Women have a significantly higher risk for developing mood disorders than men. Although reasons for this gender difference are not fully understood, it is clear that changing levels of reproductive hormones throughout women's life cycles can have direct or indirect effects on mood. Fluctuations in reproductive hormones may interactively affect neuroendocrine, neurotransmitter, and circadian systems. Reproductive hormones also may affect response to some antidepressant drugs and alter the course of rapid-cycling mood disorders. Nonpharmacologic interventions, such as light therapy and sleep deprivation, may be beneficial for mood disorders linked to the reproductive cycle. These interventions may have fewer side effects and a greater potential for patient compliance than some antidepressant drugs. (The Journal of Gender-Specific Medicine 2000;3[5]:53-58)

Women have a greater lifetime risk for depression than men, with a ratio of approximately 2:1 for unipolar depression or recurrent episodes of depression.^1,2 Men may be as likely as women to develop depression, but they are more likely to forget that they had a depressive episode.³ Although the prevalence of bipolar disorder in men and women is more equally distributed, the course of that illness may differ between the sexes. Men may be more prone to develop periods of mania, whereas women may be more likely to experience periods of depression.⁴

What are the contributing factors to the predominance of mood disturbance in women? Recent data suggest that the onset of puberty, rather than chronological age, is linked to the increase in rates of depression in women.⁵ Thus, changes in the reproductive hormonal milieu may precipitate or alleviate depression in women. This seems particularly likely in the case of rapid-cycling affective illness.

Cyclical Mood Disorders in Which Women Predominate

Rapid-cycling affective illness is a severe form of bipolar disorder in which individuals experience four or more cycles of mania and depression within a year.⁶ Approximately 92% of patients with rapid-cycling bipolar disorder are women.⁷ Thyroid impairment⁸ and treatment with a tricyclic or other antidepressant drug are risk factors for developing this form of manic-depressive illness. Women have 10 times the incidence of thyroid disease as men, and more than 90% of patients who develop lithium-induced hypothyroidism are women.^9-11 Women are also more likely than men to develop rapid cycles induced by tricyclics or other antidepressants.^12,13

Seasonal affective disorder (SAD), or recurrent winter depression, also predominates in females. Up to 80% of individuals diagnosed with SAD are women.¹⁴ The depressive symptoms in this disorder are inversely linked to the day length or photoperiod. The disorder can be treated successfully with bright light.¹⁵

Correlation With Estrogen

Given that these risk factors are correlated with sex, it is likely that reproductive hormones play an important role in the pathogenesis of rapid mood cycles. Studies of estrogen treatment for mood disorders have shown that too much or too little estrogen can alter the course of mood cycles. For example, Oppenheim¹⁶ found that estrogen induced rapid mood cycles in a postmenopausal woman with depression refractory to treatment. When the estrogen was discontinued, the rapid mood cycles ceased. The postpartum period (including the time after an abortion), when there is a rapid decline of reproductive hormone levels and possibly an increased risk for developing hypothyroidism,¹⁷ can also be associated with the induction of rapid cycles of mood.

Connection With Thyroid Impairment

There may be a tighter connection between the reproductive system and the thyroid axis in women than in men. In hypogonadal women, the thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH) is blunted.¹⁸ When a reproductive hormone such as human chorionic gonadotropin (hCG) is administered, women's response to TRH is enhanced, becoming comparable to that of control subjects. When the hCG is removed, the TSH response to TRH again becomes blunted. In contrast, hypogonadal men do not have a blunted TSH response to TRH, and adding reproductive hormones does not significantly enhance the effect. In healthy women, the TSH response to TRH also can be enhanced with the addition of oral contraceptives.¹⁹

Women may be vulnerable to thyroid impairment, predisposing them to rapid mood cycles; however, they are also more responsive to thyroid treatment. Stancer and Persad²⁰ found that higher doses of thyroid hormone can improve rapid cycling in some women but not in men.

Effect of Oral Contraceptives

Parry and Rush²¹ found that oral contraceptives - particularly pills with a high progestin content - may induce depression. In fact, atypical depressive features are one of the most common reasons women stop taking birth control pills; up to 50% of women who discontinue oral contraceptives do so because of these side effects. The mediation of the depressive effect of estrogen is thought to be through tryptophan metabolism. Tryptophan is converted to kynurenine in the liver and to serotonin in the brain. Oral contraceptives enhance the kynurenine pathway in the liver and deter the serotonin pathway in the brain. A lower level of serotonin available in the brain is associated with depressive mood, suicidal symptoms, and impulsive behaviors. Oral contraceptives given with pyridoxine, or vitamin B6 (a competitive inhibitor of estrogen), can help mitigate some of the milder depressive symptoms.^21,22

---

Premenstrual Dysphoric Disorder

What historically has been referred to as premenstrual syndrome is now defined as premenstrual dysphoric disorder (PMDD) in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV).²³ This illness occurs during the premenstrual, or late luteal, phase of the menstrual cycle; symptoms remit during the beginning of the follicular phase. In psychiatry, PMDD is one of the few disorders in which both the precipitating and the remitting influences are linked to one physiologic process.

Premenstrual dysphoric disorder is classified as a mood disorder, "Depressive Disorder, Not Otherwise Specified," in the DSM-IV. Because of political controversy surrounding the inclusion of this disorder in the DSM-IV text, its criteria are listed in Appendix B, as an area needing further research.²³ Three factors are involved in making the diagnosis of PMDD. First, the symptoms must be primarily related to mood. Currently, PMDD symptoms are listed in the DSM-IV in order of their frequency of occurrence. After pooling the ratings from several centers across the United States, the most frequently reported symptom was depression.²⁴ Second, symptom severity has to be problematic enough in the woman's personal, social, work, or school history to interfere with functioning; this criterion is also used for other psychiatric disorders. Third, the symptoms need to be documented in relationship to the timing of the menstrual cycle; they must occur premenstrually and remit shortly after the onset of menses. This cyclic pattern needs to be documented by daily mood ratings.

DeJong and colleagues²⁵ examined women who reported premenstrual symptoms. Of those women who completed daily mood ratings, 88% were diagnosed with a psychiatric disorder; the majority had a major depressive disorder. This study reflects the necessity for careful prospective screening as to the timing and severity of symptoms for women presenting with premenstrual complaints.

Role of the Serotonin System

The role of the serotonin system in discriminating PMDD patients from normal control subjects is well-supported in the literature,²⁶ and it explains the efficacy of the selective serotonin reuptake inhibitors (SSRIs) in treating this disorder.^27,28 Whether by platelet serotonin uptake or imipramine binding studies, PMDD versus healthy comparison subjects have lower serotonergic function.²⁶ In a multicenter Canadian trial, Steiner and colleagues²⁸ examined the clinical efficacy of fluoxetine at 20 mg per day versus 60 mg per day throughout the menstrual cycle in women with PMDD. The 20-mg dosage was as effective as the 60-mg dosage, with fewer side effects. Both dosages were more effective than the placebo. A multicenter sertraline trial²⁷ also showed significantly greater efficacy of active drug versus placebo. Ongoing studies are addressing whether these antidepressant medications can be effective when administered only in the luteal phase;²⁹ many women do not want a chronic treatment for a periodic illness. Additionally, side effects from these medications may still be problematic, which can lead to noncompliance.

Sleep Deprivation

For this reason, our laboratory has been investigating nonpharmacologic treatment strategies for PMDD. Based on circadian theories, we utilize sleep deprivation and phototherapy.^30-33 Gender differences in the hormonal modulation of the circadian system have been well-documented. In animal studies, estrogen has been found to shorten the free-running period (the length of the sleep/wake cycle [humans] or rest/activity cycle [animals] in temporal isolation [non-entrained conditions]), which is the length of day/night cycles in temporal isolation studies.^34,35 It also advances the timing of activity onset and helps to maintain internal phase (timing) relationships between different circadian components. In ovariectomized hamsters, circadian rhythms become desynchronized. When estrogen is reinstituted, the synchronous effect is regained.³⁶
Both estradiol and progesterone affect the development of the part of the brain that regulates circadian rhythms, the suprachiasmatic nucleus.³⁷ Estradiol and progesterone also affect the response to light that controls circadian rhythms.^38,39 In human studies, females continue to demonstrate shorter free-running periods in temporal isolation.^40,41 Desynchronization tends to occur at certain endocrine phases of the menstrual cycle.⁴² Circadian disturbances in melatonin amplitude and phase also occur during specific menstrual cycle phases.⁴³

These circadian rhythms can be realigned by using light to change the sleep cycle, or the underlying circadian clock. Sleep deprivation can improve mood in one day for patients with major depression;⁴⁴ however, they may relapse after returning to sleep. Patients with premenstrual depression improve after a night of sleep deprivation but do not relapse after a night of recovery sleep.^30,33

---

Light Therapy

Light treatment also significantly reduces depressive symptoms in patients with PMDD.^31,32 These patients remain well for up to four years on the light treatment, but relapse is likely if the light treatment is discontinued. Our laboratory also has been researching the efficacy of light treatment for childhood and adolescent depression.⁴⁵ Preliminary evidence suggests similar therapeutic effects of light; however, more work in this area is necessary.

The effects of light therapy may be mediated through melatonin. Melatonin is probably one of the best markers for circadian rhythms in humans; it is not as affected by stress, diet, or exercise as other circadian hormonal markers are. During four different phases of the menstrual cycle - the early follicular, late follicular, mid-luteal, and late luteal - women with PMDD have a lower or blunted amplitude of the melatonin rhythm, which is an important regulator of other internal rhythms.⁴⁶ This finding was replicated in a larger study.⁴³ Light treatment may improve women's mood, but the melatonin rhythm is still very blunted.

Light is perceived or responded to differently in patients with premenstrual depression compared with normal control subjects.³⁹ In the luteal phase, the melatonin rhythm does not advance in response to morning bright light as it does for normal control subjects. Instead, patients with premenstrual depression either have no response to the light or their melatonin rhythm is delayed, in the opposite direction. These findings suggest that women with PMDD have an inappropriate response to light, which is critical to synchronize rhythms. The result may be that circadian rhythms become desynchronized, thereby contributing to mood disturbances in PMDD.

Postpartum Affective Illness

The postpartum period is a highly vulnerable time for the development of mood disorders. Three postpartum psychiatric syndromes are recognized and distinguished by symptoms and severity:

1. "Maternity blues" is a relatively mild syndrome characterized by rapid mood shifts; it occurs in up to 80% of women and, therefore, is not considered a psychiatric disorder.
2. A more severe depressive syndrome with melancholia is experienced by 10% to 15% of postpartum women.
3. Postpartum psychosis, the most severe syndrome, is a medical emergency.

Postpartum depression has been recognized in the DSM-IV, although the criteria for the onset of depressive symptoms within four weeks postpartum are too limiting to be clinically accurate. Studies by Kendall and colleagues⁴⁷ and Paffenbarger⁴⁸ indicate a relatively low incidence of mental illness during pregnancy but a very dramatic rise within the first few months postpartum.

The Marc Society, an international organization for the study of psychiatric illness related to childbearing, recognizes the time of vulnerability for postpartum depression and psychosis as one year after delivery. The early episodes of postpartum psychiatric symptoms (occurring within four weeks of delivery) are often characterized by anxiety and agitation. Depressions that have a more insidious onset may not peak until three to five months postpartum and are characterized more by psychomotor retardation. Three to five months postpartum is also the peak time of postpartum hypothyroidism, which occurs in about 10% of women.¹⁴ Postpartum hypothyroidism can be predicted early in pregnancy by measuring thyroid antibodies.⁴⁹

The risk of developing postpartum psychosis is 1 in 500 to 1 in 1000 for the first delivery but increases to 1 in 3 for subsequent deliveries for those women who had it with the first delivery.⁴⁷ Unlike postpartum mood disturbances, postpartum psychosis has an acute onset. In addition to having had a previous psychotic episode, those at increased risk for developing postpartum psychosis include women who are primiparous (bearing one child), have a personal history of postpartum depression or a family history of a mood disorder, and are over 25 years of age.

In general, postpartum psychiatric episodes are characterized by a young age of onset, an increased frequency of episodes, decreased psychomotor retardation, and more confusion, which often complicates the diagnostic picture. Women with postpartum psychiatric disorders often have a family history of mood disorders. In those women with a previous history of a postpartum depression, there is at least a 50% chance of recurrence.⁵⁰ There is also a high likelihood of recurrence of depression outside the postpartum period.⁵¹ Some of the studies conducted before effective treatments were available followed these women longitudinally and found an increased incidence of depressive relapse at menopause.⁵²

---

Affective Illness at Menopause

Adhering to psychiatric diagnostic criteria, Reich and Winokur⁵⁰ found an increase in affective illness around the age of 50, the mean age for the onset of menopause. Angst⁴ also suggested that an increased frequency of cycling occurs in bipolar women around the age of 50. In a cross-national study, Weissman⁵³ found that the peak of new onsets of depressive illness occurs in the 45-to-50-year age range in women.

Controversy surrounds the diagnosis and treatment of psychiatric illness during menopause. Studies in this area are fraught with methodologic problems, particularly with regard to making careful psychiatric diagnoses using standardized criteria. Often, decisions regarding hormone replacement therapy for mood disturbances at menopause involve accessibility to the health care system. Women who have access to a specialist often receive hormone replacement; primary care physicians, however, often prescribe benzodiazepines. Women who do not have access to health care providers often follow media recommendations of vitamins and over-the-counter preparations.

