Depression to Dementia

ad-dep-0

  • (i) Individuals who develop depression at any point in their lives, sustain minimal or no depression-related neuropathology (eg, glucocorticoid neurotoxicity), and who have stable, normal cognitive functioning;
  • (ii) Individuals who develop depression at any point and who experience depression-related neuropathology that results in MCI that is stable (unless they experience additional depressive episodes);
  • (iii) Individuals who accumulate AD neuropathology over many years and who develop late-life depression (related or unrelated to AD pathology), that lowers brain reserve capacity, and results in expression of MCI earlier than otherwise would be the case, and given the underlying neuropathology, progress to AD;
  • (iv) Individuals who accumulate AD neuropathology over many years along with co-occurring cerebrovascular disease, which damages the frontostriatal circuitry, leading to late-life depression. The total neuropathologic burden, combined with depressed mood, lowers brain reserve capacity, leads to expression of MCI (eg, memory and executive dysfunction) earlier than otherwise would be the case, and, given the underlying neuropathology, progresses to AD along with co-occurring cerebrovascular disease;
  • and (v) Individuals who develop cerebrovascular disease (with variable neuropathologic burden), that damages the frontostriatal circuitry, leading to late-life depression and MCI (eg, executive dysfunction), that, will follow the course of the underlying cerebrovascular disease.
AD Alzheimer’s disease
CAD coronary artery disease
HPA hypothalamic-pituitary-adrenal
MCI mild cognitive impairment
MDE major depressive episode
WMH hyperintense white matter regions

ad-depGlucocorticoids contribute to hippocainpal atrophy and learning/episodic memory impairment

Depression is associated with neuroendocrine changes similar to those observed in animal models of chronic stress, including abnormalities within the hypothalamicpituitary-adrenal (HPA) axis. Most notably, depressed subjects have been shown to exhibit, increased HPA central drive with elevated corticotrophin-releasing hormone (CRH) and vasopressin production by cells of the hypothalamic paraventricular nucleus (PVN); impaired negative feedback regulation due to decreased expression of corticosteroid receptors in the hypothalamus and pituitary as well as upstream CNS regulatory centers; and adrenal hypertrophy (reviewed in ref 25). The net effect of these changes in HPA function is chronic elevation of adrenal glucocorticoid production with impaired negative feedback and abnormal homeostatic regulation. Such HPA dysregulation is clinically detectable (via dexamethasone nonsuppression or elevated 24-hour urinary Cortisol) in about, half of patients with major depression.2526 HPA dysregulation may be more common among older depressed individuals, as suggested by the finding of a significant correlation between age and post-dexamethasone Cortisol levels in individuals with late-life depression.27

Adrenal glucocorticoid/cortisol regulates HPA activity through both direct, negative feedback at the pituitary and hypothalamus and indirect, mechanisms involving higher central nervous system (CNS) centers. The human hippocampus, for example, contains large numbers of corticosteroid receptors and plays a critical role in downregulating CRH release via a multisynaptic pathway terminating in y-aminobutyric acid (GABA)-ergic output to the paraventricular nucleus (reviewed in ref 28). At. the same time, HPA disturbances causing prolonged hypercortisolemia may promote hippocampal atrophy and functional decline, such that HPA regulation is further compromised. ‘Iliis interaction may underlie the observed association between hypercortisolemic disease states such as Cushing’s syndrome and depression, and both hippocampal atrophy and impairment, in the verbal and spatial memory functions subserved by the hippocampus.29,30

Animal studies suggest that high-stress conditions or exogenous glucocorticoids can cause hippocampal neuronal damage31 and memory impairment.32 These changes have been observed concurrent with stress or exogenous glucocorticoid administration, and appear to progress over a lifetime of stress or glucocorticoid excess (see review in ref 33). Human studies in older adults likewise suggest that hippocampal size and function are diminished in the setting of elevated glucocorticoids,3435 and in proplemiaortion to duration of prior hypercortisolemia.36

On the basis of these findings, many have hypothesized that glucocorticoids may promote hippocampal cell injury and death when chronically elevated, as in the setting of hypercortisolemica associated with major depression. Glucocorticoid-induced cellular damage may be mediated through effects on several biochemical substrates. Postulated mechanisms include decreased glucose uptake and ATP generation, elevated intracellular calcium with increased free radical production and degradative enzyme activity, and impaired uptake of glutamate from hippocampal synapses resulting in excitotoxicity.28,37 In addition, hypercortisolemia has been linked to a decrease in neurogenesis in the dentate gyrus.38 While the combination of cell death and decreased neurogenesis may theoretically contribute to hippocampal cell loss over time, recent, evidence suggests at. most a minor role for this mechanism in hypercortisolcmic human subjects in the absence of cooccurring insults.39 Animal and human studies support the idea that glucocorticoids contribute to hippocampal atrophy and functional deficits predominantly through more subtle alterations, including reduced synapse number,40 atrophy of pyramidal cell dendrites,41derangement, of glial cells,42 and other changes.

