Postpartum depression (PPD), also called postnatal depression, is a type of mood disorder associated with childbirth, which can affect both sexes. Symptoms may include extreme sadness, low energy, anxiety, crying episodes, irritability, and changes in sleeping or eating patterns. Onset is typically between one week and one month following childbirth. PPD can also negatively affect the newborn child.
While the exact cause of PPD is unclear, the cause is believed to be a combination of physical and emotional factors. These may include factors such as hormonal changes and sleep deprivation. Risk factors include prior episodes of postpartum depression, bipolar disorder, a family history of depression, psychological stress, complications of childbirth, lack of support, or a drug use disorder. Diagnosis is based on a person’s symptoms. While most women experience a brief period of worry or unhappiness after delivery, postpartum depression should be suspected when symptoms are severe and last over two weeks.
Among those at risk, providing psychosocial support may be protective in preventing PPD. Treatment for PPD may include counseling or medications. Types of counseling that have been found to be effective include interpersonal psychotherapy (IPT), cognitive behavioral therapy (CBT), and psychodynamic therapy. Tentative evidence supports the use of selective serotonin reuptake inhibitors (SSRIs).
Postpartum depression affects about 15% of women around childbirth. Moreover, this mood disorder is estimated to affect 1% to 26% of new fathers. Postpartum psychosis, a more severe form of postpartum mood disorder, occurs in about 1 to 2 per 1,000 women following childbirth. Postpartum psychosis is one of the leading causes of the murder of children less than one year of age, which occurs in about 8 per 100,000 births in the United States.
Sabine Hazan, MD Daniel Frochtzwajg, DO Jessica Murray, BS Ventura Clinical Trials, Ventura, CA
INTRODUCTION
Cdifficile is a gram-positive, spore forming bacillus that is an obligate anaerobe and has been identified as one of the most common causes of nosocomial infection in the developed world, causing mild to severe cases of diarrheal illness to life-threatening pseudomembranous colitis and toxic megacolon,3 with increasing incidence over the last decade.2,4C. difficile infection (CDI) risk factors include extended hospital stay, protracted antibiotic regimens, other illnesses and comorbidities, and age greater than 65 years.1 In addition to the logistic complications of identifying, diagnosing, and containing infections in a hospital, and even community setting, there is substantial cost incurred as a result of CDI and the high risk of recurrent infection. In The Economic Impact of Clostridium difficile Infection: A Systemic Review, Nanwa et al. analyzed 45 cost-of-illness (COI) studies and determined that, for hospitalized patients, CDI costs range from $8,911 to $30,049.11 For decades, the standard treatment of CDI included antibiotic therapy with either metronidazole or vancomycin, however, even with the development of tapered or pulsed antibiotic regimens demonstrating improvement in recurrence rates, still some 14-31% of patients would experience repeat bouts of CDI.10 Furthermore, the risk of recurrent infection increases with every subsequent infection and by the third episode, rates become greater than 50%.4,10 Despite medical professionals’ increased awareness of the burden of CDI, there is still no consensus on treatment regimens and no standardized optimal approach to treating recurrent CDI exists.
The solution to the worsening burden of CDI may exist in the intestinal microbiome. There is already substantial evidence that fecal microbiota transplantation (FMT), the implantation of either a patient’s own stool (autologous transplant) or healthy donor stool (heterologous transplant) into a patient with gut dysbiosis caused by CDI, is a preferable alternative to traditional antibiotic therapy.7 A 2013 review and meta-analysis in the American Journal of Gastroenterology demonstrated that FMT resulted in resolution of infection in nearly 90% of patients affected by recurrent CDI.6,9 To reiterate the ideas addressed in our introduction, the suggestion of a mechanism of action is the restoration of the healthy composition of an individual’s intestinal microbiome. In addition to its efficacy, FMT presents an almost adverse event free means of cure. While some adverse events, including fever, abdominal pain, bloating, nausea, vomiting, diarrhea, flatulence, anorexia, and constipation have been reported after FMT, there have been no severe adverse events and no death attributable to FMT alone.8 Earlier research suggested that lower gastrointestinal FMT delivery resulted in high rates of clinical resolution than oral capsular implantation.6 However, in a very recent randomized controlled trial by Kao et al published in the November 2017 issue of JAMA, rates of minor adverse events were as low as 5.4%.5 In the same study, Dr. Kao demonstrates the noninferiority of oral capsule FMT to colonoscopy-delivered FMT, an important finding given that the colonoscopic method was reported as less pleasant than the capsule.5 Not only are delivery methods for FMT being refined, but models for the risk of FMT failure in the treatment of CDI have been developed. In Predictors of Early Failure After Fecal Microbiota Transplantation for the Therapy of Clostridium difficile Infection: A Multicenter Study published in the American Journal of Gastroenterology, Fischer et al. define risk score based on severity of CDI, number of CDI-related hospitalizations prior to FMT, and inpatient status.4 Although standard algorithm for the use of FMT as a treatment for recurrent CDI does not yet exist, this risk calculator will help to guide physicians as the use of FMT is pioneered.
