Survey shows negative effect of vulvovaginal atrophy symptoms on quality of life for women

With symptoms such as dryness, burning, or itching of the vagina, vulvovaginal atrophy is estimated to affect up to 98% of postmenopausal women, many of whom will fail to report symptoms to their healthcare providers or seek help. A new survey demonstrates the negative effect of these symptoms on quality of life. The study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).

Vulvovaginal atrophy (VVA) is caused by a reduction in circulating estrogen and androgen levels after menopause that leads to thinning vaginal walls, less elasticity, and lower lubrication levels. In about 50% of postmenopausal women, VVA leads to symptoms such as vaginal dryness, which is the most frequent and a major contributor to sexual dysfunction. Because of a lack of education, many women view these symptoms as a natural part of the aging process and fail to report them to their healthcare providers.

Although few studies have been conducted to understand the relationship between VVA symptoms and quality of life (QOL), some survey data suggest that VVA is associated with a clinically significant effect on QOL comparable to that seen in conditions such as arthritis, asthma, and irritable bowel syndrome. The objective of the European Vulvovaginal Epidemiology Survey (EVES) was to describe the prevalence of VVA. More recent work based on a subanalysis of the EVES study focused on assessing the correlation of VVA symptoms with QOL of postmenopausal women. The survey results from more than 2,000 women were published in the article “The burden of vulvovaginal atrophy on women’s daily living: implications on quality of life from a face-to-face real-life survey.”

The authors of the article conclude that severe VVA symptoms have a direct association with worsened QOL in postmenopausal women. They suggest that healthcare providers recognize the effect of these symptoms as equivalent to those of other conditions and pathologies for which there is greater awareness.

“Although both women and their healthcare providers are often reluctant to talk about it, vaginal atrophy (part of the genitourinary syndrome of menopause) affects quality of life, self-esteem, and the intimacy of relationships,” says Dr. JoAnn Pinkerton, NAMS executive director. “The good news is that there are over-the-counter therapies, such as lubricants and vaginal moisturizers, as well as local vaginal prescription therapies that can relieve both vaginal dryness and painful sex and improve the quality of life for women.”

Source:

https://www.menopause.org/

Posted in: Medical Research News | Women’s Health News

Tags: Androgen, Arthritis, Asthma, Education, Epidemiology, Estrogen, Healthcare, Irritable Bowel Syndrome, Medicine, Menopause, Nursing, Nutrition, Pharmacy, Psychology, Sexual Dysfunction, Sociology, Vagina, Vaginal Atrophy, Vaginal Dryness




Study reveals safety, efficacy of brexpiprazole for schizophrenia patients with severe psychotic symptoms

Otsuka Pharmaceutical Co., Ltd. (Otsuka) and H. Lundbeck A/S (Lundbeck) announced study results on the safety and efficacy of brexpiprazole in the treatment of patients with schizophrenia experiencing severe psychotic symptoms during an acute episode. The data will be presented at the upcoming Psych Congress, held in Orlando from October 25-28, 2018.

The post hoc, pooled analysis focused on three short-term studies, Vector [NCT01396421], Beacon [NCT01393613], and Lighthouse [NCT01810380], evaluating brexpiprazole in subgroups of patients with severe psychotic symptoms. Patients with severe psychotic symptoms were defined based on the total scores of the Positive and Negative Syndrome Scale (PANSS), a scale used to rate the symptoms of schizophrenia. Patients with severe psychotic symptoms were specified by having PANSS total scores of greater than 95, which was the median score of the full patient population at baseline.

The 681 patients included in the analysis exhibited an average baseline PANSS total score of 106 with 427 patients given a dose of 2-4 mg of brexpiprazole and 254 given placebo. The study demonstrated that patients receiving brexpiprazole showed a mean improvement in PANSS Total score of 24.03 vs. 17.27 for patients receiving placebo (placebo-adjusted difference of 6.76, p<0.0001). Response rates (defined as change from baseline greater than or equal to 30% in PANSS Total Score or CGI-I score of 1 or 2 at Week 6 of the study) were greater for those patients treated with brexpiprazole versus placebo (46.9% and 27.3%, respectively, p<0.0001). Similar results were observed for patients with less severe symptoms (i.e. patients with baseline PANSS score less than 95). The most common treatment emergent adverse events (occurring in greater than or equal to 5% of patients in any group) included insomnia, headache and akathisia and were similar between patients with more or less severe psychotic symptoms.

“Schizophrenia is a chronic, disabling and progressive disease, impacting approximately three million Americans, that is often challenging to treat, and the severity of schizophrenia symptoms can be a significant predictor of poor treatment outcomes,” said Nicole Meade, PhD, Senior Medical Science Liaison, Otsuka. “These results underscore the potential of brexpiprazole as an effective treatment option with a safety profile that can provide physicians the confidence to prescribe it to patients with schizophrenia with a broad range of symptoms, including those with more severe psychotic symptoms.”

Source:

https://www.otsuka-us.com/

Posted in: Drug Trial News | Medical Condition News

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Optimizing dopaminergic treatment improves non-motor symptoms

(modified; 0-276, higher = worse); D, domain. Frequencies of the modified NMSS in the “off” and the “on” state. Credit: Swedish Research Council

Non-motor symptoms are common in late stage Parkinson’s disease (PD) as the frequency and severity of most of these symptoms increase with advancing disease. Optimizing dopaminergic treatment in the most severe stages can affect non-motor symptoms and improve quality of life, report scientists in the Journal of Parkinson’s Disease.

PD is generally considered a disease that affects movement, but it also involves a large number of non-motor symptoms, which previous research has shown to have a greater impact on health-related quality of life than motor symptoms. Common non-motor symptoms include cognitive impairment, mood-related symptoms such as depression, apathy, sleep/daytime sleepiness, fatigue, and autonomic dysfunction such as urinary urgency, incontinence, and erectile dysfunction. The frequency and severity of most of these symptoms increase with advancing disease. Previous research has shown that the frequency and severity of non-motor symptoms as a whole are the most important predictors of health-related quality of life in patients with PD.

