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Depression Linked With Brain Inflammation, Opening Up New Avenues For Treatment

Diagnosing a patient with clinical depression can be difficult; depression is a complex illness that can be caused by one or a mix of many things, from environmental stressors to genetics. But a new study out of the Centre for Addiction and Mental Health (CAMH) has highlighted a link between clinical depression and brain inflammation that might be crucial in better understanding stress and depression’s physical impacts on the body, as well as in developing better treatments for these mental health issues.

In the study, published in JAMA Psychiatry, the researchers found that people with clinical depression had a 30 percent increase in brain inflammation, also referred to as neuroinflammation. It’s uncertain whether the inflammation caused the depression or vice versa, or if it’s simply a correlation. But the study makes it clear that the link should be further examined.

“This finding provides the most compelling evidence to date of brain inflammation during a major depressive episode,” Dr. Jeffrey Meyer of CAMH’s Campbell Family Mental Health Research Institute said in the press release. “Previous studies have looked at markers of inflammation in blood, but this is the first definitive evidence found in the brain.”

The authors took brain scans of 20 patients who were suffering from depression but were otherwise healthy, as well as of 20 control patients. They found that people with depression were more likely to suffer a higher rate of inflammation in their brains, and people with the most severe depression had the highest rates of all. While inflammation can protect the brain and other tissues when triggered by the immune system, too much of it can cause damage.

How Stress Fosters Inflammation

Whenever the immune system is attacked by infections (viruses or bacteria), toxins, or even physical injury (such as a knee injury), it creates an inflammatory response — sending out messengers known as cytokines, which are either pro-inflammatory or anti-inflammatory. Damaged cells release chemicals including histamine, bradykinin, and prostaglandins, which cause blood vessels to leak fluid into tissues and create tissue swelling. While acute or short-term inflammation is a protective feature of the immune system, chronic inflammation can cause simultaneous destruction and healing of the tissues, ultimately wreaking havoc on your body long-term.

It’s not only physical injury or infections that can trigger an immune response; stress and emotional trauma cause inflammation as well. Long-term or chronic stress has actually been shown to change the gene activity of immune cells before they enter the bloodstream, priming them to fight infection when there is no infection. As a result, inflammation occurs unnecessarily but still wreaks havoc on tissues and body processes. Chronic inflammation is often associated with cancer and other disorders such as heart disease and high cholesterol. Brain inflammation, meanwhile, has been linked to several disorders, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis.

Treating Inflammation To Target Depression

It’s possible that depression changes immune responses and triggers inflammation similar to how stress does. It’s not entirely certain. But the notion that depression is somehow linked to inflammation isn’t a new one. In fact, though there is currently no FDA-approved medication to treat depression-related brain inflammation, researchers have examined such therapies in the past. In a 2014 study, researchers provided patients with anti-inflammatory treatment and found that it reduced depressive symptoms.

Some physicians believe that depression and inflammation are linked by a build-up of both physical injuries and emotional stress in a person’s past, and these things can be difficult to treat with one single therapy. “When remnants of old wounds are left unresolved, they build up inside the body,” Gary Kaplan, DO, an osteopathic physician and founder of the Kaplan Center for Integrative Medicine, told Prevention. “So it makes sense that a woman who was raped as a child and gets a concussion in her 20s could develop fibromyalgia and clinical depression. These events may seem unrelated, but all of them result in chronic neuroinflammation.”

Kaplan, as an osteopathic physician who takes a more holistic approach to medicine, hasn’t been waiting for an FDA-approved drug that treats brain inflammation; he’s been attempting to treat patients who have been suffering from chronic depression and inflammation on his own. His therapies often involve a mix of acupuncture, psychotherapy, several anti-inflammatory drugs like Celebrex (which is used to treat arthritis), and craniosacral therapy (massaging the head and neck to relieve tension). But the evidence of their efficacy still remains scarce, and more studies will be needed to better mold a conclusion.

“We’re not going to help people who are depressed and in pain if we don’t spend time finding out about them as whole people with histories that greatly influence their health,” Kaplan told Prevention. “Neuroinflammation is not the answer to everything, but understanding it is extremely important. It will eventually change how we treat these reversible diseases.”

