Optimal duration of exclusive breastfeeding Kramer, Michael S; Kakuma, Ritsuko; Kramer, Michael S
Cochrane database of systematic reviews,
08/2012, Letnik:
2012, Številka:
8
Journal Article
Recenzirano
Odprti dostop
Background
Although the health benefits of breastfeeding are widely acknowledged, opinions and recommendations are strongly divided on the optimal duration of exclusive breastfeeding. Since 2001, the ...World Health Organization has recommended exclusive breastfeeding for six months. Much of the recent debate in developed countries has centred on the micronutrient adequacy, as well as the existence and magnitude of health benefits, of this practice.
Objectives
To assess the effects on child health, growth, and development, and on maternal health, of exclusive breastfeeding for six months versus exclusive breastfeeding for three to four months with mixed breastfeeding (introduction of complementary liquid or solid foods with continued breastfeeding) thereafter through six months.
Search methods
We searched The Cochrane Library (2011, Issue 6), MEDLINE (1 January 2007 to 14 June 2011), EMBASE (1 January 2007 to 14 June 2011), CINAHL (1 January 2007 to 14 June 2011), BIOSIS (1 January 2007 to 14 June 2011), African Index Medicus (searched 15 June 2011), Index Medicus for the WHO Eastern Mediterranean Region (IMEMR) (searched 15 June 2011), LILACS (Latin American and Caribbean Health Sciences) (searched 15 June 2011). We also contacted experts in the field.
The search for the first version of the review in 2000 yielded a total of 2668 unique citations. Contacts with experts in the field yielded additional published and unpublished studies. The updated literature review in December 2006 yielded 835 additional unique citations.
Selection criteria
We selected all internally‐controlled clinical trials and observational studies comparing child or maternal health outcomes with exclusive breastfeeding for six or more months versus exclusive breastfeeding for at least three to four months with continued mixed breastfeeding until at least six months. Studies were stratified according to study design (controlled trials versus observational studies), provenance (developing versus developed countries), and timing of compared feeding groups (three to seven months versus later).
Data collection and analysis
We independently assessed study quality and extracted data.
Main results
We identified 23 independent studies meeting the selection criteria: 11 from developing countries (two of which were controlled trials in Honduras) and 12 from developed countries (all observational studies). Definitions of exclusive breastfeeding varied considerably across studies. Neither the trials nor the observational studies suggest that infants who continue to be exclusively breastfed for six months show deficits in weight or length gain, although larger sample sizes would be required to rule out modest differences in risk of undernutrition. In developing‐country settings where newborn iron stores may be suboptimal, the evidence suggests that exclusive breastfeeding without iron supplementation through six months may compromise hematologic status. Based on the Belarusian study, six months of exclusive breastfeeding confers no benefit (versus three months of exclusive breastfeeding followed by continued partial breastfeeding through six months) on height, weight, body mass index, dental caries, cognitive ability, or behaviour at 6.5 years of age. Based on studies from Belarus, Iran, and Nigeria, however, infants who continue exclusive breastfeeding for six months or more appear to have a significantly reduced risk of gastrointestinal and (in the Iranian and Nigerian studies) respiratory infection. No significant reduction in risk of atopic eczema, asthma, or other atopic outcomes has been demonstrated in studies from Finland, Australia, and Belarus. Data from the two Honduran trials and from observational studies from Bangladesh and Senegal suggest that exclusive breastfeeding through six months is associated with delayed resumption of menses and, in the Honduran trials, more rapid postpartum weight loss in the mother.
Authors' conclusions
Infants who are exclusively breastfed for six months experience less morbidity from gastrointestinal infection than those who are partially breastfed as of three or four months, and no deficits have been demonstrated in growth among infants from either developing or developed countries who are exclusively breastfed for six months or longer. Moreover, the mothers of such infants have more prolonged lactational amenorrhea. Although infants should still be managed individually so that insufficient growth or other adverse outcomes are not ignored and appropriate interventions are provided, the available evidence demonstrates no apparent risks in recommending, as a general policy, exclusive breastfeeding for the first six months of life in both developing and developed‐country settings.
