20 minute read
Meet the charity
environments without placing the emphasis on individuals to change their behaviours. Within the confines of central government, the difficulty is understandable, as actions seen as removing choice gain criticism as promoting the ‘nanny state’ (removal of individual liberty and market freedoms), yet those relying on individuals to adjust lifestyles are seen as unrealistic and unfair. So how does Westminster win?
We know obesity is a structural issue – which is clearly exacerbated with widening of health inequalities – and hence the evidence base suggests the solutions should also be structural. Despite this, the largest proportion of strategies were found to put the onus on individual agency (43%). Secondly, despite the majority of strategies acknowledging that health inequalities need to be addressed, only 19% of these were set up to reduce these very inequalities from the beginning.
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POSITIVE POLICYMAKING GOING FORWARD The analysis that formed the basis for this article gives good insight into what it is reasonable to expect future government policies on obesity should include. Already, since 2018, evidencebased effective steps are being taken to improve the food environment for consumers. The SDIL (Sugary Drinks Industry Levy) is a successful example of this. An evaluation of SDIL, published in February 2020, found that the percentage of drinks with sugar over 5g per 100ml fell from an expected level of 49% to 15% over the 2015-2019 time period.8
The most recent strategy, published in July 2020, although reiterative of the previous two manifestations of strategy, provides a measurable goal with clear target audiences. It also includes a greater proportion of structural interventions than we have seen previously: the restriction of junk food advertising, removal of buy-one-get-one-free offers on high fat, sugar and salt (HFSS) products, and more.
Going forward with the 2020 Tackling Obesity strategy, in order to achieve positive outcomes, this Government must avoid repeating the mistakes of the past.
MEET THE CHARITY
Alexandra Rose Charity’s mission is to give families on low incomes access to fresh fruit and vegetables in their local communities, through their Rose Vouchers for Fruit & Veg Project.
Many of the families supported by the project struggle to provide healthy and nutritious meals for their children. One mum from Southwark shares how: “Before I had the Rose Vouchers, I didn’t have enough fruit and veg for everyone in my family. Now I do.”
Families with children under the age of five receive £3 worth of Rose Vouchers per child, (or £6 if the child is under one year of age). Vouchers can be redeemed at local markets and independent greengrocers. This means that the project also supports markets, maintaining their position as sources of healthy low-cost food, and providing the community with vital access to fruit and veg.
For more information about Alexandra Rose Charity please visit www.alexandrarose.org.uk
RENAL DISEASE AND NUTRITION
This article examines dietary approaches to the prevention and management of chronic kidney disease (CKD).
CKD is a progressive long-term condition, which describes abnormal kidney function and/or structure present for three months or more. It is classified in five stages relating to the severity of the disease, with stage 5 being classed as end stage renal disease (ESRD). CKD can progress to ESRD in a small but significant number of people. For these individuals, regular dialysis or transplantation is required to sustain life.1
Uncontrolled diabetes and hypertension remain two of the greatest risk factors for the development of CKD. The prevalence of CKD has also been found to increase with age, obesity, cardiovascular risk and in some ethnic minority groups.2 For those individuals who do progress to ESRD and start dialysis, mortality rates are significantly high at around 50-73% for those >65 years of age.3 With the growing incidence of CKD in the UK and around the world, there is now an increasing focus on the early identification and prevention of CKD. When CKD is detected early, its progression and complications can be delayed or prevented with the implementation of appropriate interventions. International guidelines now recommend that individuals are identified early to address cardiovascular risk and other risk factors, aiming to slow progression of CKD and reduce the number of patients reaching ESRD.4
DISEASE CONSEQUENCES The kidneys have a key role in maintaining homeostasis. They also have other important functions, including maintenance of fluid and electrolyte balance, removal of waste products, regulation of acid-base balance, hormone production and activation of vitamin D. There are two main consequences of CKD: the loss of kidney function resulting in complications and kidney failure, and the development of cardiovascular disease (CVD). Individuals with CKD are more likely to die from CVD than they are from progression to ESRD.5
NUTRITIONAL AIMS In the earlier stages of CKD, nutritional management aims to reduce the progression of CKD and to reduce the risk of cardiovascular events. There is evidence that good glycaemic control in diabetes, weight reduction in those with obesity and nutrition support in those with protein energy wasting (PEW) can improve patient outcomes.5 Healthy lifestyle advice should be offered to help control blood pressure, achieve good glycaemic control, achieve blood lipids within acceptable ranges and to achieve a healthy weight.4
Most individuals will be asymptomatic in the earlier stages of CKD. Complications such as fluid or electrolyte imbalances, metabolic acidosis and uraemia are more common from stage 4 onwards as residual renal function declines. Therefore, most individuals with CKD stages 1-3 will not be required to limit their fluid, potassium or phosphate intake.
