Random Thoughts on this side of Mental Illness

May is Mental Health Awareness Month and mental health has been on my mind more than normal. I come from generations of family members with mental illness including my father who had Bipolar Disorder.

I have treatment-resistant Bipolar Disorder which means medicines don’t always work on me. I live on a cocktail of nine medications and have been stable on this mix for six months.

I expect this to be an unpopular post, that’s okay I want to hear all your comments.

All people have to be held accountable for their actions. The thought that came to mind this morning was a murder case that disturbs me to this day. A woman in Texas drowned all five of her children in the bathtub. She pleaded temporary insanity. I would have to agree she was insane, how could someone kill their five children? She only spent five years in a mental health ward in the prison. Is five years of medical oversite enough punishment? Is she no longer insane? I think not. I’m responsible for all of my actions regardless of my mental state.

My father sexually abused me, was it ok because he was mentally ill? It wasn’t his fault? I don’t buy into that theory. My father never sought help for his mental illness and committed suicide at 52 years old. He made the decision to not seek treatment, at the end of his life he was too sick to see how far down he was. He’ll be held accountable by a higher power than me.

I was nine years old the first time I attempted suicide, it was the first of many attempts throughout my life. As an adult educated on my illness, I have a support system in place. I have to be disciplined in taking my medication, going to therapy, seeing my Psychiatrist, and communicate with my husband or pay the price of becoming unstable.

I have Dementia brought on by Lyme Diseases and my mind slips a little each day. I watched my granny slip away and have chosen not to live that way. I plan to commit suicide before my memory is completely gone. I don’t want my husband to have to go thru all the pain of caring for me. It’s gut-wrenching to watch someone disappear behind their eyes.

We don’t talk about it often but he accepts that he can’t change my mind. My Therapist and Psychiatrist know, they wish I felt different but know the truth, you can’t change someone’s mind. Last night I told my husband that it was selfless of me, it’s the only word I could come up with. He said it’s love, that’s exactly how I felt in my heart. I want to protect him from the pain I witnessed my gramps go thru as my granny slowly died.

I’ll be held accountable for my actions by a higher power.

Melinda

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Hope For Depression Research Foundation, Inspired by the Hope in all of us

I found out about this exciting group from a fragrance advertisement for Hope, Hope Sport, and Hope Night, all available at Bergdorf Goodman.com. All net profits support Hope For Depression Research Foundation.

Learn more at HOPEFORDEPRESSION.ORG

Please check out their site, it’s packed full of information and resources.

Melinda

Our Mission

The mission of the Hope for Depression Research Foundation (HDRF) is to fund cutting-edge, scientific research into the origins, diagnosis, treatment and prevention of depression and its related mood and other emotional disorders – bipolar disorder, postpartum depression, post-traumatic stress syndrome, anxiety disorder and suicide.

In 2010, HDRF launched its Depression Task Force (DTF) – an outstanding collaboration of seven leading scientists, at the frontiers of brain science, from different research institutions across the U.S. and Canada.  These scientists have developed an unprecedented research plan that integrates the most advanced knowledge in genetics, epigenetics, molecular biology, electrophysiology, and brain imaging. To accelerate breakthrough research, they share ongoing results, in real time, at a centralized data bank, the HDRF Data Center.

HDRF was founded in April 2006 by Audrey Gruss in memory of her mother, Hope, who suffered from clinical depression.

Every dollar raised goes directly to research.

Founder’s Message


My mother Hope suffered from depression for most of her late adult life. My sisters, father and I witnessed decades of misdiagnosis, trials of medication, troublesome side effects and the psychic pain and life-sapping loss of energy that is a mark of clinical depression.

When she passed away in December 2005, I vowed that I would do all in my power to help conquer this dreaded illness. As my mother’s patient advocate, I had consulted with leading psychopharmacologists to better understand her various treatments and medications. I soon discovered the staggering reality that in the twenty-five years since the introduction of Prozac and the other SSRI antidepressants, there has been virtually no change in the basic treatment of depression, just adjustments in the use of existing approaches.

In order to encourage more cutting-edge research at a faster pace, in 2006 I started a new foundation in memory of my mother Hope – the Hope for Depression Research Foundation (HDRF).