“Patients in late stage PD—the last four or five years of the disease—are a forgotten group, whose situation we do not know much about,” explained lead investigator Per Odin, MD, Ph.D., Professor, Department of Neurology, Lund University, Lund, Sweden, and Chairman, Department of Neurology, Central Hospital, Bremerhaven, Germany. “There is reason to believe that relatively many patients in the late stage of PD may be insufficiently treated. Since the effect of dopaminergic therapy may not be as obvious in the late stage as in earlier disease stages, there is a clear risk for undertreatment. The general aim of the present research is therefore to learn more about this group of patients, to get a basis for improving their situation.”

The goal of the present study was to find an optimal pharmacological treatment for patients with late stage PD. Investigators assessed the effect of dopaminergic therapy on non-motor symptoms in 30 patients. Participants were recruited from the southern region of Sweden through neurology departments and the municipality-based health care system. The patients were in “Hoehn and Yahr” stages IV and V; the Hoehn and Yahr scale is a commonly used system for classifying how the symptoms of PD progress.

The dopaminergic effect on non-motor symptomatology was assessed using a Non-Motor Symptoms Scale (NMSS) in the “off” and the “on” state during a standardized L-dopa test and assessing non-motor symptoms in parallel with motor function. Motor symptoms fluctuate between an “on” state, during which the patient experiences a positive response to medication, and an “off” state, during which the patient experiences a re-emergence of the Parkinson symptoms suppressed during the “on” state.

The study found that non-motor symptoms were common and many of the symptoms occurred in more than 80% of the individuals. The highest scores (frequency x severity) were seen within the NMSS domains 3: mood/apathy and 7: urinary in both the “off” and the “on” states. The differences in the NMSS score between the “off” and the “on” state were larger in general for motor responders than for motor non-responders.

The investigators concluded that there is often an L-dopa effect on both motor and non-motor symptoms even in the most severely ill PD patients, and that even if there is not a significant motor response, there was often a non-motor effect, particularly on mood or depressive symptoms. They emphasize the importance of optimizing L-dopa treatment in the late stage of the disease to give patients the best possible quality of life.

“We encourage colleagues who treat PD to pay attention so that the treatment is optimized throughout the disease progression and into the most severe disease stages,” commented Dr. Odin. “The knowledge that sufficient dopaminergic treatment may have important effects on both motor and non-motor symptoms in severe PD patients can hopefully help treating physicians improve quality of life for their patients with late stage PD.


Explore further:
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More information:
Kristina Rosqvist et al, Dopaminergic Effect on Non-Motor Symptoms in Late Stage Parkinson’s Disease, Journal of Parkinson’s Disease (2018). DOI: 10.3233/JPD-181380

Journal reference:
Journal of Parkinson’s Disease

Provided by:
IOS Press




Multi-national database can help researchers address questions about bipolar disorder throughout adult lifespan

Not much is known about how bipolar disorder (BD) affects people throughout their lives. Do women and men differ in the severity of their symptoms? Does a person’s age when a bipolar diagnosis is made have any bearing on how severe the symptoms are? How do other medical conditions affect symptoms of BD across the life-span?

These questions and others like them are the focus of an international team of researchers, joined by Martha Sajatovic, MD, professor of psychiatry and of neurology at Case Western Reserve University School of Medicine, who has received a three-year, $600,000 grant from the International Society for Bipolar Disorders. She and her colleagues will develop the first-of-its-kind multi-national database that can be used to help researchers address questions about BD throughout the adult lifespan.

“Bipolar disorder affects millions of people at all ages,” said Sajatovic. “The need for this work reflects the demographic tsunami of people living longer lives both in this country and worldwide. It is crucial to understand how bipolar disease evolves as people with the condition age. This will help us anticipate their needs better and develop appropriate treatment plans for different stages of life. In particular, this applies to older age, since by 2030, more than fifty percent of bipolar patients will be 60 and above.”

Under the grant, Sajatovic and her colleagues, aided by a steering committee of other bipolar experts, will aggregate and standardize data from more than 1,000 bipolar patients worldwide who have been previously studied. But most findings from these studies are based on research samples of no more than 50 participants from a relatively narrow geographic and age representation. By creating a single comprehensive data set, the scientific team aims to overcome these shortfalls and increase knowledge about BD, its symptoms, and changes in behavior at different stages of life.

For example, some of these studies suggest a progressive worsening of symptoms, with more depression in older age and fewer psychotic symptoms. (Many people with BD experience at least one symptom of psychosis, such as delusions and hallucinations, during their lives.) But is this the case more generally? Or is there something about the relatively small populations that were studied that rules out generalizing the findings to more people? “Having access to sufficiently large data samples will enable researchers to determine if these and other trends are valid for the population as a whole,” said Sajatovic. “It will also help uncover other patterns of and predictors for bipolar disease that we may only currently have no or little knowledge about.”

Other areas that the integrated database will allow investigators to examine include mood-symptom changes over time, common medical problems found in people with BD, long-term effects of medications on general health, and the evolution of cognitive function over time.

Sajatovic, who is the lead investigator of a team of authorities in BD and data science that will carry out the work of the grant, is also Willard Brown Chair in Neurological Outcomes Research and director of the Neurological and Behavioral Outcomes Research Center at University Hospitals Cleveland Medical Center. In addition to Sajatovic, the study leaders include Lisa Eyler, PhD, from the University of California; Annemiek Dols, MD, PhD, from the Dutch Association of Mental Health and Addiction Care in Amsterdam, the Netherlands; and. Soham Rej, MD, from McGill University in Montreal.

Also known as manic depression, BD is a mental health condition that causes unusually large shifts in mood, ranging from extreme emotional highs (mania) to debilitating lows (depression). Directly affecting more than five million people, an estimated 4.4 percent of U.S. adults experience the condition at some time in their lives, with nearly three percent having had BD episodes in the past year. The effects of the disease extend to millions more family members, co-workers, and friends.




