Towards a regulation of food advertising?

For 20 years the UK Government has recognised that food advertising plays a part in food choices and hence diets of the population, particularly for children. In 2007 the UK brought in regulations to stop the advertising of less healthy foods on television (TV) during child-specific programming. Less healthy foods were defined using the 2004/2005 nutrient profiling model (NPM) as products high in saturated fat, salt and sugar (HFSS). Evaluations showed that children were still seeing and being affected by the adverts for less healthy foods. To try to mitigate childhood obesity, in 2018, the UK Government announced its intention to consult on further restrictions on the advertising of HFSS products on TV and online. Two years later, the intention to implement a 9pm advertising ban on TV and a further consultation on restricting online advertising of HFSS products was announced. New legislative controls on the advertising of HFSS foods are expected to be brought into legislation in the UK in January 2024. In the present paper, the history of advertising restrictions in the UK and the evidence informing them is reviewed. There will also be a reflection on where further actions might be needed in due course.

Five years of national policies: progress towards tackling obesity in England.

Obesity is a major burden on the health system in England and the rest of the UK. Obesity prevalence is high in adults and children and most of the UK population are consuming more energy than required, and not meeting other dietary recommendations, including those for saturated fat, free sugars, fibre, oily fish and fruit and vegetables. Over the past 5 years, a number of cross-government policies, both promoting voluntary action and legislative, have been put in place to tackle diet-related health and obesity. The food environment is complex with many influencing factors, some of which act through individual automatic choices. Other factors such as accessibility, advertising, promotion and nudging drive increased food and drink purchases. With continual changes in the food environment favouring fast-food outlets and meal delivery companies alongside the adverse impact of the COVID-19 pandemic on diets and physical activity levels, further governmental action is likely needed to deliver sustained improvements to diet and health.

Effects of ciglitazone on energy balance, thermogenesis and brown fat activity in the rat.

Young male rats were treated with vehicle or ciglitazone (150 mg/kg/day, intragastric) for 8 or 14 days. Drug treatment did not affect food intake but reduced body weight and energy gains over 14 days, and significantly depressed energetic efficiency. Energy expenditure and resting oxygen consumption (VO2), when corrected for body size, were elevated in ciglitazone-treated rats, but the difference in VO2 was abolished by treatment of the animals with a beta-adrenergic antagonist (propranolol). The acute thermic response (postprandial rise in VO2) to a fat meal was similar for both groups, but the response to carbohydrate ingestion was greater in ciglitazone-treated rats (18%) than controls (11.5%). The mass of interscapular brown adipose tissue was not affected by drug treatment, but its protein content was increased and its thermogenic activity (mitochondrial purine nucleotide binding) was elevated by 25% after chronic treatment with ciglitazone. These results indicate that ciglitazone enhances thermogenesis via sympathetic activation of brown adipose tissue, probably as a result of improved insulin sensitivity.

The effect of islet amyloid polypeptide (amylin) and calcitonin gene-related peptide on glucose removal in the anaesthetized rat and on insulin secretion from rat pancreatic islets in vitro.

The effect of intravenous infusion of islet amyloid polypeptide (IAPP/amylin) and calcitonin gene-related peptide (CGRP) on blood glucose and plasma insulin in the basal and glucose-stimulated state was investigated in the anaesthetized rat. Both peptides had no effect on basal blood glucose or plasma insulin but following an intravenous bolus of glucose, CGRP-treated rats were hyperglycaemic and hyperinsulinaemic compared with control animals which were similar to IAPP-treated rats. IAPP had no effect on glucose-stimulated islet insulin secretion. These results suggest that CGRP, but not IAPP, alters glucose removal in vivo.

Extending breastfeeding duration through primary care: a systematic review of prenatal and postnatal interventions.

This literature review provides an overview of the effectiveness of strategies and procedures used to extend breastfeeding duration. Interventions carried out during pregnancy and/or infant care conducted in primary health care services, community settings, or hospital clinics were included. Interventions covering only the delivery period were excluded. Interventions that were most effective in extending the duration of breastfeeding generally combined information, guidance, and support and were long term and intensive. During prenatal care, group education was the only effective strategy reported. Home visits used to identify mothers' concerns with breastfeeding, assist with problem solving, and involve family members in breastfeeding support were effective during the postnatal period or both periods. Individual education sessions were also effective in these periods, as was the combination of 2 or 3 of these strategies in interventions involving both periods. Strategies that had no effect were characterized by no face-to-face interaction, practices contradicting messages, or small-scale interventions.

The effects of maternal and infant vitamin A supplementation on vitamin A status: a randomised trial in Kenya.