Our mission is two-fold: First and foremost HDRF funds advanced research to find the causes of depression, a medical diagnosis, new medications and treatments and prevention of depression. To that end, HDRF has formed the Depression Task Force — an outstanding collaboration of leading neuroscientists across the US and Canada, each a pioneer in their own field. Together they have created an unprecedented research plan – The Hope Project – that accelerates the research process by sharing ongoing results, in real time, at a new HDRF Data Center.

The second goal is to raise awareness of depression as a medical illness and to educate the public about the facts of depression. We educate and inform in order to help remove the stigma of depression.

The study of depression and the brain is the last frontier of medicine. Your support for HDRF’s pioneering research can make a difference to those you personally know and to the hundreds of millions suffering worldwide.

Although doctors couldn’t find a cure for my mother’s psychic pain in her lifetime, I feel confident that with the progressive direction of our research and the encouragement of “out-of-the-box” scientific thinking, in my lifetime we will make significant strides, providing hope and help to everyone who is touched by depression.

Sincerely,
Audrey Gruss

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When college students post about depression on Facebook

Jan 07,2020


Jeff Grabmeier Ohio State News grabmeier.1@osu.edu

Study suggests friends don’t encourage them to seek help

When college students post about feelings of depression on Facebook, their friends are unlikely to encourage them to seek help, a small study suggests.

In fact, in this study, none of the 33 participating students said their friends told them they should reach out to a mental health professional to discuss their problems.

Instead, most friends simply sent supportive or motivating messages.Scottye CashScottye CashBut that may not be good enough for people who are truly depressed – as some of the people in this study probably were, said Scottye Cash, lead author of the study and professor of social work at The Ohio State University.

“It makes me concerned that none of the Facebook friends of students in this study were proactive in helping their friend get help,” Cash said.

“We need to figure out why.”

The research, published online recently in the journal JMIR Research Protocols, is part of a larger online study of health outcomes of 287 students at four universities in the Midwest and West. This study included the 33 students in the larger study who reported that they had “reached out on Facebook for help when depressed.”

The students reported what type of post they made and how their friends responded. They also completed a measure of depression.

Results showed that nearly half of the participants reported symptoms consistent with moderate or severe depression and 33 percent indicated they had had suicidal thoughts several days in the previous few weeks.

“There’s no doubt that many of the students in our study needed mental health help,” Cash said.

The two most common themes in the participants’ Facebook posts were negative emotions (“I just said I felt so alone,” one student reported) or having a bad day (“Terrible day. Things couldn’t get any worse,” one wrote). Together, those themes appeared in about 45 percent of the posts the students reported on.

But only one of the students directly asked for help and only three mentioned “depression” or related words, Cash said.

Many participants found ways to hint at how they were feeling without being explicit: 15 percent used sad song lyrics, 5 percent used an emoji or emotion to indicate their depressed feelings and another 5 percent used a quote to express sadness.

“They didn’t use words like ‘depressed’ in their Facebook posts,” Cash said.

“It may be because of the stigma around mental illness. Or maybe they didn’t know that their symptoms indicated that they were depressed.”

Students reported that the most common responses from their friends to their posts about depression (about 35 percent of responses) were simply supportive gestures. “All my close friends were there to encourage me and letting me know that everything will be okay,” one student wrote.

The next most common response (19 percent of posts) was to ask what was wrong, which participants didn’t always take positively. “It is hard to tell who cares or who’s (just) curious this way, though,” one participant wrote.

The other three most common responses (all occurring 11 percent of the time) were contacting the depressed friend outside of Facebook, sending a private message within the app, or simply “liking” the post.

Although participants reported that none of their friends suggested they get help, Cash said she is sympathetic to the plight of these friends.

“For the friends reading these posts, they often have to read between the lines since few people came right out and said they were depressed,” Cash said.

“Many people used quotes and song lyrics to talk about how they’re feeling, so their friends really had to decode what they were saying.”

Cash said the findings point to the need for more mental health literacy among college students and others so they know how to recognize the signs of depression and how to respond.