One in ten frequent pot users experience withdrawal symptoms

Dr. Deborah Hasin, professor of epidemiology at Columbia Mailman School of Public Health, told UPI that users were asked to explain certain physical and mental symptoms.




12% of frequent marijuana smokers experience cannabis withdrawal syndrome

As the number of Americans who regularly use cannabis has climbed, so too has the number of those experiencing cannabis withdrawal symptoms. A new study by researchers at the Columbia University Mailman School of Public Health and Columbia University Irving Medical Center finds that 12 percent of frequent marijuana smokers experienced Cannabis Withdrawal Syndrome (CWS), which includes emotional, behavioral and physical symptoms. The study is published in the journal Drug and Alcohol Dependence.

CWS was first included in the Diagnostic and Statistical Manual of Mental Disorders in its most recent edition, DSM-5, published in 2013. The new study is the first large-scale report on the link between CWS and DSM-5 psychiatric disorders among frequent U.S. adult cannabis users.

“In a rapidly changing landscape of marijuana laws and attitudes, cannabis use continues to increase among American adults. As a result, more information on the prevalence and correlates of clinical withdrawal in the general population is of critical importance,” said Deborah Hasin, PhD, professor of Epidemiology at Columbia Mailman School of Public Health.

Study participants were interviewed as part of the 2012-2013 National Epidemiologic Survey on Alcohol and Related Conditions-III (NESARC-III), the only nationally representative survey that measures clinically diagnosed cannabis withdrawal syndrome, which encompasses six psychological symptoms and one or more physical symptoms. Face-to-face interviews in respondents’ homes were conducted with 36,309 participants. The final analysis was based on 1,527 participants who were frequent cannabis users, defined as using the drug three or more times a week during the year prior to the interview.

CWS symptoms were associated with numerous psychiatric disorders, significant mental disability, and a family history of depression. Psychiatric disorders included mood disorders; anxiety disorders, including social phobia, agoraphobia, and panic disorder; personality disorders; and post-traumatic stress disorder.

Among withdrawal symptoms, the most commonly reported were nervousness/anxiety (76 percent), hostility (72 percent), sleep difficulty (68 percent) and depressed mood (59 percent). While physical symptoms were reported less frequently than behavioral and emotional symptoms, headaches, shakiness/tremors, and sweating were also prevalent.

Frequent cannabis users were primarily male (66 percent), white (59 percent), aged 18-29 (50 percent), college educated (49 percent), never married (54 percent), and with low household income (45 percent). While frequency of use (within a week) was not significantly associated with withdrawal symptoms, the number of joints smoked per day was significantly associated with withdrawal symptoms.

Cannabis withdrawal syndrome was not significantly associated with family history of drug or alcohol problems, but significantly associated with family history of depression.

“Cannabis withdrawal syndrome is a highly disabling condition,” noted Hasin, who is also a professor in the Department of Psychiatry. “The syndrome’s shared symptoms with depressive and anxiety disorders call for clinician awareness of cannabis withdrawal symptoms and the factors associated with it to promote more effective treatment among frequent cannabis users.”

In an earlier study by Hasin and colleagues (LINK TK), cannabis withdrawal symptoms were prevalent and associated with psychiatric disorders and intensity of cannabis use. However, at that time,NESARC did not cover the DSM-5 cannabis withdrawal symptoms. As a new diagnosis, much remains to be learned about DSM-5 CWS, according to Hasin and colleagues.

“Most users of the newer modes of administration–vaping and edibles–also smoke cannabis. Therefore, for users in modes other than smoking, the amount of consumption could be underestimated,” said Hasin. “Given the increase in cannabis potency in recent decades, developing reliable measures to investigate the effect of cannabis concentration and mode of administration will be important in advancing our understanding of cannabis withdrawal syndrome.”

Source:

https://www.mailman.columbia.edu/




New tool improves assessment of postpartum depression symptoms

In the current issue of Family Medicine and Community Health (Volume 6,Number 3, 2018, pp.104-114; DOI:https://doi.org/10.15212/FMCH.2018.0109, researchers Ajibola A. Ishola, Chisom C. Obasi and Ismail T. Sholuke of the Department of Psychology, University of Ibadan, Ibadan, Nigeria, describes how having a baby is often marked by disturbance in mood, and the birth of a premature baby can put mothers at greater risk of psychological distress than the birth of a full-term baby.

Available screening tools assess postpartum depression symptoms without consideration of mitigating sources of postpartum stress. Edinburgh Post-natal Depression scale is the commonest measure for differential diagnosis in Nigeria but limited in screening women for suicidal ideation and anxiety.

This study developed a new tool that improves the efficiency of, and reduces the time spent diagnosing postpartum depression among mothers of preterm babies. Efficiency in diagnosing the pathological reaction of mothers of preterm babies to the child’s condition and the corresponding depression symptoms is highly important for implementation of cost-effective intervention by mental health practitioners.




Neuropsychiatric symptoms related to earliest stages of Alzheimer’s brain pathology

UC San Francisco researchers, in collaboration with the unique Brazilian Biobank for Aging Studies (BBAS) at the University of São Paulo, have shown that the earliest stages of the brain degeneration associated with Alzheimer’s disease (AD) are linked to neuropsychiatric symptoms including anxiety, depression, loss of appetite, and sleep disturbances.

The findings — published in their final version October 15, 2018 in the print edition of the Journal of Alzheimer’s Disease following preliminary online publication in September — could lead to earlier diagnosis of AD and prove a valuable biomarker in the development of therapies to slow the course of the disease, the authors say, but may also have broader implications for understanding the biological basis of psychiatric symptoms in older adults.

Though commonly associated with memory loss and dementia, Alzheimer’s disease is actually a progressive neurodegenerative condition that can be detected in a brain autopsy decades before these classic cognitive symptoms occur. A “Holy Grail” of Alzheimer’s research is to develop treatments that could be given in the disease’s earliest stages to protect brain tissue from further loss and to slow or prevent the eventual development of dementia. However, the development of such drugs will require a better understanding of the biology that drives the first stages of the disease and the ability to diagnose patients early enough to prevent extensive loss of neural tissue.