The microbiome and its associations with disease states, and hence its potential to offer insight into new cures is in a fledgling state.
References
1. Badger, V.O., et al. “Clostridium difficile: epidemiology, pathogenesis, management, and prevention of a recalcitrant healthcare-associated pathogen.” Journal of Parenteral and Enteral Nutrition, vol 36, no. 6, 2012, pp. 645-62., doi:10.1177/0148607112446703.
2. Bartlett, J.G., et al. “Historical perspectives on studies of Clostridium difficile and C. difficile infection.” Clinical Journal of Infectious Disease, vol 46, supplement 1, 2008, pp. S4-11., doi:10.1086/521865.
3. Bomers, Marije, et al. “Rapid, Accurate, and On-Site Detection of C. difficile in Stool Samples.” American Journal of Gastroenterology, vol 110, no. 4, 2015, pp. 588-94., doi:10.1038/ajg.2015.90.
4. Fischer, Monika, et al. “Predictors of Early Failure After Fecal Microbiota Transplantation for the Therapy of Clostridium Difficile Infection: A Multicenter Study.” American Journal of Gastroenterology, vol 111, no. 7, 2016, pp. 1024-31., doi:10.1038/ajg.2016.180.
5. Kao, Diana, et al. “Effect of Oral Capsule-vs Colonoscopy-Delivered Fecal Microbiota Transplantation on Recurrent Clostridium difficile Infection, A Randomized Clinical Trial.” Journal of the American Medical Association, vol 318, no. 20, 2017, pp. 1985-93., doi:10.1001/jama.2017.17077.
6. Kassam, Z., et al. “Fecal Microbiota transplantation for Clostridium difficile infection: systematic review and meta-analysis.” American Journal of Gastroenterology, vol 108, no. 4, 2013, pp. 500-8., doi:10.1038/ajg.2013.59.
7. Kelly, Colleen, et al. “Effect of Fecal Microbiota Transplantation on Recurrence in Multiply Recurrent Clostridium difficile Infection.: Annals of Internal Medicine, vol 165, no. 9, 2016, pp. 609-16., oi:10.7326/M16-0271.
8. Li, Junhua, et al. “An integrated catalog of reference genes in the human gut microbiome.” Nature Biotechnology, vol 32, no. 8, 2014, pp. 834-41., doi:10.1038/nbt.2942.
9. Mattila, E, et al. “Fecal transplantation, through colonoscopy, is effective therapy for recurrent Clostridium difficile Infection.” Gastroenterology, vol 142, no. 3, 2012, pp. 490-6., doi:10.1053/j.gastro.2011.11.037.
10. McFarland, Lynne V., et al. “Breaking the Cycle: Treatment Strategies for 163 Cases of Recurrent Clostridium difficile Disease.” American Journal of Gastroenterology, vol 97, no. 7, 2002, pp. 1769-75., doi:10.1111/j.1572-0241.2002.05839.x.
11. Nanwa, Natasha, et al. “The Economic Impact of Clostridium difficile Infection: A Systematic Review.” American Journsal of Gastroenterology, vol 110, no. 4, 2015, pp. 511-519., doi:10.1038/ajg.2015.48.