The loss of hippocampal volume and memory function observed in some elders with late -life depression suggests the possibility that depression may be a predispositional risk factor for AD in particular. Indeed, lower hippocampal volumes independently predict subsequent AD in groups of MCI and cognitively normal elderly subjects.52 Likewise, deficits in verbal learning and memory, similar to those described in cuthymic patients with history of major depression,30 also predict AD (eg, ref 53). While a primary causal role for depression in AD pathogenesis seems unlikely, depression-associated hypercortisolemia leading to decline in hippocampal size, connectivity and cognitive function may represent one of multiple links between depression and dementia as described below.

Brain and cognitive reserve are often used interchangeably, but in fact, have subtle but. distinct differences in meaning.119 Nevertheless, either may account, equally well for the relationship between depression and dementia. Tltic concept of brain reserve capacity, first proposed by Satz120 varies across individuals such that those with greater neuronal redundancy are able to tolerate more cell loss than those with less redundancy, before manifesting clinical symptoms. The concept of redundancy refers to the notion that, circuits contain more than the minimum number of neurons needed to perform an operation. Redundancy is evident when individuals incur substantial neuronal loss before the appearance of clinical symptoms. Thus, brain reserve capacity posits that individual differences in neural redundancy translate into differences in thresholds for vulnerability to or protection from clinical symptoms after brain damage. The concept of cognitive reserve developed by Stern (eg, refs 121 ,122) is similar but rather than being based on differences in brain size or neuronal count, emphasizes differences in the efficiency or manner in which tasks are performed or information is processed.

Both brain reserve and cognitive reserve explain the role of risk and protective factors for cognitive impairment (including progressive decline into dementia), associated with brain damage. For example, higher educational attainment, larger head size, larger brain volume,123 social engagement, 124 physical activity,125 and leisure cognitive activity126,127 may result in greater redundancy and/or efficiency and therefore reserve, thereby offering protection against exhibiting clinical symptoms of dementia. Similarly, lower levels of these protective factors may reduce neuronal or functional redundancy leading to earlier dementia symptom onset for a given level of CNS damage.

While certain mechanisms may alter an individual’s risk to develop (or change the rate of development of) ADrelated pathology (eg, P-amyloid deposition), other mechanisms alter the strength of association between these biological changes and the time to develop clinical disease. We propose that depression alters an individual’s risk of cognitive dysfunction, shortening the latent period between the development, of AD neuropathology and the onset, of clinical dementia, thus increasing the incidence and prevalence of AD among older adults with depression.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872078/


About Glucocorticoids

Glucocorticoids (GCs) are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor (GR),[1] that is present in almost every vertebrate animal cell. The name glucocorticoid (glucose + cortex + steroid) is composed from its role in regulation of glucose metabolism, synthesis in the adrenal cortex, and its steroidal structure (see structure to the right). A less common synonym is glucocorticosteroid.

GCs are part of the feedback mechanism in the immune system which reduces certain aspects of immune function, such as reduction of inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. GCs have many diverse (pleiotropic) effects, including potentially harmful side effects, and as a result are rarely sold over the counter.[2] They also interfere with some of the abnormal mechanisms in cancer cells, so they are used in high doses to treat cancer. This includes: inhibitory effects on lymphocyte proliferation as in the treatment of lymphomas and leukemias; and the mitigation of side effects of anticancer drugs.

GCs affect cells by binding to the glucocorticoid receptor (GR). The activated GR complex, in turn, up-regulates the expression of anti-inflammatory proteins in the nucleus (a process known as transactivation) and represses the expression of proinflammatory proteins in the cytosol by preventing the translocation of other transcription factors from the cytosol into the nucleus (transrepression).[2]

Glucocorticoids are distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects. In technical terms, “corticosteroid” refers to both glucocorticoids and mineralocorticoids (as both are mimics of hormones produced by the adrenal cortex), but is often used as a synonym for “glucocorticoid.” Glucocorticoids are chiefly produced in the zona fasciculata of the adrenal cortex, whereas mineralocorticoids are synthesized in the zona glomerulosa.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life, and it regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions. Various synthetic glucocorticoids are available; these are used either as replacement therapy in glucocorticoid deficiency or to suppress the immune system.

https://en.wikipedia.org/wiki/Glucocorticoid

Our children are not our possession, they are entrusted to us to care for

Our children are not our possession, they are entrusted to us to care for until they can independently live in this world, ready with their college degrees or creative passions.

We model our good behavior to our children or God’s children and it is our honor when they grew up as responsible citizens, loving and caring other human beings.  We are temporary caretakers of our children and we do not own or possess them. They are children of God and not our own. We are tasked to take care of them until they can take care of themselves.

Religion is a place to worship and not to limit us in the way we love or treat others. Positive cultural practices are followed and negative , dehumanized cultural norms are not followed as we are human beings, with free will and love.