Hormone replacement therapy regimens differ in their ratio of progesterone to estrogen. Progesterone is an anesthetic in animals; in women it also can be acutely "depressiogenic," especially in women who have had previous episodes of depression.^55-56 Without estrogen, the down-regulation of serotonin receptors with antidepressants does not occur in animals.⁵⁷ Similarly, in perimenopausal women with depression, there is a greater magnitude of treatment effect when estrogen is added to an SSRI than when women are treated with an SSRI (fluoxetine) alone or treated with estrogen alone.⁵⁸ Estrogen also may enhance melatonin amplitude, another possible mechanism for its beneficial effect on mood, sleep, and circadian rhythms (B.L.P. et al, unpublished data, 1999).

Conclusion

Fluctuations in reproductive hormone levels in women can have a significant impact on mood. Thyroid function also plays an important role in the regulation of mood in women, and it should be monitored during times of reproductive hormonal change, when there may be an increased risk of developing hypothyroidism.

Antidepressant drugs have proven effective for treating hormonally linked mood disorders such as PMDD. However, side effects may lead to failure to take medication. For this reason, nonpharmacologic interventions such as light therapy or sleep deprivation may be more effective for some patients.

This article appeared in the Journal of Gender Specific Medicine. Authors: Barbara L. Parry, MD, and Patricia Haynes, BA

Dr. Parry is Professor of Psychiatry at the University of California, San Diego. Ms. Haynes is a graduate student in psychology at the University of California, San Diego, and in the San Diego State University Joint Doctoral Program.

A previous study by Dr. Parry was funded by Pfizer Inc. She received speaker's fees from Eli Lilly Company.

References:

1. Weissman MM, Leaf PJ, Holzer CE, et al. The epidemiology of depression: An update on sex differences in rates. J Affect Disord 1984;7:179-188.
2. Kessler RC, McGonagle KA, Swartz M, et al. Sex and depression in the National Comorbidity Survey, Pt I: Lifetime prevalence, chronicity and recurrence. J Affect Disord 1993;29:85-96.
3. Angst J, Dobler-Mikola A. Do the diagnostic criteria determine the sex ratio in depression? J Affect Disord 1984;7:189-198.
4. Angst J. The course of affective disorders, Pt II: Typology of bipolar manic-depressive illness. Arch Gen Psychiatry, Nervankr 1978;226:65-73.
5. Angold A, Costello EF, Worthman CM. Puberty and depression: The roles of age, pubertal status and pubertal timing. Psychol Med 1998;28:51-61.
6. Dunner DL, Fieve RR. Clinical factors in lithium carbonate prophylaxis failure. Arch Gen Psychiatry 1974; 30:229-233.
7. Wehr TA, Sack DA, Rosenthal NE, Cowdrey RW. Rapid cycling affective disorder: Contributing factors and treatment responses of 51 patients. Am J Psychiatry 1988;145:179-184.
8. Cowdry RW, Wehr TA, Zis AP, Goodwin FK. Thyroid abnormalities associated with rapid-cycling bipolar illness. Arch Gen Psychiatry 1983;40:414-420.
9. Williams RH, Wilson JD, Foster DW. Williams' Textbook of Endocrinology. Philadelphia, PA: WB Saunders Co; 1992.
10. Cho JT, Bone S, Dunner DL, et al. The effects of lithium treatment on thyroid function in patients with primary affective disorder. Am J Psychiatry 1979;136:115-116.
11. Transbol I, Christiansen C, Baastrup PC. Endocrine effects of lithium, Pt I: Hypothyroidism, its prevalence in long-term treated patients. Acta Endocrinologica (Copenhagen) 1978;87:759-767.
12. Kukopulos A, Reginaldi P, Laddomada GF, et al. Course of the manic- depressive cycle and changes caused by treatments. Pharmacopsychiatry 1980;13:156-167.
13. Wehr TA, Goodwin FK. Rapid cycling in manic depressives induced by tricyclic antidepressants. Arch Gen Psychiatry 1979;36:555-559.
14. Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective disorder: A description of the syndrome and preliminary findings with light therapy. Arch Gen Psychiatry 1984:41:72-80.
15. Rosenthal NE, Sack DA, James SP, et al. Seasonal affective disorder and phototherapy. Ann N Y Acad Sci 1985;453:260-269.
16. Oppenheim G. A case of rapid mood cycling with estrogen: Implications for therapy. J Clin Psychiatry 1984;45:34-35.
17. Amino N, More H, Iwatani Y, et al. High prevalence of transient post-partum thyrotoxicosis and hypothyroidism. N Engl J Med 1982;306:849-852.
18. Spitz IM, Zylber-Haran A, Trestian S. The thyrotropin (TSH) profile in isolated gonadotropin deficiency: A model to evaluate the effect of sex steroids on TSH secretion. J Clin Endocrinol Metab 1983;57:415-420.
19. Ramey JN, Burrow GN, Polackwich RJ, Donabedian RK. The effect of oral contraceptive steroids on the response of thyroid-stimulating hormone to thyrotropin- releasing hormone. J Clin Endocrinol Metab 1975;40:712-714.
20. Stancer HC, Persad E. Treatment of intractable rapid-cycling manic- depressive disorder with levothyroxine: Clinical observations. Arch Gen Psychiatry 1982;39:311-312.
21. Parry BL, Rush AJ. Oral contraceptives and depressive symptomatology: Biologic mechanisms. Compr Psychiatry 1979;20:347-358.
22. Williams MJ, Harris RI, Dean BC. Controlled trial of pyridoxine in the premenstrual syndrome. Journal of International Medical Research 1985;13:174-179.
23. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: APA; 1994.
24. Hurt SW, Schnurr PP, Severino SK et al. Late luteal phase dysphoric disorder in 670 women evaluated for premenstrual complaints. Am J Psychiatry 1992;149:525-530.
25. DeJong R, Rubinow DR, Roy-Byrne P, et al. Premenstrual mood disorder and psychiatric illness. Am J Psychiatry 1985;142:1359-1361.
26. American Psychiatric Association. Task Force on DSM-IV. Widiger T, ed. DSM-IV Sourcebook. Washington, DC: APA; 1994.
27. Yonkers, KA, Halbreich U, Freeman E, et al, for the Sertraline Premenstrual Dysphoric Collaborative Study Group. Symptomatic improvement of premenstrual dysphoric disorder with sertraline treatment: A randomized controlled trial. JAMA 1997;278:983-988.
28. Steiner M, Steinberg S, Stewart D, et al, for the Canadian Fluoxetine/Premenstrual Dysphoria Collaborative Study Group. Fluoxetine in the treatment of premenstrual dysphoria. N Engl J Med 1995;332:1529-1534.
29. Steiner M, Korzekwa M, Lamont J, Wilkins A. Intermittent fluoxetine dosing in the treatment of women with premenstrual dysphoria. Psychopharmacol Bull 1997;33:771-774.
30. Parry BL, Wehr TA. Therapeutic effects of sleep deprivation in patients with premenstrual syndrome. Am J Psychiatry 1987;144:808-810.
31. Parry BL, Berga SL, Mostofi N, et al. Morning versus evening bright light treatment of late luteal phase dysphoric disorder. Am J Psychiatry 1989;146:1215-1217.
32. Parry BL, Mahan AM, Mostofi N, et al. Light therapy of late luteal phase dysphoric disorder: An extended study. Am J Psychiatry 1993;150:1417-1419.
33. Parry BL, Cover H, LeVeau B, et al. Early versus late partial sleep deprivation in patients with premenstrual dysphoric disorder and normal comparison subjects. Am J Psychiatry 1995;152:404-412.
34. Albers EH, Gerall AA, Axelson JF. Effect of reproductive state on circadian periodicity in the rat. Physiol Behav 1981;26:21-25.
35. Morin LP, Fitzgerald KM, Zucker I. Estradiol shortens the period of hamster circadian rhythms. Science 1977;196:305-306.
36. Thomas EM, Armstrong SM. Effect of ovariectomy and estradiol on unity of female rat circadian rhythms. Am J Physiol 1989;257:R1241-R1250.
37. Swaab DF, Fliers E, Partiman TS. The suprachiasmatic nucleus of the human brain in relation to sex, age and senile dementia. Brain Res 1985;342:37-44.
38. Davis FC, Darrow JM, Menaker M. Sex differences in the circadian control of hamster wheel-running activity. Am J Physiol 1983;244:R93-R105.
39. Parry BL, Udell C, Elliott JA, et al. Blunted phase-shift responses to morning bright light in premenstrual dysphoric disorder. J Biol Rhythms 1997;12:443-456.
40. Wever RA. Properties of human sleep-wake cycles: Parameters of internally synchronized free-running rhythms. Sleep 1984;7:27-51.
41. Wirz-Justice A, Wever RA, Aschoff J. Seasonality in freerunning circadian rhythms in man. Naturwissenschaften 1984;71:316-319.
42. Wagner DR, Monline ML, Pollack CP. Internal desynchronization of circadian rhythms in free-running young females occurs at specific phases of the menstrual cycle. Sleep Research Abstracts 1989;18:449.
43. Parry BL, Berga SL, Mostofi N, et al. Plasma melatonin circadian rhythms during the menstrual cycle and after light therapy in premenstrual dysphoric disorder and normal control subjects. J Biol Rhythms 1997;12:47-64.
44. Gillin JC. The sleep therapies of depression. Prog Neuropsychopharmacol Biol Psychiatry 1983;7:351-364.
45. Parry BL, Heyneman E, Newton RP, et al. Light therapy for childhood and adolescent depression. Paper presented at: Society for Research on Biological Rhythms; May 6-10, 1998; Jacksonville, FL.
46. Parry BL, Berga SL, Kripke DF, et al. Altered waveform of plasma nocturnal melatonin secretion in premenstrual depression. Arch Gen Psychiatry 1990;47:1139-1146.
47. Kendall RE, Chalmers JC, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry 1987;150:662-673.
48. Paffenbarger RS. Epidemiological aspects of mental illness associated with childbearing. In: Brockington IF, Kumar R, eds. Motherhood and Mental Illness. London, UK: Academic Press; 1982:21-36.
49. Jansson R, Bernander S, Karlesson A, et al. Autoimmune thyroid depression in the postpartum period. J Clin Endocrinol Metab 1984;58:681-687.
50. Reich T, Winokur G. Postpartum psychoses in patients with manic depressive disease. J Nerv Ment Dis 1970;151:60-68.
51. Cohen L. Impact of pregnancy on risk for relapse of MDD. No. 57. Presented at: Paper Session 19-Psychiatric Issues in Women. American Psychiatric Association Meeting; May 17-22, 1997; San Diego, CA.
52. Protheroe C. Puerperal psychoses: A long-term study. Br J Psychiatry 1969;115:9-30.
53. Weissman, MW. Epidemiology of major depression in women. Paper presented at: American Psychiatric Association Meeting. Women and the Controversies in Hormonal Replacement Therapy. 1996, New York, NY.
54. Sherwin BB. The impact of different doses of estrogen and progestin on mood and sexual behavior in postmenopausal women. J Clin Endocrinol Metab 1991;72:336-343.
55. Sherwin BB, Gelfand MM. A prospective one-year study of estrogen and progestin in postmenopausal women: Effects on clinical symptoms and lipoprotein lipids. Obstet Gynecol 1989;73:759-766.
56. Magos AL, Brewster E, Singh R, et al. The effects of norethisterone in postmenopausal women on estrogen replacement therapy: A model for the premenstrual syndrome. Br J Obstet Gynaecol 1986;93:1290-1296.
57. Kendall DA, Stancel AM, Enna SJ. Imipramine: Effect of ovarian steroids on modification in serotonin receptor binding. Science 1981;211:1183-1185.
58. Tam LW, Parry BL. New findings in the treatment of depression at menopause. Archives of Women's Mental Health. In press.

next: Antidepressant Medication Side-Effects in Postpartum Depression
~ depression library articles
~ all articles on depression

Part 9: Forms Of Help Beyond Triumphant Journey Cyberguide

Your Triumphant Journey through overeating to freedom will introduce you to many new feelings, ideas and opportunities. Here are listed some forms of support, help, inspiration, guidance and possible sources of joy and new friends which you can choose to access.

Some of these suggestions are obvious in that they relate directly to overeating. Others may surprise you since they relate to causes of overeating which may remain unknown to you. Still others relate to developing strength to meet your challenges. Others yet, relate to nourishing unknown wells of creativity and sources of joy within you waiting to be realized.

Experiment with these areas. Let yourself be surprised at the benefits you might reap. Give yourself, not one, but lots of opportunities to heal, grow and be happy in this life.

1. Read books and articles about overeating. They can increase your understanding of your behavior and your history with food.
2. Listen to relaxing audio tapes. They can help you internally soothe yourself.
3. Keep a journal. Writing your thoughts, feelings, reactions, dreams and fantasies can help bring unknown aspects of yourself to your attention.
4. Build and maintain contact with kind and supportive people. This can help you gain new perspectives about yourself. You can begin to learn what you have to offer others, and how you can have more positive relationships in your life.
   Programs such as Overeaters Anonymous and Al-Anon can introduce you to people who understand your struggle with overeating and too much self sacrifice..
5. Other 12 step programs may be helpful to you. When you hear people describe feelings and histories similar to your own you may be free to feel or know something that has been lost to your conscious awareness.
6. Meet regularly with a psychotherapist who understands the underlying issues of eating disorders. This can be helpful as your history unfolds and your secrets emerge.
7. Explore your relationship with your body. Give yourself the opportunity to release the tensions and emotions your body has been carrying for years. Give yourself the opportunity to discover what joy you can feel as your body becomes more strong and flexible.
   • Take a dance class.
   • Participate in a sport.
   • Do yoga on a regular basis.
   • Do some kind of aerobics exercise regularly.
8. Explore the creative arts. Give your newly emerging feelings and ideas opportunity for expression. You may not be able to say in words what these new feelings are. But you may be able to paint them or sculpt them or dance to them.
   Take a class in anything creative::
   • painting
   • sculpting
   • dance
   • gardening
   • flower arranging
   • home or office design
   • web page design
9. Take on a learning project where you are a total beginner. Start to learn a skill in which you have no previous training or background. Putting yourself in the position of being a beginner, being kind and supportive to yourself as you are awkward and open, will give you appreciation for what you can learn and become.
   It will also teach you the value of being kind to yourself as your new skills develop and become proficient over time. Patience and kindness for yourself over time is very important for a successful Triumphant Journey..
10. Read personal affirmations out loud several times every morning. Read them out loud to your furniture, garden and pets. Read them out loud to your face in the mirror.