Sabine Hazan Steinberg MD, Gastroenterology/Hepatology/Internal Medicine Physician, CEO, Ventura Clinical Trials, CEO, Malibu Specialty Center Dr. Daniel Frochtzwajg DO, Research Assistant, Ventura Clinical Trials Jessica Murray BS, Research Assistant, Ventura Clinical Trials, Ventura, CA
Ulcerative colitis (UC) and Crohn’s disease are the two chronic and progressive inflammatory states that commonly define inflammatory bowel disease (IBD). UC is typically characterized by continuous mucosal inflammation that involves that rectum and colon and often presents as bloody diarrhea. In Crohn’s disease, inflammation is spotty, transmural and can be observed in any portion of the gastrointestinal tract. IBD affects roughly 1.4 million people in the United States and some 2.2 million in Europe.5,6 The steadily increasing incidence and prevalence of IBD, as well as the association of IBD and urban living, suggests that environment plays a critical role in the development of these diseases.8,13 This hypothesis, in conjunction with the documented variations in gut microbiome associated with industrialization and geography,3 has led researchers to pursue the intestinal microbiota as an avenue for diagnostic and therapeutic intervention.
It is thought that a shift in composition of the intestinal microbiome may contribute to the development of IBD in genetically susceptible individuals. Initially hinted at by studies demonstrating such things as a reduced risk of IBD in breastfed infants or increased risk in those with low vitamin D levels,1,2,10 the new age of bioinformatics has enabled corroboration of this theory. One example of the complex genetic-microbe interplay is a study by Ijaz et al.. demonstrating that adult relatives of patients with Crohn’s disease had less diverse intestinal microbiota than healthy adults unrelated to IBD patients.4
While there is no singular microbe responsible for IBD, gut dysbiosis is clearly implicated.5 An overall reduction in microbial diversity has been observed as well as specific, relative increases and decreases in “good” and “bad” microbes.5,9,12 In Sartor and Wu’s extensive 2017 review, Roles for Intestinal Bacteria, Viruses, and Fungi in Pathogenesis of Inflammatory Bowel Disease and Therapeutic Approaches, the authors distill the latest documented genetic compositional changes in the intestinal microbiome of IBD patients.12 They identify the overarching theme of the associated dysbiosis as a decrease in known “protective” bacteria such as Bifidobacterium species and an expansion of potentially inflammatory microbes like Proteobacteria, Fusobacterium species, and invasive E. coli.12
The common treatments for UC and Crohn’s, including immunosuppressive therapies, mesalamine, glucocorticoids, and tumor necrosis factor antagonists, rarely induce remission and colectomy is too often an undesirable endpoint. Furthermore, an IBD patient’s quality of life can be significantly diminished when treated with conventional therapies.17 However, like the trend of fecal microbiota transplantation (FMT) for the treatment of Clostridium difficile infection, there is promising evidence that a similar approach will prove efficacious in treating UC and Crohn’s, especially given the increasingly predictable intestinal microbiome perturbation. In one of the premier studies of alternative treatments for IBD, Moayyedi et al. demonstrate, in a randomized controlled trial, that FMT can induce remission in UC patients.7 Researchers used the Mayo score for UC, which includes scores for stool pattern, rectal bleeding, endoscopic findings, and physician assessment (scores ranges from 0-12, with higher scores correlating with increased disease severity) to assess patients. Eligible enrollees were adults 18 years or older with active UC determined by a Mayo score ≥4 (with an endoscopic score ≥1); remission was defined as a Mayo score <3 at seven weeks. FMT from healthy donors was completed via retention enemas administered once weekly for six weeks. Overall, 9 of the 38 patients in the FMT treatment arm achieved remission, compared to 2 of the 37 patients in the placebo arm. Moreover, there was no difference in serious adverse events between the two groups. In another promising prospective, uncontrolled study, by Uygun et al. response of UC patients to FMT was examined.14 Responders were defined as a decrease in Mayo score ≥30%. 21 patients in the study, 70% of the subjects, were ultimately classified as responders. While 9 patients were categorized as non-responders, there was still improvement in CRP and hemoglobin levels after FMT.
