British Scientists Develop New Screening Test to Identify Postnatal Depression Risk

Changes in estrogen levels during pregnancy make women more sensitive to the stress hormone cortisol. Soon after the baby is born, the estrogen levels return to normal. However, women with these genetic variations are unable to do so, leading to postnatal depression.

Postnatal depression is a type of depression some women experience after they have had a baby. It usually develops in the first four to six weeks after childbirth, but in some cases, it may take months to develop.

Postnatal depression is not the same as 'baby blues' which is a mild type of depression that occurs after childbirth and lasting from a few hours to a few days. During this time, the new mother may feel tearful and irritable, but no medical treatment is needed since in milder forms it is considered normal. However, if it is more prolonged and severe, it can develop into postnatal depression.

Symptoms of postnatal depression include low mood, feeling unable to cope and difficulty with sleeping. Unfortunately, many women are not aware they have the condition. Sometimes, the new mother may feel very agitated or alternatively very apathetic or have feelings of guilt and self-blame. She may even be thinking about?harming self or the baby.

In view of this, the research is very important. 'There is evidence that if you can identify women at risk early, you could treat early or introduce measures to prevent or stop the process of the disease,' Grammatopoulos said.

Based on this research, Grammatopoulos and his team have developed the first ever blood test for postnatal depression which would allow women found to be at risk to receive treatment for the disease before they give birth.

Prof Grammatopoulos said he could test women for the genetic changes for between ?30 and ?40. But automating the test so that robots could screen large numbers of samples would bring the cost down to just ?10.

'Usually we focus on the mother, but the negative impact on the child is also immense,' Prof Grammatopoulos said. He is now looking for further genetic changes to increase the predictive power of the test.

Reference: http://www.journalofpsychiatricresearch.com/article
/S0022-3956%2813%2900143-X/abstract

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Indicators of depression can predict the Disabilty work better

by Dr.Enozia Van Daele on June 15, 2013 at 4:58 pm new Lifestyle Indications of depression may predict the inability to work in the first best discoveries, new data from arthritis.
The study showed that in a multivariate analysis none of the activity of arthritis measures or cardiovascular, metabolic or studied lung were associated with early retirement, but a statement unique depression 'having little interest or pleasure in most days during the last 2 weeks of doing things' identified more patients to ask the disability pension.

"Our results demonstrate that if patients with early arthritis consider applying for the disability pension is more dependent on the mental states that the activity of the disease. "Arthritis having a financial impact on patients and society, attention focused on welfare in the early stages of the disease may help patients remain in the labour market", commented the lead author of the study by Professor Angela Zink, head of the unit of epidemiology at the Research Centre German rheumatism in Berlin.

Musculoskeletal diseases affect at least 100 million people in Europe, represents a half of all absences European labour and 60% of incapacity for work. If poorly managed, they represent a heavy economic burden on European society, estimated at up to 2% of GDP.2

573 patients<63 years="" enrolled="" in="" an="" early="" inflammatory="" arthritis="" (ia)="" cohort=""><6 months)="" were="" analysed="" with="" respect="" to="" their="" decision="" to="" request="" disability="" pension="" within="" the="" first="" 12="" months="" of="" treatment.="" patient="" reported="" parameters="" included="" pain,="" morning="" stiffness,="" fatigue,="" functional="" capacity,="" and="" the="" depression="" statement="" "having="" little="" pleasure="" or="" interest="" in="" doing="" things="" most="" of="" the="" day.="">

Patients had duration of the symptom of 13 + 7 weeks, 67% were rheumatoid factor (RF) and/or anti-Citrullinated protein antibody (ACPA) - positive, filled with 65% the new ACR - EULAR response criteria * initially and 87% took the disease-modifying antirheumatic drugs (DMARDs) in 12 months. Less than a year of care, 21% of patients with moderate depression indicators and 45% of people with severe depression had considered or entered an early retirement.

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In COPD Patients, Inflammation Is Associated With Depression

by Bidita Debnath on? May 25, 2013 at 11:48 PM Research News In chronic obstructive pulmonary disease (COPD) patients, depression is common and has been linked with disease severity and impaired quality of life.
Now, for the first time, researchers at the University of Pittsburgh have linked the systemic inflammation associated with COPD with depression in these patients.

