[SOLVED] In what positive ways can the lifestyle change affect an individual?, assignment help – Health Medical

Research continually confirms that lifestyle changes can improve health. In this Discussion, you will address how changes in lifestyle can influence the illness-wellness continuum of an individual and a community.Choose a type of lifestyle change (e.g., an environmental, occupational, or behavioral change) that can clearly alter the health of an individual, positively or negatively.Review the two articles I attached that address lifestyle change, the type of lifestyle change I think these articles will support is behavioral change. The articles should allow you to draw evidence-based conclusions about the following questions:In what positive ways can the lifestyle change affect an individual?Are there any negative ways the change could affect an individual? If so, how?Would this lifestyle change on the part of an individual have an impact on the greater community? If so, how?How might these articles inform decisions or actions that you might take, or encourage others to take, in the future?jorc_283.qxd
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THE DIETARY MANAGEMENT OF PATIENTS WITH DIABETES
AND RENAL DISEASE: CHALLENGES AND PRACTICALITIES
Fiona Willingham, BSc (Hons), RD
Royal Derby Hospital, Derby, DE22 3NE, UK
Willingham F. (2012). The dietary management of patients with diabetes and renal disease: challenges and practicalities.
Journal of Renal Care 38(Suppl. 1), 40-51.
SUMMARY
Diabetes Mellitus is one of the major causes of chronic kidney disease and end-stage renal disease. Diet and lifestyle modification are vital components of optimal treatment for both conditions. This paper will address appropriate and often diverse
treatment for each individual, understanding that advising changes which positively impact both conditions is a major challenge for health care professionals working within either speciality. It will also highlight where overlap can be contradictory
rather than complementary, and offers practical guidance to support patients in making the necessary lifestyle changes to have
maximal positive impact upon both conditions and their overall health.
K E Y W O R D S Advice • Chronic kidney disease • Diabetes • Nutrition
INTRODUCTION
Diabetes mellitus (DM) is a complex, chronic medical condition
affecting more than 346 million people worldwide (World
Health Organisation, 2011). Worldwide prevalence is increasing rapidly in epidemic proportions, imposing a significant
health, psychological and economic burden.
DM is one of the major causes of chronic kidney disease (CKD)
and end-stage renal disease (ESRD); (USRDS; USRDS 2010;
Renal Association 2011). Diet and lifestyle modification are
vital components of optimal treatment for both conditions
(NICE 2008; Koppell et al. 2010; Renal Association 2011).
However, appropriate treatment for each individual condition
can be quite diverse, therefore advising changes which positively influence both conditions is clearly one of the major challenges for health care professionals working within either speciality, and streamlined multi-disciplinary working is essential
for effective patient care.
This paper outlines some of the important elements of dietary
treatment for patients with DM and CKD, highlighting where
overlap can be contradictory rather than complementary, and
offers practical guidance to support patients in making important changes to have maximal positive impact upon both conditions and their overall health.
TYPE 1 VERSUS TYPE 2 DIABETES
B I O D ATA
F i o n a W i l l i n g h a m is Lead Specialist
Renal Dietitian at Derby Hospitals NHS
Foundation Trust. After qualifying as a
dietitian in 1997, she commenced her first
renal dietetic post in 1998, and joined the
renal team in Derby in 2004. Her main
areas of expertise and interest are dietary
and lifestyle management in pre-dialysis
care, and nutritional screening and assessment methods in CKD.
It is important to distinguish between type 1 and type 2 DM,
as their differing pathophysiology influences the subtle differences in dietary treatment strategies between the two. Type 1
DM is usually characterised by rapid onset pancreatic insufficiency and subsequent loss of insulin production, whereas type
2 DM is a complex metabolic disorder characterised by defects
in both insulin secretion and action, and insulin resistance
(SIGN 2010; NICE 2011). Insulin deficiency is progressive over
time, and when coupled with insulin resistance, often leads to
raised blood pressure and abnormal blood lipid levels.
CORRESPONDENCE
Fiona Willingham
Lead Clinical Specialist Renal Dietitian,
Royal Derby Hospital,
Derby, DE22 3NE, UK
Tel.: 01332 786908
Fax: 01332 785133
fiona.willingham1@nhs.net
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Approximately 90% of those diagnosed with DM have type 2
DM (NICE 2008; WHO 2011), thought to be predominantly
due to the increasing prevalence of obesity and the ageing
population. Additional factors influencing risk of type 2 DM
include reduced physical activity levels and family history of
type 2 DM, with people of South Asian, African Caribbean,
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black African and Chinese descent also having an increased risk
of developing the disease (NICE 2011). Given that the majority
of patients with CKD and ESRD will have type 2 DM, this paper
will focus upon the dietary priorities for this patient group.
THE LINK BETWEEN DIABETES AND CKD
Diabetic nephropathy (DN) remains the most common cause of
ESRD in the United Kingdom, accounting for approximately
25% of patients commencing renal replacement therapy (RRT)
(UK Renal Registry 2011). The US Renal Data System (USRDS)
reports that DM is present as an additional co-morbidity in over
48% of patients with CKD stages 3–5 (USRDS 2010).
Microalbuminuria is the first clinical detectable marker of DN.
This often progresses to proteinuria, resulting from several
renal functional changes including hyperfiltration, hyperperfusion and increased capillary permeability (Raptis & Viberti
2001; van Dijk & Berl 2004). Minimising the risk of developing
the long-term complications of DM, including DN, is considered to be a cornerstone of good management (Department of
Health 2001; NICE 2008). The Diabetes Control and
Complications Trial (DCCT) and UK Prospective Diabetes Study
(UKPDS) both demonstrated the benefit of intensive glycaemic
control in delaying both the onset of microalbuminuria and
subsequent progression to proteinuria and hence renal impairment (DCCT 1993; UKPDS 1998). The Steno 2 study (Gaede
et al. 2003) highlighted the benefit of intensive multi-factorial
intervention in patients with type 2 DM and microalbuminuria,
with a 50% reduction in cardiovascular disease (CVD) risk and
microvascular complications being achieved from intensive
pharmacological therapy combined with dietary intervention
and increased exercise.
Once DN is established, tight glycaemic control and optimal
management of hypertension are vital to delay progression
towards ESRD (NICE 2008; SIGN 2010; American Diabetes
Association 2011), and diet and lifestyle modification have a
pivotal role alongside medical strategies.
KEY DIETARY ASPECTS FOR DIABETES AND KIDNEY
DISEASE
Lifestyle modification is a key component in the effective management of both DM and CKD (Mann et al. 2004; NICE 2008;
SIGN 2010; Renal Association 2011). The aim of any nutritional
advice is to provide the information required, in a way which
allows people to make informed and appropriate choices about
the type and quantity of food they consume (Diabetes Care
Advisory Committee 2003). Structured education provided by
appropriate members of the diabetes multi-disciplinary team
(MDT) is essential to ensure that patients acquire the necessary
knowledge and skills to effectively manage disease conditions.
This may consist of one to one counselling and/or group educational sessions, and care planning, which has been shown to
be beneficial in diabetes management, may also be useful in
maintaining a patient-centred approach (Department of
Health/Diabetes UK, 2006; Nice 2008).
The following section outlines the main dietary aims for both
conditions, showing not only where advice overlaps, but also
where there are contradictions.
LIFESTYLE AND DISEASE PROGRESSION
Diet and lifestyle modification is essential to prevent DN and
delay progression (NICE 2008), with several lifestyle factors
having importance and significant influence over associated
factors such as blood pressure control and obesity.
Considering that up to 50% of people with type 2 DM present
with micro- or macrovascular complications at diagnosis (UKPDS
1998), earlier identification and effective management of diabetes, or even prevention, is crucial. Lifestyle is influential in preventing onset of type 2 DM (Tuomilehto et al. 2001; Diabetes
Prevention Programme 2002). Obesity is the main contributory
factor to type 2 DM (NICE 2011), and the vast majority of those
diagnosed exhibiting signs of impaired glucose regulation (IGR)
before developing DM (Diabetes UK 2009). Tuomilehto et al.
(2001) showed that detailed, individualised advice to aid weight
reduction, decrease total and saturated fat intake, and to undertake moderate, regular exercise, reduced the cumulative incidence of DM by 58% over a four-year period, in comparison to
the control group who only received general written information
regarding diet and exercise. The Diabetes Prevention Programme
(2002) randomly assigned 3,234 subjects with elevated fasting
and post-load plasma glucose concentrations to receive metformin, placebo or a lifestyle modification programme, which
aimed to achieve 7% weight reduction and a minimum of 150
minutes of physical activity weekly. Incidence of DM was 58%
less with lifestyle intervention than in the control group.