Despite the positive findings mentioned above, there is conflicting data, and in another RCT, Rossen et al.11 did not demonstrate a difference in the remission rate of FMT vs. placebo. However, increased intestinal microbiome richness following FMT has been shown in patients with Crohn’s, and there is evidence to suggest that FMT donor species richness determines efficacy of FMT treatment for IBD.15,16
Ultimately, while current data is cause for optimism, more foundational research is necessary to characterize the microbe-gene interaction and define a treatment paradigm.
References
1. Ananthakrishnan, A.N., et al. “Higher predicted vitamin D status is associated with reduced risk of Crohn’s disease.” Gastroenterology, vol 142, no. 3, 2012, pp. 482-89., doi: 10.1053/j.gastro.2011.11.040.
2. Barclay, A.R., et al. “Systematic review: the role of breastfeeding in the development of pediatric inflammatory bowel disease.” Journal of Pediatrics, vol 155, no. 3, 2009, pp. 421-6., doi: 10.1016/j.jpeds.2009.03.017.
3. Gupta, Vinod K., et al. “Geography, Ethnicity or Subsistence-Specific Variations in Human Microbiome Composition and Diversity.” Frontiers in Microbiology, vol 8, no. 1162, 2017., doi: 10.3389/fmicb.2017.01162.
4. Ijaz, Umer Zeeshan, et al. “The distinct features of microbial ‘dysbiosis’ of Crohn’s disease do not occur to the same extent in their unaffected, geneticallylinked kindred.” PLoS ONE, vol 12, no. 2, 2017., doi: 10.137/journal.pone.0172605.
5. Lane, Erin R., et al. “The microbiota in inflammatory bowel disease: current and therapeutic insights.” Journal of Inflammation Research, vol 10, 2017, pp. 63-73., doi:10.2147/JIR.S116088.
6. Loftus, E.V. Jr. “Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology, vol 126, no. 6, 2004, pp. 1504-1517., doi: 10.1053/j.gastro.2004.01.063.
7. Moayyedi, Paul, et al. “Fecal Microbiota Transplantation Induces Remission in Patients with Active Ulcerative Colitis in a Randomized Controlled Trial.” Gastroenterology, vol 149, no. 1, 2015, pp. 102-109., doi: 10.1053/j.gastro.2015.04.001.
8. Molodecky, N.A., et al. “Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review.” Gastroenterology, vol 142, no. 1, 2012, pp. 46-54., doi: 10.1053/j.gastro.2011.10.001.
9. Morgan, X.C., et al. “Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment.” Genome Biology, vol 13, no. 9, R79, 2012., doi: 10.1186/gb-2012-13-9-r79.
10. Penders, J., et al. “Factors influencing the composition of the intestinal microbiota in early infancy.” Pediatrics, vol 118, no. 2, 2006, pp. 511-521., doi: 10.1542/peds.2005-2824.
11. Rossen, N.G., et al. “Findings from a randomized controlled trial of fecal transplantation for patients with ulcerative colitis.” Gastroenterology, vol. 149, 2015, pp. 110-118., doi: 10.1053/j.gastro.2015.03.045.
12. Sartor, R. Balfour, and Gary D. Wu. “Roles for Intestinal Bacteria, Viruses, and Fungi in Pathogenesis of Inflammatory Bowel Diseases and Therapeutic Approaches.” Gastroenterology, vol 152, no. 2, pp. 327-339., doi: 10.1053/j.gastro.2016.10.012.
13. Soon, Ing Shian, et al. “The relationship between urban environment and the inflammatory bowel diseases: a systematic review and meta-analysis.” BMC Gastroenterology, vol 12, no. 51, 2012., doi: 10.1186/1471-230X-12-51.
14. Uygen, Ahmet, et al. “Fecal microbiota transplantation is a rescue treatment modality for refractory ulcerative colitis.” Medicine, vol 96, no. 16, 2017., doi: 10.1097/MD.0000000000006479.
15. Vaughn, Byron P., et al. “Increased Intestinal Microbial Diversity following Fecal Microbiota Transplant for Active Crohn’s Disease.” Inflammatory Bowel Disease, vol 22, no. 9, 2016, pp. 2182-90., doi: 10.1097/MIB.0000000000000893.