I am sad of some honor killings in Pakistan. Let the future children believe that this world is filled with human love, not limited by cultural practices without love and compassion and not limited by religion that judges one because of abortion, marrying another without parental permission and so on.

I am sad that there is no family planning in the Philippines. A household of 6 siblings and the father and mother have no jobs. The children has to labor to put food on the table. And the older children dependent on their parents for everything. I am sad there is not enough jobs in the Philippines and not everyone can survive without help from other family members or relatives, college education is not free and other misfortunes.

I am positive that the future is bright if we have love in our hearts and passion to fulfill our dreams, to finish college and to find a better job.

I am hopeful for the USA without Trump or with Trump but still hoping that US politicians will put the people’s issues first and not their own.

 

‘Friendship Bench’ Program Proves Effective at Alleviating Mental Illness Symptoms

Summary: The ‘Friendship Bench’ approach has been able to reduce the prevalence of depression in some communities in Zimbabwe, a new study reports.

Source: Grand Challenges Canada.

In Zimbabwe study, Friendship Bench therapy reduces prevalence of depression to <14%, compared to 50% in control group; First at-scale model of community mental health care in Africa has diagnosed & treated over 27,500 people for common mental disorders.

Their offices are simple wooden seats, called Friendship Benches, located in the grounds of health clinics around Harare and other major cities in Zimbabwe.

The practitioners are lay health workers known as community “Grandmothers,” trained to listen to and support patients living with anxiety, depression and other common mental disorders.

But the impact, measured in a ground-breaking study, shows that this innovative approach holds the potential to significantly improve the lives of millions of people with moderate and severe mental health problems in countries where access to treatment is limited or nonexistent.

Funded by the Government of Canada through Grand Challenges Canada, the randomised controlled trial was conducted by the University of Zimbabwe, the London School of Hygiene & Tropical Medicine and King’s College London. The study is published today in JAMA, the world’s most widely-circulated medical journal.

Six months after undergoing six weekly “problem solving therapy” sessions on the Friendship Benches, participants showed significant differences in severity of depression, anxiety, and suicidal thoughts based on locally validated questionnaires for depression and anxiety: the Shona Symptom Questionnaire (SSQ), the Patient Health Questionnaire (PHQ) and the Generalised Anxiety Disorder scale (GAD). The results were striking.

Patients with depression or anxiety who received problem-solving therapy through the Friendship Bench were more than three times less likely to have symptoms of depression after six months, compared to patients who received standard care. They were also four times less likely to have anxiety symptoms and five times less likely to have suicidal thoughts than the control group after follow-up.

50 percent of patients who received standard care still had symptoms of depression compared to 14 percent who received Friendship Bench (based on PHQ). 48 percent of patients who received standard care still had symptoms of anxiety compared to 12 percent who received Friendship Bench (based on the GAD), and 12 percent of patients who received standard care still had suicidal thoughts compared to 2 percent who received Friendship Bench (based on SSQ).

The Friendship Bench intervention was also shown to be well suited to improve health outcomes among highly vulnerable individuals. 86 percent of the study’s participants were women, over 40 percent were HIV positive, and 70 percent had experienced domestic violence or physical illness.

Lead author of the study Dr. Dixon Chibanda, a consultant psychiatrist in Harare, co-founded the Friendship Bench network in response to the appalling shortage of evidence-based treatment for people with mental disorders in Zimbabwe, a problem common throughout Africa.

While about 25 percent of the country’s primary care patients suffer from depression, anxiety and other common mental disorders, Zimbabwe (population 15 million) has only 10 psychiatrists and 15 clinical psychologists.

“Common mental disorders impose a huge burden on all countries of sub-Saharan Africa,” says Dr. Chibanda. “Developed over 20 years of community research, the Friendship Bench empowers people to achieve a greater sense of coping and control over their lives by teaching them a structured way to identify problems and find workable solutions.”

Image shows two women talking on the friendship bench.

With CDN $1 million in funding from Grand Challenges Canada earlier this year, the Friendship Bench has since been scaled to 72 clinics in the cities of Harare, Gweru and Chitungwiza (total population 1.8 million). Through collaborating with a Médecins Sans Frontières psychiatric program in Zimbabwe, the Friendship Bench is working to create the largest comprehensive mental health program in sub-Saharan Africa.

To date, over 27,500 people have accessed treatment.

“In developing countries, nearly 90 percent of people with mental disorders are unable to access any treatment,” says Dr. Peter A. Singer, Chief Executive Officer of Grand Challenges Canada. “We need innovations like the Friendship Bench to flip the gap and go from 10 percent of people receiving treatment, to 90 percent of people receiving treatment.”

“In many parts of Africa, if you are poor and mentally ill, your chances of getting adequate treatment are close to zero,” says Dr. Karlee Silver, Vice President Programs at Grand Challenges Canada. “In Zimbabwe, that’s changing thanks to the Friendship Bench, the first project with the potential to make mental health care accessible to an entire African nation.”