Managing type 2 DM and preventing subsequent complications is challenging, therefore it is essential that strategies such
as screening high-risk individuals is implemented to enable
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early identification of IGR and type 2 DM (WHO 2003;
Diabetes UK 2008).
Several key factors, including lowering blood pressure, appropriate treatment of proteinuria, achieving optimal glycaemic
control and smoking cessation are of significant importance in
the prevention of CKD progression (NICE 2008; SIGN 2010;
Renal Association 2011). Diet and lifestyle modification are
important components in delaying progression of CKD, particularly given their positive influence upon both hypertension
and glycaemic control (Sacks et al. 2001; Diabetes Care
Advisory Committee, 2003; NICE 2008). However, the influence of both low protein diets and obesity upon CKD remains
controversial (Klahr et al. 1994; Evans et al. 2005), and both
will be subsequently discussed in more detail.
THE METABOLIC SYNDROME
The prevalence of metabolic syndrome, a common feature of
vascular and metabolic diseases is increasing (Ford et al. 2004;
Cull et al. 2007). It is characterised by insulin resistance, hyperglycaemia, hypertension, abdominal obesity and dyslipidaemia
(WHO 1999; Balkau et al. 2002; Alberti et al. 2005) and is a
commonly recognised pre-cursor for the development of type
2 DM, CVD and stroke. It may also potentially be an independent risk factor for CKD (Kurella et al. 2005; Tong et al. 2008).
Obesity and lack of physical activity are important determinants of metabolic syndrome (Ford et al. 2004), and epidemiological data indicates that low glycaemic index (GI) diets can
reduce the risk of metabolic syndrome due to the beneficial
effect they exert in lowering insulin resistance.
DIABETES
All patients with CKD and/or DM should be encouraged to eat
a well-balanced diet to provide all the energy, protein, vitamins, minerals and fibre that the body requires for optimal
health. Incorporating foods from each of the five food groups
(Figure 1) should be encouraged, in accordance with recommended food portion sizes illustrated within models used to
convey healthy eating messages, such as the EatWell plate
(Figure 2) in the United Kingdom (NHS Choices 2011) or the
‘MyPlate’ model used in the United States of America (United
States Department of Agriculture 2011).
The holistic management of DM, including optimisation of glycaemic control and risk reduction for the development of CVD
and microvascular complications strongly influences the goals
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FOOD GROUPS
1
Bread, cereals and potatoes
2
Fruit and vegetables
3
Meat, fish and alternatives
4
Milk and dairy foods
5
Fatty and sugary foods
Figure 1: Food groups.
Figure 2: EatWell plate (NHS choices 2011).
for dietary treatment of DM. Specific dietary guidelines for DM
(Mann et al. 2004; NICE 2008) are summarised in Table 1 but
generally follow the same principles as healthy eating for the
general population.
Dietary advice should focus upon reduced consumption of carbohydrate, particularly refined carbohydrates and sugars,
which often have a high GI. Particular attention should be paid
to the portion sizes of carbohydrate foods, individualising recommendations to reduce the risk of both hypoglycaemia and
hyperglycaemia. Carbohydrate foods have been shown to have
a similar effect upon glycaemic control as high sucrose intake
(Diabetes Care Advisory Committee, 2003), therefore avoiding
excessive intake, particularly in type 2 DM, is beneficial.
Promoting intake of lower GI foods such as fruit, vegetables
and pulses, along with moderate portions of wholegrain cereals and complex carbohydrate, lean meat, fish, reduced fat
dairy products and unsaturated fats are beneficial for weight
control and reducing CVD risk (Diabetes Care Advisory
Committee, 2003; Mann et al. 2004).
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1
Ensure provision of individualised, culturally acceptable nutritional advice
2
Emphasise advice based on a healthy, balanced diet which applies to the
general population
1
Dietary intervention should include appropriate education, assessment and
supervision and ensure the prevention of malnutrition
2
Achieving a healthy body weight should be encouraged, and patients with
BMI >30 kg/m2 should receive dietary advice to assist weight loss
3
Dietary advice to restrict sodium intake to ⬍2.4 g/day (100 mmol/day or ⬍6 g/day
of salt) should be provided
4
Advice to perform regular moderate exercise should be provided
5
If indicated, the risks and benefits of protein restriction should be discussed
by an appropriately trained professional
6
Specific dietary advice to restrict potassium, phosphate, protein and/or calorie
intake should be provided if indicated
2
3
Aim to achieve healthy bodyweight (BMI 20–25 kg/m ) and encourage weight
loss (5–10% initially) in those who are overweight
4
Encourage high fibre, low GI carbohydrate foods
5
Individualise recommendations for overall carbohydrate intake, and advise
limiting sucrose-containing foods to ensure avoiding excess energy intake
6
Eat plenty of fruit and vegetables
7
Include oily fish regularly within the diet
8
Reduce overall fat intake, and replace saturated fat with unsaturated fats
where possible
9
Reduce salt intake to no more than 6 g per day
10
Avoid excessive alcohol consumption
Table 1: Dietary guidelines for DM (Mann et al. 2004; NICE 2008).
CKD STAGES 1–3
Dietary advice provided to patients with CKD stages 1–3 should
focus upon the same healthy eating advice which is applicable to
both the general population and those with diabetes, with particular emphasis upon reduced sodium intake, increased physical
activity and weight reduction, to benefit overall health and
reduces risk factors for CKD. Key aspects of appropriate advice
have been included within NICE (2008) and Renal Association
(2011) guidance within the United Kingdom (Table 2).
CKD STAGES 4 AND 5
As renal function deteriorates, serum levels of both potassium
and phosphate often increase (Renal Association 2011), and
regulation of fluid balance may also be compromised. A spontaneous reduction in overall dietary intake is often observed particularly for protein and energy intake, and is usually secondary to
uraemic symptoms. The focus for dietary advice at this stage
therefore shifts towards controlling levels of waste products of
metabolism and fluid, as well as ensuring maintenance of optimal nutritional status. Malnutrition is common in patients with
CKD and is associated with adverse outcomes, including morbidity and mortality (Locatelli et al. 2002). Patients commencing RRT
in a poor nutritional state are shown to result in a poor outcomes (Leavey et al. 2001), therefore it is vital that dietary advice
is patient-specific and avoids inappropriate dietary restriction.
Fouque et al. (2007), The Renal Association (2010b) and
British Dietetic Association Renal Nutrition Group (2011) have
all produced nutritional guidelines for optimal dietary manage-
Table 2: Dietary and lifestyle modification for CKD (NICE 2008;
Renal Association 2011).
1
Screening for undernutrition in CKD stages 4 and 5 should take place at
regular intervals, including a variety of methods such as assessing actual
body weight, percentage weight loss and subjective global assessment (SGA)
2
Prevention of undernutrition in CKD stages 4 and 5 should be achieved by
recommending appropriate protein and energy intake:
• 0.75 g protein per kg ideal body weight (IBW) daily for those not on RRT,
and a minimum of 1–1.2 g/kg IBW/d protein for those on RRT
• 30–35 kcal/kgIBW/d for all patients
3
Established undernutrition in CKD stages 4 and 5 should be determined by
appropriate clinical assessment, and treatment should include appropriate use
of oral nutritional supplements or enteral or parenteral nutrition as indicated
4
Overnutrition in CKD should be determined by assessing body mass index (BMI)
Table 3: Summary of nutritional guidelines for low clearance
patients and those on RRT.
ment of patients with ESRD on RRT, the key points of which
are summarised in Table 3. However, it should be noted that
the majority of these recommendations are based on expert
opinion or lower grade evidence, highlighting the need for
research in this area.
THE DIETARY TREATMENT OF PATIENTS WITH DIABETES
AND RENAL DISEASE
The most appropriate dietary treatment for some patients with
CKD will change over time, depending on serum biochemistry
levels and current nutritional status. Furthermore, there can be
some contradiction between diet for CKD and DM, thus making the management of patients with DM challenging. It is
important to reassure patients that previous dietary advice was
appropriate for their disease status at that time, and whilst
helping them to understand changes in dietary priorities may
be difficult, it is often useful to explain the health benefits of
the different elements of dietary advice. It is likely that patients
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developing CKD as a consequence of diabetes will have been
exposed to nutrition and health information from a variety of
sources. It is therefore important that these patients are routinely referred to a registered dietitian who is qualified to assess
their overall diet and offer appropriate, individualised advice.