16. Vermeire, Severine, et al. “Donor Species Richness Determines Faecal Microbiota Transplantation Success in Inflammatory Bowel Disease.” Journal of Crohn’s and Colitis, vol 10, no. 4, 2016, pp. 387-394., doi: 10.1093/ecco-jcc/jjv203.
17. Wei, Yao, et al. “Fecal Microbiota Transplantation Improves the Quality of Life in Patients with Inflammatory Bowel Disease.” Gastroenterology Research and Practice, vol 2015, 2015., doi: 10.1155/2015/517597.
Sabine Hazan, MD Ventura Clinical Trials, Ventura, CA
Simply and elegantly defined by Lynch and Pedersen in their December 2016 article in the New England Journal of Medicine, a microbiome is the collection of all genomes of microbes in an ecosystem.3 In the context of human beings and our health, it is the vastly diverse genetic information observable in the microbes colonizing the distal GI tract. Historically, the study of human microbiology has been one of a singular relationship cause and effect, microbe and infection, and our approach to treating the disease states caused by pathogenic bacteria and viruses has been one of nearly indiscriminate eradication. The problem inherent in this approach is that no microbe is an island. A new, emerging paradigm suggests that the susceptibility, severity, and duration of some diseases, even some previously thought to be independent of microbial involvement, are mediated by a complex interplay of host and microbe genomes. Already, nearly 10 million different microbial genes have been isolated from the human gut.2 With the use of contemporary, culture – independent tools for analyzing fecal microbiota, e.g., biomarker sequencing, metagenomics, metatranscriptomics and metabolomics, the genetic diversity will likely continue to expand rapidly.3
Starting at birth and continuing throughout human life, commensal microorganisms function to aid in the development of temporally favorable phenotypes. For example, in preadolescents, the gut microbiota is relatively rich with organisms that augment vitamin B12 and folate synthesis, promoting growth.1 In adulthood, the intestinal microbiota remains comparatively constant in composition.4 In addition to biosynthesis, the gut microbiota influences immune maturation, host cell proliferation, vascularization, neurologic signaling, endocrine function, bone density, drug and food metabolism.3 Considering the seemingly global influence on host function, it is but a small leap to infer that the intestinal microbiome has indications for disease, and in turn, that interventions in microbiome makeup could aid in the treatment of disease states identified to correspond to specific dysbiosis. Despite the wealth of research to date, there are obvious limitations to our current understandings of the human microbiome and its implications in human health and disease. There are also limitations to even the most contemporary of research methods and study techniques. For example, patient stool samples are assumed to be accurately representative of intestinal microorganism content and, despite there being robust research evidence connecting changes in the microbiome to disease states, there have been few, if any, studies elucidating the biochemical mechanisms responsible for the changes in disease states with microbiome intervention.3
Many factors affect the composition of the gut microbiota. Diet, genetics, antibiotics and other medications, environment, and even geography result in differences in individual host microbiome.1,3
In this series, we aim to shed light on some of the most promising research to date that addresses the intestinal microbiome as it relates to common chronic diseases.
References
1. Hollister, EB, et al. “Structure and function of the healthy pre-adolescent pediatric gut microbiome.” Microbiome, vol 3, no. 35, 2015., doi:10.1186/s40168-015-0101-x.
2. Li, Junhua, et al. “An integrated catalog of reference genes in the human gut microbiome.” Nature Biotechnology, vol 32, no. 8, 2014, pp. 834-41., doi:10.1038/nbt.2942.
3. Lynch, Susan V., and Oluf Pedersen. “The Human Intestinal Microbiome in Health and Disease.” The New England Journal of Medicine, vol 375, no. 24, 2016, pp. 2369-79., doi:10.1056/NEJMra1600266.
4. Yatsunenko, T., et al. “Human gut microbiome viewed across age and geography.” Natrure, vol 486, no. 7402, 2012, pp. 222-27., doi:10.1038/nature11053.
Postpartum Depression Help Call 1 800 920 0016
Are you feeling anxious, withdrawn, or depressed.
It’s not your fault
Postpartum Depression is a biological complication of pregnancy.
Symptoms can be severe and should not be ignored.