Postpartum vitamin A supplementation of mothers and infants is recommended, but the efficacy has been questioned. In this double-blind, placebo-controlled trial, Kenyan mother-infant pairs were randomised to maternal vitamin A (400,000 IU) or placebo <24 h postpartum, and infant vitamin A (100,000 IU) or placebo at 14 weeks. Milk retinol was determined at weeks 4, 14 and 26, and maternal and infant serum retinol at weeks 14 and 26. Infant retinol stores were assessed at week 26, using a modified relative dose response (MRDR) test. Among 564 women, serum retinol at 36 weeks gestation was 0.81 (SD 0.21) micromol/l, and 33.3% were<0.7 micromol/l. Maternal serum retinol was not different between groups, but milk retinol was higher in the vitamin A group: (0.67 v. 0.60 micromol/l; 0.52 v. 0.44 micromol/l; 0.50 v. 0.44 micromol/l at 4, 14 and 26 weeks, respectively). When expressed per gram fat, milk retinol was higher in the vitamin A group only at 4 weeks. Infant serum retinol was not different between groups. However, although most infants had deficient vitamin A stores (MRDR>0.06%) at 26 weeks, vitamin A to infants, but not mothers, resulted in a lower proportion of infants with deficient vitamin A stores (69 v. 78 %). High-dose postpartum vitamin A supplementation failed to increase serum retinol and infant stores, despite modest effects on milk retinol. Infant supplementation, however, increased stores. There is a need for a better understanding of factors affecting absorption and metabolism of vitamin A.

Thermogenic effects of dihydrocodeine in the rat.

The object of this study was to assess the effects of dihydrocodeine on thermogenesis and brown adipose tissue activity in the rat from measurements of oxygen consumption and blood flow. Acute injection of dihydrocodeine tartrate (s.c.) stimulated resting oxygen consumption (VO2) in Sprague-Dawley rats in a dose-dependent manner (0.5-50 mg/kg), with a peak response (40-45% increase) occurring at 10-25 mg/kg. This effect was also observed in urethane-anaesthetized rats (although the effect was reduced) and in conscious animals following gastric intubation with the drug. Pretreatment of rats with either a beta-adrenergic antagonist (propranolol, 20 mg/kg), ACTH (4 g/kg), or an opiate antagonist (WIN44441-1, 2 mg/kg) significantly reduced the response to dihydrocodeine, whereas corticosterone injection (5 mg/kg) enhanced the effect. Surgical adrenalectomy or hypophysectomy (HYPX) almost completely abolished the thermogenic effect of dihydrocodeine. Dihydrocodeine also stimulated VO2 in lean (58% increase) and genetically obese Zucker rats (69% increase), and in both Zucker genotypes these responses were only slightly affected by HYPX, but enhanced in HYPX rats treated daily with corticosterone (1 mg/kg). Tissue blood flow, assessed from the distribution of radiolabelled microspheres, was unaffected in white adipose tissue, skeletal muscle, testes, kidney, brain, and liver (arterial supply) after a single injection of dihydrocodeine (25 mg/kg), but flow to interscapular and perirenal brown adipose tissue was increased by 9- to 10-fold. Surgical sympathectomy of brown adipose tissue prevented the increase in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence that use of Triton WR1339 underestimates the triacylglycerol entry rate into the plasma of lactating rats owing to continued accumulation of lipid in the mammary gland.

Measurement of the entry rate of an intragastric load of [14C]triolein into the plasma in the presence of Triton WR1339 gave similar values for virgin and weaned rats, but significantly lower values for lactating rats. This decreased entry rate (65%) in lactating compared with virgin rats was due to a failure of Triton WR1339 to inhibit the accumulation of [14C]lipid in the mammary gland. This is further evidence that mammary-gland lipoprotein lipase behaves differently from that in white adipose tissue or muscle.

Reciprocal changes in amino acid metabolism in mammary gland and liver of the lactating rat on starvation and refeeding as indicated by the tissue accumulation of alpha-amino[1-14C]isobutyrate.

Measurements of the tissue accumulation in vivo and in vitro by hepatocytes and mammary-gland acini of alpha-amino[1-14C]isobutyrate ([1-14C]AIB) were compared in virgin and lactating rats. The results indicate the existence of a reciprocal relationship between mammary gland and liver for AIB accumulation that is dependent on the lactational and the nutritional state of the rat. This suggests that amino acids are preferentially directed to the mammary gland during active lactation.

Polymyxin B diminishes blood flow to brown adipose tissue and lactating mammary gland in the rat. Possible mechanism of its action to decrease the stimulation of lipogenesis on refeeding.

Polymyxin B, a cyclic decapeptide antibiotic, increased blood glucose and lactate, and inhibited the stimulation of lipogenesis in interscapular brown adipose tissue and lactating mammary gland of starved-refed virgin and lactating rats respectively. Lipogenesis was not inhibited in white adipose tissue or liver. The antibiotic increased the haematocrit. The relative blood flow to brown adipose tissue and lactating mammary gland was decreased by polymyxin B, and this was accompanied by a decrease in tissue ATP content. In vitro polymyxin B did not affect glucose utilization or conversion into lipid, nor the stimulation by insulin of these processes in brown-adipose-tissue slices. Treatment of rats in vivo with polymyxin B resulted in decreased utilization of glucose in vitro in brown-adipose-tissue slices. Similarly, acini from mammary glands of polymyxin B-treated lactating rats had decreased rates of conversion of [1-14C]glucose to lipid. It is concluded that the effects of polymyxin B may be brought about by decreases in tissue blood flow. The possibility that these effects are secondary to inhibition of glucose utilization cannot be ruled out.