In 2017, the team will focus on expanding the model to reach other vulnerable populations, including youth and refugees. In partnership with the Swedish NGO SolidarMed, the team intends to expand implementation of this model in Masvingo province and subsequently in the refugee centres of the eastern highlands on the border with Mozambique.

“The Friendship Bench team, working with the Zimbabwe Ministry of Health, has been able to substantially scale up services for some of the most deprived people in the community,” says Dr. Shekhar Saxena, Director of Mental Health and Substance Abuse at the World Health Organization. “By supporting the uptake of mental health innovations like the Friendship Bench, Canada is helping to turn the tide in the global mental health challenge.”

The study, published today in JAMA and supported by Grand Challenges Canada, was conducted from September 2014 to June 2015, and involved:

  • Identifying participants at 24 primary care clinics in Harare, divided into an intervention group (287 participants) and a control group (286). Total participants: 573.
    Participants were all at least 18 years old (median age 33);
  • All had been assessed at 9 or higher on a 14-level “Shona Symptoms Questionnaire” (SSQ-14), an indigenous measure of common mental disorders in Zimbabwe’s Shona language . Changes in depression were measured using the PHQ-9 scale.
  • Excluded were patients with suicidal intent (those who were clinically depressed with suicidal thoughts and a plan for suicide), end-stage AIDS, were currently in psychiatric care, were pregnant or up to 3 months post-partum, presented with current psychosis, intoxication, and/or dementia (such patients were referred to a higher level clinic in Harare).
  • The control group received standard care (nurse assessment, brief support counselling, medication, referral to see a clinical psychologist and/or a psychiatrist, and Fluoxetine if warranted) plus education on common mental disorders.
  • Intervention group participants met on a wooden bench on the grounds of municipal clinics with trained, supervised lay health workers, popularly known as “grandmothers,” (median age 53) who provided problem solving therapy with three components — “opening up the mind, uplifting the individual, and further strengthening.”
  • The 45-minute sessions took place weekly for six weeks, with an optional 6-session group support program available
  • The “grandmothers” used mobile phones and tablets to link to specialist support. They also used a cloud-based platform that integrated the Friendship Bench project’s training, screening, patient referral and follow-up components
  • After three individual sessions, participants were invited to join a peer-led group called Circle Kubatana Tose, or “holding hands together,” which provided support from men and women who had benefitted from the Friendship Bench earlier. At these weekly meetings, people shared personal experiences while crocheting purses made from recycled plastic materials, the latter being an income-generating skill for participants.”
ABOUT THIS PSYCHOLOGY RESEARCH ARTICLE

Funding: The study was funded by Grand Challenges Canada.

Source: Terry Collins – Grand Challenges Canada
Image Source: NeuroscienceNews.com image is credited to Grand Challenges Canada / ZAPP.
Original Research: Abstract for “Effect of a Primary Care–Based Psychological Intervention on Symptoms of Common Mental Disorders in Zimbabwe: A Randomized Clinical Trial” by Dixon Chibanda, MD; Helen A. Weiss, DPhil; Ruth Verhey, MSc; Victoria Simms, PhD; Ronald Munjoma, SLC; Simbarashe Rusakaniko, PhD; Alfred Chingono, MSc; Epiphania Munetsi, MPhil; Tarisai Bere, BA; Ethel Manda, BSc; Melanie Abas, MD; and Ricardo Araya, PhD in JAMA. Published online December 27 2016 doi:10.1001/jama.2016.19102

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Grand Challenges Canada “‘Friendship Bench’ Program Proves Effective at Alleviating Mental Illness Symptoms.” NeuroscienceNews. NeuroscienceNews, 30 December 2016.
<http://neurosciencenews.com/friendship-bench-psychology-5835/&gt;.

Abstract

Effect of a Primary Care–Based Psychological Intervention on Symptoms of Common Mental Disorders in Zimbabwe: A Randomized Clinical Trial

Importance Depression and anxiety are common mental disorders globally but are rarely recognized or treated in low-income settings. Task-shifting of mental health care to lay health workers (LHWs) might decrease the treatment gap.

Objective To evaluate the effectiveness of a culturally adapted psychological intervention for common mental disorders delivered by LHWs in primary care.

Design, Setting, and Participants Cluster randomized clinical trial with 6 months’ follow-up conducted from September 1, 2014, to May 25, 2015, in Harare, Zimbabwe. Twenty-four clinics were randomized 1:1 to the intervention or enhanced usual care (control). Participants were clinic attenders 18 years or older who screened positive for common mental disorders on the locally validated Shona Symptom Questionnaire (SSQ-14).

Interventions The Friendship Bench intervention comprised 6 sessions of individual problem-solving therapy delivered by trained, supervised LHWs plus an optional 6-session peer support program. The control group received standard care plus information, education, and support on common mental disorders.