"Systemic inflammation is thought to be an important mediator of comorbidities in COPD, but the relationship between inflammation and depression has not been explored," said researcher Hilary Strollo, M.S., a graduate of the University of Pittsburgh School of Health and Rehabilitation Sciences. "In our study, we found a strong association between depressive symptoms and levels of the inflammatory biomarker interleukin-6 (IL-6) which was independent of the severity of airflow obstruction."

The study results will be presented at the ATS 2013 International Conference in Philadelphia.

The study included 450 tobacco-exposed patients. Assessment included the Beck Depression Inventory (BDI), the Saint George Respiratory Questionnaire (SGRQ), and the UCSD Shortness of Breath Questionnaire (SOBQ). Spirometry and multi-detector computed tomography (MDCT) of the chest were also performed.

Of 235 male patients enrolled, 37 were depressed, and of 215 females, 49 were depressed. Clinical and biological variables that were found to be significantly associated with depression included the forced expiratory volume or FEV1, a measure of the maximum amount of air that can be exhaled in one second, gender, IL-6 levels, SGRQ Total Score, UCSD SOBQ Total Score, Visual Emphysema Score, and current smoking status.

The strongest associations were seen between depressive symptoms and FEV1, followed by female gender, current smoking status and increased IL-6.

"Depression has been linked with a number of symptoms and comorbidities in COPD patients," said Ms. Strollo. "Our findings add evidence of a strong relationship between depression and one of the hallmarks of COPD, systemic inflammation, independent of the severity of disease."

"The assessment and treatment of depression should be part of the routine care of COPD patients."

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Research Links Depression to Telomere Enzyme, Aging, Chronic Disease

by Rukmani Krishna on? May 25, 2013 at 11:42 PM Mental Health News The first symptoms of major depression may be behavioral. Despite this, the common mental illness is based in biology ? and not limited to the brain. In recent years some studies have linked major, long-term depression with life-threatening chronic disease and with earlier death, even after lifestyle risk factors have been taken into account.
Now a research team led by Owen Wolkowitz, MD, professor of psychiatry at UC San Francisco, has found that within cells of the immune system, activity of an enzyme called telomerase is greater, on average, in untreated individuals with major depression. The preliminary findings from his latest, ongoing study will be reported today at the annual meeting of the American Psychiatric Association in San Francisco.

Telomerase is an enzyme that lengthens protective end caps on the chromosomes' DNA, called telomeres. Shortened telomeres have been associated with earlier death and with chronic diseases in population studies.

The heightened telomerase activity in untreated major depression might represent the body's attempt to fight back against the progression of disease, in order to prevent biological damage in long-depressed individuals, Wolkowitz said.

The researchers made another discovery that may suggest a protective role for telomerase. Using magnetic resonance imaging (MRI), they found that, in untreated, depressed study participants, the size of the hippocampus, a brain structure that is critical for learning and memory, was associated with the amount of telomerase activity measured in the white blood cells. Such an association at a single point in time cannot be used to conclude that there is a cause-and-effect relationship with telomerase helping to protect the hippocampus, but it is plausible, Wolkowitz said.

Remarkably, the researchers also found that the enzyme's activity went up when some patients began taking an antidepressant. In fact, depressed participants with lower telomerase activity at baseline ? as well as those in whom enzyme activity increased the most with treatment ? were the most likely to become less depressed with treatment.

"Our results are consistent with the beneficial effect of telomerase when it is boosted in animal studies, where it has been associated with the growth of new nerve cells in the hippocampus and with antidepressant-like effects, evidenced by increased exploratory behavior," Wolkowitz said. Wolkowitz cautions that his new findings are preliminary due to the small size of the study and must be confirmed through further research.

The researchers also measured telomere length in the same immune cells. Only very chronically depressed individuals showed telomere shortening, Wolkowitz said.

"The longer people had been depressed, the shorter their telomeres were," he said. "Shortened telomere length has been previously demonstrated in major depression in most, but not all, studies that have examined it. The duration of depression may be a critical factor."