MALNUTRITION
Malnutrition is commonly seen in CKD stages 4 and 5, with
reported prevalence up to 48% in those with CKD stage 4 and
between 20% and 70% in patients with CKD stage 5 (Fouque
et al. 2011). It often results from decreasing glomerular filtration rate (GFR) and increasing age, and is associated with
increased morbidity and mortality (Leavey et al. 2001; Pifer
et al. 2002; Dwyer et al. 2005). Several additional factors
pre-dispose to the development of malnutrition, including
symptoms associated with uraemia such as nausea and vomiting, impaired taste, anorexia and anaemia.
A meta-analysis of oral nutritional supplementation and
enteral tube feeding in dialysis patients (Stratton et al. 2005)
demonstrated that nutritional support can potentially improve
clinical outcomes in malnourished patients, therefore early
detection of malnutrition is vital, allowing timely nutritional
intervention. Since there is no ‘gold standard’ method available for assessing nutritional status, routine nutritional screening and assessment should include a variety of measures to
reflect nutritional status. If malnutrition is suspected, patients
should be referred to a registered dietitian for nutritional
assessment and support.
Patients with DM are often encouraged to reduce their carbohydrate intake to help optimise glycaemic control, or reduce
fat intake to help influence their future risk of developing CVD.
However, if they are fast approaching dialysis, struggling with
uraemia and poor appetite the current dietetic priority is maintaining an adequate energy intake rather than preventing CVD
sometime in the future. Struggling with food preparation and
reduced dietary intake is further compounded by fatigue and
nausea, hence the consequences of malnutrition become more
of a threat to the patients’ outcome than CVD. It is vital that
nutritional adequacy is achieved from an early stage, and that
patients are not subject to inappropriate dietary restriction.
DIETARY PROTEIN INTAKE
Optimal protein intake is required for growth, repair and maintenance of overall nutritional status. The benefit of protein
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Journal of Renal Care 2012
restriction in preservation of renal function remains controversial, despite being clearly implicated in the aetiology of kidney
impairment through the Brenner Hypothesis (Brenner et al.
1982). This was an important influence in the design of the
Modification of Diet in Renal Disease (MDRD) trial (Klahr et al.
1994), a comprehensive study evaluating the effect of protein
restriction as well as blood pressure upon decline in renal function. Protein intake was only found to have a minimal effect
upon the rate of decline in renal function, and only in subjects
with GFR of 25–55 mL/min. However, a meta-analysis (Fouque
et al. 2000) concluded that reduced protein intake afforded a
40% reduction in commencing RRT, and in a Cochrane
Collaboration review (Fouque & Lavill 2009), results from 10
randomised studies including a total of 2,000 patients found
that protein restriction followed for a minimum of one year,
reduced renal death (RRT or death from any cause) by 32%. In
a separate Cochrane Collaboration review of 12 studies in
patients with types 1 and 2 DM, Robertson et al. (2009) found
that lower protein intake may modestly delay progression of
DN towards ESRD, although the results were not deemed to be
clinically significant. Neither review could recommend optimal
protein intake from their findings.
Patients with CKD stages 1–4 are not advised to follow a ‘traditional’ low protein intake of ⱕ0.6 g/kg IBW per day, but to
aim for a protein intake of approximately 0.75–1 g/kg IBW per
day. For most people this would represent a protein intake of
less than 70 g per day, which represents a degree of restriction
for the majority, considering that mean protein intake is
between 66 and 88 g per day in the United Kingdom (National
Diet and Food Survey 2010) and 70–100 g per day in the
United States of America (NHANES 2008).
Patients undergoing RRT are advised to achieve a slightly
higher protein intake of 1–1.2 g/kg IBW per day (Fouque et al.
2007; Renal Association 2010; British Dietetic Association
Renal Nutrition Group 2011), in view of the increased prevalence of malnutrition in the dialysis population and to compensate protein losses on dialysis. Dietary advice regarding optimum protein intake should be given by an appropriately
trained registered dietitian, as part of routine dietary assessment (NICE 2008; Renal Association 2011).
CONTROL OF WASTE PRODUCTS
Serum potassium and phosphate levels often rise as renal function deteriorates. Patients requiring advice regarding either a
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low potassium or low phosphate diet (or both) must be
referred to a registered dietitian to enable thorough dietary
assessment upon which appropriate advice can be based
(Renal Association 2011).
POTASSIUM
High potassium levels (hyperkalaemia) are a common and
potentially dangerous complication in patients with CKD and
declining GFR, becoming increasingly common as GFR declines
below 40–60 mL /min per 1.73 m2 (Hsu & Chertow 2002).
Hyperkalaemia is associated with cardiac arrhythmias and
death, and whilst it may be preceded by other symptoms such
as muscle weakness, it often presents as cardiac arrest
(Nyirenda et al. 2009).
Dietary potassium intake is a major determinant of serum
potassium levels, and dietary potassium restriction can substantially reduce hyperkalaemia. However, non-dietary causes,
including medications commonly used in CKD and DM (e.g.
ACE inhibitors and angiotensin-II receptor antagonists), metabolic acidosis and diabetic ketoacidosis, should also be considered as potential causes of hyperkalaemia. Appropriate
dietary advice (sometimes given in conjunction with sodium
bicarbonate if metabolic acidosis is present), usually controls
hyperkalaemia in CKD stages 1–4. This potentially allows
ongoing optimal treatment of hypertension and proteinuria,
although occasionally adjustment of medications is required.
Potassium is present in many frequently consumed foods and
drink, including fruit and vegetables, fruit juices, milk and
meats, all of which are considered to be important elements
of a normal ‘healthy’ diet. This can cause particular problems
for those with DM, where increased consumption of fruit and
vegetables is encouraged. In this instance, appropriate dietary
advice regarding fruit and vegetables with a lower potassium
content (Table 4), and advice regarding suitable portion sizes
and cooking methods which will reduce the potassium content of potatoes and vegetables is required. Therefore,
patients requiring a low potassium diet should be referred for
specialist dietetic assessment and advice (Renal Association
2011). Practice varies between different renal units, but
patients will generally be referred for low potassium dietary
advice when serum potassium reaches 5.6–6.0 mmol/l. The
specific point at which dietetic referral is made often depends
upon underlying medical conditions and other treatments,
particularly those which can cause hyperkalaemia such as
ACE inhibitors or angiotensin-II receptor antagonists.
Fruits
Vegetables
(Portion size – 1 fruit unless otherwise
stated)
(Portion size – approx. 2 tablespoons)
Vegetables should be boiled where possible
Apple
Cherries (approx. 10)
Broccoli
Clementine, Satsuma or tangerine
Cabbage
1
⁄2 Grapefruit
Carrots
Nectarine
Cauliflower
1 slice fresh Pineapple
Green beans
Plum
Leeks
Raspberries (approx. 10)
Peas
Strawberries (approx. 5–6)
Runner beans
150 g any tinned fruit, drained (except
prunes)
Swede
Sweetcorn
Turnip
Small side salad (e.g. lettuce, cucumber,
1
⁄2 small tomato
Table 4: Lower potassium fruits and vegetables.
Consequently, patients with diabetes are more likely to require
earlier intervention.
PHOSPHATE
Elevated serum phosphorus levels (hyperphosphataemia) are a
common biochemical abnormality of CKD and are one of the
main factors associated with Chronic Kidney Disease–Mineral
Bone Disorder (CKD–MBD). Serum phosphorus levels increase
with declining GFR, and hyperphosphataemia becomes
increasingly common with GFR below 40 mL/min per 1.73m2
(Hsu & Chertow 2002; Moranne et al. 2009).
It is linked to cardiovascular morbidity and mortality in CKD
(Block et al. 2004; Dhingra et al. 2007; Covic et al. 2009), with
epidemiological and observational studies demonstrating a
strong association between hyperphosphataemia and mortality in dialysis patients which is thought to be mediated via vascular calcification (Covic et al. 2009).
Optimal management of hyperphosphataemia is multi-factorial, and therefore poses a number of significant challenges.