“Both Facebook and colleges and universities could do more to give these students information about resources, mental health support and how to recognize the signs of depression and anxiety,” she said.

“We need to increase mental health literacy and decrease mental health stigma.”

Co-authors of the study were Laura Marie Schwab-Reese of Purdue University; Erin Zipfel, a former graduate student at Ohio State; and Megan Wilt and Megan Moreno of the University of Wisconsin.

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Facebook posts about depression rarely spark friends to suggest counseling, a new study suggests. 

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New way to think about brain’s link to postpartum depression

Science News

Research in animals shows brain’s immune system is activated by stress during pregnancy

October 21, 2019

Source: Ohio State University

Chronic stress during pregnancy triggers an immune response in the brain that has potential to alter brain functions in ways that could contribute to postpartum depression, new research in animals suggests.

The study is the first to show evidence of this gestational stress response in the brain, which is unexpected because the immune system in both the body and the brain is suppressed during a normal pregnancy.

The Ohio State University researchers who made the discovery have been studying the brain biology behind postpartum depression for several years, creating depressive symptoms in pregnant rats by exposing them to chronic stress. Chronic stress during pregnancy is a common predictor of postpartum depression, which is characterized by extreme sadness, anxiety and exhaustion that can interfere with a mother’s ability to care for herself or her baby.

Stress is known to lead to inflammation, which prompts an immune response to protect against inflammation’s harmful effects. Based on what they already know about compromised brain signaling in rats stressed during pregnancy, the scientists suspect the immune cells in the brain responding to stress may be involved. If that’s the case, the immune changes may create circumstances in the brain that increase susceptibility to depression.

In unstressed pregnant rats, the normal suppression of the immune system in the body and the brain remained intact throughout pregnancy. In contrast, stressed rats showed evidence of neuroinflammation. The study also showed that the stressed rats’ immune response in the rest of their bodies was not active.

“That suggests there’s this disconnect between what’s happening in the body and what’s happening in the brain,” said Benedetta Leuner, associate professor of psychology at Ohio State and lead author of the study. She speculated that the signaling changes her lab has seen before in the brain and this immune response are happening in parallel, and may be directly related.

Leuner presented the findings Saturday (Oct. 19, 2019) at the Society for Neuroscience meeting in Chicago.

In this work, rats are exposed to unpredictable and varied stressful events throughout their pregnancies, a practice that adds a component of psychological stress but does not harm the health of the mother or her offspring.

In the stressed animals, the researchers found numerous pro-inflammatory compounds that indicated there was an increase in the number and activity levels of the primary immune cells in the brain called microglia. Their findings also suggested the microglia were affecting brain cells in the process.

Leuner’s lab previously determined in rats that chronic stress during pregnancy prevented motherhood-related increases in dendritic spines, which are hair-like growths on brain cells that are used to exchange information with other neurons. These same rats behaved in ways similar to what is seen in human moms with postpartum depression: They had less physical interaction with their babies and showed depressive-like symptoms.

Leuner and colleagues now plan to see whether the brain immune cells activated during gestational stress are responsible for the dendritic spine elimination. They suspect that microglia might be clearing away synaptic material on dendrites.

Leuner has partnered on this research with Kathryn Lenz, assistant professor of psychology at Ohio State, whose work explores the role of the immune system in brain development.

Though pregnancy was known to suppress the body’s immune system, Lenz and Leuner showed in a previous study that the same suppression of the immune system happens in the brain during pregnancy — the number of microglia in the brain decreases.

“By layering gestational stress onto a normal pregnancy, we’re finding this normal immunosuppression that should happen during pregnancy doesn’t occur, and in fact there’s evidence of inflammatory signaling in the brain that could be bad for dendritic spines and synapses,” Lenz said. “But we’ve also found changes in the microglia’s appetite. Every characteristic we’ve looked at in these cells has changed as a result of this stress.”

The researchers are now trying to visualize microglia while they’re performing their cleanup to see if they are eating synaptic material. They are also manipulating inflammatory changes in the brain to see if that reverses postpartum depression-like behavior in rats.