Pick one or more from the Affirmations Lists [1] and [2] and consistently read them every morning for 30 days. After 30 days, add, subtract or change your choices. Then read your new choices out loud every morning for 30 days.

Pick the statements that you want to be true for you. You can't make a mistake in which you choose or how many you choose. This is a way to nourish your deep self in precisely the way you need in the moment.

You may be spending a great deal of time, money, emotional grief, numbness and energy in isolation because of your food related behavior. How much energy you put toward the forms of help listed in this section depends on how ready and willing you are to respect and work toward a better life.

You may be willing but only ready to do a little for yourself right now. That's okay. That's your beginning and beginning is what counts.

You can choose any, all, or a combinations of these options. There need not be any competition here. Each of these avenues help empower, inform, support, encourage and allow you to become strong enough to know and appreciate yourself. Each contributes to your learning to care for yourself.

next: Eating Disorder Early Recovery: 'How Do I Begin?' The 84,000 Ways
~ all triumphant journey articles
~ eating disorders library
~ all articles on eating disorders

Brand Name: Precose
Generic Name: Acarbose

Contents:

Description
Clinical Pharmacology
Clinical Trials
Indications and Usage
Contraindications
Precautions
Adverse Reactions
Overdosage
Dosage and Administration
Supplied

Precose, acarbose, patient information (in plain English)

Description

Precose® (acarbose tablets) is an oral alpha-glucosidase inhibitor for use in the management of type 2 diabetes mellitus. Acarbose is an oligosaccharide which is obtained from fermentation processes of a microorganism, Actinoplanes utahensis, and is chemically known as O-4,6-dideoxy- 4-[[(1S,4R,5S,6S)-4,5,6-trihydroxy-3-(hydroxymethyl)-2-cyclohexen-1-yl]amino]- α-D-glucopyranosyl-(1 → 4)-O-α-D-glucopyranosyl-(1 → 4)-D-glucose. It is a white to off-white powder with a molecular weight of 645.6. Acarbose is soluble in water and has a pK_a of 5.1. Its empirical formula is C₂₅H₄₃NO₁₈ and its chemical structure is as follows:

Precose is available as 25 mg, 50 mg and 100 mg tablets for oral use. The inactive ingredients are starch, microcrystalline cellulose, magnesium stearate, and colloidal silicon dioxide.

top

Clinical Pharmacology

Acarbose is a complex oligosaccharide that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. As a consequence of plasma glucose reduction, Precose reduces levels of glycosylated hemoglobin in patients with type 2 diabetes mellitus. Systemic non-enzymatic protein glycosylation, as reflected by levels of glycosylated hemoglobin, is a function of average blood glucose concentration over time.

Mechanism of Action: In contrast to sulfonylureas, Precose does not enhance insulin secretion. The antihyperglycemic action of acarbose results from a competitive, reversible inhibition of pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolase enzymes. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine, while the membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. In diabetic patients, this enzyme inhibition results in a delayed glucose absorption and a lowering of postprandial hyperglycemia.

Because its mechanism of action is different, the effect of Precose to enhance glycemic control is additive to that of sulfonylureas, insulin or metformin when used in combination. In addition, Precose diminishes the insulinotropic and weight-increasing effects of sulfonylureas.

Acarbose has no inhibitory activity against lactase and consequently would not be expected to induce lactose intolerance.

---

 

---

Pharmacokinetics:

Absorption: In a study of 6 healthy men, less than 2% of an oral dose of acarbose was absorbed as active drug, while approximately 35% of total radioactivity from a 14C-labeled oral dose was absorbed. An average of 51% of an oral dose was excreted in the feces as unabsorbed drug-related radioactivity within 96 hours of ingestion. Because acarbose acts locally within the gastrointestinal tract, this low systemic bioavailability of parent compound is therapeutically desired. Following oral dosing of healthy volunteers with 14C-labeled acarbose, peak plasma concentrations of radioactivity were attained 14-24 hours after dosing, while peak plasma concentrations of active drug were attained at approximately 1 hour. The delayed absorption of acarbose-related radioactivity reflects the absorption of metabolites that may be formed by either intestinal bacteria or intestinal enzymatic hydrolysis.

Metabolism: Acarbose is metabolized exclusively within the gastrointestinal tract, principally by intestinal bacteria, but also by digestive enzymes. A fraction of these metabolites (approximately 34% of the dose) was absorbed and subsequently excreted in the urine. At least 13 metabolites have been separated chromatographically from urine specimens. The major metabolites have been identified as 4-methylpyrogallol derivatives (i.e., sulfate, methyl, and glucuronide conjugates). One metabolite (formed by cleavage of a glucose molecule from acarbose) also has alpha-glucosidase inhibitory activity. This metabolite, together with the parent compound, recovered from the urine, accounts for less than 2% of the total administered dose.

Excretion: The fraction of acarbose that is absorbed as intact drug is almost completely excreted by the kidneys. When acarbose was given intravenously, 89% of the dose was recovered in the urine as active drug within 48 hours. In contrast, less than 2% of an oral dose was recovered in the urine as active (i.e., parent compound and active metabolite) drug. This is consistent with the low bioavailability of the parent drug. The plasma elimination half-life of acarbose activity is approximately 2 hours in healthy volunteers. Consequently, drug accumulation does not occur with three times a day (t.i.d.) oral dosing.

Special Populations: The mean steady-state area under the curve (AUC) and maximum concentrations of acarbose were approximately 1.5 times higher in elderly compared to young volunteers; however, these differences were not statistically significant. Patients with severe renal impairment (Clcr < 25 mL/min/1.73m2) attained about 5 times higher peak plasma concentrations of acarbose and 6 times larger AUCs than volunteers with normal renal function. No studies of acarbose pharmacokinetic parameters according to race have been performed. In U.S. controlled clinical studies of Precose in patients with type 2 diabetes mellitus, reductions in glycosylated hemoglobin levels were similar in Caucasians (n=478) and African-Americans (n=167), with a trend toward a better response in Latinos (n=132).

Drug-Drug Interactions: Studies in healthy volunteers have shown that Precose has no effect on either the pharmacokinetics or pharmacodynamics of nifedipine, propranolol, or ranitidine. Precosedid not interfere with the absorption or disposition of the sulfonylurea glyburide in diabetic patients. Precosemay affect digoxin bioavailability and may require dose adjustment of digoxin by 16% (90% confidence interval: 8-23%), decrease mean Cmax of digoxin by 26% (90% confidence interval: 16-34%) and decreases mean trough concentrations of digoxin by 9% (90% confidence limit: 19% decrease to 2% increase). (See PRECAUTIONS, Drug Interactions).

The amount of metformin absorbed while taking Precosewas bioequivalent to the amount absorbed when taking placebo, as indicated by the plasma AUC values. However, the peak plasma level of metformin was reduced by approximately 20% when taking Precose due to a slight delay in the absorption of metformin. There is little if any clinically significant interaction between Precose and metformin.

top

Clinical Trials

Clinical Experience from Dose Finding Studies in Type 2 Diabetes Mellitus Patients on Dietary Treatment Only: Results from six controlled, fixed-dose, monotherapy studies of Precose in the treatment of type 2 diabetes mellitus, involving 769 Precose-treated patients, were combined and a weighted average of the difference from placebo in the mean change from baseline in glycosylated hemoglobin (HbA1c) was calculated for each dose level as presented below:

Table 1

Mean Placebo-Subtracted Change in HbA1c in Fixed-Dose Monotherapy Studies
Dose of Precose*	N	Change in HbA1c %	p-Value
* Precose was statistically significantly different from placebo at all doses. Although there were no statistically significant differences among the mean results for doses ranging from 50 to 300 mg t.i.d., some patients may derive benefit by increasing the dosage from 50 to 100 mg t.i.d.
** Although studies utilized a maximum dose of 200 or 300 mg t.i.d., the maximum recommended dose for patients 60 kg is 100 mg t.i.d.
25 mg t.i.d.	110	-0.44	0.0307
50 mg t.i.d.	131	-0.77	0.0001
100 mg t.i.d.	244	-0.74	0.0001
200 mg t.i.d.**	231	-0.86	0.0001
300 mg t.i.d.**	53	-1.00	0.0001

Results from these six fixed-dose, monotherapy studies were also combined to derive a weighted average of the difference from placebo in mean change from baseline for one-hour postprandial plasma glucose levels as shown in the following figure:

¹* Precosewas statistically significantly different from placebo at all doses with respect to effect on one-hour postprandial plasma glucose.

²** The 300 mg t.i.d. Precose regimen was superior to lower doses, but there were no statistically significant differences from 50 to 200 mg t.i.d.

Clinical Experience in Type 2 Diabetes Mellitus Patients on Monotherapy, or in Combination with Sulfonylureas, Metformin or Insulin: Precose was studied as monotherapy and as combination therapy to sulfonylurea, metformin, or insulin treatment. The treatment effects on HbA1c levels and one-hour postprandial glucose levels are summarized for four placebo-controlled, double-blind, randomized studies conducted in the United States in Tables 2 and 3, respectively. The placebo-subtracted treatment differences, which are summarized below, were statistically significant for both variables in all of these studies.

Study 1 (n=109) involved patients on background treatment with diet only. The mean effect of the addition of Precoseto diet therapy was a change in HbA1c of -0.78%, and an improvement of one-hour postprandial glucose of -74.4 mg/dL.

In Study 2 (n=137), the mean effect of the addition of Precose to maximum sulfonylurea therapy was a change in HbA1c of -0.54%, and an improvement of one-hour postprandial glucose of -33.5 mg/dL.

In Study 3 (n=147), the mean effect of the addition of Precose to maximum metformin therapy was a change in HbA1c of -0.65%, and an improvement of one-hour postprandial glucose of -34.3 mg/dL.

Study 4 (n=145) demonstrated that Precose added to patients on background treatment with insulin resulted in a mean change in HbA1c of -0.69%, and an improvement of one-hour postprandial glucose of -36.0 mg/dL.

A one year study of Precose as monotherapy or in combination with sulfonylurea, metformin or insulin treatment was conducted in Canada in which 316 patients were included in the primary efficacy analysis (Figure 2). In the diet, sulfonylurea and metformin groups, the mean decrease in HbA1c produced by the addition of Precose was statistically significant at six months, and this effect was persistent at one year. In the Precose-treated patients on insulin, there was a statistically significant reduction in HbA1c at six months, and a trend for a reduction at one year.

Table 2: Effect of Precose on HbA1c

		HbA1c (%)a
Study	Treatment	Mean Baseline	Mean change from baselineb	Treatment Difference	p-Value
a HbA1c Normal Range: 4-6%
b After four months treatment in Study 1, and six months in Studies 2, 3, and 4
c SFU, sulfonylurea, maximum dose
d Although studies utilized a maximum dose of up to 300 mg t.i.d., the maximum recommended dose for patients ≤ 60 kg is 50 mg t.i.d.; the maximum recommended dose for patients > 60 kg is 100 mg t.i.d.
e Metformin dosed at 2000 mg/day or 2500 mg/day
f Mean dose of insulin 61 U/day
g Results are adjusted to a common baseline of 8.33%
1	Placebo Plus Diet	8.67	+0.33	—	—
	Precose 100 mg t.i.d. Plus Diet	8.69	-0.45	-0.78	0.0001
2	Placebo Plus SFUc	9.56	+0.24	—	—
	Precose 50-300d mg t.i.d. Plus SFUc	9.64	-0.30	-0.54	0.0096
3	Placebo Plus Metformine	8.17	+0.08 g	—	—
	Precose 50-100 mg t.i.d. Plus Metformine	8.46	-0.57 g	-0.65	0.0001
4	Placebo Plus Insulinf	8.69	+0.11	—	—
	Precose 50-100 mg t.i.d. Plus Insulinf	8.77	-0.58	-0.69	0.0001

Table 3: Effect of Precose on Postprandial Glucose

		One-Hour Postprandial Glucose (mg/dL)
Study	Treatment	Mean Baseline	Mean change from baselinea	Treatment Difference	p-Value
a After four months treatment in Study 1, and six months in Studies 2, 3, and 4
b SFU, sulfonylurea, maximum dose
c Although studies utilized a maximum dose of up to 300 mg t.i.d., the maximum recommended dose for patients ≤ 60 kg is 50 mg t.i.d.; the maximum recommended dose for patients > 60 kg is 100 mg t.i.d.
d Metformin dosed at 2000 mg/day or 2500 mg/day
e Mean dose of insulin 61 U/day
f Results are adjusted to a common baseline of 273 mg/dL
1	Placebo Plus Diet	297.1	+31.8	—	—
	Precose 100 mg t.i.d. Plus Diet	299.1	-42.6	-74.4	0.0001
2	Placebo Plus SFUb	308.6	+6.2	—	—
	Precose 50-300c mg t.i.d. Plus SFUb	311.1	-27.3	-33.5	0.0017
3	Placebo Plus Metformind	263.9	+3.3f	—	—
	Precose 50-100 mg t.i.d. Plus Metformind	283.0	-31.0f	-34.3	0.0001
4	Placebo Plus Insuline	279.2	+8.0	—	—
	Precose 50-100 mg t.i.d. Plus Insuline	277.8	-28.0	-36.0	0.0178

Figure 2: Effects of Precose () and Placebo () on mean change in HbA1c levels from baseline throughout a one-year study in patients with type 2 diabetes mellitus when used in combination with: (A) diet alone; (B) sulfonylurea; (C) metformin; or (D) insulin. Treatment differences at 6 and 12 months were tested: * p < 0.01; # p = 0.077.

top

Indications and Usage

Precose, as monotherapy, is indicated as an adjunct to diet to lower blood glucose in patients with type 2 diabetes mellitus whose hyperglycemia cannot be managed on diet alone. Precose may also be used in combination with a sulfonylurea when diet plus either Precose or a sulfonylurea do not result in adequate glycemic control. Also, Precosemay be used in combination with insulin or metformin. The effect of Precose to enhance glycemic control is additive to that of sulfonylureas, insulin, or metformin when used in combination, presumably because its mechanism of action is different.