Elevated serum phosphate levels can usually be reduced with
advice to restrict dietary phosphorus intake in the first
instance (Combe & Aparicio 1994) however as the amount of
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phosphate found in food is closely related to its protein content, dietary advice to avoid unnecessary restriction of protein is essential (Shinaberger et al. 2008). Food additives and
soft drinks (Sullivan et al. 2007; Savica et al. 2009) are major
contributors to dietary phosphate intake which cannot be
readily identified from food labelling. Many high-fibre foods
are also higher in phosphate, although the extent to which
this is absorbed is unclear. For patients struggling to control
serum phosphate levels, reducing some high-fibre cereal
foods may be beneficial, although this can appear to contradict advice for DM patients, which is to increase dietary fibre
intake. Patients should therefore be referred to a specialist
renal dietitian who can provide specific, individualised dietary
advice (Ashurst & Dobbie 2003; Reddy et al. 2009). The point
at which dietary intervention is initiated again varies across
different renal units, but it is generally accepted that
phosphate levels should be maintained between 1.1 and
1.7 mmol/l, depending upon the stage of CKD (Renal
Association 2010).
Dietary restriction is not always sufficient to provide optimal
phosphate control, which necessitates the use of phosphate
binders (Tonelli et al. 2010), which work by inhibiting absorption of phosphate from food within the GI tract. Specialist
renal dietitians are able to advise regarding the appropriate
timing and distribution of phosphate binders with meals and
snacks. Dietetic-led CKD/MBD multi-professional clinics have
been shown to add value to management.
WEIGHT MANAGEMENT
Weight management is a vital component of treatment in both
CKD and DM. Obesity may be an independent risk factor for
the development and progression of CKD (Wang et al. 2008;
Ting et al. 2009), particularly as prevalence of CKD and ESRD
increases parallel to the rise in obesity (Ryu et al. 2008).
Conversely, in patients receiving dialysis, reduced mortality risk
has been observed in patients with higher BMI (Leavey et al.
2001; Johansen et al. 2004).
Few population-based epidemiological studies have examined
the association between obesity and CKD (Ejerblad et al.
2006; Hsu et al. 2006), although moderate weight loss has
been shown to reduce hyperfiltration and the level of metabolic stress on the kidney thereby reducing glomerular damage and proteinuria (Chagnac et al. 2003; Morales et al.
2003). Given the influence that obesity has been shown to
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exert over general health, CVD risk, hypertension and glycaemic control, it seems sensible to encourage patients with
CKD who are overweight to try and achieve a healthy BMI
(Elsayed et al. 2008).
Achieving and maintaining a healthy body weight is an important goal of therapy (Anderson et al. 2002), particularly in type
2 DM where obesity complicates management by increasing
insulin resistance and blood glucose concentrations (Klein et al.
2004), and results in decreased insulin sensitivity and deterioration in glycaemic control (Astrup et al. 2001). Weight reduction often leads to improved glycaemic control (Look AHEAD
Research Study Group 2007) along with reduction in oral
hypoglycaemic medication (Nathan et al. 2009). Even modest
weight loss of under 10% body weight improves insulin sensitivity and glucose tolerance, reducing lipid levels and blood
pressure, thereby reducing cardiovascular risk (Goldstein 1992;
Look AHEAD Study Group 2007). The Look AHEAD randomised controlled trial (RCT) in over 2,500 patients with type
2 DM demonstrated that mean weight loss of 8.6% in the
intervention group compared with 0.7% in the control group
led to subsequent improvements in glycaemic control and
reduction in CVD risk (Look AHEAD Research Study Group
2007).
Whilst a BMI in the range 20–25 kg/m2 is desirable, this may
not be achievable for all patients, particularly in those with a
significantly higher BMI. With evidence suggesting that 5–10%
weight loss can positively influence overall health, and specifically hypertension, glycaemic control and dyslipidaemia
(Goldstein 1992; Look AHEAD Study Group 2007;
Navaneethan et al., 2009), this is often a realistic initial target
for weight loss.
Obesity is multi-factorial, with psychological, genetic, behavioural and environmental influences (Anderson et al. 2001;
Ting et al. 2009). Successful prevention and treatment therefore poses a number of challenges, and appropriate consideration of psychological and lifestyle barriers to successful
weight loss is paramount. An energy deficit (overall energy
intake being less than energy expenditure) is required for successful weight loss. A commonly used practical approach is to
reduce energy intake from current intake by 500 kcals per day,
which usually results in the loss of approximately 0.5 kg of adipose tissue per week (Eckel 2008). This can be achieved by
combining a sensible structured eating programme which is
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low in fat and sugar with appropriate control of portion size.
Increasing physical activity alone can also modestly influence
weight loss (Eckel 2008), although where possible a combination of the two should be encouraged to enhance weight loss
and improve muscle mass. A steady weight loss of 0.5–1 kg
(1–2 lb) per week should be encouraged, as a faster rate of
weight loss leads to muscle loss rather than fat, and may also
prevent future weight maintenance.
HYPERTENSION
Hypertension is one of the major determinants for progression
of both CKD and DN with optimal blood pressure control
being essential to help prevent macro- and microvascular complications of DM, particularly CVD and DN (NICE 2008). The
target for optimal blood pressure control in patients with CKD
and diabetes is 130/80 mmHg (NICE 2008; SIGN 2010; Renal
Association 2011).
Several lifestyle factors, including weight loss and increased
physical activity, have been shown to reduce hypertension. A
meta-analysis of 25 studies indicating that blood pressure fell
by 1 mmHg for each kilogram of weight loss (Neter et al.
2003). It is well-established that regular, moderate exercise in
the general population reduces the risk of CVD (Paffenberger
et al. 1993; Thijssen et al. 2010). Furthermore, aerobic physical activity has been shown to be beneficial in the non-pharmacological treatment of hypertension, and is also an integral
part of a structured weight management programme, the benefits of which have also been demonstrated in renal patients
(Cook et al. 2008).
Sodium is another major determinant of blood pressure.
Western populations consume substantially higher amounts
of sodium than necessary, and this is associated with a higher
prevalence of hypertension and CVD (He & MacGregor 2009;
Bibbins-Domingo et al. 2010). A meta-analysis of 28 randomised trials investigating sodium reduction on blood pressure in normotensive and hypertensive individuals showed
that reducing sodium intake by 100 mmol/day significantly
reduced blood pressure in hypertensive individuals (He &
MacGregor 2002). The Dietary Approaches to Stop
Hypertension (DASH-sodium) RCT (Sacks et al. 2001; Vollmer
et al. 2001) found that reducing salt intake from 9 g per day
to 6 g daily gave a significant reduction in blood pressure,
with more marked effects observed in hypertensive and older
subjects, and when combining salt restriction with a diet
high in fruit and vegetables and low in fat and sugar (DASH
diet). A small study (n ⫽ 14) in the UK general population
assessed whether the DASH diet could be adapted to fit UK
food preferences (Harnden et al. 2010), and showed good
compliance with the DASH-style diet, along with reduction in
both systolic and diastolic blood pressure. However, some
elements of the DASH-style diet, particularly increasing fruit
and vegetable intake, may not be a suitable recommendation
for those following low potassium diets, and further work to
determine the safety of such diets in the CKD population
could be warranted.
An in-depth review of 16 studies investigating the effect of
sodium intake upon CKD progression (Jones-Burton et al.
2006) found relatively little evidence to suggest that a high
sodium intake specifically influences renal outcomes, however
reducing sodium intake was not found to be detrimental. A
recent study from the HONEST study group (Slagman et al.
2011), found the combination of ACE inhibition and reduction
in sodium intake from 184 to 106 mmol/day was more effective for controlling blood pressure and reducing proteinuria
than dual blockade with ACE inhibitors and angiotensin-IIreceptor blockers. This study also highlighted the difficulties in
achieving low sodium intake, as their original target for low
sodium intake was only 50 mmol/day.
The current average salt intake in the United Kingdom is
approximately 9 g (approximately 3.5 g sodium) per day
(Department of Health 2009), with current recommendations
for the general population to reduce salt intake to 6 g (2.4 g
sodium) per day. Although a greater reduction in sodium
intake is thought to be more beneficial, this realistic reduction
is expected to result in significant benefit for reduction in
hypertension and CVD (He & MacGregor 2003, 2005).
Although the effect of sodium intake upon renal outcomes
remains unclear, given the positive impact of sodium reduction on blood pressure and the known impact of high blood
pressure on renal function and proteinuria, it seems sensible
to recommend maintaining dietary sodium intake at less than
6 g per day.
