The U.S. Centers for Disease Control and Prevention reported in August that symptoms of anxiety had tripled and depression symptoms had quadrupled among a group of 5,470 adults as compared with a survey sample from 2019. Meanwhile mental health services have been stretched worldwide. One reason is that mental health personnel and the facilities they work in have been reassigned to COVID-related tasks during the crisis.
All of us need to sustain and enhance our psychological resilience to weather the daily toll of activity restrictions, rising case numbers, hospitalizations and deaths. A set of simple measures known as psychological first aid or mental health first aid can enable people to help family, friends and others in their communities who experience psychological distress from pandemic fatigue, COVID convalescence, or the loss of a friend or relative. Read the entire article at Scientific American
I am a group therapist who generally works with adults. I facilitate groups using creative arts, processing oriented, or psycho-education. Sometimes I actually sort of combine these in to a psycho-educational process oriented creative group. I provide info (psycho-educational, we talk about it from a personal perspective, and than create something out of the discussion.
One thing I have notice over the decades is that when people are stressed or overwhelmed about events in their life they tend towards a negative self perception. Below is a handout that I often use. One way of using this is to start out discussing what is positive self esteem, how you get it, maintain it, and why bother with it. I than pass out the hand out and folks write and than we share it in the group or in groups of 2 or 3 folks.
Positive Statements about you
- I like myself because:
- I’m an expert at:
- I feel good about:
- My friends would tell you I have a great:
- My favorite place is:
- I’m loved by:
- People say I am a good:
- I’ve been told I have:
Dr. Descartes Li explores the ways that culture influences mental health. He looks at the effects of cultural identify and the models of illness. He also explores the stressors and supports and the elements of the relationship with the clinicians and the resulting treatment plan. Recorded on 02/26/2020. UCTV is the broadcast and online media platform of the University of California.
Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide. Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression.
The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery.
In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.” SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds.
Now, research headed up by neuroscientists David Gurwitz and Noam Shomron of Tel Aviv University in Israel supports recent thinking that rather than a shortage of serotonin, a lack of synaptogenesis (the growth of new synapses, or nerve contacts) and neurogenesis (the generation and migration of new neurons) could cause depression. In this model lower serotonin levels would merely result when cells stopped making new connections among neurons or the brain stopped making new neurons. So, directly treating the cause of this diminished neuronal activity could prove to be a more effective therapy for depression than simply relying on drugs to increase serotonin levels.
Evidence for this line of thought came when their team found that cells in culture exposed to a 21-day course of the common SSRI paroxetine (Paxil is one of the brand names) expressed significantly more of the gene for an integrin protein called ITGB3 (integrin beta-3). Integrins are known to play a role in cell adhesion and connectivity and therefore are essential for synaptogenesis. The scientists think SSRIs might promote synaptogenesis and neurogenesis by turning on genes that make ITGB3 as well as other proteins that are involved in these processes. A microarray, which can house an entire genome on one laboratory slide, was used to pinpoint the involved genes. Of the 14 genes that showed increased activity in the paroxetine-treated cells, the gene that expresses ITGB3 showed the greatest increase in activity. That gene,ITGB3, is also crucial for the activity of SERT. Intriguingly, none of the 14 genes are related to serotonin signaling or metabolism, and, ITGB3 has never before been implicated in depression or an SSRI mode of action.
These results, published October 15 2013 in Translational Psychiatry, suggest that SSRIs do indeed work by blocking SERT. But, the bigger picture lies in the fact that in order to make up for the lull in SERT, more ITGB3 is produced, which then goes to work in bolstering synaptogenesis and neurogenesis, the true culprits behind depression. “There are many studies proposing that antidepressants act by promoting synaptogenesis and neurogenesis,” Gurwitz says. “Our work takes one big step on the road for validating such suggestions.”
The research is weakened by its reliance on observations of cells in culture rather than in actual patients. The SSRI dose typically delivered to a patient’s brain is actually a fraction of what is swallowed in a pill. “Obvious next steps are showing that what we found here is indeed viewed in patients as well,” Shomron says.
The study turned up additional drug targets for treating depression—two microRNA molecules, miR-221 and miR-222. Essentially, microRNAs are small molecules that can turn a gene off by binding to it. The microarray results showed a significant decrease in the expression of miR-221 and miR-222, both of which are predicted to target ITGB3, when cells were exposed to paroxetine. So, a drug that could prevent those molecules from inhibiting the production of the ITGB3 protein would arguably enable the growth of more new neurons and synapses. And, if the neurogenesis and synaptogenesis hypothesis holds, a drug that specifically targeted miR-221 or miR-222 could bring sunnier days to those suffering from depression.
Interesting article about Somaliland facing an ‘explosion’ of mental health conditions. From The Guardian.
Amina usually takes her brother to the clinic by force. He doesn’t like going. “I feel very bad when I take him there. I have to do it but I cry at the same time,” says the young mother who lives in downtown Hargeisa, capital of the breakaway republic of Somaliland.
“We have no choice but to take him. What else can we do for him?” Amina* adds, visibly pained.
Her 38-year-old brother Bulhan* has on four occasions been admitted to the Macruuf Relief Organisation, a privately run mental health clinic in Hargeisa, one of many that have been established in recent years.
These under-resourced private centres operate largely without scrutiny from the authorities. Chaining patients is common, as is confinement without consent, practices that Human Rights Watch saysviolate “basic international standards prohibiting ill-treatment, and may constitute torture”.
See the full article at The Guardian.