In initiating treatment for type 2 diabetes mellitus, diet should be emphasized as the primary form of treatment. Caloric restriction and weight loss are essential in the obese diabetic patient. Proper dietary management alone may be effective in controlling blood glucose and symptoms of hyperglycemia. The importance of regular physical activity when appropriate should also be stressed. If this treatment program fails to result in adequate glycemic control, the use of Precose should be considered. The use of Precose must be viewed by both the physician and patient as a treatment in addition to diet, and not as a substitute for diet or as a convenient mechanism for avoiding dietary restraint.

---

 

---

top

Contraindications

Precose is contraindicated in patients with known hypersensitivity to the drug and in patients with diabetic ketoacidosis or cirrhosis. Precose is also contraindicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or in patients predisposed to intestinal obstruction. In addition, Precose is contraindicated in patients who have chronic intestinal diseases associated with marked disorders of digestion or absorption and in patients who have conditions that may deteriorate as a result of increased gas formation in the intestine.

top

Precautions

General

Hypoglycemia: Because of its mechanism of action, Precose when administered alone should not cause hypoglycemia in the fasted or postprandial state. Sulfonylurea agents or insulin may cause hypoglycemia. Because Precose given in combination with a sulfonylurea or insulin will cause a further lowering of blood glucose, it may increase the potential for hypoglycemia. Hypoglycemia does not occur in patients receiving metformin alone under usual circumstances of use, and no increased incidence of hypoglycemia was observed in patients when Precose was added to metformin therapy. Oral glucose (dextrose), whose absorption is not inhibited by Precose , should be used instead of sucrose (cane sugar) in the treatment of mild to moderate hypoglycemia. Sucrose, whose hydrolysis to glucose and fructose is inhibited by Precose , is unsuitable for the rapid correction of hypoglycemia. Severe hypoglycemia may require the use of either intravenous glucose infusion or glucagon injection.

Elevated Serum Transaminase Levels: In long-term studies (up to 12 months, and including Precose doses up to 300 mg t.i.d.) conducted in the United States, treatment-emergent elevations of serum transaminases (AST and/or ALT) above the upper limit of normal (ULN), greater than 1.8 times the ULN, and greater than 3 times the ULN occurred in 14%, 6%, and 3%, respectively, of Precose-treated patients as compared to 7%, 2%, and 1%, respectively, of placebo-treated patients. Although these differences between treatments were statistically significant, these elevations were asymptomatic, reversible, more common in females, and, in general, were not associated with other evidence of liver dysfunction. In addition, these serum transaminase elevations appeared to be dose related. In US studies including Precose doses up to the maximum approved dose of 100 mg t.i.d., treatment-emergent elevations of AST and/or ALT at any level of severity were similar between Precose-treated patients and placebo-treated patients (p ≥ 0.496).

In approximately 3 million patient-years of international post-marketing experience with Precose, 62 cases of serum transaminase elevations > 500 IU/L (29 of which were associated with jaundice) have been reported. Forty-one of these 62 patients received treatment with 100 mg t.i.d. or greater and 33 of 45 patients for whom weight was reported weighed < 60 kg. In the 59 cases where follow-up was recorded, hepatic abnormalities improved or resolved upon discontinuation of Precose in 55 and were unchanged in two. A few cases of fulminant hepatitis with fatal outcome have been reported; the relationship to acarbose is unclear.

Loss of Control of Blood Glucose: When diabetic patients are exposed to stress such as fever, trauma, infection, or surgery, a temporary loss of control of blood glucose may occur. At such times, temporary insulin therapy may be necessary.

Information for Patients:

Patients should be told to take Precose orally three times a day at the start (with the first bite) of each main meal. It is important that patients continue to adhere to dietary instructions, a regular exercise program, and regular testing of urine and/or blood glucose.

Precose itself does not cause hypoglycemia even when administered to patients in the fasted state. Sulfonylurea drugs and insulin, however, can lower blood sugar levels enough to cause symptoms or sometimes life-threatening hypoglycemia. Because Precose given in combination with a sulfonylurea or insulin will cause a further lowering of blood sugar, it may increase the hypoglycemic potential of these agents. Hypoglycemia does not occur in patients receiving metformin alone under usual circumstances of use, and no increased incidence of hypoglycemia was observed in patients when Precose was added to metformin therapy. The risk of hypoglycemia, its symptoms and treatment, and conditions that predispose to its development should be well understood by patients and responsible family members. Because Precose prevents the breakdown of table sugar, patients should have a readily available source of glucose (dextrose, D-glucose) to treat symptoms of low blood sugar when taking Precose in combination with a sulfonylurea or insulin.

If side effects occur with Precose, they usually develop during the first few weeks of therapy. They are most commonly mild-to-moderate gastrointestinal effects, such as flatulence, diarrhea, or abdominal discomfort, and generally diminish in frequency and intensity with time.

Laboratory Tests:

Therapeutic response to Precose should be monitored by periodic blood glucose tests. Measurement of glycosylated hemoglobin levels is recommended for the monitoring of long-term glycemic control.

Precose, particularly at doses in excess of 50 mg t.i.d., may give rise to elevations of serum transaminases and, in rare instances, hyperbilirubinemia. It is recommended that serum transaminase levels be checked every 3 months during the first year of treatment with Precose and periodically thereafter. If elevated transaminases are observed, a reduction in dosage or withdrawal of therapy may be indicated, particularly if the elevations persist.

Renal Impairment:

Plasma concentrations of Precose in renally impaired volunteers were proportionally increased relative to the degree of renal dysfunction. Long-term clinical trials in diabetic patients with significant renal dysfunction (serum creatinine > 2.0 mg/dL) have not been conducted. Therefore, treatment of these patients with Precose is not recommended.

Drug Interactions:

Certain drugs tend to produce hyperglycemia and may lead to loss of blood glucose control. These drugs include the thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel-blocking drugs, and isoniazid. When such drugs are administered to a patient receiving Precose, the patient should be closely observed for loss of blood glucose control. When such drugs are withdrawn from patients receiving Precose in combination with sulfonylureas or insulin, patients should be observed closely for any evidence of hypoglycemia.

Patients Receiving Sulfonylureas or Insulin: Sulfonylurea agents or insulin may cause hypoglycemia. Precose given in combination with a sulfonylurea or insulin may cause a further lowering of blood glucose and may increase the potential for hypoglycemia. If hypoglycemia occurs, appropriate adjustments in the dosage of these agents should be made. Very rarely, individual cases of hypoglycemic shock have been reported in patients receiving Precose therapy in combination with sulfonylureas and/or insulin.

Intestinal adsorbents (e.g., charcoal) and digestive enzyme preparations containing carbohydrate-splitting enzymes (e.g., amylase, pancreatin) may reduce the effect of Precose and should not be taken concomitantly.

Precose has been shown to change the bioavailability of digoxin when they are coadministered, which may require digoxin dose adjustment. (See CLINICAL PHARMACOLOGY, Drug-Drug Interactions).

Carcinogenesis, Mutagenesis, and Impairment of Fertility:

Eight carcinogenicity studies were conducted with acarbose. Six studies were performed in rats (two strains, Sprague-Dawley and Wistar) and two studies were performed in hamsters.

In the first rat study, Sprague-Dawley rats received acarbose in feed at high doses (up to approximately 500 mg/kg body weight) for 104 weeks. Acarbose treatment resulted in a significant increase in the incidence of renal tumors (adenomas and adenocarcinomas) and benign Leydig cell tumors. This study was repeated with a similar outcome. Further studies were performed to separate direct carcinogenic effects of acarbose from indirect effects resulting from the carbohydrate malnutrition induced by the large doses of acarbose employed in the studies. In one study using Sprague-Dawley rats, acarbose was mixed with feed but carbohydrate deprivation was prevented by the addition of glucose to the diet. In a 26-month study of Sprague-Dawley rats, acarbose was administered by daily postprandial gavage so as to avoid the pharmacologic effects of the drug. In both of these studies, the increased incidence of renal tumors found in the original studies did not occur. Acarbose was also given in food and by postprandial gavage in two separate studies in Wistar rats. No increased incidence of renal tumors was found in either of these Wistar rat studies. In two feeding studies of hamsters, with and without glucose supplementation, there was also no evidence of carcinogenicity.

Acarbose did not induce any DNA damage in vitro in the CHO chromosomal aberration assay, bacterial mutagenesis (Ames) assay, or a DNA binding assay. In vivo, no DNA damage was detected in the dominant lethal test in male mice, or the mouse micronucleus test.

Fertility studies conducted in rats after oral administration produced no untoward effect on fertility or on the overall capability to reproduce.

Pregnancy:

Teratogenic Effects: Pregnancy Category B. The safety of Precose in pregnant women has not been established. Reproduction studies have been performed in rats at doses up to 480 mg/kg (corresponding to 9 times the exposure in humans, based on drug blood levels) and have revealed no evidence of impaired fertility or harm to the fetus due to acarbose. In rabbits, reduced maternal body weight gain, probably the result of the pharmacodynamic activity of high doses of acarbose in the intestines, may have been responsible for a slight increase in the number of embryonic losses. However, rabbits given 160 mg/kg acarbose (corresponding to 10 times the dose in man, based on body surface area) showed no evidence of embryotoxicity and there was no evidence of teratogenicity at a dose 32 times the dose in man (based on body surface area). There are, however, no adequate and well-controlled studies of Precose in pregnant women. Because animal reproduction studies are not always predictive of the human response, this drug should be used during pregnancy only if clearly needed. Because current information strongly suggests that abnormal blood glucose levels during pregnancy are associated with a higher incidence of congenital anomalies as well as increased neonatal morbidity and mortality, most experts recommend that insulin be used during pregnancy to maintain blood glucose levels as close to normal as possible.

Nursing Mothers: A small amount of radioactivity has been found in the milk of lactating rats after administration of radiolabeled acarbose. It is not known whether this drug is excreted in human milk. Because many drugs are excreted in human milk, Precoseshould not be administered to a nursing woman.

Pediatric Use: Safety and effectiveness of Precose in pediatric patients have not been established.

Geriatric Use: Of the total number of subjects in clinical studies of Precose in the United States, 27 percent were 65 and over, while 4 percent were 75 and over. No overall differences in safety and effectiveness were observed between these subjects and younger subjects. The mean steady-state area under the curve (AUC) and maximum concentrations of acarbose were approximately 1.5 times higher in elderly compared to young volunteers; however, these differences were not statistically significant.

top

Adverse Reactions

Digestive Tract: Gastrointestinal symptoms are the most common reactions to Precose. In U.S. placebo-controlled trials, the incidences of abdominal pain, diarrhea, and flatulence were 19%, 31%, and 74% respectively in 1255 patients treated with Precose 50-300 mg t.i.d., whereas the corresponding incidences were 9%, 12%, and 29% in 999 placebo-treated patients. In a one-year safety study, during which patients kept diaries of gastrointestinal symptoms, abdominal pain and diarrhea tended to return to pretreatment levels over time, and the frequency and intensity of flatulence tended to abate with time. The increased gastrointestinal tract symptoms in patients treated with Precose are a manifestation of the mechanism of action of Precose and are related to the presence of undigested carbohydrate in the lower GI tract.

If the prescribed diet is not observed, the intestinal side effects may be intensified. If strongly distressing symptoms develop in spite of adherence to the diabetic diet prescribed, the doctor must be consulted and the dose temporarily or permanently reduced.

Elevated Serum Transaminase Levels: See PRECAUTIONS.

Other Abnormal Laboratory Findings: Small reductions in hematocrit occurred more often in Precose-treated patients than in placebo-treated patients but were not associated with reductions in hemoglobin. Low serum calcium and low plasma vitamin B6 levels were associated with Precose therapy but are thought to be either spurious or of no clinical significance.