Reduction in dietary sodium intake can be practically achieved by:
• Limiting the amount of high salt and processed foods consumed (Table 5);
• Not adding salt to food at the table;
• Minimising the amount of salt used in cooking.
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High salt foods to reduce
Suitable alternatives
Meat and meat products: Bacon, gammon, black pudding, tinned meat (e.g. corned beef, ham, Spam),
pâté, salami, sausages, beef burgers, meat pies and most ready-made meat dishes
Plain meat (e.g. roast meats, chops and steaks) and chicken,
home-made meat pies
Fish and fish products: All smoked fish, tinned fish in brine (e.g. tuna, sardines, anchovies)
prawns, fish paste
Fresh fish (e.g. cod, haddock, halibut, lemon sole, plaice,
salmon, trout); tinned fish in spring water or oil
Cheese: Hard cheeses (e.g. Cheddar, Cheshire, Edam); soft cheeses (e.g. brie, feta); processed cheese, e.g.
cheese slices and cheese spread
Cottage cheese, cream cheese
Savoury snacks: Crisps; maize, corn and wheat snacks; salted nuts, and most other savoury snacks
(e.g. Twiglets, Bombay mix, pork scratchings, salted popcorn, salted crackers)
Unsalted crisps, nuts and crackers, plain popcorn
Soup: Packet, canned and fresh soups
Homemade soups
Miscellaneous: Soy sauce, Bovril, Marmite, gravy granules, stock cubes, olives in brine
Herbs, spices, vinegar, small amounts of chutney, pickles and
bottled sauces, salad cream and mayonnaise
Table 5: No added salt advice.
Stages 1 & 2
Aim to minimise the risk of CKD progression and cardiovascular risk:
Optimise glycaemic control (diet and medication)
Weight control (appropriate reduction in energy intake and increased physical activity)
Optimal blood pressure control (No added salt, weight control)
Optimise lipid profile (encourage oily fish, fruit and vegetables, low saturated fat intake, increased fibre intake)
Basic low potassium advice if K⫹ ⬎5.5 mmol/l
Stage 3
Aim to delay CKD progression:
As for stages 1 & 2
Treat metabolic complications if they arise, e.g. hyperkalaemia, malnutrition, renal bone disease
Stage 4
Pre-dialysis advice:
Emphasis on optimal nutritional intake & prevention of malnutrition
No added salt
Limit metabolic complications as required-–low potassium, phosphate diet, fluid restriction
Advice to optimise glycaemic control and/or achieve weight reduction as required
Stage 5
Individualised dietary advice according to biochemistry and renal replacement therapy, with emphasis on optimal nutritional intake
Table 6: Suggested dietary advice across CKD stages 1–5.
Salt substitutes contain significant amounts of potassium which
could be harmful for people with CKD and/or hyperkalaemia.
Furthermore, they still contain substantial amounts of sodium
which does not facilitate reduction in salt appetite. They should
therefore not be recommended in the general population but
this is of particular importance in those with CKD.
Considering that approximately 70–75% of sodium in the Western
diet comes from salt in processed foods (Department of Health
2009), achieving a reduction in sodium intake in the general population is challenging. However, the Food Standards Agency in the
United Kingdom (2011) has recommended a reduction in the salt
content of many processed foods, to help maintain progress
towards achieving the 6 g daily salt intake target.
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Journal of Renal Care 2012
KEY POINTS
Dietary and lifestyle advice for people with CKD and DM
(Table 6) should focus on:
• Eating a varied diet;
• Achieving a healthy weight;
• Encouraging regular physical activity;
• Reducing salt intake;
• Control of metabolic complications as they arise;
• Referral to a registered dietitian working within the
renal and/or diabetes MDT for specialist dietary
intervention.
CONFLICT OF INTEREST
The author confirms no conflict of interest.
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REFERENCES
Alberti K.G., Zimmet P. & Shaw J. (2005). The metabolic syndrome: a
new worldwide definition. Lancet 3 6 6, 1059-1062.
American Diabetes Association. (2011). Standards of medical care in
diabetes-2011. Diabetes Care 3 4(Suppl 1), S11-S61.
Anderson J.W., Konz E.C., Frederich R.C. et al. (2002). Long term
weight loss maintenance: a meta-analysis of US studies. American
Journal of Clinical Nutrition 7 4, 579-584.
Ashurst I. & Dobbie H. (2003). A randomized controlled trial of an educational intervention to improve phosphate levels in hemodialysis
patients. Journal of Renal Nutrition 1 3(4), 267-274.
Astrup A., Grunwald G.K., Melanson E.L. et al. (2001). The role of lowfat diets in the body weight control: a meta-analysis of ad libitum
dietary intervention studies. International Journal of Obesity 2 4,
1545-1552.
Balkau B., Charles M.A., Drivsholm T. et al. (2002). Frequency of the
WHO metabolic syndrome in European cohorts, and an alternative definition of an insulin resistance syndrome. Diabetes and
Metabolism 2 8, 364 -376.
Bibbins-Domingo K., Chertow G.M., Coxson P.G. et al. (2010).
Projected effect of dietary salt reductions on future cardiovascular disease. The New England Journal of Medicine 3 6 2, 590-599.
Block G., Klassen P., Lazarus J. et al. (2004). Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. Journal of the
American Society of Nephrology 1 5, 2208-2218.
Brenner B.M., Meyer T.W. & Hostetter T.H. (1982). Dietary protein
intake and the progressive nature of kidney disease: the role of
hemodynamically mediated glomerular injury in the pathogenesis
of progressive glomerular sclerosis in aging, renal ablation, and
intrinsic renal disease. The New England Journal of Medicine
3 0 7(11), 652-659.
British Dietetic Association Renal Nutrition Group. (2011). Evidence
Based Dietetic Guidelines: Protein Requirements of Adults on
Haemodialysis and Peritoneal Dialysis.
Chagnac A., Weinstein T., Herman M. et al. (2003). The effects of
weight loss on renal function in patients with severe obesity.
Journal of the American Society of Nephrology 1 4, 1480-1486.
Combe C. & Aparicio M. (1994). Phosphorus and protein restriction
and parathyroid function in chronic renal failure. Kidney
International 4 6, 1381-1386.
Cook S., MacLaughlin H. & MacDougall I.C. (2008). A structured weight
management programme can achieve improved functional ability
and significant weight loss in obese patients with chronic kidney
disease. Nephrology Dialysis Transplantation 2 3, 263-268.
Covic A., Kothawala P., Bernal M. et al. (2009). Systematic review of
the evidence underlying the association between mineral metabolism disturbances and risk of all-cause mortality, cardiovascular
mortality and cardiovascular events in chronic kidney disease.
Nephrology Dialysis Transplantation 2 4, 1506-1523.
Department of Health. (2001). The National Service Framework for
Diabetes. www.dh.gov.uk (accessed 6 June 2011).
Department of Health. (2009). Blood Pressure. www.dh.gov.uk
(Accessed 6 June 2011).
Department of Health and Diabetes UK Joint Report. (2006). Care
Planning in Diabetes.
Diabetes Control and Complications Trial Research Group. (1993). The
effect of intensive treatment of diabetes on the development and
progression of long-term complications in insulin-dependent
diabetes mellitus. The New England Journal of Medicine 3 2 9,
977-986.
Diabetes UK. (2008). Position paper on vascular risk factors.
Dhingra R., Sullivan L., Fox C.S. et al. (2007). Relations of serum
phosphorus and calcium levels to the incidence of cardiovascular
disease in the community. Archives of Internal Medicine 1 6 7,
879-884.
Dwyer J.T., Larvine B., Leung J. et al. (2005). Are nutritional status indicators associated with mortality in the hemodialysis (HEMO)
study? Kidney International 6 8, 1766-1776.
Eckel R.H. (2008). Clinical practice. Non-surgical management of obesity
3 5 8, 1941-1950.
in adults. The New England Journal of Medicine3
Ejerblad E., Fored C.M., Lindblad P. et al. (2006). Obesity and risk for
chronic renal failure. Journal of the American Society of
Nephrology 1 7, 1695-1702.
Elsayed E.F., Tighiouart H., Weiner D.E. et al. (2008). Waist-to-hip ratio
and body mass index as risk factors for cardiovascular events in
CKD. American Journal of Kidney Diseases 5 2, 49-57.
