Association of prenatal counselling and immediate postnatal support with early initiation of breastfeeding in Uttar Pradesh, India.

BACKGROUND: Timely initiation of breastfeeding, also known as early initiation of breastfeeding, is a well-recognized life-saving intervention to reduce neonatal mortality. However, only one quarter of newborns in Uttar Pradesh, India were breastfed in the first hour of life. This paper aims to understand the association of community-based prenatal counselling and postnatal support at place of delivery with early initiation of breastfeeding in Uttar Pradesh, India. METHODS: Data from a cross-sectional survey of 9124 eligible women (who had a live birth in 59 days preceding the survey) conducted in 25 districts of Uttar Pradesh, India, in 2018, were used. Simple random sampling was used to randomly select 40 Community Development Blocks (sub district administrative units) in 25 districts. The Primary Sampling Units (PSUs), health service delivery unit for frontline workers, were selected randomly from a linelisting of PSUs in each selected Community Development Block. Bivariate and multivariate logistic regression analyses were performed to assess the association of prenatal counselling and postnatal support on early initiation of breastfeeding in public, private and home deliveries. RESULTS: Overall 48.1% of mothers initiated breastfeeding within an hour, with major variation by place of delivery (61.2% public, 23.6% private and 32.6% home). The adjusted odds ratio (aOR) of early initiation of breastfeeding was highest among mothers who received both counselling and support (aOR 2.67; 95% CI 2.30, 3.11), followed by those who received only support (aOR 1.99; 95% CI 1.73, 2.28), and only counselling (aOR 1.40; 95% CI 1.18, 1.67) compared to mothers who received none. The odds of early initiation of breastfeeding was highest among mothers who received both prenatal counselling and postnatal support irrespective of delivery at public health facilities (aOR 2.49; 95% CI 2.07, 3.01), private health facilities (aOR 3.50; 95% CI 2.25, 5.44), or home (aOR 2.84; 95% CI 2.02, 3.98). CONCLUSIONS: A significant association of prenatal counselling and postnatal support immediately after birth on improving early initiation of breastfeeding, irrespective of place of delivery, indicates the importance of enhancing coverage of both the interventions through community and facility-based programs in Uttar Pradesh.

Visualizing participant experiences in maternal and child nutrition studies using timeline mapping.

Iron and folic acid (IFA) supplementation is one of the most cost-effective interventions to prevent and treat anemia during pregnancy. Despite having the highest global burden of anemia among pregnant women, rates of IFA uptake in pregnancy in India are still very low, particularly in the state of Uttar Pradesh. Timeline maps were developed as a visual qualitative tool to explore the nuances of health behaviors among pregnant women with respect to antenatal care (ANC) services, including IFA consumption.  Timeline maps were used to elicit and visually document critical events pertaining to ANC services chronologically, including details on contact points with the health system and events specific to IFA distribution, consumption and counselling. The tool consists of a horizontal straight line with nine suspended boxes corresponding to each month of pregnancy, with legends on how to illustrate IFA receipt and consumption. In this instance, the woman's last menstrual period and expected date of delivery were used as a frame of reference for the duration of pregnancy.  Six research assistants (RAs) were trained on how to use timeline maps to elicit and record participant narratives. The RAs later participated in a focus group discussion to gain insight about their experiences using the tool. The timeline maps were easy-to-use and facilitated in-depth conversations with participants. RAs were able to actively engage the participants in co-creating the maps. The visual nature of the tool prompted participants' recall of key pregnancy events and reflexivity. Challenges reported with the tool/process included recollection of past events and potential misrepresentation of information. These highlight a need to restructure training processes. Our findings indicate that timeline maps have the potential to be used in a variety of other program contexts, and merit further exploration.

Enhancing the capacity and effectiveness of community health volunteers to improve maternal, newborn and child health: Experience from Kenya.