CVD RISK REDUCTION Given that hypertension is one of the greatest risk factors for CKD, it is understandable that lowering blood
Danielle Nott RD
Danielle currently works for Airedale NHS Trust and Leeds Teaching Hospitals NHS Trust as a Specialist Diabetes and Cystic Fibrosis Dietitian. Prior to this, she specialised in Renal for a number of years, gaining a variety of experience with all stages of CKD and posttransplantation.
REFERENCES Please visit: nhdmag.com/ references.html
pressure will have favourable outcomes on CKD progression and cardiovascular outcomes. Individuals are advised to limit their salt intake to <5g/day.4 The majority of salt consumed comes from processed foods, therefore education may be needed on interpreting food labels. Salt substitutes are not recommended as they contain potassium additives that can increase the risk of hyperkalemia.
Evidence relating to weight loss interventions in CKD have been found to reduce blood pressure, proteinuria and rate of renal function decline.6 Other benefits associated with weight loss include improved insulin resistance, diabetes, dyslipidaemia and left ventricular hypertrophy.7 It is recommended that individuals with a BMI of >30kg/m2 should receive advice to help them lose weight.8 Weight reduction advice may also be given to help improve glycaemic control in individuals with or at risk of diabetes. A target HbA1c of 53mmol/mol is suggested to prevent or delay progression of the microvascular complications of diabetes.4
PROTEIN INTAKE Approximately 250g of protein is catabolised by the body on a daily basis. The breakdown of protein leads to the development of urea and other compounds, which, in a healthy functioning individual, would normally be cleared by the kidney and excreted in the urine. However, in CKD these by-products can accumulate in the blood and can lead to uraemic symptoms.9 High- protein diets have also been found to increase hyperfiltration, worsen proteinuria and increase the rate of decline in kidney function.10
There is insufficient evidence to support the use of low-protein diets in CKD stages 1-3; however, high-protein intakes (>1.3g/kg/day) are not recommended in those with CKD at risk of progression. Previous guidelines have suggested intakes of 0.8-1.0g/kg in stages 4-5 to be acceptable.4 However, more recent guidelines have suggested lower protein diets in stages 3-5 may offer benefits, such as postponing the need for dialysis and improving quality of life through the reduction of uraemic toxins. These guidelines have suggested 0.55-0.60g/kg body weight per day may be considered for individuals without diabetes who are metabolically stable.9
There are some safety concerns associated with lower protein diets. Previously, NICE has advised against low-protein diets (<0.6-0.8g/ kg/day) in CKD, partly due to the risk of PEW.1 PEW is a major problem in the later stages of CKD. Its onset and severity is related to the glomerular filtration rate (GFR), becoming more common with GFR <60ml/min and affecting 2040% of patients with stages 4-5 CKD.11 Energy
metabolism may also be impaired in CKD, therefore adequate energy is essential to reduce the risk of PEW. This becomes more important with lower protein intakes in order to promote protein sparing. However, it has been suggested that nitrogen balance and nutritional status can be maintained with energy intake in the range of 30-35kcal/kg with appropriate surveillance and nutrition education.9 Lower protein diets may not be suitable for all individuals, such as those at significant risk of malnutrition. Similarly, energy requirements are influenced by a multitude of factors and may vary depending on treatment goals. Therefore, dietary advice should always be individualised as there is no ‘one-size-fits-all’ approach.
There is currently limited evidence in relation to the type of protein that is consumed. However, there is increasing interest in the use of plant-based diets in CKD. Plant proteins are less likely to result in hyperphosphataemia, as this type of phosphate is less bioavailable than in animal sources.