Many studies have identified correlations between neuropsychiatric symptoms such as depression, anxiety, and sleep disturbances and an eventual Alzheimer’s diagnosis, and some have even proposed that these symptoms could be used as biomarkers for the disease in its earliest stages. But the relationship between the two has remained murky. In fact, some researchers have proposed that depression and other psychiatric conditions, or even the drugs used to treat these conditions, could themselves be triggers that lead to the onset of dementia decades later, much like occasional seizures can contribute to the development of chronic epilepsy.

Now members of the lab of Lea Grinberg, MD, PhD in the UCSF Weill Institute for Neurosciences’ Memory and Aging Center, working with their Brazilian colleagues, have shown that psychiatric symptoms are tightly linked to the earliest stages of Alzheimer’s brain pathology. These results strongly suggest that neuropsychiatric conditions or treatments do not cause Alzheimer’s, but could be the earliest warning signs of the disease.

“The discovery that the biological basis for these symptoms is the early Alzheimer’s pathology itself was quite surprising,” Grinberg said. “It suggests these people with neuropsychiatric symptoms are not at risk of developing Alzheimer’s disease — they already have it.”

The research took advantage of São Paulo’s unique century-old autopsy service, which is mandated in all deaths and conducts approximately 15,000 autopsies per year. In 2003, as part of her doctoral research, Grinberg co-founded the BBAS to collect brain tissue samples from these autopsies, and BBAS has since grown to become the largest such resource in the world.

Most postmortem brain studies of AD use relatively small “convenience samples” from older individuals who already show signs of memory loss or dementia. Because multiple brain pathologies can accumulate with age, it can be difficult to tightly link specific AD-related symptoms to brain abnormalities detected in these samples. Thanks to the BBAS collaboration, however, Grinberg’s team was able to avoid these potential pitfalls by drawing from a much larger population, selecting brains from younger and healthier individuals, and excluding tissue samples with multiple competing pathologies.

In the new study, lead author Alex Ehrenberg, a neuropathology research associate in the Grinberg lab, worked closely with Claudia Suemoto MD, PhD, and other colleagues from the University of São Paulo to study the brains of 1092 seemingly healthy adults over the age of 50 who closely represented the general population of São Paulo. The researchers excluded 637 brains that showed neurological signs of brain abnormalities not related to AD, leaving 455 brains with either no signs of degeneration or a range of AD-related pathology.

AD pathology is characterized by buildup of telltale neurofibrillary (NF) tangles and amyloid-beta (Aβ) plaques, paralleled by the atrophy of brain tissue in associated regions. The disease nearly always progresses in the same fashion, with NF tangles first appearing in brainstem regions associated with sleep, appetite, and emotional processing, while Aβ plaques first appear in cortical regions and then spread to deeper parts of the brain.

Ehrenberg and colleagues classified each of the 455 brains using standard scales of AD progression based on NF tangle and Aβ plaque accumulation. They then used statistical algorithms to test for a relationship between AD stage and reported changes in the brain donor’s cognitive and emotional status prior to their death, based on interviews with informants — typically relatives and caretakers — who had been in at least weekly contact with the deceased in the six months before their deaths, a gold-standard approach for neuropathological studies of degenerative brain diseases such as AD.

Ehrenberg’s computational analysis of the results found that in individuals whose brainstems showed the very earliest stages of NF tangles but lacked memory changes, family members and caretakers reported increased rates of one or more neuropsychiatric symptoms including agitation, anxiety, appetite changes, depression, and sleep disturbances, but lacked any noticeable memory problems. The next stage of the disease, as NF buildup increased in the brainstem and began to spread to other brain regions, was associated with increased odds of agitation, while only in later stages, as NF buildup began to reach the brain’s outer cortex, did the individuals begin showing signs of the dementia-like delusions and the cognitive and memory decline typically associated with AD.

Tellingly, the researchers found no link between buildup of Aβ plaques and these neuropsychiatric symptoms. Alzheimer’s researchers have long debated whether Aβ plaques or NF tangles — made up of clumps of a protein called “tau” — play an earlier or more central role in driving neurodegeneration in AD, and the authors believe the new findings add additional support for focusing on developing tau-targeted treatments, particularly given disappointing results from many recent trials of A?-targeted AD therapies.

“These results could have major implications for Alzheimer’s drug trials focused on early degenerative changes, where people have been seeking tractable clinical outcomes to target in addition to early cognitive decline,” Ehrenberg said. He added that the findings will also be valuable as new technologies become available for detecting early stages of AD pathology in living patients – such as blood biopsies or PET brain imaging of tau — to aid the implementation of such novel biomarkers into clinical practice.

To Grinberg, the discovery that psychiatric symptoms such as depression or sleep disturbance in older adults may be linked to a specific biological phenomenon — namely accumulation of tau protein into NF tangles in the brainstem — is as exciting as the implications for Alzheimer’s disease itself.

“Because we generally don’t know the biological basis for most psychiatric conditions, we can’t do what we do for other diseases like diabetes or cancer — we can’t say, ‘You are having depression or sleep problems because of this disease in your brain, so let’s see if we can treat that disease,'” Grinberg said. “If we could use this new knowledge to find a way to reduce the burden of these conditions in aging adults it would be absolutely huge.”




What causes schizophrenia? What we know, don’t know and suspect

Symptoms include delusions and hallucinations (“psychotic” symptoms), diminished emotional expression, poverty of speech and lack of purposeful action (known as “negative” symptoms), and incoherent speech and disorganised behaviour (“disorganised” symptoms). A diagnosis of schizophrenia requires at least two symptoms, including one psychotic or disorganised, to be present for at least six months. These must result in significant social or occupational dysfunction.

It is thought disruptions in brain development early in life may underlie the emergence of schizophrenia in later years. While the causes of these disruptions aren’t exactly clear, research points to several possible reasons.