Indeed, Meyer and his team who’ve published the most recent study on brain inflammation feel the same way. “Depression is a complex illness and we know that it takes more than one biological change to tip someone into an episode,” Meyer said in the press release. “But we now believe that inflammation in the brain is one of these changes that’s an important step forward.”

Source: Setiawan E, Wilson A, Mizrahi R, Rusjan P, Miler L, Rajkowska G. “Role of Translocator Protein Density, a Marker of Neuroinflammation, in the Brain During Major Depressive Episodes.” JAMA Psychiatry, 2015.

Role of Translocator Protein Density, a Marker of neuroinflammation in the brain during major depression episodes

The Brain on Fire: Inflammation and Depression

Inflammation and Its Effects on Mood

We have all had the flu or at least know what it feels like.

The miserable collection of symptoms includes lack of energy, difficulty concentrating, sleepiness, loss of appetite, and general malaise.

For most of us these symptoms disappear within a few days. For some, it takes much longer. Although we tend to blame the influenza virus for making us feel miserable, the symptoms are actually a result of our immune system trying to combat the virus.

The symptoms of the flu are brought on by proteins, pro-inflammatory cytokines, our bodies produce in order to fight the flu and other infections.

When the immune system is under attack from physical injury, infections, or toxins, the immune system generates an inflammatory response. Inflammation is a normal physiological process that is now understood to play a major role in many chronic medical illnesses, including cancer, heart disease, diabetes, asthma, and obesity. In each of these cases inflammation causes the release of cytokines. Cytokines, which come in many different classes, including anti- and pro-inflammatory, behave as messengers and signal cells of the immune system.

The effects of pro-inflammatory cytokines can cause a diverse array of physical and psychological symptoms. When this happens it is referred to as sickness behavior.

Recently, scientists have been able to demonstrate how the symptoms of sickness behavior mirror those of depression. Researchers and healthprofessionals are now beginning to understand the connection between inflammation and depression.

  1. One study found that patients with major depressive disorder had significantly higher levels of the pro-inflammatory cytokine TNF-alpha than their non-depressed counterparts. In addition, patients with depression had low levels of anti-inflammatory cytokines.
  2. Researchers have also found that eight weeks of Zoloft treatment was able to decrease some pro-inflammatory cytokines seen in depressed patients. On Zoloft, the depressed patients also saw an increase in anti-inflammatory cytokines.
  3. A study involving depressed patients classified as non-responders supplemented the patients’ standard antidepressant treatment with the addition of aspirin, an anti-inflammatory. More than 50% of these patients responded to this combination treatment. At the end of the study more than 80% of the group responsive to the anti-inflammatory went into remission.

Cytokines, the messengers during inflammation, are also used to treat infections and autoimmune disorders. So-called autoimmune disorders are clear examples of how an unregulated immune system can cause destructive damage to many different organs and tissues. Some of the most common autoimmune diseases include rheumatoid arthritis, multiple sclerosis, thyroid disease, and celiac disease.

Interferons, a form of cytokines which activate the immune system and act as antiviral agents, is a common treatment for hepatitis C infection.  Research and clinical studies have shown that interferon therapy can actually lead to depression in patients who have hepatitis C. It’s been reported that between 20% and 30% of patients who have hepatitis C and who receive interferon treatment are at risk for depression.

In one study, nearly a third of patients with chronic hepatitis C who received interferon treatment displayed psychiatric symptoms after four weeks of treatment. Symptoms included mania, hypomania, and depression.  Over the years I have had to admit patients for inpatient psychiatric treatment for depression and suicidal behavior following interferon therapy.

It appears that inflammation and the complicated collection of immune system chemical messengers called cytokines play an important role in brain function and may cause psychological symptoms.

When the brain is aggravated by any source-stress, infections, trauma, stroke, poisons, or nutritional deficiencies-inflammation spurs the release of pro- inflammatory cytokines, which may affect mood. Scientists have proposed many mechanisms as to how this may occur.

One mechanism as to how an unregulated immune system may contribute to depression is quite well understood. Cytokines activate an enzyme, indoleamine 2,3-dioxygenase (IDO), which degrades serotonin resulting in low levels of the neurotransmitter. IDO also degrades the precursor to serotonin, tryptophan. Decreased levels of the neurotransmitter serotonin are likely the contributing factor to the development of depressive symptoms. The inflammatory process’ contribution to the constant destruction of serotonin decreases the chances of recovery.

