RESULTS: The decline in breastfeeding in the Philippines in the mid-twentieth Century associated with intensive BMS marketing via health systems and consumer advertising. As regulations tightened, the industry more aggressively promoted CMFs for older infants and young children, thereby 'marketing around' the Milk Code. It established front groups to implement political strategies intended to weaken the country's breastfeeding policy framework while also fostering a favourable image. This included lobbying government officials and international organizations, emphasising its economic importance and threats to foreign investment and trade, direct litigation against the government, messaging that framed marketing in terms of women's choice and empowerment, and forging partnerships. A resurgence in breastfeeding from the mid-1980s onwards reflected strengthening political commitment for a national breastfeeding policy framework and Milk Code, resulting in-turn, from collective actions by breastfeeding coalitions, advocates and mothers.
CONCLUSION: The Philippines illustrates the continuing battle for worldwide Code implementation, and in particular, how the baby food industry uses and adapts its market and political practices to promote and sustain CMF markets. Our results demonstrate that this industry's political practices require much greater scrutiny. Furthermore, that mobilizing breastfeeding coalitions, advocacy groups and mothers is crucial to continually strengthen and protect national breastfeeding policy frameworks and Code implementation.
METHODS: We performed a randomized, double-blind, placebo-controlled trial of consecutive adults with biopsy-proven NASH and a NAFLD activity score (NAS) of 4 or more at a tertiary care hospital in Kuala Lumpur, Malaysia, from November 2012 through August 2014. Patients were randomly assigned to groups given silymarin (700 mg; n = 49 patients) or placebo (n = 50 patients) 3 times daily for 48 weeks. After this 48-week period, liver biopsies were repeated. The primary efficacy outcome was a decrease of 30% or more in NAS; findings from 48-week liver biopsies were compared with those from the baseline biopsy. Secondary outcomes included changes in steatosis, lobular inflammation, hepatocyte ballooning, NAS and fibrosis score, and anthropometric measurements, as well as glycemic, lipid, and liver profiles and liver stiffness measurements.
RESULTS: The percentage of patients achieving the primary efficacy outcome did not differ significantly between the groups (32.7% in the silymarin group vs 26.0% in the placebo group; P = .467). A significantly higher proportion of patients in the silymarin group had reductions in fibrosis based on histology (reductions of 1 point or more; 22.4%) than did the placebo group (6.0%; P = .023), and based on liver stiffness measurements (decrease of 30% or more; 24.2%) than did the placebo group (2.3%; P = .002). The silymarin group also had significant reductions in mean aspartate aminotransferase to platelet ratio index (reduction of 0.14, P = .011 compared with baseline), fibrosis-4 score (reduction of 0.20, P = .041 compared with baseline), and NAFLD fibrosis score (reduction of 0.30, P < .001 compared with baseline); these changes were not observed in the placebo group (reduction of 0.07, P = .154; increase of 0.18, P = .389; and reduction of 0.05, P = .845, respectively). There was no significant difference between groups in number of adverse events; adverse events that occurred were not attributed to silymarin.
CONCLUSIONS: In a randomized trial of 99 patients, we found that silymarin (700 mg, given 3 times daily for 48 weeks) did not reduce NAS scores by 30% or more in a significantly larger proportion of patients with NASH than placebo. Silymarin may reduce liver fibrosis but this remains to be confirmed in a larger trial. It appears to be safe and well tolerated. ClinicalTrials.gov: NCT02006498.