Genes

Hundreds of genes have been linked to schizophrenia, but do not appear to follow typical patterns of inheritance across generations, where disorders can be predicted with confidence. Like diabetes and coronary heart disease, schizophrenia cannot be predicted from family history alone. This is because no one gene, or set of genes, has definitively been identified as causing the disorder.

Family studies do provide robust evidence of a genetic contribution. For instance, across the population, a person’s risk of developing schizophrenia is 1%. If one of their parents has the disorder, the risk increases to 15%.

Twin studies have found a 50% increase in the risk of schizophrenia in the identical twin of a person with schizophrenia. Because identical twins share 100% of their DNA, this means environmental risk factors must also be involved. We do not currently know exactly which genes interact with which environmental factors, nor the extent of these interactions.

There is also an association between the age of the father at the time the child is born and an increased risk of schizophrenia in the child. If the father is over the age of 55, the child’s risk of schizophrenia increases by 50%. This may be due to rare mutations in paternal sperm that could lead to abnormal development, or to family factors associated with having an older father.

Obstetric complications

Various obstetric complications in utero and at birth have also been identified as risk factors for schizophrenia in the offspring. Complications during pregnancy include maternal bleeding, diabetes, rhesus incompatibility (when the mother has Rh-negative blood and the fetus Rh-positive, or vice versa), pre-eclampsia and abnormal fetal growth and development.

Maternal exposure to famine during pregnancy has been linked to schizophrenia in the offspring. Complications at delivery include uterine atony (failure of the uterus to contract after delivery), lack of oxygen to the fetus and emergency caesarean.

Most of these obstetric associations are small, and other potential influencing factors weren’t controlled for. For example, exposure to maternal infections, such as upper respiratory tract and genital or reproductive infections, has been linked to schizophrenia in the offspring. If exposed to these infections, these could be the real culprits rather than the obstetric complications described above.

Exposure to infections in childhood, such as Toxoplasma gondii (a parasitic organism carried by domestic cats) and viral central nervous system infections (such as meningitis), have also been linked to schizophrenia in adulthood. Again, if exposed, these could have led to the mental illness as opposed to complications in delivery.

Immune markers

Markers of infection and inflammation are often increased in adults with schizophrenia. This means immune system dysfunction may be involved in the development of the disorder.

Drug use

Studies following people from birth to adulthood have identified cannabis use in childhood or adolescence as a likely risk factor.

These studies have adjusted for other risk factors and taken into account intoxication effects and reverse causation (that schizophrenia may cause cannabis use). They found a dose-response effect, which means the risk of psychosis increased as the frequency of cannabis use increased. Such dose-response effects provide the most robust evidence of causation.

The neurological and biological mechanisms of cannabis use are similar to those in schizophrenia, with the same neurons showing activity.

Methamphetamines, particularly ice or crystal methamphetamine, have been linked to increased risk of persistent psychosis, and not just substance-induced psychosis. Controlled amphetamine administration that triggers temporary psychosis in healthy individuals can also be blocked by antipsychotics. This further strengthens the evidence of association.

Social factors

There is solid evidence supporting the link between having experienced child abuse, or any type of abuse that includes bullying, and schizophrenia. Stressful life events in adulthood have been associated with schizophrenia too.

People living in urban areas, particularly areas with high income inequality, also show increased risk, which may be associated with social fragmentation. Both first- and second-generation immigrants show increased risk, with surprisingly greater risk seen in the second generation.

Studies have also found a greater risk of schizophrenia in ethnic minority groups living in areas of low ethnic density than those living in high ethnic density areas. These finding indicate that sustained social marginalisation, particularly from early childhood, may have greater adverse effects than migration itself.

Stress

Social stressors can lead to biological disruptions. For instance, stress increases the release of dopamine. And evidence shows people with schizophrenia have increased dopamine production and release.

Stress is also associated with dysregulation of a brain network known as the hypothalamic-pituitary-adrenal (HPA) axis, which is sensitised in people with schizophrenia.

Stress associated with being raised in a harsh environment has been linked to the emergence of an inflammatory gene expression in adolescents. And people with schizophrenia show immune system dysfunction in both the early and late stages of the disorder.

Disruption to these biological systems can cause paranoid ideas, social withdrawal and other behavioural problems. These in turn cause additional stress and further biological disruption. In time, paranoid ideas can become delusional and fixed, signalling schizophrenia, particularly in the presence of other symptoms.

While much progress has been made in identifying the potential causes of schizophrenia, most of the evidence comes from population-level studies that may or may not be applicable to a particular individual. More research is required to determine the various individual pathways to schizophrenia.


Explore further:
Scientists identify 35 genes associated with cannabis use

Provided by:
The Conversation




Patient-friendly and accurate cardiac damage diagnosis

3D Model of the heart by Dr. Matthew Bramlet. Credit: NIH

Systemic inflammatory diseases, such as lupus, often cause cardiac damage that goes undetected. An international research team headed by the Institute for Experimental and Translational Cardiovascular Imaging at the University Hospital Frankfurt was now able to show via heart imaging that cardiac damage can be diagnosed in a patient-friendly way ahead of the clinical symptoms.

The number of diagnoses of systemic lupus erythematodes (SLE) has tripled over the past 45 years, due in part to improved diagnostic methods. Lupus is a systemic inflammatory disease that can affect several organs, most frequently, the kidneys, skin, brain and the heart. Involvement of the heart is important, as it determines the outcome, yet can remain undetected and untreated for a long time.

This problematic situation has several causes. First, the natural course of lupus-caused heart disease often has few or no symptoms—this subclinical course represents a major challenge for diagnosis. It also predominantly affects young female patients, for whom heart disease is unusual in the first place. Moreover, if symptoms occur, they are not classical symptoms of heart disease, such as angina. More commonly, symptoms are atypical—in other words, they do not explicitly indicate heart disease. Examples of symptoms are tiredness, dyspnoea, or sharp pain of the chest wall. Lupus patients are also frequently overwhelmed by symptoms in other organ systems, especially the kidneys, which are significantly more pronounced. As a result, clinicians may mistakenly focus on these organs instead of the heart during diagnosis and treatment. Ultimately, a small percentage of patients develops heart failure, which is often resistant to therapy.