Main Outcomes and Measures Primary outcome was common mental disorder measured at 6 months as a continuous variable via the SSQ-14 score, with a range of 0 (best) to 14 and a cutpoint of 9. The secondary outcome was depression symptoms measured as a binary variable via the 9-item Patient Health Questionnaire, with a range of 0 (best) to 27 and a cutpoint of 11. Outcomes were analyzed by modified intention-to-treat.

Results Among 573 randomized patients (286 in the intervention group and 287 in the control group), 495 (86.4%) were women, median age was 33 years (interquartile range, 27-41 years), 238 (41.7%) were human immunodeficiency virus positive, and 521 (90.9%) completed follow-up at 6 months. Intervention group participants had fewer symptoms than control group participants on the SSQ-14 (3.81; 95% CI, 3.28 to 4.34 vs 8.90; 95% CI, 8.33 to 9.47; adjusted mean difference, −4.86; 95% CI, −5.63 to −4.10; P < .001; adjusted risk ratio [ARR], 0.21; 95% CI, 0.15 to 0.29; P < .001). Intervention group participants also had lower risk of symptoms of depression (13.7% vs 49.9%; ARR, 0.28; 95% CI, 0.22 to 0.34; P < .001).

Conclusions and Relevance Among individuals screening positive for common mental disorders in Zimbabwe, LHW-administered, primary care–based problem-solving therapy with education and support compared with standard care plus education and support resulted in improved symptoms at 6 months. Scaled-up primary care integration of this intervention should be evaluated.

“Effect of a Primary Care–Based Psychological Intervention on Symptoms of Common Mental Disorders in Zimbabwe: A Randomized Clinical Trial” by Dixon Chibanda, MD; Helen A. Weiss, DPhil; Ruth Verhey, MSc; Victoria Simms, PhD; Ronald Munjoma, SLC; Simbarashe Rusakaniko, PhD; Alfred Chingono, MSc; Epiphania Munetsi, MPhil; Tarisai Bere, BA; Ethel Manda, BSc; Melanie Abas, MD; and Ricardo Araya, PhD in JAMA. Published online December 27 2016 doi:10.1001/jama.2016.19102

Maternal Depression Across Child’s Early Years Impacts Neural Basis of Empathy

Summary: Children whose mothers experienced depression early in their life are more susceptable to socio-emotional problems and a reduction in empathy toward others, a new study reports.

Source: Elsevier.

Exposure to early and chronic maternal depression markedly increases a child’s susceptibility to psychopathology and social-emotional problems, including social withdrawal, poor emotion regulation, and reduced empathy to others. Since 15-18% of women in industrial societies and up to 30% in developing countries suffer from maternal depression, it is of clinical and public health concern to understand the effects of maternal depression on children’s development. A study published in the January 2017 issue of the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP) followed children of mothers with depression from birth to preadolescence and tested depression’s impact on children’s neural empathic response to others’ distress.

While previous studies have demonstrated the effects of maternal depression on children’s limited response to other’s pain, this new study is the first to examine this topic in a longitudinal sample of mother-child pairs followed from birth to age 11. This carefully selected sample of women with no comorbid contextual risk, who were repeatedly assessed for maternal depression across the first years of life, was utilized in order to compare children of mothers who were chronically depressed and children who were never exposed to any maternal psychopathology. 27 children of mothers with depression took part in the study, as well as 45 controls. They were home-visited at 9 months and 6 years to examine mother-child interaction patterns and were invited to a magnetoencephalography (MEG) session at age 11 in order to evaluate their neural reaction to pain in others.

“We were amazed to see that maternal depression in and of itself was related to differential neural processing of others’ pain in 11-year-old children. We found that the neural reaction to pain in children of depressed mothers stops earlier than in controls, in an area related to socio-cognitive processing, so that children of depressed mothers seem to reduce mentalizing-related processing of others’ pain, perhaps because of difficulty in regulating the high arousal associated with observing distress in others,” said Prof. Ruth Feldman, director of the Developmental Social Neuroscience Lab and the Irving B. Harris Early Childhood Community Clinic at Bar-Ilan University and lead author of the study.

The researchers also found that mother-child interaction patterns had a crucial role on this effect. When mother-child interactions were more synchronous, that is, mother and child were better attuned to one another, and when mothers were less intrusive, children showed higher mentalizing-related processing in this crucial brain area.

Image shows a crying woman.

“It is encouraging to see the role of mother-child interactions in our findings. Depressed mothers are repeatedly found to show less synchronous and more intrusive interactions with their children, and so it might explain some of the differences found between children of depressed mothers and their peer controls in our study,” added Prof. Feldman. “If so, our findings highlight a point of entry, where future interventions can focus their attention to help reduce the effects of maternal depression on children’s psychosocial development.”