OBJECTIVE: To determine whether a simple monitoring and tracking tool, Mwanzo Mwema Monitoring and Tracking Tool (MMATT), would enable community health volunteers (CHVs) in Kenya to 1) plan their workloads and activities, 2) identify the women, newborns and children most in need of accessing critical maternal, newborn and child health (MNCH) interventions and 3) improve key MNCH indicators. METHODS: A mixed methods approach was used. Household surveys at baseline (n = 912) and endline (n = 1143) collected data on key MNCH indicators in the four subcounties of Taita Taveta County, Kenya. Eight focus group discussions were held with 40 CHVs to ascertain their perspectives on using the tool. RESULTS: Qualitative findings revealed that the CHVs found the MMATT to be useful in planning their activities and prioritizing beneficiaries requiring more support to access MNCH services. They also identified potential barriers to care at both the community and health system levels. At endline, previously pregnant women were more likely to have received four or more antenatal care visits, facility delivery, postnatal care within two weeks of delivery and a complete package of care than baseline respondents. Among women with children under 24 months, those at endline were more likely to report early breastfeeding and exclusive breastfeeding for the first six months. These results remained after adjustment for age, subcounty, gravida, mother's education and asset index. CONCLUSION: Our results demonstrate that simple tools enable CHVs to identify disparities in service delivery and health outcomes, and to identify barriers to MNCH care. Tools that enhance CHVs' ability to plan and prioritize the women and children most in need increase CHVs' potential impact.

Dietary soy protein selectively reduces renal prostanoids and cyclooxygenases in polycystic kidney disease.

Increasing evidence in human chronic kidney disease and in animal models indicates the potential utility of dietary soy protein in the treatment of this disorder. A model in which a beneficial soy protein effect has been consistently demonstrated is the Han:SPRD-cy rat model of polycystic kidney disease. Therefore, since dietary soy protein alters renal hemodynamics and prostanoid production, the effects of dietary soy protein on renal prostanoids and related rate-limiting enzymes were examined. Normal and diseased weanling rats were given diets containing casein or soy protein for 7 wk. At 10 wk of age, renal levels of thromboxane B(2) (TXB(2), stable metabolite of TXA(2)), prostaglandin E(2) (PGE(2)) and 6-keto PGF(1alpha) (stable metabolite of PGI(2)) and activities of cyclooxygenase 1 (COX1) and COX2 were elevated in diseased compared to normal kidneys. Soy protein feeding resulted in 49% lower in vitro steady-state levels of TXB(2), and 76% less 6-keto PGF(1alpha) produced by COX1 activity in diseased kidneys, while not altering these parameters in normal kidneys. It also resulted in 47% less TXB(2) and 36% lower 6-keto PGF(1alpha) produced by COX2 activity in diseased kidneys. The relative effect of soy protein feeding on COX2 activity was in the order of TXB(2) > 6-keto PGF(1alpha) > PGE(2). Diseased kidneys had elevated protein and mRNA levels of cytosolic phospholipase A(2) (cPLA(2)) and COX1 and lower levels of COX2. Dietary soy protein attenuated the protein levels of cPLA(2) in diseased kidneys, and reduced COX2 mRNA expression in both normal and diseased kidneys. Dietary soy protein therefore reduced the levels of specific renal prostanoids, cPLA(2) and COX enzymes in this model of polycystic kidney disease, a model in which soy protein has been demonstrated to reduce disease progression.

Late dietary intervention limits benefits of soy protein or flax oil in experimental polycystic kidney disease.

BACKGROUND/AIMS: Dietary soy protein and flax oil retard kidney disease progression when initiated in the early stages of disease in several experimental models, including the Han:SPRD-cy rat. However, individuals with kidney disease often do not become aware of their condition until injury to the kidney is extensive. The objective of this study was to determine whether initiating these interventions in established disease would alter further progression of renal injury. METHODS: Two-month-old adult male Han:SPRD-cy rats were given either a flax oil diet (7% flax oil), a soy protein diet (20% soy protein) or a control diet (7% corn oil, 20% casein) for 4 months. Renal disease progression was assessed by examining morphological, immunohistochemical and biochemical parameters. RESULTS: Compared to controls, there was 21-24% less staining of proliferating cells, 21-24% less oxidative damage and 13-15% less renal inflammation in kidneys from rats given dietary soy protein and flax oil. Renal cystic growth and fibrosis and serum creatinine levels were not altered by these dietary treatments. CONCLUSIONS: Late intervention with dietary soy protein and flax oil reduces some disease-associated pathologies in established renal disease in Han:SPRD-cy rats. The potential benefits of the antioxidant and anti-inflammatory effects on ultimate renal disease outcome in the long term remains to be determined.

Selective COX-2 inhibition markedly slows disease progression and attenuates altered prostanoid production in Han:SPRD-cy rats with inherited kidney disease.