A study by the University Hospital Frankfurt in collaboration with partners from London and Tübingen has shown that imaging with cardiac magnetic resonance (CMR) can improve detection of subclinical cardiac injury in lupus patients. The study was published in the Annals of the Rheumatic Diseases. In the present study, the authors demonstrated that inflammation of heart muscle and the vessels is the defining underlying pathophysiological mechanism of heart injury and impairment in lupus patients, and not, as previously assumed, as a result of the accelerated atherosclerotic blockage of the coronary blood vessels. The research team developed and validated an imaging signature of disease presence and activity of involvement. Thus, they have shown that heart inflammation can be detected and monitored in a noninvasive way without radiation using CMR imaging. Furthermore, CMR imaging can help clinicians to adjust the anti-inflammatory treatment to treat the heart involvement directly.

The study has significant potential for a real change in the clinical care of heart involvement in patients with lupus, replacing the current less sensitive, highly invasive and radiation-intensive methods with patient-friendly and secure diagnostic approaches that are noninvasive, radiation-free, and aside from the baseline investigation, also largely free from contrast agents. The new diagnostic method accurately assesses disease presence, stage and severity, and gauges the treatment response.

Ninety-two patients with lupus were examined using the CMR imaging; 78 healthy individuals served as a control group. This multicentre and multidisciplinary study was headed by Dr. Valentina Puntmann from the Institute for Experimental and Translational Cardiovascular Imagery (Goethe CVI) at the University Hospital Frankfurt and builds on a decade-long record of investigation into cardiac inflammation by noninvasive imaging in systemic inflammatory diseases. In addition to the Goethe CVI, University Hospital Frankfurt’s Rheumatology, Cardiology and Radiology were also involved.

The heart muscle, its volume, and function were examined in all participants using CMR imaging. Various other blood values, such as troponin and NT-proBNP, which serve as biomarkers for heart impairment, were also examined. These markers were raised in 81 percent of lupus patients, but only in eight percent to a degree we usually see in the course of a heart attack. However, CMR imaging was able to point towards the presence of relevant inflammation of heart muscle much more frequently, making it more suited to detect inflammation, even if the blood tests remain only mildly raised. In addition, changes to the clinical activity can be more quickly detected using the imaging than with blood values, as these may remain raised for weeks on end. There are no disadvantages to CMR, as no invasive procedures or radiation are involved.


Explore further:
Study reveals early warning signs of heart problems in patients with newly diagnosed lupus

More information:
Lea Winau et al, High-sensitive troponin is associated with subclinical imaging biosignature of inflammatory cardiovascular involvement in systemic lupus erythematosus, Annals of the Rheumatic Diseases (2018). DOI: 10.1136/annrheumdis-2018-213661

Journal reference:
Annals of the Rheumatic Diseases

Provided by:
Goethe University Frankfurt am Main




Quitting junk food produces similar withdrawal-type symptoms as drug addiction

Credit: CC0 Public Domain

If you plan to try and quit junk food, expect to suffer similar withdrawal-type symptoms—at least during the initial week—like addicts experience when they attempt to quit using drugs.

A new study by University of Michigan is believed to be the first of its kind to evaluate withdrawal symptoms people incur when they stop devouring highly processed foods, such as pastries, French fries and pizza.

Previous studies have focused on sugar withdrawal among animals and the literature regarding humans offered only anecdotal evidence, said Erica Schulte, the study’s lead author and U-M psychology doctoral candidate.

What all researchers can agree upon is that the addictive qualities of tobacco, drugs or alcohol affect the brain similarly and cutting back can lead to negative side effects that can make it difficult to reduce intake. Anxiety, headaches, irritability and depression are some of those outcomes.

Understanding whether withdrawal may also occur with highly processed foods was an essential next step in evaluating whether these foods might be capable of triggering similar addictive processes.

Schulte and colleagues created the first self-report tool to measure the physical and psychological withdrawal symptoms among people, then asked 231 adults to report what happened when they reduced the amount of highly processed foods they ate in the past year.

The participants reported that sadness, irritability, tiredness and cravings peaked during the initial two to five days after they quit eating junk food, then the negative side effects tapered off, which parallels the time course of drug withdrawal symptoms, the study found.

The U-M researchers did not focus on the method used to change their eating behavior, such as participants quitting “cold turkey” or gradually phasing out junk food. Schulte said future studies will analyze the behavior in real time rather than a retrospective approach as in the current findings.

The study implications suggest that withdrawal symptoms may make dietary changes challenging, which may contribute to people reverting back to bad eating habits, said Ashley Gearhardt, associate professor of psychology and co-author, along with U-M graduates Julia Smeal and Jessi Lewis.

The findings appear in the current issue of Appetite.


Explore further:
Highly processed foods linked to addictive eating

More information:
Erica M. Schulte et al. Development of the Highly Processed Food Withdrawal Scale, Appetite (2018). DOI: 10.1016/j.appet.2018.09.013

Journal reference:
Appetite

Provided by:
University of Michigan




Optimizing dopaminergic treatment improves non-motor symptoms and quality of life

Non-motor symptoms are common in late stage Parkinson’s disease (PD) as the frequency and severity of most of these symptoms increase with advancing disease. Optimizing dopaminergic treatment in the most severe stages can affect non-motor symptoms and improve quality of life, report scientists in the Journal of Parkinson’s Disease.

PD is generally considered a disease that affects movement, but it also involves a large number of non-motor symptoms, which previous research has shown to have a greater impact on health-related quality of life than motor symptoms. Common non-motor symptoms include cognitive impairment, mood-related symptoms such as depression, apathy, sleep/daytime sleepiness, fatigue, and autonomic dysfunction such as urinary urgency, incontinence, and erectile dysfunction. The frequency and severity of most of these symptoms increase with advancing disease. Previous research has shown that the frequency and severity of non-motor symptoms as a whole are the most important predictors of health-related quality of life in patients with PD.

