It’s important to differentiate between depressed mood and depressive disorder when correlating depression with menopausal symptoms. Depressed mood refers to familiar sadness, low spirits, or despondency, while depressive disorder is a more serious syndrome. The lack of distinction between these two conditions could pose challenges in interpretation. Clinical depression during the climacteric is often associated with a pre-existing major mood disorder. Most research on menopausal depression uses measurement scales such as the Beck Depression Inventory (BDI) and the Hamilton Rating Scales of Clinical Anxiety and Depression (Greene, 1998), which can make it difficult to differentiate between depressive disorder and depressed mood.
Caspar (1998) found inconclusive evidence when linking depressive episodes directly to lower estrogen levels or hot flashes, although it’s recognized that hormonal fluctuations may contribute to psychological distress. It’s possible that lack of sleep may be the link between hot flashes and mood changes, but a direct cause-and-effect relationship between hot flashes and depression has not been established. Luaritzen and van Keep (Lobo, 1997) suggest that depressed mood may be related to night sweats when they cause sleep deprivation. Similarly, Baker, Simpson, and Dawson (1996) found that perimenopausal women experienced disrupted sleep, correlated with higher anxiety, but their study did not specifically identify night sweats as the cause of disrupted sleep. Nonetheless, it seems likely that psychological symptoms do result from disturbed sleep indirectly related to hot flashes or night sweats. Since yoga, with its deep breathing techniques, can help reduce hot flashes, it may also improve sleep and subsequently mood. At least, that was my experience of practicing deep breathing at night when I was unable to sleep because of a hot flash.
On a more serious note, a history of mood disorder may impact how perimenopausal symptoms are experienced. Tam and colleagues (1999) found that perimenopausal women had higher scores of depression on the Beck Depression Inventory compared to pre- or postmenopausal women, and attributed these scores to a prior history of mood disorder (Tam, Stucky, Hanson, & Parry, 1999). According to the DSM-IV criteria for major depression, five or more of the following symptoms must be present in the same 2-week period: depressed mood most of the day, diminished interest or pleasure, weight loss, insomnia, psychomotor retardation, fatigue, feelings of worthlessness or excessive guilt, diminished ability to concentrate or indecisiveness, and recurrent thoughts of death. These symptoms would be considered clinical if they cause impairment in social, occupational, or other important areas of functioning, and cannot be explained by bereavement, drug use, or a general medical condition.
According to Beck (1967), the development of depressed mood depends on the negative attitudes one forms about oneself, the outside world, and the future based on past experiences. If women perceive the loss of reproductive ability during perimenopause as a personal deficiency, it may lead to a negative attitude towards menopause. Depression then becomes a symptom of perimenopause and not solely a result of other major life stressors. In depression, the cognitive pattern or schema is negative, involving a person’s health, worth, performance, personality, or expectations of the future. Negative schemas may not necessarily arise solely from experiencing hot flashes, but women with pre-existing mood disorders may be particularly sensitive to the stress of perimenopause.
In contrast to North American studies showing a higher prevalence of depression during perimenopause, a Turkish study (Sagsoz, Oguzturk, Bayram, & Kamaci, 2001) found that depression is higher among postmenopausal women. Sagsoz and colleagues state that this may be due to the correlation between childbearing and depression, as depression was higher among women who had born children compared to those who had not. This type of depression may be a result of specific cultural values and could be exacerbated by the loss of social support or family role changes. The study also found no correlation between blood hormone or lipid levels and anxiety or depression, but did find that depression was higher in women who had born children than in those who had not born children. This contrasts with depression associated with night sweats and sleep deprivation, or even cyclical depression.
In North America, depression related to menopause is believed to be largely biochemical in nature, with some researchers suggesting that a decline in estrogen levels leads to changes in brain chemistry that can result in mood changes (Lobo, 1997). This is supported by research indicating that mood changes, such as those experienced during pre-menstrual syndrome (PMS), are related to hormone levels throughout the life cycle. Comparisons have also been made between the pathophysiology of depression and the neurobiologic effects of estrogen.