For too many years we have tried to correlate depression with a deficiency of serotonin and related neurotransmitters in the brain. Using medications based on this theory has yielded dismal results, barely better than a placebo.  If we understand the underlying physiological abnormalities contributing to mood disorders, then we are likely to benefit from more effective solutions.

Understanding the connection between depression and inflammation gives researchers and pharmaceutical companies incentive to look for alternative medications to treat depression. In the meantime there are, however, well-researched lifestyle and nutritional interventions that are known to decrease inflammation and improve mood: exercise, stress reduction, nutritional supplements (i.e. omega-3 fatty acids), and optimizing vitamin D levels. Chronic stress is one of the major preventable contributors to inflammation and immune dysregulation.

For each individual the inflammatory response is likely precipitated by a unique and complex interaction of causative agents. Infection, stress, nutritional deficiencies, and sedentary lifestyles are the most common factors. Individual, personalized understanding of inflammation and its contributions to the physiology of mood disorders is a critical, but often neglected component of integrative therapies for depression. By neglecting the underlying cause of depression, recovery is less likely.

The immune-mediated alteration of serotonin and glutamate towards an integrated view of depression

Shortened onset of action of antidepressants in major depression using acetylsalicylic acid augmentation a pilot open-label study

Therapeutic Strategies for Treatment of Inflammation-related Depression

Pro- and Anti-Inflammatory Cytokine Balance in Major Depression



Chronic Stress Changes Immune Cell Genes, Leading To Inflammation: Study

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A new study provides a better understanding of why chronic stress leads to high levels of inflammation in the body.

Researchers found that chronic stress changes gene activity of immune cells before they enter the bloodstream so that they’re ready to fight infection or trauma — even when there is no infection or trauma to fight. This then leads to increased inflammation.

This phenomenon was seen in mice, as well as in blood samples from people with poor socioeconomic statuses (a predictor of chronic stress), reported the researchers from Ohio State University, the University of California, Los Angeles, Northwestern University and the University of British Columbia.

“There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that’s going to be pro-inflammatory,” study researcher John Sheridan, a professor at Ohio State University and associate director of the university’s Institute for Behavioral Medicine Research, said in a statement. “So what this suggests is that if you’re working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system.”

Inflammation isn’t always bad, particularly acute inflammation in response to an injury or infection. But chronic inflammation, on the other hand, has been linked with a range of conditions such as heart disease, depression and even cancer.

For the mouse part of this study, published in the journal Proceedings of the National Academy of Sciences, researchers induced chronic stress in mice by having a bunch of male mice live together for a certain period of time. This time was enough for the mice to establish a hierarchy. Then, they introduced an aggressive male mouse to this group for periods of two hours to induce chronic stress in the mice.

After that, researchers looked at the immune cells circulating in the stressed mice’s blood stream, and found that they had four times the frequency of immune cells in their blood and spleen, versus non-stressed mice.

Researchers completed genome-wide analysis of the immune cells taken from the stressed mice’s blood. They found that compared with the non-stressed mice, 3,000 genes in the stressed mice’s immune cells were either expressed at higher or lower levels — and 1,142 of the up-regulated genes played a role in making the immune cells become more inflammatory.

Similar results were found in humans. The University of California, Los Angeles researchers looked at blood samples from both the stressed mice, as well as humans who came from differing socioeconomic statuses. Just like in the mouse part of the experiment, 387 genes were identified that had differences in activity between the people who came from low socioeconomic backgrounds and those who came from high socioeconomic backgrounds. And just like in the mice, the up-regulated genes in those who came from low socioeconomic backgrounds were pro-inflammatory.

In addition, a third of the genes that seemed to be affected by chronic stress were the same in both the humans and mice.

“This study provides a nice mechanism for how psychology impacts biology,” study researcher Nicole Powell, a research scientist in oral biology at Ohio State University, said in a statement. “Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it’s directly due to the sympathetic nervous system.”

Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis

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The Intersection of Eating and Alcohol Disorders: Detecting and Managing “Drunkorexia”

“Drunkorexia,” a term introduced by the media in 2008 referring to “limiting food intake before alcohol consumption,”1 is a “trend among college students.”2

Drunkorexia is more typically associated with binge drinking (defined as ≥4 drinks for women and ≥5 drinks for men in ~2 hours) than with moderate drinking.3 Binge drinking is a serious problem on college campuses.4 According to a review of several national datasets examining alcohol use among college students, approximately 70% of college students report using alcohol in the past month and approximately 40% report binge drinking.5 Eating disorders (EDs) are likewise a serious issue on college campuses. For example, one 13-year study of college students found that total EDs increased from 23% to 32% in female students and from 7.9% to 25% in male students during the study period.6

Drunkorexia, which is the intersection of alcohol use and EDs, may affect as many as 46% of college students, according to one study of 3409 students.7 Another study of 1184 college students found that that 8 of 10 were affected.8

Drunkorexia is characterized by food restrictions, extreme exercising, or purging with a goal of either trading food calories for those consumed by drinking alcohol to heighten the inebriating effects of alcohol, or both.8

“We are seeing an increasing number of cases of ‘drunkorexia’ at our clinic at Rutgers University,” Petros Levounis, MD, MA, Chair, Department of Psychiatry, Rutgers New Jersey Medical School, told Psychiatry Advisor.

He noted that although this trend may be taking place outside the university, it seems to primarily affect college students and “there are no good epidemiological studies to show how extensive it might be outside of the college setting.”

Who Is Affected?

Some research has suggested that first-year college students are at particularly high risk.4

“It is often quite a common occurrence that many college students are so fearful to gain the dreaded ‘freshmen 15′ [pounds] that, in order to save calories and also not to gain weight while consuming alcohol, they try to manage eating behaviors by drinking more instead of eating,” Alison Chase, PhD, CEDS, Regional Managing Clinical Director, Eating Recovery Center, and Insight Behavioral Center, Austin, Texas, told Psychiatry Advisor.

Drunkorexia tends to affect women more than men, especially if they were already engaging in restrictive eating behaviors. One study of college students found that 80.7% reported some type of drunkorexia behavior during the previous 3 months, of whom 78.0% were male and 82.7% were female.8 Another study of 63 students found that women were more likely than men to engage in drunkorexia because they were more likely to be concerned about weight.1 The greatest risk was found in women who drank more heavily.1

Nevertheless, it is important not to underestimate the impact of this disorder on men, Dr Chase cautioned.

“People have stereotypes about eating disorders — especially those with anorexia — that they are primarily female and white, but our centers get a diverse population of males and a variety of ethnicities,” she said.

Financial Factors

Although the more typical reason for drunkorexia is fear of weight gain, one reason that Dr Levounis has noticed is that “some college students have difficulty affording food and find it cheaper to get their calories through cheap alcohol rather than food, so there is a poverty component, apart from the strictly psychiatric one.”

Dr Levounis admitted that this is “not the major component of the problem, nor does it even affect the majority of people, but it has been brought up more than once in our clinic and practitioners should be aware and alert for this potential situation.”

Detecting Drunkorexia

Interviewing is generally the most important tool in diagnosing alcohol use disorders [AUDs] and substance use disorders  in people with EDs.9 Components include:

  • Personal history (including lifetime and current substance use as well as heaviest period of use)
  • Information from third-party sources, if possible
  • Physical signs of alcohol or substance use
  • Urine toxicology screening to determine drug use
  • Liver function tests (especially glutaryl transaminase  and mean corpuscular volume  in the complete blood count  maybe elevated in patients with AUDs)

Screening tests may be helpful as well, including the CAGE10 detecting alcohol use, the SCOFF11for detecting Eds, and the Drunkorexia Motives and Behaviors Scales.1

“Clinicians working in an academic setting should be vigilant regarding the possibility of drunkorexia and should proactively inquire about students’ drinking and eating habits,” Dr Chase said.

General questions are not sufficient, she emphasized.

“Inquire about what the student’s eating behaviors are, if they are over-exercising, purging, or restricting their eating,” she advised.

Additionally, “ascertain their drinking behaviors — how much do they drink? When do they drink? How often do they party?”