The 20 depressed participants enrolled in the study had been untreated for at least six weeks and had an average lifetime duration of depression of about 13 years. After baseline evaluation and laboratory measures, 16 of the depressed participants were treated with sertraline, a member of the most popular class of anti-depressants, the serotonin-selective-reuptake-inhibitors (SSRIs), and then evaluated again after eight weeks. There were 20 healthy participants who served as controls.

The ongoing study still is accepting depressed participants who are not now taking antidepressants. Wolkowitz's team also studies chronic inflammation and the biochemical phenomenon of oxidative stress, which he said have often been reported in major depression. Wolkowitz is exploring the hypothesis that inflammation and oxidative stress play a role in telomere shortening and accelerated aging in depression.

"New insights into the mechanisms of these processes may well lead to new treatments ? both pharmacological and behavioral ? that will be distinctly different from the current generation of drugs prescribed to treat depression," he said. "Additional studies might lead to simple blood tests that can measure accelerated immune-cell aging."

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People With Treatment-Resistant Depression Benefit Significantly With Ketamine

by Kathy Jones on? May 19, 2013 at 3:38 PM General Health News The largest ketamine clinical trial to-date led by researchers from the Icahn School of Medicine at Mount Sinai has revealed that patients with treatment-resistant major depression saw dramatic improvement in their illness after treatment with ketamine.
The antidepressant benefits of ketamine were seen within 24 hours, whereas traditional antidepressants can take days or weeks to demonstrate a reduction in depression.

The research will be discussed at the American Psychiatric Association meeting on Monday, May 20, 2013 at 12:30 pm in the Press Briefing Room at the Moscone Center in San Franscico.

Led by Dan Iosifescu, MD, Associate Professor of Psychiatry at Mount Sinai; Sanjay Mathew, MD, Associate Professor of Psychiatry at Baylor College of Medicine; and James Murrough, MD Assistant Professor of Psychiatry at Mount Sinai, the research team evaluated 72 people with treatment-resistant depression-meaning their depression has failed to respond to two or more medications-who were administered a single intravenous infusion of ketamine for 40 minutes or an active placebo of midazolam, another type of anesthetic without antidepressant properties. Patients were interviewed after 24 hours and again after seven days. After 24 hours, the response rate was 63.8 percent in the ketamine group compared to 28 percent in the placebo group. The response to ketamine was durable after seven days, with a 45.7 percent response in the ketamine group versus 18.2 percent in the placebo group. Both drugs were well tolerated.

"Using midazolam as an active placebo allowed us to independently assess the antidepressant benefit of ketamine, excluding any anesthetic effects," said Dr. Murrough, who is first author on the new report. "Ketamine continues to show significant promise as a new treatment option for patients with severe and refractory forms of depression."

Major depression is caused by a breakdown in communication between nerve cells in the brain, a process that is controlled by chemicals called neurotransmitters. Traditional antidepressants such as selective serotonin reuptake inhibitors (SSRIs) influence the activity of the neurotransmitters serotonin and noreprenephrine to reduce depression. In these medicines, response is often significantly delayed and up to 60 percent of people do not respond to treatment, according to the U.S Department of Health and Human Services. Ketamine works differently than traditional antidepressants in that it influences the activity of the glutamine neurotransmitter to help restore the dysfunctional communication between nerve cells in the depressed brain, and much more quickly than traditional antidepressants.

Future studies are needed to investigate the longer term safety and efficacy of a course of ketamine in refractory depression. Dr. Murrough recently published a preliminary report in the journal Biological Psychiatry on the safety and efficacy of ketamine given three times weekly for two weeks in patients with treatment-resistant depression.

"We found that ketamine was safe and well tolerated and that patients who demonstrated a rapid antidepressant effect after starting ketamine were able to maintain the response throughout the course of the study," Dr. Murrough said. "Larger placebo-controlled studies will be required to more fully determine the safety and efficacy profile of ketamine in depression."

The potential of ketamine was discovered by Dennis S. Charney, MD, Anne and Joel Ehrenkranz Dean of the Icahn School of Medicine at Mount Sinai, and Executive Vice President for Academic Affairs of The Mount Sinai Medical Center, in collaboration with John H. Krystal, MD, Chair of the Department of Psychiatry at Yale University.

"Major depression is one of the most prevalent and costly illnesses in the world, and yet currently available treatments fall far short of alleviating this burden," said Dr. Charney. "There is an urgent need for new, fast-acting therapies, and ketamine shows important potential in filling that void."