The pathophysiology of depression refers to the underlying biological processes and mechanisms that contribute to the development and manifestation of depression, which is a complex mental health disorder. While the exact cause of depression is not fully understood, research suggests that multiple factors, including genetic, environmental, and neurobiological factors, play a role in its development.
One of the neurobiological factors that has been implicated in depression is the role of neurotransmitters in the brain, which are chemical messengers that transmit signals between nerve cells. Serotonin, dopamine, and norepinephrine are among the neurotransmitters that are believed to play a role in depression. Alterations in the levels or functioning of these neurotransmitters have been observed in individuals with depression, and antidepressant medications often work by targeting these neurotransmitter systems to help regulate mood.
Estrogen, which is a female sex hormone, has also been implicated in the neurobiological effects of depression. Estrogen receptors are found throughout the brain, including areas that are involved in mood regulation, such as the hippocampus, amygdala, and prefrontal cortex. Estrogen has been shown to have a complex and multifaceted role in the brain, influencing neurotransmitter systems, neuroplasticity (the brain's ability to change and adapt), and inflammation, among other processes.
Research suggests that estrogen may have antidepressant effects, as it has been shown to increase serotonin levels in the brain, promote neuroplasticity, and have anti-inflammatory effects. Estrogen levels fluctuate during the menstrual cycle, and some women may experience mood changes during the pre-menstrual phase, commonly known as pre-menstrual syndrome (PMS). Similarly, during perimenopause and menopause, there is a decline in estrogen levels, and this hormonal fluctuation may contribute to the development of mood changes and depressive symptoms in some women.
One wonders if it may be possible to counteract the effect of lowered levels of serotonin by increasing brain chemicals that have the opposite effect such as beta-endorphins..
Beta-endorphins are a type of endogenous opioid peptide that are naturally produced by the body and are known to play a role in mood regulation. They are often associated with feelings of well-being and can have an analgesic, or pain-relieving, effect. Beta-endorphins are released in response to various stimuli, including exercise, meditation, and stress.
Research has shown that exercise and meditation can increase the levels of beta-endorphins in the brain. For example, studies have found that regular exercise can lead to an increase in beta-endorphins, which may contribute to the mood-enhancing effects of exercise and the phenomenon known as “runner’s high,” which is a state of euphoria or heightened well-being experienced by some individuals during or after intense exercise.
Similarly, meditation has also been shown to increase beta-endorphin levels in some studies. Corticotropin-releasing hormone (CRH), which is a stress hormone, has been found to stimulate the release of beta-endorphins during meditation, leading to increased levels of these brain chemicals. This may help explain the reported mood-enhancing effects of meditation and the similarities between the effects of meditation and exercise on beta-endorphin levels.
The idea of counteracting the effect of lowered serotonin levels by increasing other brain chemicals, such as beta-endorphins, is an interesting concept. However, it’s important to note that the neurobiology of depression is complex and involves multiple neurotransmitters, receptors, and other molecular and cellular processes. The relationship between serotonin, beta-endorphins, and other brain chemicals in the context of depression is still an area of ongoing research and further investigation is needed to fully understand the mechanisms involved.
It’s also worth noting that while exercise and meditation have been shown to have potential mood-enhancing effects through the release of beta-endorphins, they are not standalone treatments for depression. Depression is a multifaceted condition that requires a comprehensive approach to treatment, which may include a combination of medication, therapy, lifestyle changes, and other interventions, tailored to the individual’s needs and severity of symptoms.
And as related to hot flashes, the data on beta-endorphin levels during hot flashes is inconsistent according to Freedman (Lobo, 1997), Sternfeld and colleagues have suggested that decreases in hypothalamic beta-endorphin levels during perimenopause may be implicated in the pathogenesis of hot flashes (Sternfeld, Quesenberry, & Husson, 1999). The correlation between beta-endorphin levels and hot flashes is encouraging, as it suggests that increasing beta-endorphin levels could potentially be a therapeutic approach for managing hot flashes.