Post Marketing Adverse Event Reports:

Additional adverse events reported from worldwide post marketing experience include hypersensitive skin reactions (e.g. rash, erythema, exanthema and uticaria), edema, ileus/subileus, jaundice and/or hepatitis and associated liver damage (See PRECAUTIONS.)

top

Overdosage

Unlike sulfonylureas or insulin, an overdose of Precose will not result in hypoglycemia. An overdose may result in transient increases in flatulence, diarrhea, and abdominal discomfort which shortly subside. In cases of overdosage the patient should not be given drinks or meals containing carbohydrates (polysaccharides, oligosaccharides and disaccharidees) for the next 4-6 hours.

top

Dosage and Administration

There is no fixed dosage regimen for the management of diabetes mellitus with Precose or any other pharmacologic agent. Dosage of Precose must be individualized on the basis of both effectiveness and tolerance while not exceeding the maximum recommended dose of 100 mg t.i.d. Precose should be taken three times daily at the start (with the first bite) of each main meal. Precose should be started at a low dose, with gradual dose escalation as described below, both to reduce gastrointestinal side effects and to permit identification of the minimum dose required for adequate glycemic control of the patient.

During treatment initiation and dose titration (see below), one-hour postprandial plasma glucose may be used to determine the therapeutic response to Precose and identify the minimum effective dose for the patient. Thereafter, glycosylated hemoglobin should be measured at intervals of approximately three months. The therapeutic goal should be to decrease both postprandial plasma glucose and glycosylated hemoglobin levels to normal or near normal by using the lowest effective dose of Precose, either as monotherapy or in combination with sulfonylureas, insulin or metformin.

Initial Dosage: The recommended starting dosage of Precose is 25 mg given orally three times daily at the start (with the first bite) of each main meal. However, some patients may benefit from more gradual dose titration to minimize gastrointestinal side effects. This may be achieved by initiating treatment at 25 mg once per day and subsequently increasing the frequency of administration to achieve 25 mg t.i.d.

Maintenance Dosage: Once a 25 mg t.i.d. dosage regimen is reached, dosage of Precoseshould be adjusted at 4-8 week intervals based on one-hour postprandial glucose or glycosylated hemoglobin levels, and on tolerance. The dosage can be increased from 25 mg t.i.d. to 50 mg t.i.d. Some patients may benefit from further increasing the dosage to 100 mg t.i.d. The maintenance dose ranges from 50 mg t.i.d. to 100 mg t.i.d. However, since patients with low body weight may be at increased risk for elevated serum transaminases, only patients with body weight > 60 kg should be considered for dose titration above 50 mg t.i.d. (see PRECAUTIONS). If no further reduction in postprandial glucose or glycosylated hemoglobin levels is observed with titration to 100 mg t.i.d., consideration should be given to lowering the dose. Once an effective and tolerated dosage is established, it should be maintained.

Maximum Dosage: The maximum recommended dose for patients ≤ 60 kg is 50 mg t.i.d. The maximum recommended dose for patients > 60 kg is 100 mg t.i.d.

Patients Receiving Sulfonylureas or Insulin: Sulfonylurea agents or insulin may cause hypoglycemia. Precose given in combination with a sulfonylurea or insulin will cause a further lowering of blood glucose and may increase the potential for hypoglycemia. If hypoglycemia occurs, appropriate adjustments in the dosage of these agents should be made.

top

How is Supplied

Precose is available as 25 mg, 50 mg or 100 mg round, unscored tablets. Each tablet strength is white to yellow-tinged in color. The 25 mg tablet is coded with the word "Precose" on one side and "25" on the other side. The 50 mg tablet is coded with the word "Precose" and "50" on the same side. The 100 mg tablet is coded with the word "Precose" and "100" on the same side. Precose is available in bottles of 100 and 50 mg strength in unit dose packages of 100.

Strength	NDC	Tablet Identification
Bottles of 100:	25 mg	0026-2863-51	Precose 25
	50 mg	0026-2861-51	Precose 50
	100 mg	0026-2862-51	Precose 100
Unit Dose Packages of 100:	50 mg	0026-2861-48	Precose 50

Do not store above 25°C (77°F). Protect from moisture. For bottles, keep container tightly closed.

Bayer Pharmaceuticals Corporation
400 Morgan Lane
West Haven, CT 06516

Made in Germany

08753825, R.3

©2004 Bayer Pharmaceuticals Corporation

Printed in U.S.A.

last updated 11/2008

Precose, acarbose, patient information (in plain English)

Detailed Info on Signs, Symptoms, Causes, Treatments of Diabetes

---

The information in this monograph is not intended to cover all possible uses, directions, precautions, drug interactions or adverse effects. This information is generalized and is not intended as specific medical advice. If you have questions about the medicines you are taking or would like more information, check with your doctor, pharmacist, or nurse.

back to: Browse all Medications for Diabetes

Information on the safety of antidepressants and mood stablizers during breastfeeding.

Bupropion and Breastfeeding (December 2002)

Q. I'm looking for further information regarding postpartum depression and the use of Wellbutrin (bupropion). Prior to my pregnancy I was taking Wellbutrin for depression and had relief of my symptoms. (I had also tried Celexa and Paxil with no success). When I became pregnant, I discontinued all medications but still felt really good and had a healthy pregnancy. I delivered my son about 6 weeks ago; I'm breastfeeding but I'm really starting to feel pretty down and overwhelmed. I'm wondering if I can go back on Wellbutrin and still continue breastfeeding?

A. Data have accumulated over the last few years on the use of antidepressants in nursing mothers. It appears that all antidepressants are secreted into the breast milk; however, the amount of medication to which the nursing child is exposed appears to be relatively small. We have the most information is available for fluoxetine (Prozac), , paroxetine (Paxil), and the tricyclic antidepressants. In general, one should try to choose an antidepressant for which there are data to support its safety during breastfeeding. However, there are often situations where one may choose another antidepressant that has not been as well characterized. For instance, if a woman has not responded well to any of the above medications.

To date, there has been only one report on the use of bupropion in two breastfeeding mothers. Serum levels of bupropion and its metabolite were undetectable in the infants, and there were no observed adverse events in the nursing infants. While this information is reassuring, further study is needed to fully determine the effects of bupropion in nursing infants.

In general, the risk of adverse events in the nursing infant appears to be low. The child should be monitored for any changes in behavior, level of alertness, or sleep and feeding patterns. In this setting, collaboration with the child's pediatrician is essential.

Source: Baab SW, Peindl KS, Piontek CM, Wisner KL. 2002. Serum bupropion levels in two breastfeeding mother-infant pairs. J Clin Psychiatry 63: 910-1.

Paxil and Breastfeeding (August 2002)

Q. I am trying to get more information about the effects of Paxil (Paroxetine) and breastfeeding. How safe is it? Any side effects for the baby? My daughter is 7 months old and is down to 2-3 feedings a day. I plan to start Paxil and would like to continue with two feedings a day if it is safe to do so. If I take the Paxil at bedtime, is there a time of day when the level is lower in my body and less of the drug would be passed on to the baby, or is the level constant so the time of feeding and time of taking the Paxil do not matter? I would appreciate any information. My daughter had a very hard first five months and I don't want to pass along the Paxil to her if it is not safe or if it may cause her any side effects. Thanks.

A. All medications are secreted into the breast milk, although concentrations appear to vary. There is a fair amount of information on the use of Paxil in nursing women. While Paxil may be detected in the breast milk, there have been no reports of adverse events in the nursing infant. The only situation where one may want to avoid breastfeeding is when the baby is premature or has signs of hepatic immaturity, which may make it more difficult for the infant to metabolize the medication to which he or she is exposed. Premature babies are also probably more vulnerable to the toxic effects of these medications.

There may be some ways to minimize the amount of medication to which the nursing infant is exposed. First, the lowest dose of medication that is effective should be used. Second, in older infants, it may be possible to time the feedings so as to minimize exposure. The levels of Paxil in the breast milk peak about 8 hours after ingestion of medication and decline thereafter, reaching the lowest levels immediately before the next dose of medication is to be taken. Theoretically, the amount of medication to which the infant is exposed could be reduced by avoiding nursing during times at which the medication concentration in the breast milk would be the highest (i.e., 8 hours after taking the medication). Studies with indicate that this approach leads to a 20% reduction in the amount of medication to which the infant is exposed.

Sources: Burt VK, Suri R, Altshuler L, Stowe Z, Hendrick VC, Muntean E. The use of psychotropic medications during breast-feeding. Am J Psychiatry 2001; 158(7): 1001-9.
Newport DJ, Hostetter A, Arnold A, Stowe ZN. The treatment of postpartum depression: minimizing infant exposures. J Clin Psychiatry 2002; 63(7): 31-44.

---

Breastfeeding and Bipolar Disorder (June 2002)

Q. I was diagnosed with bipolar disorder (manic depression) in July of 2001. In January, I became pregnant and immediately stopped my Lithium. I am now 18 weeks along and my psychiatrist would like me to start on Lithium again. I do not want to, as I would like to breastfeed. It seems that the biggest concern is that I will experience postpartum depression. One suggestion was to start an antidepressant at 8 months and to continue it through breastfeeding. What is a safe antidepressant to use while breastfeeding? Also are there any safe mood stabilizers to use while breastfeeding?

A. Women with bipolar disorder are particularly vulnerable during the postpartum period. Studies indicate at least 50% of women with bipolar disorder relapse during the first few months after childbirth. While most women present with depressive symptoms, there is also a significant risk of hypomania or mania. Prophylactic treatment with a mood stabilizer, initiated either towards the end of pregnancy or at the time of delivery, significantly reduces the risk of postpartum illness. Thus far we have no data on the use of antidepressants in this setting. Although antidepressants may help reduce the risk of recurrent illness in women with unipolar depression, there is evidence that using antidepressants without a mood stabilizer in patients with bipolar disorder may increase the likelihood of having a hypomanic or manic episode.

We often recommend that women with bipolar disorder remain on a mood stabilizer during the postpartum period; however, the use of medications during the postpartum period is complicated by the issue of breastfeeding. All medications are secreted into the breast milk, although their concentrations appear to vary. Lithium is found in the breast milk at relatively high concentrations, and there have been reports of toxicity in nursing infants exposed to lithium in the breast milk. Symptoms of toxicity in these infants include lethargy, poor muscle tone, and changes on the electrocardiogram. While there are risks associated with breastfeeding on lithium, it is probably the safest mood stabilizer to use in this setting. Other mood stabilizers, like valproic acid and carbamazepine, may cause liver damage in the nursing infant, which is a serious and potentially life-threatening complication.

For women with bipolar disorder, breastfeeding raises concerns for another reason. For a young infant, breastfeeding entails multiple feedings during the night. Sleep deprivation is destabilizing for those with bipolar disorder and may help to precipitate a relapse during this vulnerable time. For women with bipolar disorder, we recommend that somebody else take over the nighttime feedings in order to protect the mother's sleep and to increase her chances of staying well.

Sources: Cohen LS, Sichel DA, Roberston LM, et al: Postpartum prophylaxis for women with bipolar disoder. Am J Psychiatry 1995; 152: 1641-1645.
Viguera AC, Nonacs R, Cohen LS, Tondo L, Murray A, Baldessarni RJ: Risk of Recurrence of Bipolar Disorder in Pregnant and Nonpregnant Women After Discontinuing Lithium Maintenance. Am J Psychiatry 2000; 157: 179-184.

Breastfeeding and Antidepressants (January 2002)

Q. For women who are breastfeeding, it appears that certain antidepressants are safer than others. Researching the American Journal of Psychiatry and the New England Journal of Medicine, data point to as the drug of choice. What is your recommendation for breastfeeding women? Should any blood tests be conducted on mother and nursing infant?

A. When discussing the use of antidepressant medications by breastfeeding women, It is somewhat misleading to say that certain medications are "safer" than others. All medications taken by the mother are secreted into the breast milk. The amount of drug to which the infant is exposed depends on many factors, including the medication dosage, as well as the infant's age and feeding schedule. To date, we have not found that certain medications are found at lower levels in the breast milk and may therefore pose less of a risk to the nursing infant. Nor have we found that any antidepressant medication has been associated with serious adverse events in the baby.

In general, one should try to choose an antidepressant for which there are data to support its safety during breastfeeding. The most information is available on fluoxetine (Prozac), followed by , paroxetine (Paxil), and the tricyclic antidepressants. Other antidepressant medications have not been studied as well.

We do not regularly measure drug levels in the breastfeeding mother or baby; however, there may be certain situations where information on exposure to drug in the child may help make decisions regarding treatment. If there is a significant change in the child's behavior (e.g., irritability, sedation, feeding problems, or sleep disturbance) an infant serum drug level may be obtained. If levels are high, breastfeeding may be suspended. Similarly if the mother is taking a particularly high dosage of medication, it may be helpful to measure drug levels in the infant to determine the degree of exposure.

Source: Burt VK, Suri R, Altshuler L, Stowe Z, Hendrick VC, Muntean E. The use of psychotropic medications during breast-feeding. Am J Psychiatry 2001; 158: 1001-9.

About the author: Ruta M Nonacs, MD, PhD, is Associate Director of the Perinatal Psychiatry Clinical Research Program, Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School.

next: Preventing Against Postpartum Relapse of Bipolar Disorder
~ bipolar disorder library
~ all bipolar disorder articles

The importance of "living in the moment" to my recovery needs to be emphasized. Before recovery, I lived in constant fear. I was obsessed with finding security; financial security, emotional security, job security, etc. I wanted to ensure that nothing rocked the boat in my carefully constructed little world. Yet the more I pursued such goals, the faster they eluded me. As I desperately tried to cling to material and physical stuff, I saw it literally vaporize between my fingers.