DIETARY PATTERNS Historically, nutritional intervention has focused on individual nutrients such as potassium, phosphate and sodium. However, evidence suggests that certain dietary patterns, such as those with a focus on the quality and diversity of the diet, with liberal consumption of plant foods, may be relevant for the prevention and management of CKD. As there is no widely accepted definition of the term ‘plant-based’, there are no guidelines to suggest the minimum amount of meat a diet requires in order to qualify as plant-based. However, in individuals with CKD, a diet with a higher proportion of plant sources (emphasising fruit, vegetables, nuts, seeds, oils, wholegrains, legumes and beans) has been associated with improved outcomes, including reduced mortality and delayed progression of CKD.12
There may also be additional benefits in preventing and managing some of the metabolic complications of CKD. Proposed benefits of this diet include the increased fibre content, which can shift the gut microbiota towards increased production of anti-inflammatory compounds and reduced production of uraemic toxins.13 As previously discussed, this may help to improve quality of life and delay the need for renal replacement therapy. Higher fibre diets may also increase stool volume and decrease transit time which can increase faecal potassium excretion.14
Metabolic acidosis is a common complication of advanced CKD and is associated with an increased risk of muscle wasting, progression of renal failure and mortality.15 The reduced net endogenous acid production of plant-based diets
may have favourable outcomes on acid-base balance. One recent RCT in patients with CKD not on dialysis found that increasing alkali-rich plant foods resulted in improved metabolic acidosis and reduced decline in kidney function when compared with oral bicarbonate supplementation. Those following the plant-based diet were also found to have lower blood pressure, improved lipid profile and better body weight control than those receiving the bicarbonate supplementation or usual care.16
There is the concern that following a plantbased diet may lead to higher incidences of hyperkalemia due to the increase in potassiumrich foods such as fruit, vegetables, nuts and seeds. However, electrolyte disturbances are more common in the later stages of CKD as kidney function declines. Compensatory mechanisms are said to maintain potassium homeostasis until the very late stages of CKD.13 In addition, nondietary factors, such as uncontrolled diabetes, metabolic acidosis and constipation, can have a significant impact on potassium levels. Where possible, these should be addressed before considering dietary modification.
Only a well-balanced plant-based diet is likely to offer the above benefits. Not all plantbased diets are of high quality, as some may contain lower intakes of fruit and vegetables and higher intakes of processed foods. Therefore, this approach may not be suitable for all individuals and may require extensive dietary education and support. As with all successful dietary interventions, advice should be patient-centred allowing flexibility and considering, for example, the patient’s ability to implement changes, their cooking skills, finances and access to food.
CONCLUSION Nutrition plays a key role in the prevention and management of CKD. In order to prevent and delay progression to ESRD as well as risk of CVD, dietary advice should focus on salt reduction, achieving good glycaemic control in those with diabetes, reduction of blood lipids to optimal levels and weight reduction to achieve a healthy BMI.
Optimal protein intake is debated, but high- protein intakes are not advised in those with CKD at risk of progression. Lower protein intakes may have a place in delaying the need for dialysis and reducing production of uraemic toxins, though close monitoring and dietary counselling would be needed to ensure nutritional adequacy and to reduce the risk of PEW.
Re-emerging evidence supports the use of plant-based diets in delaying progression of CKD and its metabolic complications. Caution should be taken in those with advanced CKD stages 4-5, as the evidence for their safety is not yet well established. However, in the earlier stages of CKD, well-balanced plant-based diets may be beneficial, as they have been associated with lower cholesterol levels, blood pressure levels, rates of Type 2 diabetes and BMI, all of which are key recommendations in the prevention and management of CKD.
