An additional 12% of these relatives had major depression.
  • (Note that this quoted 8% concordance rate for bipolar disorder is lower than the rates mentioned in the handout).

    Quoting Torrey (Surviving Manic Depression, 1st Edition, page 282):

    The offspring of two parents who have manic-depressive illness or schizophrenia have a much greater probability of developing one of these disease (at least 40%) than the offspring of parents among whom only one is affected (approximately 8%).

    Given these finding, a person with manic depressive illness who is planning to have children should select as a partner a person who does not have a severe psychiatric disorder.

  • What is the risk of depression if I only have one relative (an aunt) with depression?
  • We found a reference in Understanding Depression by Paul Richard Robbins, page 44. If a family member develops depression, then...:

    …"Among such relatives as aunts, uncles, and grandparents, the risk of depression runs around 7%, which is close to the risk of anyone in the general population."

    Since the risk in the general population (per the handouts) is about 5%, having an ill aunt, uncle, or grandparent only slightly increases the risk of developing depression.

    Yet another way to "estimate probabilities" is that you share some genetic heritage with your aunt, uncle, and grandparent - but not as much as with a brother. So the risk of developing depression is somewhere between the general population risk (5%) and the brother/sister risk (15%).

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    Answers to April 4 Family-to-Family Class Questions:

    #1: Is Thorazine still used for medication for consumers?


    According to Wikipedia, Thorazine (Chlorpromazine)is still in use for various purposes, but for psychiatric disorders other meds have largely replaced it:


    #2: What exactly does dopamine do in a normal brain? What does seratonin do? What does norepinephrine do? What does gAmino-butyric acid (GABA) do?


    The following web page contains an excellent table (Section 4. "Transmitters") that lists the neurotransmitters, their function in the body and in the brain, and what can happen if they get out of balance.



    Although there are over 80 known different "transmitters" in the brain, each nerve ending only has one type. These "neurotransmitters" tend to be grouped together and each seems to have specific roles e.g.;-

    Transmitter What it seems to do Problems if it gets out of balance
    Serotonin or 5-HT In the body, 5-HT is involved with blood pressure and gut control.

    In the brain, it controls mood, emotions, sleep/wake, feeding, temperature regulation, etc.

    Too much serotonin and you feel sick, less hungry, get headaches or migraines

    Too little and you feel depressed, drowsy etc.



    - there are three main groups (or pathways) of dopamine neurones in the brain

    In the brain, one group controls muscle tension and another controls e.g. emotions, perceptions, sorting out what is real/important/imaginary etc. Not enough dopamine in the first group and your muscles tighten up (e.g. as in Parkinson's Disease).

    Too much dopamine in the second group gives you an overactive brain i.e. too much "perception e.g. you may see, hear or imagine things that are not real

    Noradrenaline (NA)

    (sometimes called "norepinephrine" or NE)

    In the body, it controls the heart and blood pressure.

    In the brain, it controls sleep, wakefulness, arousal, mood, emotion and drive

    Too much noradrenaline and you may feel anxious, jittery etc.

    Too little and you may feel depressed, sedated, dizzy, have low blood pressure etc.

    Acetylcholine (ACh) In the body, acetyl choline passes the messages which make muscles contract.

    In the brain, it controls arousal, the ability to use memory, learning tasks etc.

    Too much in your body and your muscles tighten up.

    Too little can produce dry mouth, blurred vision and constipation, as well as becoming confused, drowsy, slow at learning etc.

    Glutamate Acts as an "accelerator" in the brain Too much and you become anxious, excited and some parts of your brain may become overactive.

    Too little and you may become drowsy or sedated

    GABA Acts as a "brake" in the brain Too much and you become drowsy or sedated.

    Too little and you may become anxious and excited

    In many mental health problems, it is known that some of these transmitters get out of balance e.g. you have too much or too little of a particular transmitter.


    The following section discusses GABA specifically (an answer to a question asked in the 2005 Family-to-Family course):


    GABA is a "brake" on the other neurotransmitters.

    p. 4.33: GABA: What influences the level in the body? Does it change in level throughout the day for all people? Or is it in a steady state with a different amount for ill people?

    (Webmaster note: Jan 2012:   the GABA links listed below are "dead", and I haven't been able to find websites that give similar information without shilling some type of health

    This web page (link is dead as of May 2014) gives a pretty detailed overview of GABA. The article says that GABA levels can change due to diet, prolonged stress, and genetics.

    GABA Levels can also change throughout the day (GABA levels seem to vary with the body's circadian rhythm). The above reference table lists neurotransmitter variation during the day, as measured via urine analysis:

    GABA (units are ug/grCr)

    6AM = 5.5
    9AM = 8.0
    12AM = 4.2
    3PM = 4.3
    6PM = 3.1
    9PM = 4.4

    Note that GABA in urine doesn't necessarily mean those same levels are also maintained in the brain. For that people try to use PET and other types of imaging scans. Here are some good links describing PET scans and other brain imaging technologies:

    Information on PET (Positron Emission Tomography) Scans

  • Overview of PET and other Brain Scan Technologies
  • PET isn't widely available because the machines were only recently introduced commercially, and you need a special lab to prepare the radioactive substances that are mixed with sugar water (which must be injected or ingested by the patient).

    Finally, are the GABA levels different in mentally ill vs. normal people?

    The answer is yes for folks with bipolar and depression, unclear for schizophrenia.

    This brain imaging study says that people suffering from depression have very low cortical GABA levels:

    And the following article says that Bipolar patients also have low GABA levels...

    GABA: Mania and Seizures to Relaxation and Impulse Control

    Gamma-Aminobutyric Acid (GABA) is a neurotransmitter that is inhibitory, that is, it decreases the ability of other neurotransmitters to work. GABA is involved in our level of excitability. Rather than encouraging communication between cells such as Dopamine, Serotonin or Norepinephrine - GABA reduces, discourages, and blocks communication. This neurotransmitter is important in brain areas involving emotion and anxiety.