Evans M., Fryzek J.P., Elinder C.G. et al. (2005). The natural history of
chronic renal failure: results from an unselected, populationbased, inception cohort in Sweden. American Journal of Kidney
Diseases 4 6, 863-870.
Food Standards Agency. (2011). Salt. www.food.gov.uk (Accessed 3
June 2011).
Fouque D. & Lavill M. (2009). Low protein diets for chronic kidney disease in non diabetic adults (Review). The Cochrane Collaboration.
Fouque D., Pelletier S., Mafra D. et al. (2011). Nutrition and chronic
kidney disease. Kidney International 8 0, 348-357.
Fouque D., Vennegoor M., Wee P.T. et al.(2007). EBPG guideline on
nutrition. Nephrology Dialysis Transplantation 2 2, ii45-ii87.
Gaede P., Vdel P., Larsen N. et al. (2003). Multifactorial intervention
and cardiovascular disease in patients with type 2 diabetes. The
3 4 8(5), 383-393.
New England Journal of Medicine3
Goldstein D.J. (1992). Beneficial health effects of modest weight loss.
International Journal of Obesity and Related Metabolic Disorders
1 6, 397-415.
Harnden K.E., Frayn K.N. & Hodson L. (2010). Dietary Approaches to Stop
Hypertension (DASH) diet: applicability and acceptability to a UK
population. Journal of Human Nutrition and Dietetics 2 3(1), 3-10.
He F.J. & MacGregor G.A. (2002). Effect of modest salt reduction on
blood pressure: a meta-analysis of randomised trials. Implications
for public health. Journal of Human Hypertension 1 6, 761-770.
He F.J. & MacGregor G.A. (2003). How far should salt intake be
reduced? Hypertension 4 2, 1093-1099.
He F.J. & MacGregor G.A. (2005). Modest salt reduction lowers blood
pressure in isolated systolic hypertension and combined hypertension. Hypertension 4 6, 66-70.
© 2012 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2012
49
jorc_283.qxd
2/2/12
10:34 AM
Page 50
Willingham
He F.J. & MacGregor G.A. (2009). A comprehensive review on salt and
health and current experience of worldwide salt reduction programmes. Journal of Human Hypertension 2 3, 363-384.
Hsu C.Y. & Chertow G.M. (2002). Elevations of serum phosphorus and
potassium in mild to moderate chronic renal insufficiency.
Nephrology Dialysis Transplantation 1 7, 1419-1425.
Hsu C., McCulloch C.E., Iribarren C. et al. (2006). Body mass index and
risk for end-stage renal disease. Annals of Internal Medicine 1 4 4,
21-28.
Johansen K.L., Young B., Kaysen G.A. et al. (2004). Association of body
size with outcomes among patients beginning dialysis. The
American Journal of Clinical Nutrition 8 0, 324-332.
Jones-Burton C., Mishra S.I., Fink J.C. et al. (2006). An in-depth review
of the evidence linking dietary salt intake and progression of
chronic kidney disease. American Journal of Nephrology 2 6, 268275.
Klahr S., Levey A.S., Beck G.J. et al. (1994). For the Modification of Diet
in Renal Disease Study Group. The effects of dietary protein
restriction and blood pressure control on the progression of
chronic renal disease. The New England Journal of Medicine
3 3 0(13), 877-884.
Klein S., Sheard N.F., Pi-Sunyer X. et al. (2004). Weight management
through lifestyle modification for the prevention and management of type 2 diabetes: rationale and strategies. Diabetes Care
2 7(8), 2067-2073.
Knowler, Stratton R.J., Bircher G., Rouque D. et al. (2002). Diabetes
Prevention Program Research Group. Reduction in the incidence
of type 2 diabetes with lifestyle intervention or metformin. The
New England Journal of Medicine 3 4 6(6), 393-403.
Koppell K.J., Kataoka M., Williams S.M. et al. (2010). Nutritional intervention in patients with type 2 diabetes who are hyperglycaemic
despite optimised drug treatment-Lifestyle Over and Above Drugs
in Diabetes (LOADD) study: randomised controlled trial. BMJ
3 4 1, 3337-43.
Leavey S., McCullough K., Hecking E. et al. (2001). Body mass index
and mortality in ‘healthier’ as compared with ‘sicker’ haemodialysis patients: results from the Dialysis Outcomes and Practice
Patterns Study (DOPPS). Nephrology Dialysis Transplantation 1 6,
2386-2394.
Locatelli F., Fouque D., Heimburger O. et al. (2002). Nutritional status
in dialysis patients: a European consensus. Nephrology Dialysis
Transplantation 1 7, 563-572.
Look AHEAD Research Study Group. (2007). Reduction in weight
and cardiovascular disease risk factors in individuals with type
2 diabetes: one-year results of the Look AHEAD trial. Diabetes
Care, 3 0 : 1374-83.
Mann J.I., De Leeuw I., Hermansen K. et al. (2004). Evidence-based
nutritional approaches to the treatment and prevention of diabetes mellitus. Nutrition Metabolism and Cardiovascular Diseases
1 4, 373-394.
Morales E., Valero M.A., Leon M. et al. (2003). Beneficial effects of
weight loss in overweight patients with chronic proteinuric
nephropathies. American Journal of Kidney Diseases 4 1, 319327.
50
Journal of Renal Care 2012
Moranne O., Froissart M., Rossert J. et al. (2009). Timing of onset of
CKD-related metabolic complications. Journal of the American
Society of Nephrology 2 0, 164-167.
Nathan D.M., Buse J.B., Davidson M.B. et al. (2009). Medical management of hyperglycaemia in type 2 diabetes mellitus: a consensus
algorithm for the initiation and adjustment of therapy (A consensus statement from the American Diabetes Association and the
European Association for the Study of Diabetes). Diabetologia
5 2, 17-30.
National Collaborating Centre for Chronic Conditions-on behalf of
NICE. (2008). Type 2 Diabetes – National Clinical Guideline for
Management in Primary and Secondary Care (Update). London:
Royal College of Physicians.
National Diet and Food Survey. (2010). www.data.gov.uk/dataset/
national_diet_and_nutrition_survey_rolling_programme
(accessed June 2011).
National Institute for Clinical Excellence. (2008). Chronic kidney disease –
early identification and management of chronic kidney disease in
adults in primary and secondary care. NICE Clinical Guideline 73.
National Institute for Clinical Excellence. (2011). Preventing type 2 diabetes: population and community interventions. NICE Public
Health Guidance 35.
Navaneethan S.D., Yehnert H., Moustarah F. et al. (2009). Weight loss
interventions in chronic kidney disease: a systematic review and
meta-analysis. Clinical Journal of the American Society of
Nephrology 4 , 1565-1574.
Neter J.E., Stam B.E., Kok F.J. et al. (2003). Influence of weight reduction on blood pressure: a meta analysis of randomised controlled
trials. Hypertension 4 2, 878-884.
NHS Choices. (2011). EatWell plate. www.nhs.uk/Livewell/healthy-eating (accessed 29 November 2011).
Nutritional Subcommittee of the Diabetes Care Advisory Committee of
Diabetes U.K. (2003). The implementation of nutritional advice
for people with diabetes. Diabetes Medicine 2 0, 786-807.
Nyirenda M.J., Tang J.I., Padfield P.L. et al. (2009). Hyperkalaemia. BMJ
3 3 9, b4114.
Paffenberger R.S. Jr., Hyde R.T., Wing A.L. et al. (1993). The association
of changes in physical-activity level and other lifestyle characteristics with mortality among men. The New England Journal of
Medicine 3 2 8, 538-545.
Pifer T.B., McCullough K.P, Port F.K. et al. (2002). Mortality risk in
hemodialysis patients and changes in nutritional indicators:
DOPPS. Kidney International 6 2, 2238-2245.
Raptis A.E., and Viberti G. (2001). Pathogenesis of Diabetic Nephropathy.
Exp. Clin. Endocrinol. Diabetes 1 0 9(Suppl 2): 5424-37.
Reddy V., Symes F., Sethi N. et al. (2009). Dietitian-led education program to improve phosphate control in a single-center hemodialysis population. Journal of Renal Nutrition 1 9(4), 314-320.
Renal Association. (2010a). 13th Report of the UK Renal Registry.
www.renalreg.com/Reports/2010 (Accessed 30 May 2011).
Renal Association. (2010b). Nutrition in CKD Clinical Practice
Guidelines. www.renal.org/guidelines (Accessed 14 June 2011).