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Iron deficiency is the most common nutritional disorder in the world, affecting around 42% of children under five globally.1,2 In the UK alone, research has found that up to 60% of infants aged 6-12 months have inadequate dietary iron intake.1
Infant iron deficiency anaemia (IDA) in the developed world is a serious issue. This is particularly concerning when we consider that infants are easily accessible to primary care services and IDA is a preventable condition.3 Research spanning the last 20 years does not show a reduction in the prevalence of IDA, despite advances in healthcare provision.1,4
Early screening and nutrition education are imperative in reducing the risk of infants developing IDA.5 Adequate nutrition can be achieved in infancy by using breast milk, first infant formula milk and iron-enriched foods.6
IDA IN INFANTS Iron is essential for fundamental cellular processes. Studies show that inadequate iron leads to developmental delays, cognitive impairment and increased infant mortality rates.1,3,4,7
Infants often exhibit no symptoms in the early stages of iron deficiency, so IDA commonly goes undiagnosed.8 Left untreated, the cognitive impairments caused by IDA can remain present at all stages of life and are unlikely to be corrected by subsequent iron supplementation.3 Therefore, preventative programmes are essential for improving public health in the long term.3
IRON REQUIREMENTS DURING INFANCY As nutritional requirements increase throughout infancy, so does the risk of developing IDA.8 In early infancy (0-6 months), IDA is rare because endogenous iron stores from the perinatal stage are sufficient to support growth during this time.3 Between 6-12 months, iron requirements are higher than at any other stage of development.1,5 Neonatal iron stores reduce by 50% and exogenous iron is required to maintain the optimal haemoglobin concentration during this phase of rapid growth.4
Maternal nutrition status, the timing of cord clamping, birth weight and growth rate, all influence infant iron requirements.5 The Department of Health recommends specific requirements for each stage of life.9 However, primary care practitioners should identify whether any adjustments are required on a case-by-case basis, as preterm infants and those born to mothers with anaemia need extra consideration.
Notably, the SACN Iron and Health Report (2010) considers that dietary reference values from 0-6 months may be redundant due to endogenous iron supplies being sufficient during this period of development.5 Providing guidelines for infant iron intake at this age may cause confusion and added
Jessica Paradine ANutr
Jessica is a Freelance Nutritionist who recently graduated from Bath Spa University with a degree in Human Nutrition. She is working towards Registered Nutritionist accreditation and has a specific interest in paediatric nutrition and public health.
REFERENCES Please visit: nhdmag.com/ references.html
Age (months)
0-3
Iron (mg/day)
1.7
4-6
7-12 4.3
7.8
13-36 6.9
needless stress for new parents, leading to unnecessary supplementation in the first few months of life.
IRON SOURCES AND ABSORPTION Iron absorption varies depending on the source. Breast milk contains a relatively low iron concentration (0.2-0.4mg/L); however, absorption levels are optimal, so breastfed babies are at low risk of IDA in their first months of life.3,5
In sources other than breast milk, the bioavailability of iron is low, therefore diet needs to be optimised with ascorbic acid to promote higher absorption.3
The consumption of cow’s milk in the first year of life is considered the greatest dietary risk factor for developing IDA.10-11 Cow’s milk contains around 0.5-0.6mg/L of iron.5 This is more than breast milk, but it is well established that iron in cow’s milk is poorly absorbed.5 The high bioavailability of iron in breast milk compensates for the lower concentration.5
Iron in infant formula milk is only absorbed in moderate amounts, but it can be added at higher concentrations to make up for this.6 This makes formula milk a reliable source of iron when breast milk is unavailable or in short supply. It can also provide additional nutrition after six months.
Although the exact data is uncertain, it is estimated that around 95% of UK adults have adequate iron in their diet.5 These overall healthy levels are partially due to the introduction of iron-fortified foods.5 Iron content is lost during the processing of wheat flour, so the Bread and Flour Regulations Act of 1998 was introduced to ensure that all wheat flour is fortified to contain at least 1.65mg iron/100g.5 During the infant weaning process, fortified cereals can help to ensure that infants are getting adequate levels of iron in their diet.1,4
EDUCATION AS A METHOD OF PREVENTION With simple nutrition education and supplementation, IDA and associated developmental delays are both preventable and correctable.4 Nevertheless, the general approach to IDA must be preventative rather than reactive. Many infants do not show any symptoms of IDA until it has progressed to stages where the effects are potentially long term and more serious than if treated sooner.3-4
Breast milk has been established as the ideal feeding method for a variety of reasons, including reducing the risk of IDA.5 From 0-6 months, the risk of IDA in exclusively breastfed babies is minimal unless the infant has complex needs. However, infants who are not breastfed should be given iron-enriched first infant formula milk.12 The Infant Formula and Followon Formula Regulations Act (England) 2007, requires all infant milk to have an iron content of 0.3-1.3mg/100kcal.6
For infants with additional needs, there are other types of formulas available. These include high-energy, easy-to-digest, anti-reflux, lactosefree, soy-based and hypoallergenic formulations. However, these formulas are not necessarily appropriate unless specifically instructed by a healthcare professional or health visitor.6
From six months, it is agreed that breastfed infants should also be introduced to foods to help meet increased iron requirements, whereas infants fed with formula should continue on infant milk alongside the standard weaning process.6
To encourage the exclusive use of breast milk, advertising infant formulas to the general public is illegal in the UK.6 However, follow-on milk is not subject to the same stringent regulation. Follow-on milk has minor nutritional differences that reflect the increased nutritional requirements of infants after six months. However, the WHO and the UK Department of Health advise against the use of follow-on milk.6
Advertising of follow-on milk has caused controversy in the media and amongst healthcare professionals.6 Parents of young children will sometimes feel pressured to make the switch to follow-on milk, while healthcare professionals will attempt to educate about the guidance issued by the WHO and the UK Department of Health. With conflicting information from all angles, it can be difficult for new parents to fully understand what the best way is to prevent iron deficiency in weaning infants.