Objective Because the diagnosis of postpartum hemorrhage (PPH) depends on the accoucheur's subjective estimate of blood loss and varies according to mode of delivery, we examined temporal trends in ...severe PPH, defined as PPH plus receipt of a blood transfusion, hysterectomy, and/or surgical repair of the uterus. Study Design We analyzed 8.5 million hospital deliveries in the US Nationwide Inpatient Sample from 1999 to 2008 for temporal trends in, and risk factors for, severe PPH, based on International Classification of Diseases, 9th revision, clinical modification diagnosis and procedure codes. Sequential logistic regression models that account for the stratified random sampling design were used to assess the extent to which changes in risk factors explain the trend in severe PPH. Results Of the total 8,571,209 deliveries, 25,906 (3.0 per 1000) were complicated by severe PPH. The rate rose from 1.9 to 4.2 per 1000 from 1999 to 2008 ( P for yearly trend < .0001), with increases in severe atonic and nonatonic PPH, due especially to PPH with transfusion, but also PPH with hysterectomy. Significant risk factors included maternal age ≥35 years (adjusted odds ratio aOR, 1.5; 95% confidence interval CI, 1.5–1.6), multiple pregnancy (aOR, 2.8; 95% CI, 2.6–3.0), fibroids (aOR, 2.0; 95% CI, 1.8–2.2), preeclampsia (aOR, 3.1; 95% CI, 2.9–3.3), amnionitis (aOR, 2.9; 95% CI, 2.5–3.4), placenta previa or abruption (aOR, 7.0; 95% CI, 6.6–7.3), cervical laceration (aOR, 94.0; 95% CI, 87.3–101.2), uterine rupture (aOR, 11.6; 95% CI, 9.7–13.8), instrumental vaginal delivery (aOR, 1.5; 95% CI, 1.4–1.6), and cesarean delivery (aOR, 1.4; 95% CI, 1.3–1.5). Changes in risk factors, however, accounted for only 5.6% of the increase in severe PPH. Conclusion A doubling in incidence of severe PPH over 10 years was not explained by contemporaneous changes in studied risk factors.
Background
Some breastfed infants with atopic eczema benefit from elimination of cow milk, egg, or other antigens from their mother's diet. Maternal dietary antigens are also known to cross the ...placenta.
Objectives
To assess the effects of prescribing an antigen avoidance diet during pregnancy or lactation, or both, on maternal and infant nutrition and on the prevention or treatment of atopic disease in the child.
Search methods
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (6 July 2012).
Selection criteria
All randomized or quasi‐randomized comparisons of maternal dietary antigen avoidance prescribed to pregnant or lactating women. We excluded trials of multimodal interventions that included manipulation of the infant's diet other than breast milk or of non‐dietary aspects of the infant's environment.
Data collection and analysis
We extracted data from published reports, supplemented by additional information received from the trialists we contacted.
Main results
The evidence from five trials, involving 952 participants, does not suggest a protective effect of maternal dietary antigen avoidance during pregnancy on the incidence of atopic eczema during the first 18 months of life. Data on allergic rhinitis or conjunctivitis, or both, and urticaria are limited to a single trial each and are insufficient to draw meaningful inferences. Longer‐term atopic outcomes have not been reported. The restricted diet during pregnancy was associated with a slightly but statistically significantly lower mean gestational weight gain, a non‐significantly higher risk of preterm birth, and a non‐significant reduction in mean birthweight.
The evidence from two trials, involving 523 participants, did not observe a significant protective effect of maternal antigen avoidance during lactation on the incidence of atopic eczema during the first 18 months or on positive skin‐prick tests to cow milk, egg, or peanut antigen at one, two, or seven years.
One crossover trial involving 17 lactating mothers of infants with established atopic eczema found that maternal dietary antigen avoidance was associated with a non‐significant reduction in eczema severity.
Authors' conclusions
Prescription of an antigen avoidance diet to a high‐risk woman during pregnancy is unlikely to reduce substantially her child's risk of atopic diseases, and such a diet may adversely affect maternal or fetal nutrition, or both. Prescription of an antigen avoidance diet to a high‐risk woman during lactation may reduce her child's risk of developing atopic eczema, but better trials are needed.
Dietary antigen avoidance by lactating mothers of infants with atopic eczema may reduce the severity of the eczema, but larger trials are needed.
One of the United Nations' Millennium Development Goals of 2000 was to reduce maternal mortality by 75% in 15 y; however, this challenge was not met by many industrialized countries. As average ...maternal age continues to rise in these countries, associated potentially life-threatening severe maternal morbidity has been understudied. Our primary objective was to examine the associations between maternal age and severe maternal morbidities. The secondary objective was to compare these associations with those for adverse fetal/infant outcomes.