“We’ve seen the depressive-like symptoms and neural changes in terms of dendritic spines and synapses, and now we have neuroimmune changes suggesting that those microglia could be contributing to the neural changes — which we think ultimately underlie the behaviors,” Leuner said.

The research was supported by the National Institutes of Health.

Ohio State current and former students Caitlin Goodpaster, Nicholas Deems and Rachel Gilfarb also worked on the study.

Story Source:

Materials provided by Ohio State University. Original written by Emily Caldwell. Note: Content may be edited for style and length.

Cite This Page:

Ohio State University. “New way to think about brain’s link to postpartum depression: Research in animals shows brain’s immune system is activated by stress during pregnancy.” ScienceDaily. ScienceDaily, 21 October 2019. <www.sciencedaily.com/releases/2019/10/191021151538.htm>.

 

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Ketamine and Future Depression Treatments

October 16, 2019

Psychiatry Advisor Contributing Writer

doctor holding nasal spray
Most antidepressants take time to alleviate symptoms, but ketamine reduces symptoms quickly in most patients with major depressive disorder.

Researchers are hailing ketamine as the most significant new development in psychiatry given its high efficacy for treating major depression. Recent evidence has shown that in addition to depression, ketamine may also be a promising treatment for obsessive-compulsive disorder, post-traumatic stress disorder, and a number of other treatment-refractory neuropsychiatric disorders. In a recent paper published in Drug Discovery Today, researchers explore ketamine’s role in revolutionizing new mental health treatments and discuss how this drug’s mechanism of action has led to an influx of new research and studies on depression treatment.

Ketamine was approved by the US Food and Drug Administration (FDA) in 1970 as an anesthetic and safe alternative to phencyclidine. The therapeutic benefits of ketamine as an antidepressant were explored years later because of a stigma on from its widespread recreational use during the late 1960s and 1970s, and this agent was initially only administered intravenously.

In 2000, researchers found that ketamine had strong, fast-acting, and long-term effects in depression. In a randomized, placebo-controlled, crossover design study, patients with depression received 0.5 mg/kg of ketamine or saline on the first day of testing. Treatments were switched 1 week later. Researchers found that the antidepressant effects of ketamine began within 4 hours, peaked at 72 hours, and lasted for 1 to 2 weeks thereafter.1 In a 2006 study, this finding was replicated in an independent group of 18 patients with major depressive disorder who were resistant to other treatments. Compared with participants who received placebo, those who received ketamine showed significant improvement in symptoms within 110 minutes, with 35% maintaining significant response for at least 1 week.2

In subsequent years, results from a number of placebo-controlled studies revealed that ketamine is largely effective and long-acting in treatment of bipolar disorder and treatment-resistant major depressive disorder and produces antisuicidal and anti-anhedonic effects in mood disorders.

Many of today’s depression treatments are monoaminergic-based, including monoamine oxidase inhibitors, tricyclic antidepressants, selective serotonin reuptake inhibitors, and serotonin-norepinephrine reuptake inhibitors. These treatments have been proven effective for a large number of patients. However, a significant subset of patients with major depressive disorder do not respond to these agents.1 When compared with ketamine, these agents have a delayed onset of action that can take up to several weeks — increasing the risk for organ failure and suicide in this subset.

A single dose of ketamine is shown to produce rapid and robust effects within hours to days of administration. This agent is also shown to rapidly reduce suicidal ideation, fatigue, and anhedonia, and improve circadian rhythm and sleep patterns in major depressive disorder.1 Researchers point out that these symptoms are synonymous across several psychiatric disorders but remain inadequately treated by monoaminergic-based agents.

The notable differences between ketamine and standard antidepressants have spurred researchers to develop new ketamine treatments that are less invasive than those involving intravenous administration. In March 2019, the FDA approved an intranasal version of ketamine called esketamine for adults with treatment-resistant depression.