Although a switch to follow-on milk is not generally recommended, exclusive breastfeeding beyond six months can actually increase the risk of IDA.4 In later infancy, it is advised that a combination approach of breast milk, infant formulas and/or iron-enriched foods should be used to achieve and maintain optimal iron levels.4
THE ROLE OF PRIMARY CARE FOR PREVENTION Primary care has a significant role to play in preventing IDA. However, a multidisciplinary approach must be taken to identify the ongoing potential risk of IDA in infants.8 For optimal preventative results, comprehensive overviews of maternal iron status, infant diet, birth weight and any other medical history must be taken into account with every primary care contact.8
Educating parents about infant nutrition is undoubtedly the single most influential thing that can be done to prevent IDA in the early stages.3,10 Wherever possible, we must encourage parents to breastfeed exclusively up to six months of age.6 However, it is important to raise awareness of the increased nutritional requirements after six months, and the various methods available for iron supplementation.6
It is advised that infants with IDA risk factors or presenting with symptoms be screened regularly, including tracking haematological and biochemical markers to identify any changes in nutritional status that may lead to IDA. Once diagnosed, treatment should commence immediately with regular follow-ups to monitor progress.10
THERAPEUTIC SUPPLEMENTATION OF IRON It is important to distinguish between preventative supplementation and therapeutic supplementation. Preventative supplementation through enriched food and infant formula is recommended on a population level, whereas therapeutic supplementation is only used to correct diagnosed IDA.3
The WHO has published guidelines for iron consumption for high-risk infants and for correcting established IDA. Between 2-23 months, it is advised that infants with a low birth weight should be given 2mg/kg.3 In high prevalence areas, or in the absence of enriched foods, 6-23 month infants should also be given 2mg/kg.3 In diagnosed IDA, these requirements increase to 3mg/kg, up to a maximum of 60mg per day. This is a significant increase from the usual recommendation in the first year (1.7-7.8mg daily).3 However, as a therapeutic dose, this is considered appropriate and aims to correct the long-term adverse effects of IDA.3,10
AN URGENT CALL TO ACTION The prevalence of infant IDA is unacceptably high. IDA is preventable with adequate nutrition and infants are one of the most accessible patient groups to primary care services.3 Instead of correcting IDA, a multidisciplinary and preventative approach is needed to identify risk factors for developing IDA at all stages of infant development. This involves: making education on the importance of iron status more accessible to parents and all women of childbearing age who may become pregnant;1,3 prioritising early recognition of IDA in infancy;5,10 and regular screening of infants with risk factors for IDA as standard practice.5,10
Evidence is lacking regarding the true prevalence of IDA, the effectiveness of regular supplementation and alternative methods of delivering iron at an absorption rate comparable to breast milk. More research is required to understand the full effects of the current burden of IDA and to evaluate the benefits of reducing prevalence. Furthermore, to implement the best preventative strategies, the cost-effectiveness of public health iron supplementation interventions needs to be assessed.3
The responsibility lies with healthcare professionals, parents, educators and researchers, to increase awareness of IDA. As healthcare professionals, our role is vital in educating the public about the importance of iron status in infancy and providing simple, accessible solutions to combating infant IDA.