Dr. Murrough will present his research on Sunday, May 19, 2013 from 1:00 pm to 3:00 pm in the Moscone exhibit hall at the APA meeting.

About The Mount Sinai Medical Center
The Mount Sinai Medical Center encompasses both The Mount Sinai Hospital and Icahn School of Medicine at Mount Sinai. Established in 1968, the Icahn School of Medicine at Mount Sinai is one of the leading medical schools in the United States. The Icahn School of Medicine is noted for innovation in education, biomedical research, clinical care delivery, and local and global community service. It has more than 3,400 faculty members in 32 departments and 14 research institutes, and ranks among the top 20 medical schools both in National Institutes of Health (NIH) funding and by U.S. News & World Report.

The Mount Sinai Hospital, founded in 1852, is a 1,171-bed tertiary- and quaternary-care teaching facility and one of the nation''s oldest, largest and most-respected voluntary hospitals. In 2012, U.S. News & World Report ranked The Mount Sinai Hospital 14th on its elite Honor Roll of the nation''s top hospitals based on reputation, safety, and other patient-care factors. Mount Sinai is one of just 12 integrated academic medical centers whose medical school ranks among the top 20 in NIH funding and by U.S. News & World Report and whose hospital is on the U.S. News & World Report Honor Roll. Nearly 60,000 people were treated at Mount Sinai as inpatients last year, and approximately 560,000 outpatient visits took place.

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Treating Depression Naturally with Sam-E

Over the past decade I’ve suffered through bouts of depression. Within the past year I felt myself spiraling into a depression that I was unable to pull myself out of. I had started seeing a therapist but I was beginning to be open to the possibility of taking anti-depressants. I have never taken anti-depressants before except for a very brief (one week) trial of Lexapro. At the time I decided to stop taking Methadone, which I was taking for an injury. The doctor at the pain clinic that prescribed it to me insisted it was much better than morphine for my type of injury. It wasn’t and she’s a liar. When I came off the Methadone I had such a horrific withdrawal that I decided to stop taking the Lexapro because if I had to have a horrible withdrawal, I wanted to get it all over at once. I made this decision on my own, and in the end I was glad to be off of everything.

Several months ago when I was researching psychiatrists I came across SAM-e. I had purchased some and kept it for many weeks because I was actually scared to take it. Some of the potential side effects include anxiety and insomnia, and I am very afraid of anything that might cause me not to sleep. But since I was on the verge of taking an anti-depressant, which have much more side effects than SAM-e, I figured I better exhaust the natural route and give it a try.

I can only speak for my experience, but within a week of starting the SAM-e, I noticed the heavy sadness in my heart lifted a significant amount. I was better able to handle stressful events and my mood felt lighter in general.

“SAM-e (S-Adenosylmethionine) is an amino acid derivative that has been clinically proven to benefit brain and joint function. Found in all living cells, SAM-e is also called “activated methionine” since it is formed by reacting ATP and methionine (an essential amino acid).*” (Jarrow)

Sam-e has been used throughout Europe for over 20 years. It is sold as a prescription drug over there.

Clinical trials have shown that SAM-e may help with depression, joint pain, as well as liver function.

Here is a NY Times article from 2010 that discusses SAM-e’s beneficial use in treating patients with depression who do not respond to prescription anti-depressants.

For more information read “10 Things You Should Know About SAM-e.”

Jarrow Formulas makes the brand of SAM-e that I take. I get it at Vitacost, where it is much cheaper than other online outlets or health food stores. There has been a surge in SAM-e’s popularity because many companies are out of stock and Jarrow is trying to keep up with demand. As I said before, this has been my experience. I am not a doctor and this is not medical advice. I am a big proponent of exhausting natural and alternative therapies if modern medicine and prescriptions can be avoided.

Here is a video from Bastyr University’s Living Naturally Series entitled Overcoming Depression and Anxiety. It is an hour long lecture on natural ways to treat depression and anxiety.

Tags: Anti-Depressants, Anxiety, Brain, Brain Chemistry, Depression, Dopamine, Jarrow, Joint Pain, Liver Function, Natural, Naturally, Sadness, Sam-e, Seratonin, Side-Effects

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