Renal Association. (2011). Chronic Kidney Disease Clinical Practice
Guidelines. www.renal.org/guidelines (Accessed 14 June 2011).
© 2012 European Dialysis and Transplant Nurses Association/European Renal Care Association
jorc_283.qxd
2/2/12
10:34 AM
Page 51
THE DIETARY MANAGEMENT OF PATIENTS WITH DIABETES
AND RENAL DISEASE: CHALLENGES AND PRACTICALITIES
Robertson L.M., Waugh N. & Robertson A. (2009). Protein restriction
for diabetic renal disease (review). The Cochrane Collaboration.
Ryu S., Chang Y., Woo H.Y. et al. (2008). Changes in body weight predict CKD in healthy men. Journal of the American Society of
Nephrology 1 9, 1798-1805.
Sacks F.M., Svetkey L.P., Vollmer W.M. et al. (2001). For the DASHSodium Collaborative Research Group. Effects on blood pressure
of reduced dietary sodium and the dietary approaches to stop
hypertension (DASH) diet. The New England Journal of Medicine
3 4 4(1), 3-10 .
Savica V., Calo L.A., Monardo P. et al. (2009). Salivary phosphorus and
phosphate content of beverages: implications for the treatment
of uremic hyperphosphatemia. Journal of Renal Nutrition 1 9, 6972.
Shinaberger C.S., Greenland S., Kopple J.D. et al. (2008). Is controlling
phosphorus by decreasing dietary protein intake beneficial or
harmful in persons with chronic kidney disease? American Journal
of Clinical Nutrition 8 8, 1511-1518.
Scottish Intercollegiate Guidelines Network (SIGN) Guideline 116 (2010).
Management of Diabetes – A National Clinical Guideline. ISBN
978 1 905813 58 2
Slagman M.C.J., Waanders F., Hemmelder M.H. et al. (2011).
Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial.
BMJ 3 4 3, d4366.
Stratton R.J., Bircher G., Fouque. et al. (2005). Multinutrient oral supplements & tube feeding in maintenance dialysis: a systematic
review & meta-analysis. American Journal of Kidney Diseases 4 6
(3), 387 – 405.
Sullivan C.M., Leon J.B. & Sehgal A.R. (2007). Phosphorus-containing food additives and the accuracy of nutrient databases:
implications for renal patients. Journal of Renal Nutrition 1 7 ,
350-354.
The National Health and Nutrition Examination Survey NHANES. (2008).
www.uk.ask.com/web?q ⫽ NHANES&o (accessed May 2011).
Thijssen D.H., Maiorana A.J., O’Driscoll G. et al (2010). Impact of inactivity and exercise on the vasculature in humans. European
Journal of Applied Physiology 1 0 8, 845-875.
Ting S.M.S., Nair H., Ching I. et al. (2009). Overweight, obesity and
chronic kidney disease. Nephron Clinical Practice 1 1 2, c121-127.
Tonelli M., Pannu N. & Manns B. (2010). Oral phosphate binders in
patients with kidney failure. The New England Journal of
Medicine 3 6 2, 1312-1324.
Tong P., Luk A., So W.Y. et al. (2008). Metabolic syndrome predicts
new onset of chronic kidney disease in 5,829 patients with type
2 diabetes: a 5-year prospective analysis of the Hong Kong
Diabetes Registry. Diabetes Care 3 1, 2357-2361.
Tuomilehto J., Lindstrom J., Eriksson J.G. et al. (2001). (for the Finnish
Diabetes Prevention Study Group). Prevention of type 2 diabetes
mellitus by changes in lifestyle among subjects with impaired glucose tolerance. The New England Journal of Medicine 3 4 4(18),
1343-1350.
United Kingdom Prospective Diabetes Study Group. (1998). Intensive
blood-glucose control with sulphonylureas or insulin compared
with conventional treatment and risk of complications in patients
with type 2 diabetes (UKPDS 33). Lancet 3 5 2, 837-853.
United States Department of Agriculture. (2011). MyPlate.
www.choosemyplate.gov (accessed 29 November 2011).
United States Renal Data System. (2010). USRD 2008 Annual Report.
Vollmer W.M., Sacks F.M., Ard J. et al. (2001). Effects of diet and
sodium intake on blood pressure: subgroup analysis of the
DASH-sodium trial. Annals of Internal Medicine 1 3 5, 10191028.
Wang Y., Chen X., Song Y. et al. (2008). Association between obesity
and kidney disease: a systematic review and meta-analysis. Kidney
International 7 3, 19-33.
World Health Organization. (1999). Definition, Diagnosis and
Classification of Diabetes Mellitus and Its Complications: Report of a
WHO Consultation, Part 1: Diagnosis and Classification of Diabetes
Mellitus. Geneva, Switzerland: World Health Organization.
World Health Organization. (2003). Screening for Type 2 Diabetes:
Report of a World Health Organization and International Diabetes
Federation Meeting. Geneva: Department of Noncommunicable
Disease Management, World Health Organization.
World Health Organization. (2011). Diabetes – Fact sheet 312. Available
at: www.who.int/medicentre/factsheets/fs312 (Accessed 30
December 2011)
© 2012 European Dialysis and Transplant Nurses Association/European Renal Care Association
Journal of Renal Care 2012
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Mash et al. BMC Family Practice 2012, 13:126
http://www.biomedcentral.com/1471-2296/13/126
STUDY PROTOCOL
Open Access
Effectiveness of a group diabetes education
programme in underserved communities in South
Africa: pragmatic cluster randomized control trial
Bob Mash1*, Naomi Levitt2, Krisela Steyn3, Merrick Zwarenstein4 and Stephen Rollnick5
Abstract
Background: Diabetes is an important contributor to the burden of disease in South Africa and prevalence rates as
high as 33% have been recorded in Cape Town. Previous studies show that quality of care and health outcomes
are poor. The development of an effective education programme should impact on self-care, lifestyle change and
adherence to medication; and lead to better control of diabetes, fewer complications and better quality of life.
Methods: Trial design: Pragmatic cluster randomized controlled trial
Participants: Type 2 diabetic patients attending 45 public sector community health centres in Cape Town
Interventions: The intervention group will receive 4 sessions of group diabetes education delivered by a health
promotion officer in a guiding style. The control group will receive usual care which consists of ad hoc advice
during consultations and occasional educational talks in the waiting room.
Objective: To evaluate the effectiveness of the group diabetes education programme
Outcomes: Primary outcomes: diabetes self-care activities, 5% weight loss, 1% reduction in HbA1c. Secondary
outcomes: self-efficacy, locus of control, mean blood pressure, mean weight loss, mean waist circumference, mean
HbA1c, mean total cholesterol, quality of life
Randomisation: Computer generated random numbers
Blinding: Patients, health promoters and research assistants could not be blinded to the health centre’s allocation
Numbers randomized: Seventeen health centres (34 in total) will be randomly assigned to either control or
intervention groups. A sample size of 1360 patients in 34 clusters of 40 patients will give a power of 80% to detect
the primary outcomes with 5% precision. Altogether 720 patients were recruited in the intervention arm and 850 in
the control arm giving a total of 1570.
Discussion: The study will inform policy makers and managers of the district health system, particularly in low to
middle income countries, if this programme can be implemented more widely.
Trial register: Pan African Clinical Trial Registry PACTR201205000380384
Keywords: Diabetes, Group education, Health education, Motivational interviewing, Mid-level health workers, South
Africa, Primary care
* Correspondence: rm@sun.ac.za
1
Family Medicine and Primary Care, Stellenbosch University, Box 19063,
Tygerberg 7505, South Africa
Full list of author information is available at the end of the article
© 2012 Mash et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Mash et al. BMC Family Practice 2012, 13:126
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Background
Diabetes is a significant contributor to the burden of disease in South Africa [1] and the prevalence in Africa is
expected to increase by 80% over the next 15 years [2].
Self-reported prevalence rates for diabetes of 2.4% in
men and 3.7% in women have been reported in South
Africa [3]. However, studies in the Western Cape, one of
the nine provinces of South Africa, suggest rates in
urban areas as high as 33% [4].