The Hummingbird Study is a research study evaluating an investigational medication in women with moderate to severe postpartum depression.
You May Qualify to Participate if you:
Are between 18 to 45 years old
Gave birth within the last 6 months
Frequently feel extremely sad, anxious, or overwhelmed and these symptoms are associated with postpartum depression.
IF YOU QUALIFY AND DECIDE TO PARTICIPATE, YOU WILL RECEIVE:
Study-related care during the 3-day, in-patient period
All study-related care medical care and medication at no cost
All Transportation is provided if needed
For more information please call Ventura Clinical Trials at 1 800 920 0016
Are you feeling Anxious, withdrawn or depressed ? It is not your fault and you could have Postpartum depression. Learn more about a new Research study that could make a difference by calling Ventura clinical trials at 1 866 947 6815
Postpartum depression (PPD), also called postnatal depression, is a type of clinical depression which can affect both sexes after childbirth. Symptoms may include sadness, low energy, changes in sleeping and eating patterns, reduced desire for sex, crying episodes, anxiety, and irritability. While many women experience self-limited, mild symptoms postpartum, postpartum depression should be suspected when symptoms are severe and have lasted over two weeks.
Although a number of risk factors have been identified, the causes of PPD are not well understood. Hormonal change is hypothesized to contribute as one cause of postpartum depression. The emotional effects of postpartum depression can include sleep deprivation, anxiety about parenthood and caring for an infant, identity crisis, a feeling of loss of control over life, and anxiety due to lack of support from a romantic or sexual partner. Many women recover with treatment such as a support group, counseling, or medication.
Between 0.5% to 61% of women will experience depression after delivery. Postpartum psychosis occurs in about 1–2 per thousand women following childbirth. Among men, in particular new fathers, the incidence of postpartum depression has been estimated to be between 1% and 25.5%.
Onset and duration
Postpartum depression usually begins between two weeks to a month after delivery. Recent studies have shown that fifty percent of postpartum depressive episodes actually begin prior to delivery. Therefore, in the DSM-5, postpartum depression is diagnosed under “depressive disorder with peripartum onset”, in which “peripartum onset” is defined as anytime either during pregnancy or within the four weeks following delivery. PPD may last several months or even a year.Postpartum depression can also occur in women who have suffered a miscarriage.
Parent-infant relationship
Postpartum depression can interfere with normal maternal-infant bonding and adversely affect child development. Postpartum depression may lead mothers to be inconsistent with childcare.Children of mothers with PPD have been found to have higher rates of emotional problems, behavioral problems, psychiatric diagnoses (such as oppositional defiant disorder and conduct disorder), and hyperactivity.
In rare cases, or about 1 to 2 per 1,000, the postpartum depression appears as postpartum psychosis which may adversely affect the infant’s health. In these, or among women with a history of previous psychiatric hospital admissions, may occur. In the United States, postpartum depression is one of the leading causes of annual reported infanticide incidence rate of about 8 per 100,000 births.
To find out if you qualify for our Study please call 1 866 947 6815
We can take on the flu as soon as the flu takes on you!
When you reach for the tissues this flu season, think CAPSTONE-2 the CAPSTONE-2 clinical research study will try to find out if an investigational flu drug can speed up the recovery to people with the flu who are at risk of further complications,when compared to a placebo (a look-alike containing no medication) and a drug already approved to treat the flu called Tamiflu ( also know as oseltamivir).
Those taking part must: Have flu symptoms (such as fever, aches, pains, cough, sore throat) for less than 48 hours
Be at least 12 years old
Be at risk of developing further complications (for example, those with another health condition and those over the age of 65)
Taking part in the study means visiting a clinic between 7 and 9 times for health checks.
these checks, along with any study-related drugs, will be provided at no additional cost.
you do not need health insurance, and compensation for time or travel will be provided up to $900
Because you need to enroll in the study 48 hours of becoming ill, it is important to get in touch with the study team as soon as possible after symptoms appear.