    When GABA is in the normal range in the brain, we are not overly aroused or anxious. At the same time, we have appropriate reactions to situations in our environment. GABA is the communication speed controller, making sure all brain communications are operating at the right speed and with the correct intensity. Too little GABA in the brain, the communication becomes out of control, overstimulated, and chemically unstable. Too much GABA and we are overly relaxed and sedated, often to the point that normal reactions are impaired.

    Low levels of GABA are associated with Bipolar Disorder, Mania. With GABA levels below average, the brain is too stimulated. We begin talking rapidly, staying up for days at a time, and develop wild and grandiose ideas. In a Manic state, we are so "high" and out of control that social problems are quick to develop, often due to hypersexuality, excessive spending, reckless decisions, risk-taking behavior, and grandiose ideas.

    We may feel so good that we think we are a heavenly spirit, an intellectual genius, or possessing extraordinary powers. I personally had one patient who locked himself in his mobile home and spent one week rewriting the New Testament in "hillbilly". Another, with limited education, began purchasing books on the Theory of Relativity by Albert Einstein, sensing he may "warp drive".

    Low levels of GABA are also associated with problems of poor impulse control, including clinical conditions such as gambling, temper tantrums, and stealing. When GABA is low in the brain, impulsive behaviors are not inhibited (stopped) by logical or reasonable thinking.

    Low levels of GABA are also associated with epilepsy or seizure disorders. If we imagine a seizure as a type of electrical storm, the seizure begins at one location in the brain then rushes across and through the brain like a sudden storm. Low levels of GABA make it easy for the brain to develop seizures which is why seizures are part of the withdrawal syndrome for many substances that work with GABA such as alcohol and tranquilizers (benzodiazepines – Xanax, Ativan, Librium, Valium, etc.). Substances that artificially maintain a high level of GABA, when stopped, create a dramatic drop in GABA levels, thus creating the risk for withdrawal seizures due to the chemical instability that is created.

    High levels of GABA produce more control, relaxation, and even sedation. Alcohol works by increasing GABA levels, which is why all body systems are relaxed at first – then sedated to the point of slurred speech, unsteady gait, and foggy thinking. Alcohol withdrawal, or the sudden severe drop of high GABA levels, produce a low GABA level and the possibility of seizures. Withdrawal from benzodiazepines is known to follow the same pattern. Taking forty milligrams of Valium for two years, suddenly stopping all medication, will likely produce a seizure.

    Medications for anxiety create relaxation and a decrease in anxiety by increasing GABA levels in the brain. Alcoholic beverages work in the same manner; the alcohol increasing GABA levels to produce mild euphoria, loss of social anxiety, and other symptoms of intoxication. Excessive intake of benzodiazepines and/or alcohol is extremely dangerous as the high GABA level actually smothers the communication between brain neurons – sometimes to the point of a total lack of communication between neurons – also known as death.

    Medications for seizures, impulse control problems, and Bipolar Disorder, Mania all work by increasing the GABA levels without accompanying euphoria. Lithium and anti-seizure medications all increase GABA into the normal range, thus lowering the possibility of seizures and producing brain chemical stability. As GABA is the neurotransmitter policeman, changes in GABA can influence all neurotransmitters but especially norepinephrine.

    #3: Are transdermal patches approved by the FDA? (Selegiline Transdermal System) Brand name EMSAM It's an MAO inhibitor used as an antidepressant. Our handout from May 2004 (student handout 6.27 on the bottom) says that FDA


    The Selegiline Transdermal System was approved by the FDA in 2006 as a treatment for major depressive disorder. As of May 2014 - here is the Medline page describing its use, precautions, and side effects.

    March 6, 2006

    Bristol-Myers Squibb Company (NYSE: BMY) and Somerset Pharmaceuticals, Inc., a joint venture between Mylan Laboratories Inc. (NYSE: MYL) and Watson Pharmaceuticals, Inc., (NYSE:WPI), announced today that the U.S. Food and Drug Administration (FDA) approved EMSAM(R) (selegiline transdermal system), the first transdermal patch for the treatment of major depressive disorder (MDD) in adults. EMSAM, a transdermal delivery system manufactured by Mylan Technologies, Inc. for Somerset, is a monoamine oxidase inhibitor (MAOI) that has been shown to relieve depressive symptoms in patients with MDD.

    #4: Any extra information you can provide about Repetitive Transcranial Magnetic Stimulation (rTMS) beyond what is on 6.29?  "rTMS involves placing an electromagnetic coil on the forehead for 20 minutes to stimulate the left frontal cortex. No anesthesia is required; no memory loss occurs. In one study, 56% of subjects with depression responded to rTMS, administered on a daily basis. Trials for this new therapy are now in progress."


    rTMS appears to be safe, but questions linger regarding how well it works. The FDA and the National Institutes of Health may answer this question in 2007, per the following references.

  • From the Wikipedia entry for rTMS:
  • The FDA convened its Neurological Devices Panel on January 26, 2007 to review the TMS Therapy application. The results of this panel meeting were mixed with no concerns regarding the safety of this treatment, however, there was clear questioning of the efficacy of this treatment.[6]. A final decision from the FDA in regard to approving TMS as a treatment for depression is expected in the first half of 2007.

    In 2006 the National Institute of Mental Health recently completed a 10-year, 91 patient study. Evaluation of Repetitive Transcranial Magnetic Stimulation (rTMS) in the Treatment of Mood Disorders.

    You could probably see papers on this study emerging in 2007/2008. The earlier papers indicate a pretty well controlled study (double-blind with placebo).

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