Clinicians who encounter a potential substance use disorder should also inquire about eating habits, and those who encounter potential EDs should inquire about drinking habits, “since there is so much crossover,” she added.

This index of suspicion should be maintained if a student is receiving help for one of the disorders and appears to be improving, she cautioned.

“As one disorder improves, it’s not unusual for the other issue to pop up or worsen, since the person may turn to one unhealthy behavior to manage the feelings they were trying to manage through the other unhealthy behavior.”

Chicken and Egg?

EDs frequently occur comorbidly with other psychiatric conditions, including depression, anxiety, posttraumatic stress disorder , attention-deficit/hyperactivity disorder , body dysmorphic disorder, and other underlying conditions, and people often try to self-medicate with alcohol, Dr Levounis noted.

For this reason, it is difficult to determine which is the primary and which is the secondary disorder, he continued.

“However, we are no longer worried about which is the chicken and which is the egg, because these types of considerations and deliberations are not relevant to treatment.”

Instead, he recommended, “treat both conditions independently and together at the same time.”

Pharmacotherapies for Treating Drunkorexia

“The primary treatments for eating disorders are psychosocial, but there nevertheless is some role that medication can play even for anorexia and certainly for alcohol abuse,” Dr Levounis declared.

He noted that there are 3 oral agents (naltrexone, acamprosate, and disulfiram) that are approved by the US Food and Drug Administration  for treatment of AUD.12

Some evidence points to selective serotonin reuptake inhibitors  as promising treatments for EDs,9,13 “enabling us to kill two birds with one stone, so to say, by addressing the depression and anxiety that so often drive these behaviors,” he said.

Additional pharmacotherapies that have shown utility as adjunctive therapies in anorexia nervosa are atypical antipsychotics — specifically olanzapine — and zinc supplementation.14

Dr Chase agreed that medication has a role to play in drunkorexia treatment. “Medication can be very useful in helping manage the symptoms that exist with eating disorders, particularly managing mood and anxiety issues. Once those symptoms are stabilized, it is easier to manage working through the other aspects of the eating disorder.”

Evidence-Based Psychotherapies

“Most of the evidence-based treatment approaches for treating disorders that we use at our centers are based in some fashion on cognitive behavioral therapy (CBT) approaches,” Dr Chase said.

“We use third waves of evidence-based CBT, including dialectical behavior therapy , acceptance and commitment therapy , and exposure plus response prevention,” she said.15-19

CBT has also been found affective in treating alcohol disorders,20 “making it a treatment of choice for these comorbid conditions,” Dr Levounis said.

He added that motivational interviewing can often be an important precursor to CBT in this population “because some patients might not even be motivated to participate in CBT interventions, since some of them do not see their behavior as problematic.”21,22

In addition, Dr Chase noted that their work with adolescents always includes family-based treatments, since EDs do not take place in a vacuum and often include issues of self-esteem that can have a basis in family relationships. This holds true even for college students, many of whom are no longer living with their families.

Tips for Psychiatrists

Be nonjudgmental

Both experts stressed the critical importance of approaching individuals with AUD and/or EDs nonjudgmentally because many encounter judgment and blame both in and out of medical settings. People who feel judged or blamed are less likely to open up and trust their providers and less likely to participate in treatments. It is important to recognize that these individuals are experiencing low self-esteem, depression, anxiety, or other issues that drive their behaviors and to demonstrate the same compassion toward them as would be demonstrated toward any other patient with a mood or other psychiatric disorder.

Engage in multidisciplinary collaboration

The most effective interventions include several professionals, including psychiatrists, psychotherapists, dietitians, and others who may play a role in addressing the multiple complex components of this condition.

“It is important to collaborate and make sure all treatment professionals are working together,” Dr Chase emphasized.

Consider recommending support groups

Twelve-step support groups can be helpful for individuals with both EDs and AUD, Dr Chase noted.

SMART Recovery® is another support forum for individuals recovering from addiction as an adjunct or alternative to more traditional 12-step approaches (


The ready availability of alcohol on college campuses and high prevalence of student drinking23has many serious risks, including increased risk for comorbid EDs. Education, proactive screening, early intervention, and multidisciplinary collaboration are essential in addressing this serious and growing problem.