I've read somewhere that living is really about giving up. The final thing we give up or surrender is our very life (i.e., we eventually surrender to physical death). I remember when my Grandfather died in 1982, the doctors said, "He fought hard for life, but his heart was just too weak." The same principle applies to other areas: no matter how hard we fight to hang on to someone or something, we eventually give in and give up.

In a sense, as soon as we are born, we begin the lifelong process of giving up. We give up the warmth and security of the womb; we give up the bond with our mother; we give up baby food; we give up being carried everywhere; we give up crawling; we give up holding a parent's hand; we give three-wheels for two-wheels; and so on throughout all of life. Life is constantly changing, moment by moment, all around us. Every passing minute is one less to call our own.

Thus, every moment is indeed precious. Every moment has a lesson to learn. Every moment brings me closer to something else I must eventually give up. Every moment must be embraced and lived fully, and then released. Maybe fully embracing each moment is the only way to surrender each moment.

Yesterday was Father's Day. My children are twelve and nine. Only a moment ago, they were newborn. Only a moment from now, they'll graduating college, creating lives of their own. I try to embrace every moment I spend with them, but I also surrender and let each moment go. For example, my 1997 Father's Day was very special. I spent the day with friends who care about me, because the kids are off vacationing with their mother in another state.

Sure, I missed seeing them, but all the times we've spent together are here in my heart. All the moments we'll spend together in the future still await.

I've learned how to embrace the moment, in the now, and my life is better for having done so. I'm no longer dependent on the past or the future. I'm no longer chasing the illusion of security. I accept things as they come; I release things as they go. This is balance. This is peace. This is serenity. This is recovery.

---

continue story below

---

next: Letting Go of the Past

Contents in the Adders.org Site:

• Adders.org Homepage
• A.D.D./A.D.H.D. Possible Causes and Diagnosis
• Things College Students With ADHD Would Like Their Teachers To Know
• 50 Tips for Managing Attention Deficit Disorder in the Classroom
• A British Perspective on the Psychological Assessment of Childhood AD/HD
• Access to School Records in the UK
• A.D.D. / A.D.H.D. Treatment Options
• ADDvice for ADDults
• ADHD-LD Adults and Success in the Workplace
• ADHD Medication and Sports in the UK
• ADHD Medication, Behavior Therapy Best For ADHD Children
• ADHD Students and Getting Ready for College
• ADHD Tips for Time and Mood Management
• An Inclusive Learning Handbook for Prisons and Young Offender Institutions
• Appealing Exclusion From School
• Atomoxetine and Stimulants in Combination for Treatment of Attention Deficit Hyperactivity Disorder: Four Case Reports
• Cards for Explaining ADHD Child's Behaviour to Others
• Long Term Medical Conditions: Career Prospects for People with ADHD
• Comparative Study of Cerebral White Matter in Autism and Attention-deficit/Hyperactivity Disorder by Means of Magnetic Resonance Spectroscopy
• Danger of Using SPECT Scan to Diagnose ADHD
• Early Years Action
• Natural Alternatives: EEG Biofeedback or Neurofeedback
• Effectiveness of Boarding Schools for ADHD Teens
• Feingold Diet and Fresh Lemon Balm for ADHD
• Guide to ADHD Coaching
• Health Visitor Training Paper
• Home Education Information
• How a Partner's Untreated Attention-Deficit/Hyperactivity (ADHD) Affects Relationships
• Hyperkinesis and Breakdown of Parenting
• Impact of ADHD on School Performance
• Link Between ADHD and Addiction
• Reality of ADHD
• Recent Advances in the Genetics of Attention Deficit Hyperactivity Disorder
• Relationship Issues for Adults with ADHD
• Developmental Neuropsychopathology of Attention Deficit and Impulsiveness
• Respite Care for People with ADHD
• Risk Genes for ADHD
• Safe Storage and Administration of Methylphenidate
• School Exclusion Laws in the UK
• Serotonin May Hold Key to ADHD Treatment
• Six Pillars to Treating ADD from Jason Alster
• Special Educational Needs and Disabilty Act 2001
• Special Educational Needs Code of Practice 2002
• Strattera Plus Stimulants for Treatment of ADHD
• Study Confirms Concerta (methylphenidate HCl) Effective, Safe Treatment For Attention Deficit Hyperactivity Disorder
• Supporting an ADHD Child in the Classroom
• The Role of Disability Living Allowance in the Management of ADHD
• Treating Children's Sleep Disorders Improves Attention Deficit Symptoms
• Understanding and Recognizing ADHD in Children
• Vitamin C and Niacinamide for Treating ADHD
• Natural Alternatives: 5-HTP for Treating ADHD Symptoms
• Activities for ADHD Children and Family Members
• ADD and Intimate Relationships
• Adderall More Effective Than Ritalin in Treating ADHD
• ADHD Accommodations for a Driving Test
• ADHD and Self Esteem Issues
• ADHD Children and Exam Taking
• ADHD Children and Immature Social Skills
• Concerta For ADHD Children Safe and Effective
• ADHD Teens and Relationship Problems
• ADHD Teens: School Issues, Career Choices
• ADHD Teens: Help for School and Social Skills Difficulties
• Nonstimulant Therapy Shows Effectiveness in ADHD
• Assessment for ADD-ADHD Adults in the UK
• Attention Deficit Hyperactivity Disorder: Minimal Brain Dysfunction
• Brain Areas Critical To Human Time Sense Identified
• Brain Scan Shows ADHD
• Natural Alternatives: Calm Focus, Calmplex 2000
• Child Profile For Use At School
• Claiming Disability Living Allowance Benefits
• Common ADHD Myths and Facts
• Conduct Disorder - European Description
• Confusion About ADHD
• Corporal Punishment From A Religious Viewpoint
• Natural Alternatives: Defend-OL, Developmental Integration Technique
• Diagnosing ADHD Takes Time, Insight and Experience
• Disability Discrimination and Schools
• Disability Rights UK
• Disclosing ADHD Disability to Employer
• Do Benefits of Intensive ADHD Medication Management Last
• Early Years Action
• Natural Alternatives: EEG Biofeedback or Neurofeedback
• Natural Alternatives: Efalex
• E Numbers - Eliminating Additives from Your ADHD Child's Diet
• Employment Accommodations for Adults with ADHD
• Natural Alternatives: Evening Primrose Oil for Treating ADHD
• Natural Alternatives: Eye Q for Treating ADHD Symptoms
• Frequently Asked Questions About Methylphenidate, ADHD Diagnosis
• Financial Aid for ADHD Children and Families
• Finding the Right School for Your Special Needs Child
• Further Study on ADDerall
• Natural Alternatives: G.P.4.o,, Ginko Biloba for Treating ADHD
• Natural Alternatives: Gotu Kola, Guarana for Treating ADHD
• Help for Eating Problems in Children with ADHD
• How a Partner's Untreated Attention-Deficit/Hyperactivity (ADHD) Affects Relationships
• How Do I Know If I have ADD/ADHD? (Children)
• How Do You Cope With An ADHD Spouse?
• Impact of ADHD on the Family
• An Introduction to ADHD Coaching
• Introduction to Disability Assessment by Social Services
• Legal Help for ADHD-Related Issues in UK
• The Link Between ADHD and Addiction
• The Link Between ADHD and Eating Disorders
• Natural Alternatives: Low Phosphate Diet, Magnets For Treating ADHD
• Making ADHD-Friendly Career Choices
• Natural Alternatives: Melatonin for Treating ADHD Sleep Problems
• Melatonin for Treating ADHD Sleep Problems
• Mini CV for Dr. Billy Levin
• Modeling ADHD Child and Family Relationships
• My Top Tips For Dealing With My ADD Son, Richard
• Natural Alternatives: AD-FX, AiA, Attend
• Natural Alternatives: beCALM'd, Buried Treasure ADD Attention, Bioflow
• Natural Alternatives: Biometics, Calm Child
• Natural Alternatives: SerenAid, Skullcap for Treating ADHD
• Natural Alternatives: Neuro 911, Neurofeedback for ADHD
• New Results from the MTA Study - Do treatment effects persist?
• NHS and Community Care Act 1990
• Natural Alternatives: Nikken Sleep Systems, Nux Vomica for Treating ADHD
• Parent Coaching for Children with ADHD and Learning Disabilities
• Parenting Teenagers with ADHD: Surviving the Ride
• Natural Alternatives: Passionflower, Pedi-Active for ADHD
• Pastoral Support Programme
• Natural Alternatives: Pycnogenol-Proanthocyanadin for ADHD
• Relationship Between ADHD Stimulant Therapy and Substance Abuse
• Natural Alternatives: Reliv, St. John's Wort for ADHD, Depression
• Requesting an Assessment of Special Educational Needs
• Requesting Workplace Accommodations for Disability
• Ropinirole in a Child With ADHD and Restless Legs Syndrome
• Siblings of Children with Special Needs
• Strategies for Enhancing Social Interaction in ADHD Children
• Natural Alternatives: Super Blue Green Algae for ADHD
• Supporting Teenagers with ADHD
• Taking ADHD Medication on Holiday Abroad
• Ten Steps for Student Success for College and Adult Students with ADHD
• The Impact of ADHD on Marriage
• Top Coping Strategies For Teenagers and Adults With ADHD
• Types of ADD/ADHD in the form of the characters from Winnie the Pooh!
• Tyrosine for Treatment of ADHD
• Crime & Disorder Act with Reference to School Attendance
• Natural Alternatives: Vitamin B Complex and Magnesium for ADHD
• What a Whole School Policy on Disability Equality and Inclusion Should Cover
• Natural Alternatives: Wild Oat Seed, ZAN, Zinc Sulphate for ADHD
• You Know You Have ADHD When...
• Natural Alternatives: Nambudripad's Allergy Elimination Techniques for ADHD
• About Us

---

---

 

Self-Therapy For People Who ENJOY Learning About Themselves

PROBLEMS WITH NATURAL SADNESS

Unfortunately, when we are confronted with a huge amount of sadness we are likely to fear that it will last forever.

No matter how deeply you believe that it will last forever, it won't! You need to trust that this is true.

Ideally, all of the energy that comes to us when we are sad should be used to replace what we've lost.

But some people believe that they can't replace certain losses. And believing this can make them give up on even trying.

You can always replace what you've lost!

When you experience grief from the loss of a person you have loved, you may be very tempted to believe you can't replace such a good person. Once you are finished with your sadness, you'll find that you can replace the roles that person served in your life!

Think of what the person did for you (i.e. - "they loved me," "they supported me," "they advised me," etc.) and be willing to accept those same functions from others.

Another problem with natural sadness is that you may be living your life around people who do not encourage you to feel your sadness completely. If this is the problem, spend time with others who are more respectful of your feelings.

PROBLEMS WITH UNNATURAL SADNESS

Remember that unnatural sadness is, by definition, sadness you create in your mind.

It might be due to some completely imaginary loss, or perhaps you really did lose something important and you are continually "recycling" the memory of that loss in your mind.

---

 

---

People who are always sad: If you know someone who seems to always be sad, know that they are not really sad! (If they were really sad, there would have been a natural duration to the sadness and they'd be done by now...!)

These people are usually angry down-deep although they may be hiding some other emotion from themselves as well.

They are extremely afraid of the deeper, more real feeling. A therapist who understands and who offers a safe haven might be necessary.

The most common problem: By far the most common problem with sadness comes in the form of
people who talk about "hurt feelings" and act sad as they tell you about it.

While it is indeed possible for people to hurt your feelings, the natural reaction to this is to be angry!

If you find yourself wanting to tell someone that they hurt your feelings start out by saying: "I'm angry about what you did!" Then notice how much better you feel! And notice how much more willing the other person is to take your feelings seriously.

BIG BOYS DON'T CRY

Unfortunately, men often have a very hard time expressing their sadness.

The best advice I can give, of course, would be that they should let themselves cry.

But I've found that this often doesn't help with people who fear looking foolish, etc.

So, I offer the second best advice I can give: "Express your sadness in your own way. If you don't express it by crying, express it some other way... your way!"

People who don't allow themselves to cry tend to need a lot of alone time while they are sad.

"I'LL GIVE YOU SOMETHING TO CRY ABOUT, YOUNG LADY!"

When we needed to cry as children it was usually because one of our parents had just hurt us.
Since they didn't want to admit their responsibility, they hated to see us cry.

It might help to remember them frightening you with threats when you needed to cry. Then imagine yourself telling them off! Then cry as a way of expressing your freedom from these teachings.

"I LOOK SO UGLY WHEN I CRY!"

This is one of the more pitiful excuses I hear.

It shows that the person believes their appearance is more important than their feelings.

This simple statement often indicates some pretty serious problems.

A REMINDER

We all confuse our feelings sometimes.

If you thought you had a problem with sadness but these words don't fit, your problem may be related to one of the other feelings.

Enjoy Your Changes!

Everything here is designed to help you do just that!

next: Problems With Scare

Recovery has only recently become a word used in relation to the experience of psychiatric symptoms. Those of us who experience psychiatric symptoms are commonly told that these symptoms are incurable, that we will have to live with them for the rest of our lives, that the medications, if they (health care professionals) can find the right ones or the right combination, may help, and that we will always have to take the medications. Many of us have even been told that these symptoms will worsen as we get older. Nothing about recovery was ever mentioned. Nothing about hope. Nothing about anything we can do to help ourselves. Nothing about empowerment. Nothing about wellness.