If you think you/your child may be suitable, please contact Ventura Clinical Trials
1835 knoll Dr., Ventura Ca 93003 Influenza Ventura California Call 1 866 947 6815
Postpartum depression (PPD), also called postnatal depression, is a type of clinical depression which can affect both sexes after childbirth. Symptoms may include sadness, low energy, changes in sleeping and eating patterns, reduced desire for sex, crying episodes, anxiety, and irritability. While many women experience self-limited, mild symptoms postpartum, postpartum depression should be suspected when symptoms are severe and have lasted over two weeks.
Although a number of risk factors have been identified, the causes of PPD are not well understood. Hormonal change is hypothesized to contribute as one cause of postpartum depression. The emotional effects of postpartum depression can include sleep deprivation, anxiety about parenthood and caring for an infant, identity crisis, a feeling of loss of control over life, and anxiety due to lack of support from a romantic or sexual partner. Many women recover with treatment such as a support group, counseling, or medication.
Between 0.5% to 61% of women will experience depression after delivery. Postpartum psychosis occurs in about 1–2 per thousand women following childbirth. Among men, in particular new fathers, the incidence of postpartum depression has been estimated to be between 1% and 25.5%.
Onset and duration
Postpartum depression usually begins between two weeks to a month after delivery. Recent studies have shown that fifty percent of postpartum depressive episodes actually begin prior to delivery. Therefore, in the DSM-5, postpartum depression is diagnosed under “depressive disorder with peripartum onset”, in which “peripartum onset” is defined as anytime either during pregnancy or within the four weeks following delivery. PPD may last several months or even a year.Postpartum depression can also occur in women who have suffered a miscarriage.
Parent-infant relationship
Postpartum depression can interfere with normal maternal-infant bonding and adversely affect child development. Postpartum depression may lead mothers to be inconsistent with childcare.Children of mothers with PPD have been found to have higher rates of emotional problems, behavioral problems, psychiatric diagnoses (such as oppositional defiant disorder and conduct disorder), and hyperactivity.
In rare cases, or about 1 to 2 per 1,000, the postpartum depression appears as postpartum psychosis which may adversely affect the infant’s health. In these, or among women with a history of previous psychiatric hospital admissions, may occur. In the United States, postpartum depression is one of the leading causes of annual reported infanticide incidence rate of about 8 per 100,000 births.
To find out if you qualify for our Study please call 1 866 947 6815
ULCERATIVE COLITIS? If you take Mesalamine for UC, but continue to struggle with your disease, learn more about this study evaluating a novel investigational UC food product.
-To pre-qualify for this study, you must be:
18 to 70 years of age and diagnosed with Ulcerative Colitis
Currently taking Mesalamine
Having an Ulcerative Colitis flare (increased UC symptoms)
-All study related visits, tests, and drugs will be provided to the participants at no cost. In addition, compensation for study related time and travel may be provided. Compensation can be up to $1,460 for qualifying patients.
To find out if you qualify for this study and compensation please call 1 800 920 0016
Symptoms
Ulcerative colitis symptoms can vary, depending on the severity of inflammation and where it occurs. Therefore, doctors often classify ulcerative colitis according to its location.
You may have the following signs and symptoms, depending on which part of the colon is inflamed:
Diarrhea, often with blood or pus
Abdominal pain and cramping
Rectal pain
Rectal bleeding — passing small amount of blood with stool
Urgency to defecate
Inability to defecate despite urgency
Weight loss
Fatigue
Fever
In children, failure to grow
Most people with ulcerative colitis have mild to moderate symptoms. The course of ulcerative colitis may vary, with some people having long periods of remission.
Types
Ulcerative colitis is classified according to how much of your colon is affected. The condition can be mild and limited to the rectum (ulcerative proctitis). Or it can affect additional parts of your colon, generally with more severe symptoms. People who develop ulcerative colitis at a younger age are more likely to have severe symptoms.
When to see a doctor
See your doctor if you experience a persistent change in your bowel habits or if you have signs and symptoms such as:
Abdominal pain
Blood in your stool
Ongoing diarrhea that doesn’t respond to over-the-counter medications
Diarrhea that awakens you from sleep
An unexplained fever lasting more than a day or two
Although ulcerative colitis usually isn’t fatal, it’s a serious disease that, in some cases, may cause life-threatening complications.
Sabine Hazan, MD Ventura Clinical Trials, Ventura, CA