Researchers say that ketamine’s mechanism of action in the context of clinical antidepressant efficacy is only partially clear. At present, researchers understand that ketamine’s mechanism of action goes beyond modulating the neurotransmission of glutamate and includes direct and indirect high affinity antagonistic binding properties at the N-methyl-D-aspartate receptor, as well as a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid throughput modulation.1 Researchers have also noted that ketamine is a weak agonist at the mu, delta, and kappa opioid receptors.1

Other mechanisms that may contribute to ketamine’s efficacy for depression treatment include agonism at the dopamine receptor, antagonism at the M1–3 muscarinic receptors, and inhibition of the reuptake of serotonin, dopamine, and norepinephrine.1

Researchers are continuing to investigate ketamine’s underlying mechanism of action so they can progress with identifying and developing new agents that work similarly and that offer fewer side effects, as well as prolonged therapeutic effects.

Ketamine has influenced researchers to place more focus on the glutamatergic system when developing new therapies, since it is thought that rapid-acting antidepressants may trigger neurobiological events deeply rooted in the rapid reconfiguration of limbic circuitries.1 In addition to intranasal esketamine, other examples of rapid-acting glutamatergic agents that show promising results are nitrous oxide and sarcosine.

Nitrous oxide has been used as an anesthetic for more than 150 years and offers many of the same mechanisms as ketamine. Results from a 2015 study revealed that patients with treatment-resistant depression who received nitrous oxide experienced significant improvement in symptoms at 2 hours and 24 hours compared with placebo. Symptoms that showed the largest changes in improvement were depressed mood, guilt, suicidal ideation, and psychic anxiety.3 Additional trials are being conducted to determine the safety, efficacy, and optimal dosing of nitrous oxide for depression.

Sarcosine is an amino acid that functions as a glycine transporter-1 inhibitor and has co-agonistic properties at the N-methyl-D-aspartate receptor. Results from clinical trials have shown that sarcosine is a promising treatment for major depressive disorder and produces no adverse events. However, compared with ketamine, sarcosine does not produce the same rapid-acting effects within the same amount of time.1 Studies are currently underway to replicate the effects of both nitrous oxide and sarcosine in depression.

Ketamine has been found to enhance the transmission of gamma-aminobutyric acid (GABA) to reduce depression. Shortly after approving intranasal esketamine, the FDA approved an agent called brexanolone that acts as a positive allosteric modulator of GABA receptors. Brexanolone is currently being used to treat postpartum depression since this therapy produces rapid- and long-acting antidepressant effects similar to that produced by ketamine. The exact mechanism of action of brexanolone remains unclear, though researchers theorize that it binds to synaptic and extrasynaptic GABA receptors to increase functionality. Brexanolone is still being tested in clinical trials, since this agent has been associated with serious adverse events including syncope, altered state of consciousness, suicidal ideation, and intentional overdose.1

Related Articles

Buprenorphine, an opioidergic agent currently used to treat opioid use disorder, is also being studied for treatment of depression. Opioidergic agents were once used to treat melancholia during the 1950s before less addictive therapies became available and are shown to have a wide variety of actions in the brain that reduce depression. Studies evaluating the effects of buprenorphine by itself and combined with other agents on depression have produced promising results, though the FDA has stated it needs additional clinical data before this agent can be used to treat major depressive disorder.

Given what studies have since revealed about the efficacy of ketamine in depression, many researchers are reconsidering the potential benefits of banned or scheduled drugs for psychiatric patients.

Psychoactive drugs being reevaluated include lysergic acid diethylamide (LSD), 3,4-methylenedioxy-methamphetamine, and psilocybin. Researchers are determining whether microdosing these substances could produce therapeutic benefits without harmful side effects or abuse. Results from a 2011 study revealed that psilocybin was successful at significantly reducing symptoms of depression for up to 6 months in patients treated for advanced-stage cancer.1 In a 2015 study that examined the effects of LSD in patients with life-threatening diseases who were experiencing anxiety, LSD was safe, well-tolerated, and effective at reducing psychiatric symptoms.1

Researchers say that the recent FDA approval of intranasal ketamine represents a major breakthrough in psychiatry and that advances in ketamine or ketamine-like treatments may greatly improve the quality of life for patients with depression who do not respond to current treatments. Studies conducted on ketamine have paved the way for research evaluating novel approaches for the prevention and treatment of depression.

Disclosure: One author is listed as a co-inventor on a patent for the use of ketamine in major depression and suicidal ideation, among others. Please see original reference for a full list of authors’ disclosures.