Mary Ellen Copeland says:

When I was first diagnosed with manic depression at the age of 37, I was told that if I just kept taking these pills - pills that I would need to take for the rest of my life - I would be OK. So I did just that. And I was "OK" for about 10 years until a stomach virus caused severe lithium toxicity. After that I could no longer take the medication. During the time I was taking the medication, I could have been learning how to manage my moods. I could have been learning that relaxation and stress reduction techniques and fun activities can help reduce the psychiatric symptoms. I could have been learning that I would probably feel a lot better if my life wasn't so hectic and chaotic, if I wasn't living with an abusive husband, if I spent more time with people who affirmed and validated me, and that support from other people who have experienced these symptoms helps a lot. I was never told that I could learn how to relieve, reduce and even get rid of troubling feelings and perceptions. Perhaps if I had learned these things and had been exposed to others who where working their way through these kinds of symptoms, I would not have spent weeks, months and years experiencing extreme psychotic mood swings while doctors searched diligently to find effective medications.

Now the times have changed. Those of us who have experienced these symptoms are sharing information and learning from each other that these symptoms do not have to mean that we must give up our dreams and our goals, and that they don't have to go on forever. We have learned that we are in charge of our own lives and can go forward and do whatever it is we want to do. People who have experienced even the most severe psychiatric symptoms are doctors of all kinds, lawyers, teachers, accountants, advocates, social workers. We are successfully establishing and maintaining intimate relationships. We are good parents. We have warm relationships with our partners, parents, siblings, friends and colleagues. We are climbing mountains, planting gardens, painting pictures, writing books, making quilts, and creating positive change in the world. And it is only with this vision and belief for all people that we can bring hope for everyone.

Support From Health Care Professionals

Sometimes our health care professionals are reluctant to assist us in this journey - afraid that we are setting ourselves up for failure. But more and more of them are providing us with valuable assistance and support as we make our way out of the system and back to the life we want. Recently I (Mary Ellen) spent a full day visiting with health care professionals of all kinds at a major regional mental health center. It was exciting to hear over and over the word "recovery". They were talking about educating the people they work with, about providing temporary assistance and support for as long as is necessary during the hard times, about working with people to take responsibility for their own wellness, exploring with them the many options available to address their symptoms and issues and then sending them on their way, back to their loved ones and into the community.

A word that these dedicated health care professionals used over and over again was "normalize". They are trying to see for themselves, and help the people they work with to see, these symptoms on a continuum of the norm rather than an aberration - that these are symptoms that everyone experiences in some form or other. That when, either from physical causes or stress in our lives, they become so severe that they are intolerable, we can work together to find ways to reduce and relieve them. They are talking about less traumatic ways to deal with crises where symptoms become frightening and dangerous. They are talking about respite centers, guest homes and supportive assistance so a person can work through these hard times at home and in the community rather than in the frightening scenario of a psychiatric hospital.

What Are The Key Facets Of A Recovery Scenario?

1. There is hope. A vision of hope that includes no limits. That even when someone says to us, "You can't do that because you've had or have those symptoms, dear!" - we know it's not true. It is only when we feel and believe that we are fragile and out of control that we find it hard to move ahead. Those of us who experience psychiatric symptoms can and do get well. I (Mary Ellen) learned about hope from my mother. She was told she was incurably insane. She had wild, psychotic mood swings unremittingly for eight years. And then they went away. After that she worked very successfully as a dietitian in a large school lunch program and spent her retirement helping my brother raise seven children as a single parent and volunteering for a variety of church and community organizations.

   We don't need dire predictions about the course of our symptoms - something which no one else, regardless of their credentials can ever know. We need assistance, encouragement and support as we work to relieve these symptoms and get on with our lives. We need a caring environment without feeling the need to be taken care of.

   Too many people have internalized the messages that there is no hope, that they are simply victims to their illness, and that the only relationships they can hope for are one-way and infantalizing. As people are introduced to communities and services that focus on recovery, relationships change to being more equal and supportive in both directions. As we feel valued for the help we can offer as well as receive, our self-definitions are expanded. We try out new behaviors with each other, find ways in which we can take positive risks and find that we have more self-knowledge and more to offer than we were led to believe.

---

1. It's up to each individual to take responsibility for their own wellness. There is no one else who can do this for us. When our perspective changes from reaching out to be saved to one in which we work to heal ourselves and our relationships, the pace of our recovery increases dramatically.

   Taking personal responsibility can be very difficult when symptoms are severe and persistent. In these cases, it is most helpful when our health care professionals and supporters work with us to find and take even the smallest steps to work our way out of this frightening situation.

2. Education is a process that must accompany us on this journey. We search for sources of information that will help us to figure out what will work for us and the steps we need to take in our own behalf. Many of us would like health care professionals to play a key role in this educational process - directing us to helpful resources, setting up educational workshops and seminars, working with us to understand information, and helping us to find a course that resonates with our wishes and beliefs.

3. Each of us must advocate for ourselves to get what it is we want, need and deserve. Often people who have experienced psychiatric symptoms have the mistaken belief that we have lost our rights as individuals. As a result, our rights are often violated, and these violations are consistently overlooked. Self-advocacy becomes much easier as we repair our self-esteem, so damaged by years of chronic instability, and come to understand that we are often as intelligent as anyone else, and always as worthwhile and unique, with special gifts to offer the world, and that we deserve all the very best that life has to offer. It is also much easier if we are supported by health care professionals, family members and supporters as we reach out to get our personal needs met.

   All people grow through taking positive risks. We need to support people in:

   • making life and treatment choices for themselves, no matter how different they look from traditional treatment,

   • building their own crisis and treatment plans,

   • having the ability to obtain all their records,

   • accessing information around medication side effects,

   • refusing any treatment (particularly those treatments that are potentially hazardous),

   • choosing their own relationships and spiritual practices,

   • being treated with dignity, respect and compassion, and,

   • creating the life of their choice.

4. Mutual relationship and support is a necessary component of the journey to wellness. The nationwide focus on peer support is a result of the recognition of the role of support in working toward recovery. Throughout New Hampshire, peer support centers are providing a safe community where people can go even when their symptoms are most severe, and feel safe and secure.

   Beyond this, peer support holds few, if any, assumptions about people's capabilities and limits. There is no categorizing and no hierarchical roles (eg. doctor/patient), with the result being that people move from focusing on themselves to trying out new behaviors with one another and ultimately committing to a larger process of building community. The crisis respite center at Stepping Stones Peer Support Center, in Claremont, New Hampshire, carries this concept a step further by providing around-the-clock peer support and education in a safe, supportive atmosphere. Instead of feeling out of control and pathologized, peers support one another in moving through and beyond difficult situations, and help each other learn how crisis can be an opportunity for growth and change. An example of this was when a member who was having lots of difficult thoughts came into the center to avoid hospitalization. His goal was to be able to talk through his thoughts without feeling judged, categorized or told to increase his medication. After several days he went home feeling more comfortable and connected to others with whom he could continue to interact. He committed to staying in and expanding on the relationships that he built while in the respite program.

   Through the use of support groups and building community that defines itself as it grows, many people find that their whole sense of who they are expands. As people grow they move ahead in other parts of their lives.

   Support, in a recovery based environment, is never a crutch or a situation in which one person defines or dictates the outcome. Mutual support is a process in which the people in the relationship strive to use the relationship to become fuller, richer human beings. Although we all come to relationships with some assumptions, support works best when both people are willing to grow and change.

   This need for mutual and appropriate support extends into the clinical community. Though clinical relationships may never truly be mutual, or without some assumptions, we can all work to change our roles with each other in order to further move away from the kinds of paternalistic relationships some of us have had in the past. Some of the questions health care professionals can ask themselves in this regard are:

   • How much of our own discomfort are we willing to sit with while someone is trying out new choices?

   • How are our boundaries continuously being redefined as we struggle to deepen each individual relationship?

   • What are the assumptions we already hold about this person, by virtue of his/her diagnosis, history, lifestyle? How can we put aside our assumptions and predictions in order to be fully present to the situation and open to the possibility for the other person to do the same?

   • What are the things that might get in the way of both of us stretching and growing?

   Support begins with honesty and a willingness to revisit all of our assumptions about what it means to be helpful and supportive. Support means that at the same time clinicians hold someone in "the palm of their hand," they also hold them absolutely accountable for their behavior and believe in their ability to change (and have the same self-reflective tools to monitor themselves).

   No one is beyond hope. Everyone has the ability to make choices. Even though health care professionals have traditionally been asked to define treatment and prognosis, they have to look through the layers of learned helplessness, years of institutionalization, and difficult behaviors. Then they can creatively begin to help a person reconstruct a life narrative that is defined by hope, challenge, accountability, mutual relationship and an ever changing self-concept.

   As part of our support system, health care professionals need to continue to see if they are looking at their own roadblocks to change, understand where they get "stuck" and dependent, and look at their own less than healthy ways of coping. Health care professionals need to relate to us that they have their own struggles and own that change is hard for all. They need to look at our willingness to "recover" and not perpetuate the myth that there is a big difference between themselves and people they work with. Support then becomes truly a mutual phenomenon where the relationship itself becomes a framework in which both people feel supported in challenging themselves. The desire to change is nurtured through the relationship, not dictated by one person's plan for another. The outcome is that people don't continue to feel separate, different and alone.

---

How Can Health Care Professionals Address Learned Helplessness?

Clinicians often ask us, "What about people who aren't interested in recovery, and who have no interest in peer support and other recovery concepts?" What we often forget is that MOST people find it undesirable to change. It's hard work! People have gotten used to their identities and roles as ill, victims, fragile, dependent and even as unhappy. Long ago we learned to "accept" our illnesses, give over control to others and tolerate the way of life. Think how many people live like this in one way or another that don't have diagnosed illnesses. It's easier to live in the safety of what we know, even if it hurts, than it is to do the hard work of change or develop hope that conceivably could be crushed.

Our clinical mistake, up to this point, has been thinking that if we ask people what they need and want, they will instinctively have the answer AND want to change their way of being. People who have been in the mental health system for many years have developed a way of being in the world, and particularly being in relationship with professionals, where their self-definition as patient has become their most important role.

Our only hope for accessing internal resources that have been buried by layers of imposed limitations is to be supported in making leaps of faith, redefining who we'd like to become and taking risks that aren't calculated by someone else. We need to be asked if our idea of who we'd like to become is based on what we know about our "illnesses". We need to be asked what supports we would need to take new risks and change our assumptions about our fragility and our limitations. When we see our closest friends and supporters willing to change, we begin to try out our own incremental changes. Even if this means buying ingredients for supper instead of a TV dinner, we need to be fully supported in taking the steps to recreating our own sense of self and be challenged to continue to grow.

Recovery is a personal choice. It is often very difficult for health care providers who are trying to promote a person's recovery when they find resistance and apathy. Severity of symptoms, motivation, personality type, accessibility of information, perceived benefits of maintaining the status quo rather than creating life change (sometimes to maintain disability benefits), along with the quantity and quality of personal and professional support, can all effect a person's ability to work toward recovery. Some people choose to work at it very intensively, especially when they first become aware of these new options and perspectives. Others approach it much more slowly. It is not up to the provider to determine when a person is making progress - it is up to the person.

What Are Some Of The Most Commonly Used Recovery Skills And Strategies?

Through an extensive ongoing research process, Mary Ellen Copeland has learned that people who experience psychiatric symptoms commonly use the following skills and strategies to relieve and eliminate symptoms:

• reaching out for support: connecting with a non-judgmental, non-critical person who is willing to avoid giving advice, who will listen while the person figures out for themselves what to do.

• being in a supportive environment surrounded by people who are positive and affirming, but at the same time are direct and challenging; avoiding people who are critical, judgmental or abusive.

• peer counseling: sharing with another person who has experienced similar symptoms.

• stress reduction and relaxation techniques: deep breathing, progressive relaxation and visualization exercises.

• exercise: anything from walking and climbing stairs to running, biking, swimming.

• creative and fun activities: doing things that are personally enjoyable like reading, creative arts, crafts, listening to or making music, gardening, and woodworking.

• journaling: writing in a journal anything you want, for as long as you want.

• dietary changes: limiting or avoiding the use of foods like caffeine, sugar, sodium and fat that worsen symptoms.

• exposure to light: getting outdoor light for at least 1/2 hour per day, enhancing that with a light box when necessary.

• learning and using systems for changing negative thoughts to positive ones: working on a structured system for making changes in thought processes.

• increasing or decreasing environmental stimulation: responding to symptoms as they occur by either becoming more or less active.

• daily planning: developing a generic plan for a day, to use when symptoms are more difficult to manage and decision making is difficult.

• developing and using a symptom identification and response system which includes:

  1. a list of things to do every day to maintain wellness,

  2. identifying triggers that might cause or increase symptoms and a preventive action plan,

  3. identifying early warning signs of an increase in symptoms and a preventive action plan,

  4. identifying symptoms that indicate the situation has worsened and formulating an action plan to reverse this trend,

  5. crisis planning to maintain control even when the situation is out of control.

In self-help recovery groups, people who experience symptoms are working together to redefine the meaning of these symptoms, and to discover skills, strategies and techniques that have worked for them in the past and that could be helpful in the future.

---

What Is The Role Of Medication In The Recovery Scenario?

Many people feel that medications can be helpful in slowing down the most difficult symptoms. While in the past, medications have been seen as the only rational option for reducing psychiatric symptoms, in the recovery scenario, medications are one of many options and choices for reducing symptoms. Others include the recovery skills, strategies and techniques listed above, along with treatments that address health related issues. Though medications are certainly a choice, these authors believe that medication compliance as the primary goal is not appropriate.