This was a population-based retrospective cohort study, including all singleton births to women residing in Washington State, US, 1 January 2003-31 December 2013 (n = 828,269). We compared age-specific rates of maternal mortality/severe morbidity (e.g., obstetric shock) and adverse fetal/infant outcomes (e.g., perinatal death). Logistic regression was used to adjust for parity, body mass index, assisted conception, and other potential confounders. We compared crude odds ratios (ORs) and adjusted ORs (AORs) and risk differences and their 95% CIs. Severe maternal morbidity was significantly higher among teenage mothers than among those 25-29 y (crude OR = 1.5, 95% CI 1.5-1.6) and increased exponentially with maternal age over 39 y, from OR = 1.2 (95% CI 1.2-1.3) among women aged 35-39 y to OR = 5.4 (95% CI 2.4-12.5) among women aged ≥50 y. The elevated risk of severe morbidity among teen mothers disappeared after adjustment for confounders, except for maternal sepsis (AOR = 1.2, 95% CI 1.1-1.4). Adjusted rates of severe morbidity remained increased among mothers ≥35 y, namely, the rates of amniotic fluid embolism (AOR = 8.0, 95% CI 2.7-23.7) and obstetric shock (AOR = 2.9, 95% CI 1.3-6.6) among mothers ≥40 y, and renal failure (AOR = 15.9, 95% CI 4.8-52.0), complications of obstetric interventions (AOR = 4.7, 95% CI 2.3-9.5), and intensive care unit (ICU) admission (AOR = 4.8, 95% CI 2.0-11.9) among those 45-49 y. The adjusted risk difference in severe maternal morbidity compared to mothers 25-29 y was 0.9% (95% CI 0.7%-1.2%) for mothers 40-44 y, 1.6% (95% CI 0.7%-2.8%) for mothers 45-49 y, and 6.4% for mothers ≥50 y (95% CI 1.7%-18.2%). Similar associations were observed for fetal and infant outcomes; neonatal mortality was elevated in teen mothers (AOR = 1.5, 95% CI 1.2-1.7), while mothers over 29 y had higher risk of stillbirth. The rate of severe maternal morbidity among women over 49 y was higher than the rate of mortality/serious morbidity of their offspring. Despite the large sample size, statistical power was insufficient to examine the association between maternal age and maternal death or very rare severe morbidities.
Maternal age-specific incidence of severe morbidity varied by outcome. Older women (≥40 y) had significantly elevated rates of some of the most severe, potentially life-threatening morbidities, including renal failure, shock, acute cardiac morbidity, serious complications of obstetric interventions, and ICU admission. These results should improve counselling to women who contemplate delaying childbirth until their forties and provide useful information to their health care providers. This information is also useful for preventive strategies to lower maternal mortality and severe maternal morbidity in developed countries.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
In a Perspective, Sarka Lisonkova and Michael Kramer discuss the accompanying study by Kathryn Fitzpatrick and co-authors on management of amniotic fluid embolism.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Hexanucleotide-repeat expansions in the C9ORF72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD). The nucleotide-repeat expansions are ...translated into dipeptide-repeat (DPR) proteins, which are aggregation prone and may contribute to neurodegeneration. We used the CRISPR-Cas9 system to perform genome-wide gene-knockout screens for suppressors and enhancers of C9ORF72 DPR toxicity in human cells. We validated hits by performing secondary CRISPR-Cas9 screens in primary mouse neurons. We uncovered potent modifiers of DPR toxicity whose gene products function in nucleocytoplasmic transport, the endoplasmic reticulum (ER), proteasome, RNA-processing pathways, and chromatin modification. One modifier, TMX2, modulated the ER-stress signature elicited by C9ORF72 DPRs in neurons and improved survival of human induced motor neurons from patients with C9ORF72 ALS. Together, our results demonstrate the promise of CRISPR-Cas9 screens in defining mechanisms of neurodegenerative diseases.
To explore international differences in the classification of births at extremely low gestation and the subsequent impact on the calculation of survival rates.
We used national data on births at 22 ...to 25 weeks' gestation from the United States (2014;
= 11 144), Canada (2009-2014;
= 5668), the United Kingdom (2014-2015;
= 2992), Norway (2010-2014;
= 409), Finland (2010-2015;
= 348), Sweden (2011-2014;
= 489), and Japan (2014-2015;
= 2288) to compare neonatal survival rates using different denominators: all births, births alive at the onset of labor, live births, live births surviving to 1 hour, and live births surviving to 24 hours.
For births at 22 weeks' gestation, neonatal survival rates for which we used live births as the denominator varied from 3.7% to 56.7% among the 7 countries. This variation decreased when the denominator was changed to include stillbirths (ie, all births 1.8%-22.3% and fetuses alive at the onset of labor 3.7%-38.2%) or exclude early deaths and limited to births surviving at least 12 hours (50.0%-77.8%). Similar trends were seen for infants born at 23 weeks' gestation. Variation diminished considerably at 24 and 25 weeks' gestation.
International variation in neonatal survival rates at 22 to 23 weeks' gestation diminished considerably when including stillbirths in the denominator, revealing the variation arises in part from differences in the proportion of births reported as live births, which itself is closely connected to the provision of active care.