References

1. Kraus C, Wasserman D, Henter ID, Acevedo-Diaz E, Kadriu B, Zarate CA Jr. The influence of ketamine on drug discovery in depression [published online August 2, 2019]. Drug Discov Today. doi: 10.1016/j.drudis.2019.07.007

2. Zarate CA Jr, Singh JB, Carlson PJ, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry. 2006;63(8):856-64.

3. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trial. Biol Psychiatry. 2015;78(1):10-18.

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Billie Eilish opens up about mental health: ‘I didn’t think that I would even make it’ to 17

Charles Trepany, USA TODAYPublished 10:22 a.m. ET Sept. 5, 2019

Billie Eilish is getting real on her mental health.

The “Bury a Friend” songstress confessed in her cover story for Elle magazine that, despite early career success, she hasn’t always been happy. 

“Two years ago, I felt like nothing mattered; every single thing was pointless,” she said in the article published Thursday. “Not just in my life, but everything in the whole world. I was fully clinically depressed. It’s insane to look back and not be anymore.”

Eilish has been accused by trolls of faking her depression, which she admitted have been painful to read.

“It hurt me to see that,” she said. “I was a 16-year-old girl who was really unstable. I’m in the happiest place of my life, and I didn’t think that I would even make it to this age.”

More: Billie Eilish, 17, rips Nylon Germany for topless cover: I ‘did not consent in any way’

The 17-year-old said her mental health has since improved, calling happiness a “crazy” feeling.

“I haven’t been happy for years,” she said. “I didn’t think I would be happy again. And here I am—I’ve gotten to a point where I’m finally okay. It’s not because I’m famous. It’s not because I have a little more money. It’s so many different things: growing up, people coming into your life, certain people leaving your life.”

More: Believe the hype: Billie Eilish proves she’s a once-in-a-generation talent at NYC concert

The singer added she wants people to know there’s hope on the other side of depression.

“For anybody who isn’t doing well, it will get better,” she said. “Have hope. I did this (expletive) with fame riding on my shoulders. And I love fame! Being famous is great, but it was horrible for a year. Now I love what I do, and I’m me again. The good me. And I love the eyes on me.”

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We Don’t Talk Much About Debt and Depression. This Blogger Is Changing That

Melanie Lockert remembers checking the traffic for her blog, Dear Debt, and feeling shocked at the results.

Someone had found her site by searching, “I want to kill myself because of debt.”

Lockert started Dear Debt in January 2013 after spending the previous year feeling depressed about her student loans. She posted monthly updates about her efforts to pay off $81,000 while working temporary hourly gigs before she landed a role running communications and planning events for a nonprofit. Along the way, she was open about her mental health struggles and how they were tied to her debt.

She had created her blog as a way to stay positive while she paid off the debt. But looking at the search terms that brought readers to her site made her recognize that her accountability stretched far beyond herself.

“It gave me an instant sense of purpose,” Lockert said.

She had attended counseling the previous year, after negotiating with a graduate student clinic to pay $5 per session while she was underemployed. She knew how much her debt affected her outlook.

She read up on the link between debt and depression. She saw she was far from alone.

“I found out that people who die by suicide are eight times more likely to have debt,” Lockert said. “From the emails I get, I know that debt is really affecting families and their mental health and their ability to find joy.”

People with debt are three times more likely to suffer from depression, according to a 2013 study published in the Clinical Psychology Review.

Lockert wrote a short post for people with debt who were feeling hopeless.

“You are not alone,” she declared. “You are not a loan.”

Still thinking about those search terms, she wrote another post.

“I want to jump through my computer and give you a hug,” she wrote. “Shake you and say your life is worth so much more.”

Then, she started getting emails from people who were desperate and afraid.

What Happened When She Wrote a Letter to Her Debt

A few months into blogging, Lockert wrote her first breakup letter to her debt.

“Dear Debt,” the letter reads. “You do not define me. My worth is more important than the value of your number. Love, M.”

After writing her own breakup letter with debt, Lockert then published an estimated 100 breakup letters with debt from her readers. Photo courtesy of Melanie Lockert

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