Selective cyclooxygenase-2 (COX-2) inhibitors appear to have beneficial renoprotective effects in most, but not all, renal disease conditions. The objective of our study was to examine the effects of COX-2 inhibition in a rat model of polycystic kidney disease. Four-week-old Han:SPRD-cy rats were given a standard rodent diet containing NS-398 (3 mg.kg body wt(-1).day(-1)) or a control diet without NS-398 for 7 wk. In diseased rats, selective COX-2 inhibition resulted in 18% and 67% reduction in cystic expansion and interstitial fibrosis, respectively, but no change in renal function. NS-398 also ameliorated disease-associated pathologies, such as renal inflammation, cell proliferation, and oxidant injury (by 33, 38, and 59%, respectively). Kidney disease was associated with elevated renal COX-1 and COX-2 enzyme activities, and NS-398 blunted the increase in COX-2 enzyme activity (as indicated by 21 and 28% lower renal thromboxane B2 and PGE2 levels, respectively). NS-398 reduced urinary excretion of prostanoid metabolites in diseased rats. In summary, COX-2 inhibition attenuated renal injury, reduced the elevated renal COX-2 activity, and ameliorated disease-related alterations in prostanoid production in this rat model of chronic renal disease.

COX-2 expression in cystic kidneys is dependent on dietary n-3 fatty acid composition.

Dietary n-3 fatty acids generally attenuate elevated cyclooxygenase-2 (COX-2) levels in disease states. However, models of renal cystic disease (RCD) exhibit reduced renal COX-2 expression. Therefore, the in vivo regulation of COX-2 expression by dietary n-3 fatty acids was examined. In archived tissues from dietary studies, COX-2 protein and gene expression was up-regulated in diseased pcy mouse and Han:SPRD-cy rat kidneys when given diets containing eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA), but not those containing alpha-linolenic acid (ALA), compared to control diets with linoleic acid (LA). The presence of disease was necessary to elicit these effects as COX-2 expression was unaltered by diet in normal kidneys. The effects were specific for COX-2, since COX-1 levels were unaltered by these dietary manipulations in either model. Thus, in RCD, diets containing EPA and DHA but not ALA appear to specifically up-regulate renal COX-2 gene and protein levels in vivo.

Dietary soya protein during pregnancy and lactation in rats with hereditary kidney disease attenuates disease progression in offspring.

Dietary soya protein substitution for casein initiated at weaning slows disease progression in animal models of chronic renal disease. As there is increasing evidence that fetal programming can have a significant impact on kidney physiology and function in offspring, the objective of the current study was to determine whether exposure to soya protein in the diet earlier than weaning would have further benefits. Han:SPRD-cy (cy/+) breeder rats were fed a casein-based or soya protein-based diet 2 weeks prior to mating, throughout pregnancy and during lactation. Following this maternal period, 3-week-old pups were given either the same or the alternate diet for a 7-week weaning period. Dietary soya protein compared with casein in the maternal or weaning period both independently resulted in less renal inflammation (macrophage infiltration lower by 24% (P=0.0003) and 32% (P<0.001), respectively). When soya protein was given in both feeding periods, the effect was additive. Soya protein substitution for casein resulted in less oxidative damages as indicated by 28% lower oxidized-LDL staining (P=0.013) when present in the maternal period, or in the weaning period (by 56%, P<0.0001). Renal cell proliferation was reduced by 29-33% (P<0.05) in rats given soya protein whether the exposure was during the maternal or weaning period. Soya protein compared with casein in the maternal period also resulted in 33% (P=0.0013) less proteinuria, indicating superior renal function. Dietary soya protein during pregnancy and lactation represents a potential preventative approach in treating for those with congenital kidney diseases.

Dietary flax oil during pregnancy and lactation retards disease progression in rat offspring with inherited kidney disease.

Dietary flax oil (FO) retards disease progression in growing or adult animal models of kidney disease. To determine whether dietary flax oil during the perinatal period would alter renal disease progression in offspring, Han-SPRD-cy rats with inherited cystic kidney disease were given diets with either 7% FO or corn oil (CO), throughout pregnancy and lactation. At 3 wk of age, offspring were then given either the same or the alternate diet for 7 wk. Rats given FO during the maternal period had 15% less renal cyst growth compared with rats given FO only in the postweaning period. Dietary FO, compared with CO, in the maternal period also resulted in 12% lower cell proliferation and 15% less oxidant injury in diseased kidneys of offspring. Including FO in both the maternal and postweaning period resulted in 29-34% less renal interstitial fibrosis and 22-23% lower glomerular hypertrophy. Along with improved histology, these rats exhibited 13% less proteinuria and 30% lower creatinine clearance when dietary FO was given in the maternal period. The potential for dietary FO during pregnancy and lactation to positively modulate adult renal disease has significant implications for the 1 in 1000 individuals with congenital cystic kidney disease.