  1. Eisenberg MH, Fitz CC. “Drunkorexia”: exploring the who and why of a disturbing trend in college students’ eating and drinking behaviors. J Am Coll Health. 2014;62(8):570-577.
  2. Ward RM, Galante M. Development and initial validation of the Drunkorexia Motives and Behaviors scalesEat Behav. 2015 ;18:66-70.
  3. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Drinking Levels Defined. Available at: Accessed November 14, 2018.
  4. Burke SC, Cremeens J, Vail-Smith K,  Woolsey C. Drunkorexia: Calorie restriction prior to alcohol consumption among college freshman. J Alcohol Drug Educ. 2010;54(2):17-35.
  5. O’Malley PM, Johnston LD. Epidemiology of alcohol and other drug use among American college students. J Stud Alcohol Suppl. 2002;(14):23-39.
  6. White S, Reynolds-Malear JB, Cordero E. Disordered eating and the use of unhealthy weight control methods in college students: 1995, 2002, and 2008. Eat Disord.2011;19(4):323-334.
  7. Roosen KM, Mills JS. Exploring the motives and mental health correlates of intentional food restriction prior to alcohol use in university students. J Health Psychol. 2015;20(6):875-886.
  8. Rinker DV, Neighbors C. Examining the association between “drunkorexia,” perceived norms, and drinking motives.” Paper presented at: 39th Annual Research Society on Alcoholism Scientific Meeting; June 27, 2016; New Orleans, LA.
  9. Conason AH, Brunstein Klomek A, Sher L. Recognizing alcohol and drug abuse in patients with eating disorders. QJM. 2006;99(5):335-339.
  10. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Screening Tests. Available at: Accessed November 13, 2018.
  11. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: a new screening tool for eating disorders. West J Med. 2000;172(3):164-165.
  12. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Helping Patients Who Drink Too Much: A Clinician’s Guide. Available at: Updated October 2008. Accessed November 14, 2018.
  13. Marvanova M, Gramith K. Role of antidepressants in the treatment of adults with anorexia nervosaMent Health Clin. 2018;8(3):127-137.
  14. Flament MF, Bissada H, Spettigue W. Evidence-based pharmacotherapy of eating disorders. Int J Neuropsychopharmacol. 2012;15(2):189-207.
  15. Murphy R, Straebler S, Cooper Z, Fairburn CG. Cognitive behavioral therapy for eating disordersPsychiatr Clin North Am. 2010;33(3):611-627.
  16. Jenkins PE, Morgan C, Houlihan C. Outpatient CBT for underweight patients with eating disorders: effectiveness within a National Health Service (NHS) eating disorders service.Behav Cogn Psychother. 2018:1-13.
  17. Groff SE. Is enhanced cognitive behavioral therapy an effective intervention in eating disorders? A reviewJ Evid Inf Soc Work. 2015;12(3):272-288.
  18. Mac Neil BA, Hudson CC. Patient experience and satisfaction with acceptance and commitment therapy delivered in a complimentary open group format for adults with eating disorders. J Patient Exp. 2018;5(3):189-194.
  19. Steinglass JE, Sysko R, Glasofer D, Albano AM, Simpson HB, Walsh BT. Rationale for the application of exposure and response prevention to the treatment of anorexia nervosa.Int J Eat Disord. 2011;44(2):134-141.
  20. McHugh RK, Hearon BA, Otto MW. Cognitive-behavioral therapy for substance use disordersPsychiatr Clin North Am. 2010;33(3):511-525.
  21. Macdonald P, Hibbs R, Corfield F, Treasure J. The use of motivational interviewing in eating disorders: a systematic review. Psychiatry Res. 2012;200(1):1-11.
  22. Nyamathi A, Shoptaw S, Cohen A, et al. Effect of motivational interviewing on reduction of alcohol use. Drug Alcohol Depend. 2010;107(1):23-30.
  23. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. College Drinking. Available at: December 2015. Accessed November 14, 2018.

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Can We stop Suicides?