Asked what next steps should be taken, Feldman responded: “The main clinical question now becomes: what strategies are most effective to improve mother-child interaction patterns for depressed mothers and their offspring. Moreover, if we are able to help these mothers be more attuned and less intrusive, will it be enough in order to enable resilience in the offspring? In addition, there are further scientific questions about the manner in which patterns of maternal care implement in the development of children’s brain, endocrine systems, behavior, and relationships.”

To that end, Feldman and her team are studying how maternal depression and mother-child interactions are associated with children’s stress hormones, behavioral empathy, hormones related to bond formation, and their neural reaction to affiliative cues. Feldman is planning to study intervention strategies that focus on the mother-child interaction pattern, and is hopeful that if successful, these strategies will improve mental health and social adjustment in children of mothers with depression. “Wouldn’t it be interesting and promising if an intervention focused on synchronous mother-child interactions could also reduce the prevalence of psychopathology in the children of depressed mothers?” she concluded.

ABOUT THIS GENETICS RESEARCH ARTICLE

Source: Mary Billingsley – Elsevier
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Maternal Depression Across the First Years of Life Impacts the Neural Basis of Empathy in Preadolescence” by Maayan Pratt, MA, Abraham Goldstein, PhD, Jonathan Levy, PhD, Ruth Feldman, PhD in Journal of American Academy of Child and Adolescent Psychiatry. Published online January 3 2017 doi:10.1016/j.jaac.2016.10.012

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Elsevier “Maternal Depression Across Child’s Early Years Impacts Neural Basis of Empathy.” NeuroscienceNews. NeuroscienceNews, 3 January 2017.
<http://neurosciencenews.com/maternal-depression-empathy-children-5851/&gt;.

Abstract

Maternal Depression Across the First Years of Life Impacts the Neural Basis of Empathy in Preadolescence

Objective
Exposure to maternal depression across the first years of life markedly increases children’s susceptibility to psychopathology, yet no study has tested its effects on the maturation of children’s social brain.

Method
Using a birth cohort of mothers with no contextual risk (N = 1,983), families were followed at 7 time points from birth to 11 years and repeatedly assessed for maternal depression across the first 6 years to form 2 cohorts: mothers continuously depressed from birth to 6 years and controls without depression. At 11 years of age, children’s (n = 72; depressed, n = 27; nondepressed, n = 45) brain response to others’ pain was measured by magnetoencephalography.

Results
Preadolescents displayed a unique oscillatory pattern with higher alpha power to pain versus no pain expressing as alpha rebound, not alpha suppression, at a late time window (1,100–1,300 ms post-stimulus) in the supplementary motor area. This suggests that top-down processing in areas of the pain matrix can underpin the maturation of vicarious empathy. Children of mothers with depression showed enhanced alpha rebound to pain in the right posterior superior temporal gyrus, which was unrelated to emotion detection abilities, pointing to decreased late processing of others’ overwhelming experiences in socio-cognitive areas. Alpha power in the posterior superior temporal gyrus was predicted by higher maternal intrusiveness and lower synchrony across early childhood.

Conclusion
These findings, from the first study to examine maternal depression and early caregiving as long-term predictors of children’s neural empathic response, pinpoint a decrease in top-down socio-cognitive mechanisms as potential pathways for the cross-generational transfer of vulnerability from mothers with depression to their offspring and highlight the need for early interventions focused on enhancing maternal attunement.

“Maternal Depression Across the First Years of Life Impacts the Neural Basis of Empathy in Preadolescence” by Maayan Pratt, MA, Abraham Goldstein, PhD, Jonathan Levy, PhD, Ruth Feldman, PhD in Journal of American Academy of Child and Adolescent Psychiatry. Published online January 3 2017 doi:10.1016/j.jaac.2016.10.012

Depression in Pregnancy and Low Birth Weight Tied to Biomarker

Summary: Researchers discover a link between low levels of BDNF protein, depression in pregnant women and low birth weight.

Source: Mediasource.

Depression is very common during pregnancy, with as many as one in seven women suffering from the illness and more than a half million women impacted by postpartum depression in the U.S. alone. The disorder not only affects the mother’s mood, but has also been linked to influencing the newborn’s development, according to recent research.

Lower blood levels of a biomarker called brain-derived neurotrophic factor (BDNF) have been associated with depression in multiple studies, mainly in non-pregnant adults.

Now, in a study published in the journal Psychoneuroendocrinology, research from The Ohio State University Wexner Medical Center found that BDNF levels change during pregnancy, and can cause depression in the mother and low birth weight in the baby.

“Our research shows BDNF levels change considerably across pregnancy and provide predictive value for depressive symptoms in women, as well as poor fetal growth. It’s notable that we observed a significant difference in BDNF in women of different races,” said Lisa M. Christian , an associate professor of psychiatry in the Institute for Behavioral Medicine Research at Ohio State’s Wexner Medical Center and principal investigator of the study.

