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Labor markets and economic development in Malaysia

Smith JP

Res Popul Econ, 1991;7:131-56.
PMID: 12317026
Climate Change and Infant Nutrition: Estimates of Greenhouse Gas Emissions From Milk Formula Sold in Selected Asia Pacific Countries

Dadhich JP, Smith JP, Iellamo A, Suleiman A

J Hum Lact, 2021 May;37(2):314-322.
PMID: 33586512 DOI: 10.1177/0890334421994769

BACKGROUND: There is growing recognition that current food systems and policies are environmentally unsustainable. There is an identified need to integrate sustainability objectives into national food policy and dietary recommendations.
RESEARCH AIMS: To (1) describe exploratory estimates of greenhouse gas emission factors for all infant and young child milk formula products and (2) estimate national greenhouse gas emission association with commercial milk formulas sold in selected countries in the Asia Pacific region.
METHOD: We used a secondary data analysis descriptive design incorporating a Life Cycle Assessment (LCA) concepts and methodology to estimate kg CO2 eq. emissions per kg of milk formula, using greenhouse gas emission factors for milk powder, vegetable oils, and sugars identified from a literature review. Proportions of ingredients were calculated using FAO Codex Alimentarius guidance on milk formula products. Estimates were calculated for production and processing of individual ingredients from cradle to factory gate. Annual retail sales data for 2012-2017 was sourced from Euromonitor International for six purposively selected countries; Australia, South Korea, China, Malaysia, India, Philippines.
RESULTS: Annual emissions for milk formula products ranged from 3.95-4.04 kg CO2 eq. Milk formula sold in the six countries in 2012 contributed 2,893,030 tons CO2 eq. to global greenhouse gas emissions. Aggregate emissions were highest for products (e.g., toddler formula), which dominated sales growth. Projected 2017 emissions for milk formula retailed in China alone were 4,219,052 tons CO2 eq.
CONCLUSIONS: Policies, programs and investments to shift infant and young child diets towards less manufactured milk formula and more breastfeeding are "Triple Duty Actions" that help improve dietary quality and population health and improve the sustainability of the global food system.
ABM Position Statement: Paid Maternity Leave-Importance to Society, Breastfeeding, and Sustainable Development

Bettinelli ME, Smith JP, Haider R, Sulaiman Z, Stehel E, Young M, et al.

Breastfeed Med, 2024 Mar;19(3):141-151.
PMID: 38489526 DOI: 10.1089/bfm.2024.29266.meb

Background: Paid maternity leave benefits all of society, reducing infant mortality and providing economic gains. It is endorsed by international treaties. Paid maternity leave is important for breastfeeding, bonding, and recovery from childbirth. Not all mothers have access to adequate paid maternity leave. Key Information: Paid leave helps meet several of the 17 United Nations' Sustainable Development Goals (2, 3, 4, 5, 8, and 10), including fostering economic growth. A family's expenses will rise with the arrival of an infant. Paid leave is often granted with partial pay. Many low-wage workers earn barely enough to meet their needs and are unable to take advantage of paid leave. Undocumented immigrants and self-employed persons, including those engaging in informal work, are often omitted from maternity leave programs. Recommendations: Six months of paid leave at 100% pay, or cash equivalent, should be available to mothers regardless of income, employment, or immigration status. At the very minimum, 18 weeks of fully paid leave should be granted. Partial pay for low-wage workers is insufficient. Leave and work arrangements should be flexible whenever possible. Longer flexible leave for parents of sick and preterm infants is essential. Providing adequate paid leave for partners has multiple benefits. Increasing minimum wages can help more families utilize paid leave. Cash benefits per birth can help informal workers and undocumented mothers afford to take leave. Equitable paid maternity leave must be primarily provided by governments and cannot be accomplished by employers alone.
Fulltext The political economy of infant and young child feeding: confronting corporate power, overcoming structural barriers, and accelerating progress

Baker P, Smith JP, Garde A, Grummer-Strawn LM, Wood B, Sen G, et al.

Lancet, 2023 Feb 11;401(10375):503-524.
PMID: 36764315 DOI: 10.1016/S0140-6736(22)01933-X

Despite increasing evidence about the value and importance of breastfeeding, less than half of the world's infants and young children (aged 0-36 months) are breastfed as recommended. This Series paper examines the social, political, and economic reasons for this problem. First, this paper highlights the power of the commercial milk formula (CMF) industry to commodify the feeding of infants and young children; influence policy at both national and international levels in ways that grow and sustain CMF markets; and externalise the social, environmental, and economic costs of CMF. Second, this paper examines how breastfeeding is undermined by economic policies and systems that ignore the value of care work by women, including breastfeeding, and by the inadequacy of maternity rights protection across the world, especially for poorer women. Third, this paper presents three reasons why health systems often do not provide adequate breastfeeding protection, promotion, and support. These reasons are the gendered and biomedical power systems that deny women-centred and culturally appropriate care; the economic and ideological factors that accept, and even encourage, commercial influence and conflicts of interest; and the fiscal and economic policies that leave governments with insufficient funds to adequately protect, promote, and support breastfeeding. We outline six sets of wide-ranging social, political, and economic reforms required to overcome these deeply embedded commercial and structural barriers to breastfeeding.
Fulltext Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer

Klein AP, Wolpin BM, Risch HA, Stolzenberg-Solomon RZ, Mocci E, Zhang M, et al.

Nat Commun, 2018 02 08;9(1):556.
PMID: 29422604 DOI: 10.1038/s41467-018-02942-5

In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10-8). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10-14), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10-10), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10-8), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10-8). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene.
Fulltext A Transcriptome-Wide Association Study Identifies Novel Candidate Susceptibility Genes for Pancreatic Cancer

Zhong J, Jermusyk A, Wu L, Hoskins JW, Collins I, Mocci E, et al.

J Natl Cancer Inst, 2020 Oct 01;112(10):1003-1012.
PMID: 31917448 DOI: 10.1093/jnci/djz246

BACKGROUND: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown.
METHODS: To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples).
RESULTS: We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate < .05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22: RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction.
CONCLUSIONS: By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.