The link above attached to the New York Times article opinion section that discusses Ketamine and its transforming ability for depression and related mood  disorders. Below is the excerpt:

In May of 2017, Louise decided that her life was just too difficult, so she’d end it. In the previous four years, three siblings and a half-sibling had died, two from disease, one from fire and one from choking. Close friends had moved away. She felt painfully, unbearably alone. It would be the fourth time Louise (I’m using her middle name to protect her privacy), then 68, would attempt suicide, and she was determined to get it right.

She wrote a letter with instructions on where to find important documents and who should inherit what. She packed up her jewelry and artwork, addressing each box to particular friends and family members. Then she checked into a motel — homes where people have committed suicide lose value and she didn’t want hers to sell below market — put a plastic sheet on the bed, lay down and swallowed what she figured was an overdose of prescription pills with champagne.

A few days later, she woke up in a psychiatric ward in Albuquerque. The motel maid had found her. “I was very upset I had failed,” she told me recently. So she tried to cut her wrists with a bracelet she was wearing — unsuccessfully.

The suicide rate has been rising in the United States since the beginning of the century, and is now the 10th leading cause of death, according to the Centers for Disease Control and Prevention. It’s often called a public health crisis. And yet no new classes of drugs have been developed to treat depression (and by extension suicidality) in about 30 years, since the advent of selective serotonin reuptake inhibitors like Prozac.

The trend most likely has social causes — lack of access to mental health care, economic stress, loneliness and despair, the opioid epidemic, and the unique difficulties facing small-town America. These are serious problems that need long-term solutions. But in the meantime, the field of psychiatry desperately needs new treatment options for patients who show up with a stomach full of pills.

Now, scientists think that they may have found one — an old anesthetic called ketamine that, at low doses, can halt suicidal thoughts almost immediately

Depression ran in Louise’s family. It had afflicted all her siblings, both of her parents and her grandmother. Prozac had helped Louise for a time, but stopped working for her in the late 2000s, as it sometimes does. No other drug seemed able to lift her dark moods.

After her suicide attempt, Louise’s psychiatrist suggested she try ketamine. She agreed, and received an infusion intravenously. Within hours, her sense of well-being improved. The hospital discharged her. Back home, she discovered that going to the market was no longer a “herculean task.” Getting her car washed wasn’t an insurmountable chore. “Life was better,” she said. “Life was doable.”

Using ketamine to treat depression and suicidality is somewhat controversial. Numerous small studies suggest that it holds great promise, but it’s only now being tested in placebo-controlled trials with hundreds of patients. It is also popular as a club drug in some circles. Like morphine, it may operate on the opioid system, and it can induce feelings of euphoria. Occasionally ketamine abusers develop severe symptoms, including brain damage, persistent hallucinations and a painful inflammation of the bladder called cystitis.

Nonetheless, if proven safe and effective in small doses, ketamine stands to transform how doctors deal with suicidal patients and depression generally.

The drug seems to address a longstanding problem in emergency psychiatry. Sedation and physical restraint aside, doctors have few ways to quickly stop suicidal ideation, or thoughts of killing oneself. The current crop of anti-depressants can take weeks and sometimes months to work, if they work at all. They may also, paradoxically, increase suicidality in some patients. Talk therapy takes time to help as well (assuming it does). Here’s a sobering fact: Some studies indicate that suicide risk peaks soon after patients have been discharged from a medical facility.

Antidepressants and Suicide Risk A Comprehensive Overview

Suicide risk peaks in first week of psychiatric hospitalisation and post discharge  <, See commentary excerpt at bottom of this page


Researchers at Yale discovered ketamine’s potential as an antidepressant in the late 1990s and scientists at the National Institute of Mental Health confirmed it the mid 2000s. Numerous studies followed suggesting that the drug helps precisely with that subset of depressive patients — about a third — for whom nothing else works. It doesn’t work for everyone in this group, but when it does, it works within hours, not weeks.

A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression<<<Carlos Zarate

Suicidality doesn’t perfectly overlap with depression. Many people attempt suicide not because they’re clinically depressed, but rather impulsively, because they’ve been fired or they’ve broken up with girl- and boyfriends, or sometimes because they’re just really drunk. I’ve heard people who show up in the hospital in this state — despondent, angry and uninhibited more than depressed — described as “drunkicidal.”