Researchers took blood serum samples during and after pregnancy from 139 women and observed that BDNF levels dropped considerably from the first through the third trimesters, and subsequently increased at postpartum.

Image shows a pregnant woman.

Overall, black women exhibited significantly higher BDNF than white women during the perinatal period.

Controlling for race, lower BDNF levels at both the second and third trimesters predicted greater depressive symptoms in the third trimester. In addition, women delivering low versus healthy weight infants showed significantly lower BDNF in the third trimester, but didn’t differ in depressive symptoms at any point during pregnancy, which suggests separate effects.

“The good news is there are some good ways to address the issue,” Christian said. “Antidepressant medications have been shown to increase BDNF levels. This may be appropriate for some pregnant women, but is not without potential risks and side effects.”

“Luckily, another very effective way to increase BDNF levels is through exercise,” she said.” With approval from your physician, staying physically active during pregnancy can help maintain BDNF levels, which has benefits for a woman’s mood, as well as for her baby’s development.”

Other Ohio State researchers who participated in this study were Amanda M. Mitchell, Shannon L. Gillespie and Marilly Palettas.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Funding from the Eunice Kennedy Shriver National Institute for Child Health and Human Development supported this research.

Source: Drew Schaar – Mediasource
Image Source: NeuroscienceNews.com image is credited to The Ohio State University Wexner Medical Center.
Video Source: Video credited to OSU Wexner Medical Center.
Original Research: Abstract for “Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight” by Lisa M. Christian, Amanda M. Mitchell, Shannon L. Gillespie, and Marilly Palettas in Psychoneuroendocrinology. Published online August 27 2016 doi:10.1016/j.psyneuen.2016.08.025

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Mediasource “Depression in Pregnancy and Low Birth Weight Tied to Biomarker.” NeuroscienceNews. NeuroscienceNews, 12 January 2017.
<http://neurosciencenews.com/bdnf-depression-weight-birth-5926/&gt;.

Abstract

Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight

Background
Brain-derived neurotrophic factor (BDNF) is implicated as a causal factor in major depression and is critical to placental development during pregnancy. Longitudinal data on BDNF across the perinatal period are lacking. These data are of interest given the potential implications for maternal mood and fetal growth, particularly among Black women who show ∼2-fold greater risk for delivering low birth weight infants.

Methods
Serum BDNF, serum cortisol, and depressive symptoms (per CES-D) were assessed during each trimester and 4–11 weeks postpartum among 139 women (77 Black, 62 White). Low birth weight (<2500 g) was determined via medical record. Results Serum BDNF declined considerably from 1st through 3rd trimesters (ps ≤ 0.008) and subsequently increased at postpartum (p < 0.001). Black women exhibited significantly higher serum BDNF during the 1st trimester, 2nd trimester, and postpartum (ps ≤ 0.032) as well as lower serum cortisol during the 2nd and 3rd trimester (ps ≤ 0.01). Higher serum cortisol was concurrently associated with lower serum BDNF in the 2nd trimester only (p < 0.05). Controlling for race, serum BDNF at both the 2nd and 3rd trimester was negatively associated with 3rd trimester depressive symptoms (ps ≤ 0.02). In addition, women delivering low versus healthy weight infants showed significantly lower serum BDNF in the 3rd trimester (p = 0.004). Women delivering low versus healthy weight infants did not differ in depressive symptoms at any time point during pregnancy (ps ≥ 0.34).

Conclusions
Serum BDNF declines considerably across pregnancy in Black and White women, with overall higher levels in Blacks. Lower serum BDNF in late pregnancy corresponds with higher depressive symptoms and risk for low birth weight in Black and White women. However, the predictive value of serum BDNF in pregnancy is specific to within-race comparisons. Potential links between racial differences in serum BDNF and differential pregnancy-related cortisol adaptation require further investigation.

“Serum brain-derived neurotrophic factor (BDNF) across pregnancy and postpartum: Associations with race, depressive symptoms, and low birth weight” by Lisa M. Christian, Amanda M. Mitchell, Shannon L. Gillespie, and Marilly Palettas in Psychoneuroendocrinology. Published online August 27 2016 doi:10.1016/j.psyneuen.2016.08.025

How Depression May Compound Risk of Type 2 Diabetes

Depression, metabolic factors combine to boost risk of developing diabetes, study finds.

Depression may compound the risk of developing type 2 diabetes in people with such early warning signs of metabolic disease as obesity, high blood pressure and unhealthy cholesterol levels, according to researchers from McGill University, l’Université de Montréal, the Institut de recherches cliniques de Montréal and the University of Calgary.

While previous studies have pointed to a link between depression and diabetes, the new findings, published in the journal Molecular Psychiatry, suggest that when depression combines with metabolic risk factors the risk of developing diabetes rises to a level beyond the sum of its parts.