“Patients in late stage PD – the last four or five years of the disease – are a forgotten group, whose situation we do not know much about,” explained lead investigator Per Odin, MD, PhD, Professor, Department of Neurology, Lund University, Lund, Sweden, and Chairman, Department of Neurology, Central Hospital, Bremerhaven, Germany. “There is reason to believe that relatively many patients in the late stage of PD may be insufficiently treated. Since the effect of dopaminergic therapy may not be as obvious in the late stage as in earlier disease stages, there is a clear risk for undertreatment. The general aim of the present research is therefore to learn more about this group of patients, to get a basis for improving their situation.”

The goal of the present study was to find an optimal pharmacological treatment for patients with late stage PD. Investigators assessed the effect of dopaminergic therapy on non-motor symptoms in 30 patients. Participants were recruited from the southern region of Sweden through neurology departments and the municipality-based health care system. The patients were in “Hoehn and Yahr” stages IV and V; the Hoehn and Yahr scale is a commonly used system for classifying how the symptoms of PD progress.

The dopaminergic effect on non-motor symptomatology was assessed using a Non-Motor Symptoms Scale (NMSS) in the “off” and the “on” state during a standardized L-dopa test and assessing non-motor symptoms in parallel with motor function. Motor symptoms fluctuate between an “on” state, during which the patient experiences a positive response to medication, and an “off” state, during which the patient experiences a re-emergence of the Parkinson symptoms suppressed during the “on” state.

The study found that non-motor symptoms were common and many of the symptoms occurred in more than 80% of the individuals. The highest scores (frequency x severity) were seen within the NMSS domains 3: mood/apathy and 7: urinary in both the “off” and the “on” states. The differences in the NMSS score between the “off” and the “on” state were larger in general for motor responders than for motor non-responders.

The investigators concluded that there is often an L-dopa effect on both motor and non-motor symptoms even in the most severely ill PD patients, and that even if there is not a significant motor response, there was often a non-motor effect, particularly on mood or depressive symptoms. They emphasize the importance of optimizing L-dopa treatment in the late stage of the disease to give patients the best possible quality of life.

“We encourage colleagues who treat PD to pay attention so that the treatment is optimized throughout the disease progression and into the most severe disease stages,” commented Dr. Odin. “The knowledge that sufficient dopaminergic treatment may have important effects on both motor and non-motor symptoms in severe PD patients can hopefully help treating physicians improve quality of life for their patients with late stage PD.




Alzheimer’s drug may stop disease if used before symptoms develop

The reddish-blue mouse neurons in this image have reentered the cell cycle after exposure to amyloid beta oligomers, and thus are primed for death. Credit: Erin Kodis and George Bloom

About 50 percent of people who reach the age of 85 will develop Alzheimer’s disease. Most will die within about five years of exhibiting the hallmark symptoms of the disease – severe memory loss and a precipitous decline in cognitive function.

But the molecular processes that lead to the disease will have begun years earlier.

Currently, there are no known ways to prevent the disease or to stop its progression once it has begun. But research at the University of Virginia offers new understanding of how the disease develops at the molecular level, long before extensive neuronal damage occurs and symptoms show up.

Additionally, the researchers have found that an FDA-approved drug, memantine, currently used only for alleviating the symptoms of moderate-to-severe Alzheimer’s disease, might be used to prevent or slow the progression of the disease if used before symptoms appear. The research also offers, based on extensive experimentation, a hypothesis as to why this might work.

The findings are published currently online in the journal Alzheimer’s & Dementia.

“Based on what we’ve learned so far, it is my opinion that we will never be able to cure Alzheimer’s disease by treating patients once they become symptomatic,” said George Bloom, a UVA professor and chair of the Department of Biology, who oversaw the study in his lab. “The best hope for conquering this disease is to first recognize patients who are at risk, and begin treating them prophylactically with new drugs and perhaps lifestyle adjustments that would reduce the rate at which the silent phase of the disease progresses.

“Ideally, we would prevent it from starting in the first place.”

As Alzheimer’s disease begins, there is a lengthy period of time, perhaps a decade or longer, when brain neurons affected by the disease attempt to divide, possibly as a way to compensate for the death of neurons. This is unusual in that most neurons develop prenatally and then never divide again. But in Alzheimer’s the cells make the attempt, and then die.

“It’s been estimated that as much as 90 percent of neuron death that occurs in the Alzheimer’s brain follows this cell cycle reentry process, which is an abnormal attempt to divide,” Bloom said. “By the end of the course of the disease, the patient will have lost about 30 percent of the neurons in the frontal lobes of the brain.”

Erin Kodis, a former Ph.D. student in Bloom’s lab and now a scientific editor at AlphaBioCom, hypothesized that excess calcium entering neurons through calcium channels on their surface drive those neurons back into the cell cycle. This occurs before a chain of events that ultimately produce the plaques found in the Alzheimer’s brain. Several experiments by Kodis ultimately proved her theory correct.

The building blocks of the plaques are a protein called amyloid beta oligomers. Kodis found that when neurons are exposed to toxic amyloid oligomers, the channel, called the NMDA receptor, opens, thus allowing the calcium flow that drives neurons back into the cell cycle.

Memantine blocks cell cycle reentry by closing the NMDA receptor, Kodis found.

“The experiments suggest that memantine might have potent disease-modifying properties if it could be administered to patients long before they have become symptomatic and diagnosed with Alzheimer’s disease,” Bloom said. “Perhaps this could prevent the disease or slow its progression long enough that the average age of symptom onset could be significantly later, if it happens at all.”

Side effects of the drug appear to be infrequent and modest.

Bloom said potential patients would need to be screened for Alzheimer’s biomarkers years before symptoms appear. Selected patients then would need to be treated with memantine, possibly for life, in hopes of stopping the disease from ever developing, or further developing.