Many are fine once they sober up. For those who aren’t, ketamine may help independent of its effect on depression. And because ketamine is already approved by the Food and Drug Administration, doctors can prescribe it off-label. Meaning that not only does a drug exist right now that could help with depression and suicidality, it’s theoretically available to patients.

I kept thinking about this during the recent spate of high-profile suicides: the chef Anthony Bourdain, the designer Kate Spade, the actress Margot Kidder. Could ketamine have saved any of them? Did they know about it? Did their psychiatrists?

Dealing with Chronic Pain in Sobriety


Dealing with Chronic Pain in Sobriety

by Cassidy Webb

Much of the opioid epidemic that the country is facing today has been attributed to pharmaceutical companies over prescribing pain medications. Opioid dependence can occur in just 5 days of taking opiates. Unfortunately, chronic pain does not subside as people get sober. However, there are many ways that one can manage chronic pain in sobriety without taking addictive prescription drugs.




Though physical exercise may seem counterproductive when it comes to pain management, it is actually shown to be beneficial in preventing pain from getting worse by keeping muscles strong, loose, and active.


Stretching increases flexibility and loosens tight or stiff muscles, easing day to day movements and preventing further muscle pain. Having tight muscles only creates more pain. Stretching also increases blood flow and aligns the spine resulting in better posture. One shouldn’t force these stretches, but should move slowly into stretches. These should be held for 30-45 seconds and repeated 5-10 times. One should only feel a stretch, if there is any pain in the stretch then it should not be continued.


There are several kinds of low impact exercises that aren’t as physically demanding as others. For example, swimming provides light aerobic exercise and warm water can help relax the muscles. The weightlessness of water helps with movement and lessens physical demand on joints. Exercising in warm water allows spine and limbs to expand, relieving painful pressure in the lower and upper back. Other forms of low impact exercises include walking and biking.




Acupuncture consists of needles, heat, and pressure being applied to certain areas on body. It has been shown to have several benefits such as reduced inflammation and increased blood flow. The NIH claims it can ease many types of chronic pain including the lower back, neck, osteoarthritis, knee pain, and persistent headaches. Through stimulation of the nerves, endorphins are released into the body which are the body’s natural pain killers. This stimulation also releases serotonin which controls ones mood. When serotonin and endorphins are released simultaneously, one’s pain can be dramatically alleviated. Evidence also suggests that acupuncture stimulates the vagus nerve which results in decreased inflammation in the body.


Though acupuncture may seem painful to some, the needles used are thinner than a strand of hair and don’t normally hurt, many people even fall asleep and feel extremely relaxed during the process. It is a safe practice, but should be conducted in a reputable office where sterile equipment is used each session by an experienced practitioner.


Healthy eating


There are several healthy foods that can decrease inflammation in the body and help ease chronic pain. Cherries and ginger reduce inflammation in muscles by up to 25%. They hinder pain enzymes causing an effect similar to that of aspirin and other anti inflammatories. Consuming fish that are low in mercury, such as salmon or herring, can help relieve back pain because omega-3s improve blood flow and lower inflammation in blood vessels and nerves. Coffee has been suggested as relief for headaches for many years, because it narrows the enlarged blood vessels that cause headaches, just be sure to drink a glass of water with that coffee to prevent dehydration. Edamame and hot peppers are great foods to eat for those suffering with arthritis because they stimulate nerve endings and deplete chemicals that relay pain signals to the brain.


Holistic therapy


Yoga and meditation are two great forms of holistic therapy that can be used to ease and cope with chronic pain. Using these techniques, one can learn to focus on their breath which can put pain into perspective. By learning to focus on mindfulness, one is able to listen to body’s demands and create a plan of how to treat the pain. Bringing this kind of awareness to any unnecessary strain that is placed on certain areas of body can help alleviate the pain in those areas. In addition, holding yoga poses releases any unnecessary tension that may be causing more pain. Similar to stretching and swimming, one can utilize the muscles in their body to become stronger and more resilient. Yoga also helps develop a strengthened spine and neck which takes the pressure off of the joints and bones.


Cassidy Webb is an avid writer from South Florida.  She works for a digital marketing company that advocates spreading awareness on the disease of addiction. Her passion in life is to help others by sharing her experience, strength, and hope.