Selectivity of cyclooxygenase isoform activity and prostanoid production in normal and diseased Han:SPRD-cy rat kidneys.

Renal prostanoids are important regulators of normal renal function and maintenance of renal homeostasis. In diseased kidneys, renal cylooxygenase (COX) expression and prostanoid formation are altered. With the use of the Han:Sprague-Dawley-cy rat, the aim of this study was to determine the relative contribution of renal COX isoforms (protein, gene expression, and activity) on renal prostanoid production [thromboxane B(2) (TXB(2), stable metabolite of TXA(2)), prostaglandin E(2) (PGE(2)), and 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha), stable metabolite of PGI(2))] in normal and diseased kidneys. In diseased kidneys, COX-1-immunoreactive protein and mRNA levels were higher and COX-2 levels were lower compared with normal kidneys. In contrast, COX activities were higher in diseased compared with normal kidneys for both COX-1 [0.05 +/- 0.02 vs. 0.45 +/- 0.11 ng prostanoids x min(-1) x mg protein(-1) (P < 0.001)] and COX-2 [0.64 +/- 0.10 vs. 2.32 +/- 0.22 ng prostanoids x min(-1).mg protein(-1) (P < 0.001)]. As the relative difference in activity was greater for COX-1, the ratio of COX-1/COX-2 was higher in diseased compared with normal kidneys, although the predominant activity was still due to the COX-2 isoform in both genotypes. Endogenous and steady-state in vitro levels of prostanoids were approximately 2-10 times higher in diseased compared with normal kidneys. The differences between normal and diseased kidney prostanoids were in the order of TXB(2) > 6-keto-PGF(1alpha) > PGE(2), as determined by higher renal prostanoid levels and COX activity ratios of TXB(2)/6-keto-PGF(1alpha), TXB(2)/PGE(2), and 6-keto-PGF(1alpha)/PGE(2). This specificity in both the COX isoform type and for the prostanoids produced has implications for normal and diseased kidneys in treatments involving selective inhibition of COX isoforms.

Modulation of renal injury in pcy mice by dietary fat containing n-3 fatty acids depends on the level and type of fat.

Low-fat diets and diets containing n-3 fatty acids (FA) slow the progression of renal injury in the male Han:Sprague-Dawley (SPRD)-cy rat model of polycystic kidney disease. To determine whether these dietary fat effects are similar in females and in another model of renal cystic disease, in this study we used both male and female pcy mice to examine the effects of fat level and type on disease progression. Adult pcy mice were fed 4, 10, or 20 g soybean oil/100 g diet for 130 d in study 1. In study 2, weanling pcy mice were fed high or low levels of fat rich in 18:2n-6 (corn oil, CO), 18:3n-3 (flaxseed oil/CO 4:1 g/g, FO), or 22:6n-3 (algal oil/CO 4:1 g/g, DO) for 8 wk. In adult pcy mice, low- compared with high-fat diets lowered kidney weights (2.4 +/- 0.2 vs. 3.1 +/- 0.2 g/100 g body weight, P = 0.006) and serum urea nitrogen (SUN) (9.6 +/- 0.6 vs. 11.9 +/- 0.6 mmol/L, P = 0.009), whereas in young pcy mice it reduced renal fibrosis volumes (0.44 +/- 0.04 vs. 0.62 +/- 0.04 mL/kg body weight, P < 0.0001). FO feeding in young pcy mice mitigated the detrimental effects of high fat on fibrosis while not altering kidney size, function, and oxidative damage when compared with the CO-fed mice. In contrast, DO- compared with CO-fed mice had higher kidney weights (2.64 +/- 0.07 vs. 2.24 +/- 0.08 g/100 g body weight, P = 0.005), SUN (9.4 +/- 0.57 vs. 7.0 +/- 0.62 mmol/L, P < 0.0001), and cyst volumes (7.9 +/- 0.28 vs. 6.2 +/- 0.30 mL/kg body weight, P < 0.0001) and similar levels of oxidative damage and fibrosis. The FA compositions of the diets were reflected in the kidneys: 18:2n-6, 18:3n-3, and 22:6n-3 were the highest in the CO, FO, and DO diets, respectively. Dietary effects on kidney disease progression were similar in males and females. A low-fat diet slows progression of renal injury in male and female pcy mice, consistent with findings in the male Han:SPRD-cy rat. Dietary fat type also influenced renal injury, with flaxseed oil diets rich in 18:3n-3 slowing early fibrosis progression compared with diets rich in 18:2n-6 or in 22:6n-3.