“Emerging evidence suggests that not depression, per se, but depression in combination with behavioral and metabolic risk factors increases the risk of developing type 2 diabetes and cardiovascular conditions,” said lead author Norbert Schmitz, an Associate Professor in McGill’s Department of Psychiatry and a researcher at its affiliated Douglas Mental Health University Institute. “The aim of our study was to evaluate characteristics of individuals with both depressive symptoms and metabolic risk factors.”

Over 2,500 adults studied

The four-and-a-half year study divided 2,525 participants in Quebec, aged between 40 and 69, into four groups: those with both depression and three or more metabolic risk factors; two groups, each with one of these conditions but not the other; and a reference group with neither condition.

In a departure from previous findings, the researchers discovered that participants with depression, alone, were not at significantly greater risk of developing diabetes than those in the reference group. The group with metabolic symptoms but not depression was around four times more likely to develop diabetes. Those with both depression and metabolic risk factors, on the other hand, were more than six times more likely to develop diabetes, with the analysis showing the combined effect of depression and metabolic symptoms was greater than the sum of the individual effects.

A vicious cycle?

The researchers believe depression, metabolic symptoms and the risk of developing diabetes interact in a number of ways. In some cases, a vicious cycle may emerge with depression and metabolic risk factors aggravating one another.

Evidence shows people suffering from depression are less likely to adhere to medical advice aimed at tackling metabolic symptoms, whether it be taking medication, quitting smoking, getting more exercise or eating a healthier diet. Without effective management, metabolic symptoms often worsen and this can in turn exacerbate the symptoms of depression.

woman looking depressed.

Beyond these behavioral aspects, some forms of depression are associated with changes in the body’s metabolic systems which can lead to weight gain, high blood pressure and problems with glucose metabolism. Meanwhile, some antidepressant medications can also cause weight gain.

Integrated treatment key to prevention

The researchers emphasize that not all cases of depression are the same – only some people with depression also suffer from metabolic problems. When it comes to improving health outcomes, identifying those patients who suffer from both depression and metabolic symptoms as a subgroup and adopting an integrated treatment approach may be crucial to breaking the cycle.

“Focussing on depression alone might not change lifestyle/metabolic factors, so people are still at an increased risk of developing poor health outcomes, which in turn increases the risk of developing recurrent depression,” Prof. Schmitz said.

ABOUT THIS PSYCHOLOGY RESEARCH

This research was supported by the Canadian Institutes of Health Research (CIHR), and the Fonds de recherche du Québec – Santé, Canada.

Source: Katherine Gombay – McGill University
Image Credit: The image is in the public domain.
Original Research: Abstract for “Depression and risk of type 2 diabetes: the potential role of metabolic factors” by N Schmitz, S S Deschênes, R J Burns, K J Smith, A Lesage, I Strychar, R Rabasa-Lhoret, C Freitas, E Graham, P Awadalla and J L Wang in Molecular Psychiatry. Published online February 23 2016 doi:10.1038/mp.2016.7


Abstract

Depression and risk of type 2 diabetes: the potential role of metabolic factors

The aim of the present study was to evaluate the interaction between depressive symptoms and metabolic dysregulations as risk factors for type 2 diabetes. The sample comprised of 2525 adults who participated in a baseline and a follow-up assessment over a 4.5-year period in the Emotional Health and Wellbeing Study (EMHS) in Quebec, Canada. A two-way stratified sampling design was used, on the basis of the presence of depressive symptoms and metabolic dysregulation (obesity, elevated blood sugar, high blood pressure, high levels of triglycerides and decreased high-density lipoprotein). A total of 87 (3.5%) individuals developed diabetes. Participants with both depressive symptoms and metabolic dysregulation had the highest risk of diabetes (adjusted odds ratio=6.61, 95% confidence interval (CI): 4.86–9.01), compared with those without depressive symptoms and metabolic dysregulation (reference group). The risk of diabetes in individuals with depressive symptoms and without metabolic dysregulation did not differ from the reference group (adjusted odds ratio=1.28, 95% CI: 0.81–2.03), whereas the adjusted odds ratio for those with metabolic dysregulation and without depressive symptoms was 4.40 (95% CI: 3.42–5.67). The Synergy Index (SI=1.52; 95% CI: 1.07–2.17) suggested that the combined effect of depressive symptoms and metabolic dysregulation was greater than the sum of individual effects. An interaction between depression and metabolic dysregulation was also suggested by a structural equation model. Our study highlights the interaction between depressive symptoms and metabolic dysregulation as a risk factor for type 2 diabetes. Early identification, monitoring and a comprehensive management approach of both conditions might be an important diabetes prevention strategy.

“Depression and risk of type 2 diabetes: the potential role of metabolic factors” by N Schmitz, S S Deschênes, R J Burns, K J Smith, A Lesage, I Strychar, R Rabasa-Lhoret, C Freitas, E Graham, P Awadalla and J L Wang in Molecular Psychiatry. Published online February 23 2016 doi:10.1038/mp.2016.7