People who experience psychiatric symptoms have a hard time dealing with the side-effects of medications designed to reduce these symptoms - side effects like obesity, lack of sexual function, dry mouth, constipation, extreme lethargy and fatigue. In addition, they fear the long term side-effects of the medications. Those of us who experience these symptoms know that many of the medications we are taking have been on the market for a short time - so short that no one really knows the long term side-effects. We know that Tardive's Dyskinesia was not recognized as a side-effect of neuroleptic medication for many years. We fear that we are at risk of similar irreversible and destructive side-effects. We want to be respected by health care professionals for having these fears and for choosing not to use medications that are compromising the quality of our lives.

When people who have shared similar experiences get together, they begin to talk about their concerns about medications and about alternatives that have been helpful. They build up a kind of group empowerment that begins to challenge the notion of prophylactic medication or medication as the only way to address their symptoms. Many physicians, on the other hand, worry that people who come to them blame the medication for the illness and they fear that stopping the medication will worsen symptoms. These become fairly polarized views and amplify the hierarchical relationship. People feel that if they question their doctors about decreasing or getting off medications, they will be threatened with involuntary hospitalization or treatment. Doctors fear that people are jumping on an unreliable band wagon that will lead to out of control symptoms, jeopardizing the person's safety. Consequently, talk about medication often goes on without counsel with doctors.

In a recovery based environment, more effort needs to be spent focusing on choice and self-responsibility around behavior. If the complaint is that medications control behavior and thoughts while extinguishing all pleasurable, motivational kinds of feelings, there is a need to develop a way we talk about symptoms so that each of us has many choices and options for dealing with them.

Shery Mead has developed a visual image of a car wash that has been useful to her and many others. She says:

If I think about early stages of symptoms as driving towards the car wash, there are still many choices I can make before my wheels engage in the automatic treads. I can veer off to the side, stop the car or back up. I am also aware that once my wheels are engaged in the car wash - though it feels out of my control - the situation, based on self observation, is time limited and I can ride it out and will eventually come out on the other side. My behavior, even when I am "white knuckling it" through the car wash, is still my choice and in my control. This kind of process has helped others define triggers, watch their automatic response, develop self critical skills about their own defense mechanisms, and ultimately even ride out the car wash better. Although medications can be helpful in making it through the car wash without ending up in a dangerous situation, there are many more proactive skills that help each of us develop our own techniques, making personal responsibility a more desirable outcome.

What Are The Risks And Benefits Of Using A "Recovery" Vision For Mental Health Services?

Because the feelings and symptoms that have been commonly referred to as "mental illness" are very unpredictable, our health care professionals may fear that we will "decompensate" (a nasty word to many of us) and may put ourselves or others at risk. Health care professionals become fearful that, if they do not continue to provide the kind of caretaking and protective services they have provided in the past, people will become discouraged, disappointed and may even harm themselves. It must be recognized that risk is inherent in the experience of life. It is up to us to make choices about how we will live our lives and it is not up to health care professionals to protect us from the real world. We need our health care professionals to believe that we are capable of taking risks and support us as we take them.

More clinicians working in a recovery based environment will enjoy the positive reinforcement of successful experiences in working with people who are growing, changing and moving on with their lives. The recovery focus and the increased wellness of more of us will give health care professionals more time to spend with those who experience the most severe and persistent symptoms, giving them the intense support they need to achieve the highest levels of wellness possible.

In addition, health care professionals will find that instead of providing direct care for people who experience psychiatric symptoms, they will be educating, assisting and learning from them as they make decisions and take positive action in their own behalf. These caregivers will find themselves in the rewarding position of accompanying those of us who experience psychiatric symptoms as we grow, learn and change.

The implications of a recovery vision for services to adults with severe "mental illness" will be that providers of services, instead of coming from a paternalistic framework with often harsh, invasive and seemingly punitive "treatments," will learn from us as we work together to define what wellness is for each of us on an individual basis and explore how to address and relieve those symptoms which prevent us from leading full and rich lives.

The hierarchical health care system will gradually become non-hierarchical as people understand that health care professionals will not only provide care, but will also work with a person to make decisions about their own course of treatment and their own lives. Those of us who experience symptoms are demanding positive, adult treatment as partners. This progression will be enhanced as more people who have experienced symptoms become providers themselves.

While the benefits of a recovery vision for mental health services defy definition, they obviously include:

• Cost effectiveness. As we learn safe, simple, inexpensive, non-invasive ways to reduce and eliminate our symptoms, there will be less need for costly, invasive interventions and therapies. We will live and work interdependently in the community, supporting ourselves and our family members.

• Reduced need for hospitalization, time away from home and personal supports, and the use of harsh, traumatic and dangerous treatment which often exacerbate rather than relieve symptoms, as we learn to manage our symptoms using normal activities and supports.

• Increased possibility of positive outcomes. As we recover from these pervasive and debilitating symptoms, we can do more and more of the things we want to do with our lives, and work toward meet our life goals and dreams.

• As we normalize people's feelings and symptoms, we build a more accepting, diverse culture.

---

Does Recovery Work Do Anything To Specifically Help A Person Avoid Situations Of Being Personally Unsafe Or A Danger To Others?

With the increased focus on recovery and the use of self-help skills to alleviate symptoms, it is hoped that fewer and fewer people will find themselves in a situation where they are a danger to themselves or someone else.

If the symptoms should become that severe, people may have developed their own personal crisis plan - a comprehensive plan that would tell close supporters what needs to happen to ward off disaster. Some of these things might include 24-hour peer support, phone line availability or speaking for or against some types of treatment. These plans, when developed and used collaboratively with supporters, are helping people maintain control even when it seems that things are out of control.

While disagreement about any kind of coercive treatment is widespread, the authors, both of whom have been in these kinds of high-risk situations, agree that any kind of forced treatment is NOT helpful. The long-range effects of coercive, unwanted treatment can be devastating, humiliating and ultimately ineffective and can leave people more untrusting of the relationships that should have been supportive and healing. Although both authors feel that all people are responsible for their behavior and should be held accountable, we believe that the development of humane, caring protocols should be everyone's focus.

Guidelines For A Recovery Focus In Service Provision

The following guidelines for health care professionals should guide and enhance all recovery work while decreasing resistance and lack of motivation:

• Treat the person as a fully competent equal with equal capacity to learn, change, make life decisions and take action to create life change - no matter how severe their symptoms.

• Never scold, threaten, punish, patronize, judge or condescend to the person, while being honest about how you feel when that person threatens or condescends to you.

• Focus on how the person feels, what the person is experiencing and what the person wants rather than on diagnosis, labeling, and predictions about the course of the person's life.

• Share simple, safe, practical, non-invasive and inexpensive or free self-help skills and strategies that people can use on their own or with the help of their supporters.

• When necessary, break tasks down into the smallest steps to insure success.

• Limit the sharing of ideas and advice. One piece of advice a day or visit is plenty. Avoid nagging and overwhelming the person with feedback.

• Pay close attention to individual needs and preferences, accepting individual differences.

• Assure that planning and treatment is a truly collaborative process with the person who is receiving the services as the "bottom line".

• Recognize strengths and even the smallest bit of progress without being paternalistic.

• Accept that a person's life path is up to them.

• As the first step toward recovery, listen to the person, let them talk, hear what they say and what they want, making sure their goals are truly theirs and not yours. Understand that what you might see as being good for them may not be what they really want.

• Ask yourself, "Is there something going on in their life which is getting in the way of change or moving toward wellness, eg., learned helplessness," or are there medical problems that are getting in the way of recovery?

• Encourage and support connection with others who experience psychiatric symptoms.

• Ask yourself, "Would this person benefit from being in a group led by others who have experienced psychiatric symptoms?"

The person who experiences psychiatric symptoms is the determiner of their own life. No one else, even the most highly skilled health care professional, can do this work for us. We need to do it for ourselves, with your guidance, assistance and support.

Copyright 2000, Plenum Publishers, New York, NY.

About The Authors

Mary Ellen Copeland, MA, MS

Mary Ellen Copeland has experienced episodes of severe mania and depression for most of her life. She is the author of:

• The Depression Workbook: A Guide to Living with Depression and Manic Depression

• Living without Depression and Manic Depression: A Guide to Maintaining Mood Stability

• Wellness Recovery Action Plan

• Adolescent Depression Workbook

• Winning Against Relapse

• The Worry Control Workbook

• Healing the Trauma of Abuse

• The Loneliness Workbook

She is also co-author of the book Fibromyalgia and Chronic Myofascial Pain Syndrome, co-producer of the video Coping with Depression, and producer of the audio tape Strategies for Living with Depression and Manic Depression. These resources are based on her ongoing study of the day-to-day coping strategies of people who experience psychiatric symptoms and of how people have gotten well and stayed well. She has achieved long term wellness and stability by using many of the coping strategies she learned while writing her books. Mary Ellen has presented numerous workshops for people who experience psychiatric symptoms and their supporters.

Shery Mead, MSW

Ms. Mead is the founder and past Executive Director of three highly regarded peer support service program for persons with serious mental illness. Ms Mead is highly experienced in training, staff skill development, administration, management, advocacy, program design and evaluation. In addition to peer support program development, she has been a pioneer in establishing innovative peer operated respite programs that offer an alternative to psychiatric hospitalization. She has pioneered in the establishment of trauma survivor support groups and ongoing education initiatives for mental health professionals and court judges about recovery and parenting issues. Shery has recently become a full time consultant and educator to help other communities develop effective peer support and professional services.

next: Developing a Wellness Toolbox
~ back to Mental Health Recovery homepage
~ depression library articles
~ all articles on depression

People with eating disorders often refuse treatment for many reasons including fear of weight gain and the stigma of being hospitalized. But if eating disorders go untreated, they can have serious medical consequences -- death being one of them.

If an adult refuses treatment for a life-threatening illness, he or she can be legally required to enter a treatment program. But involuntary treatment of eating disorders, including anorexia nervosa and bulimia nervosa, is controversial, mostly because some experts suggest that it is counterproductive if the patient isn't willing to cooperate.

Now new research suggests that such involuntary treatment may be just as effective as voluntary treatment -- at least in the short run. The findings appear in the November issue of the American Journal of Psychiatry.

Of nearly 400 patients admitted to an eating disorders program during a seven-year period, the 66 patients who were involuntarily committed were hospitalized for an average of more than two weeks longer than the voluntary patients, mostly because they were in worse shape and weighed less. However, both groups gained weight at the same rate on a weekly basis.

The study did not assess how patients did in the long term, but a new study is now under way looking at how such patients fare five to 20 years after treatment.

"The short-term response of the legally committed patients was just as good as the response of the patients admitted for voluntary treatment," concludes Tureka L. Watson, MS, a psychiatry researcher the University of Iowa in Iowa City, and colleagues. "Further, the majority of those involuntarily treated later affirmed the necessity of their treatment and showed goodwill toward the treatment process."

Craig Johnson, PhD, says that he has no difficulty admitting adolescents, or even adults, involuntarily if they have had previous intensive treatment. "If their anorexia is severe ... their ability to think clearly is compromised, and they don't have the skills to make good judgments." Johnson is the director of the eating disorder program at the Laureate Clinic and Hospital in Tulsa, Okla.

In these cases, one should intervene as aggressively as possible, he says. "The courts, of course, view this differently ... they are far less prepared to commit people over not eating," he adds.

"There is tremendous resistance even in people who are ... eager to get better," says Abigail H. Natenshon, an eating disorder psychotherapist in private practice in Highland Park, Ill., and founder and director of Eating Disorder Specialists of Illinois.

"In a sense, the eating disorder makes them feel better than being healed because the eating disorder gives them a sense of control and power over their lives," says Natensohn, author of When Your Child Has an Eating Disorder: A Step-by-Step Workbook for Parents and Other Caregivers.

Even a patient who voluntarily gets treatment is afraid to give up this disease, she says. Some may be afraid that they will lose control over all of their life if they gain weight and/or get better.

But the first step in any eating disorder recovery is to get the patient's weight back into the healthy range, she says "Even medications will not have an effect on a person who is malnourished because their brain is malnourished and their perceptions are distorted," she says.

A hospital will force feed if it has to, Natenshon says. "Once hospitalized, a patient has no choice but to restore enough body weight so they are no longer in danger of dying." She explains that because patients are being fed, they eventually become more accepting of treatment willing patients.

About 10 million adolescent females and one million males struggle with eating disorders and conditions that border on eating disorders, according to Eating Disorders Awareness and Prevention Inc. of Seattle.

next: Eating Disorders Conference Transcripts Toc
~ eating disorders library
~ all articles on eating disorders

Parent shares personal experience with tyrosine supplement for treating ADHD.

Catherine writes.......

"One of my favorite supplements for ADHD/ADD is tyrosine. it helps to improve the dopamine levels in the brain which is what the stimulant meds do. Depending on the severity of the ADHD/ADD, you may still need to have stimulant meds but with both my kids I was able to cut the meds by half and cut the side effects by at least half.

Having taken the stimulant meds and tyrosine myself, I can tell you how much better I feel with tyrosine rather than the stimulant medications. I would much rather be on tyrosine you feel much more alert and able to think even first thing in the morning.

Been on it for 5 year and still believe in it benefits.

It should not be combined with antidepressants without doctor's understanding.

And for a small handfull of people, it makes them anxious or cranky... be aware and if it occures simply stop the tyrosine for a week and try again. Might have been a bad day... if it happens again, it may not be for you or your child.

When it works, it is wonderful."

---

Ed. Note: Please remember we do not endorse any treatments and strongly advise you to check with your doctor before using, stopping or changing a treatment.

---

 

---

next: Crime & Disorder Act with Reference to School Attendance
~ back to adders.org homepage
~ adhd library articles
~ all add/adhd articles