Introduction
The Alzheimer's disease (AD) continuum begins with a long asymptomatic or preclinical stage, during which amyloid beta (Aβ) is accumulating for more than a decade prior to widespread ...cortical tauopathy, neurodegeneration, and manifestation of clinical symptoms. The AHEAD 3‐45 Study (BAN2401‐G000‐303) is testing whether intervention with lecanemab (BAN2401), a humanized immunoglobulin 1 (IgG1) monoclonal antibody that preferentially targets soluble aggregated Aβ, initiated during this asymptomatic stage can slow biomarker changes and/or cognitive decline. The AHEAD 3‐45 Study is conducted as a Public‐Private Partnership of the Alzheimer's Clinical Trial Consortium (ACTC), funded by the National Institute on Aging, National Institutes of Health (NIH), and Eisai Inc.
Methods
The AHEAD 3‐45 Study was launched on July 14, 2020, and consists of two sister trials (A3 and A45) in cognitively unimpaired (CU) individuals ages 55 to 80 with specific dosing regimens tailored to baseline brain amyloid levels on screening positron emission tomography (PET) scans: intermediate amyloid (≈20 to 40 Centiloids) for A3 and elevated amyloid (>40 Centiloids) for A45. Both trials are being conducted under a single protocol, with a shared screening process and common schedule of assessments. A3 is a Phase 2 trial with PET‐imaging end points, whereas A45 is a Phase 3 trial with a cognitive composite primary end point. The treatment period is 4 years. The study utilizes innovative approaches to enriching the sample with individuals who have elevated brain amyloid. These include recruiting from the Trial‐Ready Cohort for Preclinical and Prodromal Alzheimer's disease (TRC‐PAD), the Australian Dementia Network (ADNeT) Registry, and the Japanese Trial Ready Cohort (J‐TRC), as well as incorporation of plasma screening with the C2N mass spectrometry platform to quantitate the Aβ 42/40 ratio (Aβ 42/40), which has been shown previously to reliably identify cognitively normal participants not likely to have elevated brain amyloid levels. A blood sample collected at a brief first visit is utilized to "screen out" individuals who are less likely to have elevated brain amyloid, and to determine the participant's eligibility to proceed to PET imaging. Eligibility to randomize into the A3 Trial or A45 Trial is based on the screening PET imaging results.
Result
The focus of this article is on the innovative design of the study.
Discussion
The AHEAD 3‐45 Study will test whether with lecanemab (BAN2401) can slow the accumulation of tau and prevent the cognitive decline associated with AD during its preclinical stage. It is specifically targeting both the preclinical and the early preclinical (intermediate amyloid) stages of AD and is the first secondary prevention trial to employ plasma‐based biomarkers to accelerate the screening process and potentially substantially reduce the number of screening PET scans.
Analyze the relation of gestational diabetes and maternal blood glucose levels to early cognitive functions in the first two years of life.
In a prospective Singaporean birth cohort study, pregnant ...women were screened for gestational diabetes at 26-28 weeks gestation using a 75-g oral glucose tolerance test. Four hundred and seventy three children (n = 74 and n = 399 born to mothers with and without gestational diabetes respectively) underwent neurocognitive assessments at 6, 18, and/or 24 month, including electrophysiology during an attentional task and behavioral measures of attention, memory and cognition.
Gestational diabetes is related to left hemisphere EPmax amplitude differences (oddball versus standard) at both six (P = 0.039) and eighteen months (P = 0.039), with mean amplitudes suggesting offspring of mothers with gestational diabetes exhibit greater neuronal activity to standard stimuli and less to oddball stimuli. Associations between 2-hour maternal glucose levels and the difference in EPmax amplitude were marginal at 6 months adjusted β = -0.19 (95% CI: -0.42 to +0.04) μV, P = 0.100 and significant at 18 months adjusted β = -0.27 (95% CI: -0.49 to -0.06) μV, P = 0.014, and the EPmax amplitude difference (oddball-standard) associated with the Bayley Scales of Infant and toddler Development-III cognitive score at 24 months β = 0.598 (95% CI: 0.158 to 1.038), P = 0.008.
Gestational diabetes and maternal blood glucose levels are associated with offspring neuronal activity during an attentional task at both six and eighteen months. Such electrophysiological differences are likely functionally important, having been previously linked to attention problems later in life.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Normal fetal growth is a critical component of a healthy pregnancy and influences the long-term health of the offspring. However, defining normal and abnormal fetal growth has been a long-standing ...challenge in clinical practice and research. We review various references and standards that are used widely to evaluate fetal growth and discuss common pitfalls of current definitions of abnormal fetal growth. Pros and cons of different approaches to customize fetal growth standards are described. We further discuss recent advances toward an integrated definition for fetal growth restriction . Such a definition may incorporate fetal size with the status of placental health that is measured by maternal and fetal Doppler velocimetry and biomarkers, biophysical findings, and genetics. Although the concept of an integrated definition appears promising, further development and testing are required. An improved definition of abnormal fetal growth should benefit both research and clinical practice.
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