Menopause, which is defined as the cessation of menses for at least 1 year, begins at an average age of 50 to 51 years.[34] A direct link between menopause and depression has not been substantiated. In fact, epidemiologic studies suggest that the risk of depression decreases in women after age 50. A large 5-year longitudinal prospective study of women between the ages of 45 and 55 years examined the effect of menopause on depression.The study, which controlled for prior depression, menopausal symptoms, and concurrent hormonal treatment, showed that the onset of natural menopause was not associated with an increased risk of depression.

Perimenopause, which typically occurs between the ages of 45 to 50 years, is the transition time between premenopause (the period when women normally have menstrual cycles) and menopause. Several studies and community surveys have reported a peak in the prevalence of MD during perimenopause.[55] For example, Ballinger et al.[55] reported a significant increase in psychiatric morbidity among perimenopausal women ages 45 to 49 years. Similarly, in a longitudinal study, Avis et al.

reported that women who experienced increased menopausal symptoms during a prolonged perimenopausal period (at least 27 months) had a moderately increased risk of developing transitory depression. More recent evidence, based on international Epidemiologic Catchment Area data, also suggested a peak in the onset of depressive illness during the perimenopausal years.[56] Affective changes at the time of menopause may be secondary to the occurrence of vasomotor or other physical symptoms, rather than menopausal status itself.

Environmental events and developmental life stressors, such as changes in family structure, caring for an elderly parent, having children leave or return home, involvement in outside work in addition to running a household, and reappraisal of one’s future role, also have been shown to affect mental health during this life stage.

These psychosocial factors may contribute more to such common menopausal symptoms as fatigue, anxiety, and sadness than the physiologic changes of menopause.[55,57] Women with a previous history of PPD, premenstrual syndrome, or prior depressive episodes are at increased risk for developing a depressive illness at menopause.[58] In a longitudinal study by Avis et al.,[54] prior depression was the variable most predictive of subsequent depression in postmenopausal women.

Antidepressants have been the hot ticket in psychiatry, making it seem like psychotherapy’s time was up. But the 50-minute-hour may be coming back into fashion. A growing body of research is showing that combining antidepressants and psychotherapy is significantly better at driving away despair than either treatment alone. “Psychiatry’s discovery that depression could be attacked by drugs that alter the distribution of brain chemicals is an extraordinary achievement, ” says Martin B. Keller, MD, chairman of psychiatry at Brown University Medical School. But in the pursuit of biological causes to explain mental illness, he adds, “Our profession may have fallen behind in its efforts to test the value of new psychotherapies.”

Dr. Keller is the lead author of a breakthrough study published in the New England Journal of Medicine in May, comparing psychotherapy and antidepressants for the treatment of chronic depression. It is the largest study of its kind. “Our profession may have fallen behind in its efforts to test the value of new psychotherapies.” The Chronic Depression study, conducted at 12 sites across the United States, involved 519 patients who had been continuously depressed for at least 2 years.

(Most had battled depression their entire adult lives.) The researchers found that 85% of those treated with both psychotherapy and the antidepressant Serzone for 3 months experienced remission or showed major improvement in their symptoms. Patients who received psychotherapy or medication alone didn’t fare as well: 55% of those in the drug group and 52% in the psychotherapy group recovered or improved significantly. For some of these patients, “It was the first time in 20 years that they felt joy or optimism or woke up in the morning wanting to face the day,” says Dr. Keller.

The controversy about whether Fibromyalgia and Chronic Fatigue Syndrome are simply psychological disorders persists despite the fact that an abundance of research has shown otherwise. Last week’s article focused on the distinction between Fibromyalgia Syndrome (FMS) and depression. There is an even greater body of research that compares patients diagnosed with primary depression to those who fit the criteria for Chronic Fatigue Syndrome. According to CFS expert Dr. Anthony Komaroff of Harvard Medical School, studies of CFS patients around the world show evidence of abnormalities in the brain and immune system.

Although we still do not understand the cause of these problems in CFS patients, Komaroff points out that it is not “all in their heads.” Says Komaroff, “There is no evidence of any psychiatric disorder in a sizable number of patients with this illness.” In fact, research has distinguished between depression and CFS on both a biological and psychiatric basis. Studies of brain pathology have revealed abnormalities in patients with CFS that are not characteristic of depression. For example, a 1992 study showed that CFS patients exhibit more alpha electroencephalographic (EEG) activity during non-REM sleep.

This irregularity is not found in patients with major depressive disorders. In addition, a greater number of CFS patients (53%) report difficulty falling asleep, while this number is only 26% for depressed patients. Immunological and neurological findings also differ between CFS and depression. A 1995 study indicated that CFS patients with more severe cognitive problems exhibited more abnormalities in their immune systems. Since the study statistically controlled for depression, this finding indicates that the presence of cognitive dysfunction in CFS sufferers cannot be explained merely by depressive symptoms.

According to the abstract and methods, they screened their patients with chronic fatigue syndrome (CFS) to exclude those with depression. Then they examined this group further using a standardized psychiatric interview (Schedule for Affective Disorders and Schizophrenia) in order to “exclude subjects with current psychiatric illness, with a particular emphasis on depression”. The data from the Hamilton Depression Rating scale are difficult to interpret given the number of illness-related items, but the scores did not indicate a significant degree of depression either.

So, having excluded “subjects with depression or anxiety”, why did the authors claim in their discussion that “the main limitation of the present study is that our CFS subjects had high levels of depression”? If this is correct, why was their depression not picked up by the three measures? Why were these patients not excluded from the research as stated by the authors, or funds permitting, used as a comparison group (cf. Costa et al 1995, Fischler et al 1998)?

How depressed were the ten patients on antidepressants and if these were not effective, could their suboptimal treatment have contributed to their ongoing fatigue? I was also baffled by the authors’ suggestion that the thalamic hyperperfusion may reflect “increased attention to motor and cognitive tasks”. What were the patients doing? The abstract states that the scans were conducted at rest.

If the subjects had just completed a battery of cognitive tests, why did the authors not check to see if the data available supported their hypothesis (cf. Fischler et al)? If this paper was subjected to peer review, why did no one challenge the obvious inconsistencies? Why did no one query the selective discussion of the findings and the misrepresentation of the literature on CFS and psychopathology? Does British Psychiatry no longer value scientific objectivity and attention to detail?