“I don’t want to raise false hopes,” Bloom said, but “if this idea of using memantine as a prophylactic pans out, it will be because we now understand that calcium is one of the agents that gets the disease started, and we may be able to stop or slow the process if done very early.”

Bloom currently is working with colleagues at the UVA School of Medicine to design a clinical trial to investigate the feasibility of using memantine as an early intervention.


Explore further:
New mechanism by which Alzheimer’s disease spreads through the brain discovered

More information:
Erin J. Kodis et al, N-methyl-D-aspartate receptor–mediated calcium influx connects amyloid-β oligomers to ectopic neuronal cell cycle reentry in Alzheimer’s disease, Alzheimer’s & Dementia (2018). DOI: 10.1016/j.jalz.2018.05.017 , dx.doi.org/10.1016/j.jalz.2018.05.017

Provided by:
University of Virginia




Concussion symptoms last for longer time in kids than adults

Concussion symptoms for children under 13 years old typically last three times longer than they do for older teens and adults, but keeping them out of the classroom during recovery is not necessarily the preferred treatment, according to a comprehensive research review in The Journal of the American Osteopathic Association.

Parents should be aware that significant changes in the treatment of concussion–including a major shift to promoting active recovery–have emerged in recent years, said Hallie Zwibel, DO, Director of Sports Medicine at New York Institute of Technology College of Osteopathic Medicine, and lead researcher on this study.

“It used to be thought that rest was best for a concussion. Kids were told to stay home from school and sit in a dark room for two weeks,” says Dr. Zwibel. “Now we encourage them to get back to school after two days and progressively get more active, so long as symptoms don’t return or worsen.”

The article also cites children’s vulnerability to prolonged symptoms due to underlying conditions, including ADHD, depression, anxiety and stress. Study authors hope their findings can help parents manage expectations and know their best options for treatment.

“It’s important parents understand that symptoms persist in kids for about four weeks on average,” says Dr. Zwibel. “This can be alarming and feel like a long time, especially compared to adults whose symptoms last closer to a week, but it is well within a normal recovery time.”

Researchers say rehabilitation has also proven effective for mitigating symptoms such as dizziness and changes in vision, like difficulty with focus. This includes engaging in visual and vestibular exercises, which assist with balance and spatial orientation. Therapy can help the brain to establish new neurologic pathways to regain function or to bypass disturbing signals.

While active recovery has emerged as the standard of treatment, Dr. Zwibel says athletes should not compete while they are experiencing concussion symptoms. Brain swelling and death can result if an athlete receives a concussive blow while recovering from an earlier concussion. However, getting young athletes to stay off the field during recovery remains a challenge, Dr. Zwibel noted.

“There’s not a good administrative structure to prevent an injured high school athlete from playing for another league,” says Dr. Zwibel. “At this point, parents are in the best position to prevent that and we strongly encourage them to follow return-to-sport protocols.”

Dr. Zwibel also encourages youth sports leagues to adopt and implement these standardized guidelines and seek medical providers’ input when establishing policies and practices.​




Most parents aren’t able to recognize meningitis until it’s too late

  • The majority of people surveyed believe that a rash, dislike of bright lights and stiff neck are the early signs and symptoms of meningitis – these are important indicators of the disease but typically appear later – or not at all.
  • The campaign calls for greater awareness of the steps that parents can take to protect their children against meningitis when going back-to-school or starting university, including how to identify the early signs and symptoms of meningitis, understanding the risks, and prevention including vaccination.

Parents do not always know the early signs and symptoms of meningitis which if known, could potentially help children receive medical attention more quickly, independent research commissioned by GSK shows.

The research, which was carried out among parents of 3-5-year olds, 14-15-year olds and 18-19-year olds, shows that a dislike of bright lights, a stiff neck and a rash were the three most commonly identified early signs and symptoms of meningitis by a majority of people surveyed.

While these are all important indicators of the disease, they may indicate late progression of the infection, may not be present at all or only occur after other symptoms including a headache, vomiting, fever, muscle pain and cold hands and feet.

The new research was carried out as part of GSK’s Cotton-on to Meningitis: Let’s Tackle it Together campaign, which is run in partnership with former England Rugby player, Matt Dawson, and supported by UK charities Meningitis Research Foundation and Meningitis Now.

As children and young people return to school or start university, the campaign emphasizes that wrapping a child up in cotton wool won’t be protected against the many causes of meningitis, but we can help tackle the disease by knowing the early signs and symptoms, getting treatment quickly, and seeking advice on prevention including available vaccines.

Babies, children and young adults are all at risk of meningitis and parents want to do the best for their children, so it’s important that they are fully aware of the symptoms.

The rash is commonly thought of as an early sign but often appears later-on or not at all. I urge parents not to wait for the rash, but to learn about early symptoms and to speak with a GP or pharmacist about ways to prevent meningitis.”

Matt Dawson

Meningitis is a rare and potentially life-threatening disease that can become fatal if not treated quickly. Older teenagers are the second most vulnerable group to infection after babies and young children because they mix socially with lots of other people who may be carrying the bacteria that cause meningitis.

As parents start to prepare their children for a new school term or going to university, it’s important to know the signs and symptoms of meningitis, understand the risks, and be aware of preventive measures.

The research data showed that over two-thirds of respondents are aware that meningitis can be prevented through vaccination, however, 40 percent of respondents were not aware that there is more than one vaccine to protect a child against the different strains of the disease.

The research also shows that when preparing for school or university, a lower priority is given to vaccinations the older the child gets.

In the first three months of 2018, Public Health England confirmed 287 cases of invasive meningococcal disease, a rise of 7.9 percent compared to the same period in 2017.

Since 2015, the NHS vaccination programme has offered vaccines for Meningitis B to babies, and Meningitis ACWY for children aged 13/14 years old. Both vaccines are available privately for those who are not eligible under the NHS scheme and advice is available from your local GP or pharmacist.

Meningitis Awareness Week (17-24 September 2018) is run by the Meningitis Research Foundation.