Approximately 80% of the 3,1 million population in
the Cape Town Metropole are uninsured and rely on
public sector facilities to manage their diabetes. Several
previous studies in the Western Cape have illustrated
the poor quality of care and outcomes for diabetic
patients [5,6]. Almost 80% of patients were uncontrolled
(HbA1c≥7%) in an audit of type 2 diabetes in Cape
Town’s public sector in 2011 [6]. Deficiencies in knowledge and self-care amongst patients and the inability of
primary care providers to ameliorate this, have been
identified as part of the problem. The population served
by the public sector is characterized by low socioeconomic status, low levels of education and low health
literacy. The population served come from historically
disadvantaged communities and speak mainly Afrikaans
or Xhosa.
Primary care services in the country are largely nurseled with the support of doctors. Other health workers,
appropriate to the management of diabetes, such as dieticians and podiatrists, are usually not available. A variety of mid-level workers, such as health promoters,
have been trained and employed in community health
centres. Currently the education of diabetic patients and
support of self-care has been left to the varied initiatives
of individual health workers and there is no structured
programme of education for people with diabetes in the
Western Cape. Chronic care teams have identified that
the health promoter should be the key person in delivering such a programme [7].
Community health centres in the Western Cape are
usually found in larger metropolitan areas or rural
towns. Diabetic patients are often seen in such large
numbers that a specific day is set aside each week for
them to attend a diabetic “club”. At a given health centre
patients are usually scheduled to attend the “club” as a
group and are given appointments to be seen for review
every 3 months.
During 2006–2008 the investigators were involved in
an appreciative inquiry project to improve the annual
review of the diabetic patients in the Cape Town
Metropole. During this project the quality of care in
the annual audit in terms of assessment of HbA1c,
serum creatinine and cholesterol, retinal screening,
foot screening and calculation of body mass index significantly improved [7]. At the end of this project staff
Page 2 of 7
articulated the need for a better approach to diabetes
education and collaborated in designing the content of
a more structured programme to be delievered by
health promoters [7].
Health promoters have a secondary school education
up to at least Grade 8 and once employed have additional training in the knowledge and skills required to
deliver health education messages and promote health.
There are currently 120 health promoters in the Province and the policy of the Department of Health is to
have a health promoter at every community health
centre. A recent study showed that the current health
promoters have a good knowledge of key diabetes education messages for patients [8].
Although a variety of individual and group educational
materials are available from non-government organizations and pharmaceutical companies, no materials are
officially disseminated or recommended by the national
or provincial Department of Health.
The relationship between health care provider and patient is recognized to have an important influence on patient understanding and adherence [9]. Motivational
interviewing has been recommended as a more skilful
guiding approach to eliciting lifestyle change and promoting self-care [10] and a recent systematic review
concluded that it out-performs traditional advice-giving
in 80% of studies [11,12]. Professors Rollnick and Mash
are members of the International Network of Motivational Interviewing Trainers and have experience with
training and researching in this area [10,13]. Studies of
individually-delivered motivational interviewing for diabetic patients have produced promising results [14,15].
A recent study of individual motivational interviewing
for the prevention of diabetes also demonstrated a significant effect on achieving 5% weight loss [16].
Group interactions have been found to be effective in
diabetes education [17] and local chronic care staff have
indicated that this is the most practical approach in their
very busy health centres [7]. A systematic review of group
education in diabetes concluded that “The results of the
meta-analyses in favour of group-based diabetes education
programmes were: reduced glycated haemoglobin at four
to six months (1.4%; 95% confidence interval (CI) 0.8 to
1.9; P < 0.00001), at 12–14 months (0.8%; 95% CI 0.7 to 1.0; P < 0.00001) and two years (1.0%; 95% CI 0.5 to 1.4; P< 0.00001); reduced fasting blood glucose levels at 12 months (1.2 mmol/L; 95% CI 0.7 to 1.6; P < 0.00001); reduced body weight at 12–14 months (1.6 Kg; 95% CI 0.3 to 3.0; P = 0.02); improved diabetes knowledge at 12–14 months (SMD 1.0; 95% CI 0.7 to1.2; P < 0.00001) and reduced systolic blood pressure at four to six months (5 mmHg: 95% CI 1 to 10; P = 0.01). There was also a reduced need for diabetes medication (odds ratio 11.8, 95% CI 5.2 to 26.9; P < 0.00001; RD = 0.2; NNT = 5). Mash et al. BMC Family Practice 2012, 13:126 http://www.biomedcentral.com/1471-2296/13/126 Therefore, for every five patients attending a groupbased education programme we could expect one patient to reduce diabetes medication” [17]. Motivational interviewing in group format is a relatively new development; 12 published reports have emerged [18,19], which include three randomized trials and one study in the diabetes field [20]. Despite evidence of the effectiveness of group diabetes education all of the trials have been conducted in high-income countries and by health professionals such as doctors or nurses. This trial will be the first in an African context and delivered by mid-level health workers. In addition the incorporation of group motivational interviewing will add to a small evidence base on this topic. If the study demonstrates effectiveness of this educational intervention then it can be implemented throughout the Western Cape and may well be replicated in the rest of the country and possibly within the southern African Region. The study intends to inform policy makers and managers of the district health services and help them decide whether to implement the programme more widely. Page 3 of 7 The CONSORT statement on pragmatic trials was used to assist with the design [21]. Target population Patients with Type 2 Diabetes attending 45 Community Health Centres in the Cape Town Metropole were the target population. Thirty eight health promoters are currently employed within these facilities. Sample size Data from a previous study in the same population (n=450, 18 clinics) showed that the mean HbA1c was 8.8% (SD 3.3) and intraclass correlation 0.1 [22]. Similarly the mean weight was 78.2Kg (SD 16.7) and intraclass correlation 0.05. These figures were used to calculate the sample and cluster size for a 5% weight reduction and a 1% reduction in HbA1c. Based on a level of significance of 0.05 and a power of 0.8 the study required 17 clusters in each arm with 40 patients per cluster. The total sample size therefore would be 34 clusters (health centres) and 1360 patients. Sample selection process Aim and objectives Aim: To evaluate, by means of a pragmatic cluster randomized controlled trial, the effectiveness of a group diabetes education programme delivered by trained health promoters with a guiding (motivational interviewing) style, in community health centres in Cape Town, South Africa. Objective 1: To evaluate effectiveness by assessing group changes in the following: Primary outcomes: improved diabetes self-care activities, 5% weight loss, HbA1c reduction of 1 percentage point Secondary outcomes: improved diabetes-specific selfefficacy, locus of control, mean blood pressure, mean weight loss, mean waist circumference, mean HbA1c, mean total cholesterol and quality of life Objective 2: To evaluate fidelity to the educational programme and motivational interviewing by use of audiotapes and scoring health promoters with the Motivational Interviewing Integrity Code. Objective 3: To explore the experiences of the health promoters with regards to their training and delivery of the diabetes education programme. Objective 4: To explore the experiences of patients who attend the diabetes education sessions. Methods Study design Pragmatic cluster randomized controlled trial with additional qualitative and quantitative process evaluations. Community health centres that agreed to participate were randomly allocated by computer generated random numbers to either control or intervention groups. All type 2 diabetic patients attending the selected health centre on the recruitment days were invited to participate in the study. Recruitment days were when the health centre had a diabetic club. Centres were visited weekly until the sample of 40 patients per health centre was obtained. Altogether 720 patients were recruited in the intervention arm and 850 in the control arm giving a total of 1570. Inclusion and exclusion criteria Inclusion: All type 2 diabetic patients who gave consent, regardless of the type of medication (oral and/or insulin) or time since diagnosis. Exclusion: Type 1 diabetic patients, those who refused consent, those who were judged by the clinical nurse practitioner or medical officer as unable to participate in the intervention (for example due to acute illness, mental illness, dementia or another justifiable reason). Design of intervention The intervention was developed by the researchers with assistance from a diabetes nurse educator and social scientist with an interest in behaviour change counseling. The sessions were piloted with a group of diabetic patients attending Groote Schuur Tertiary Hospital. The following overall structure was suggested by the chronic care teams (including health promoters) in a previous study [7]. Patients should receive 4 educational Mash et al. BMC Family Practice 2012, 13:126 http://www.biomedcentral.com/1471-2296/13/126 sessions each lasting between 20–60 minutes. Sessions should be offered when the patients are scheduled for a routine visit to the health centre by a health promoter. Groups should have between 10 and 15 people who would remain together throughout the programme: Page 4 of 7 elicit-provide-elicit was emphasized as a strategy and in fact the sessions themselves were structured according to this model. This model involves the following three steps in a cyclical process [10]. Elicit either the groups prior knowledge or what Session Session Session Session 1: 2: 3: 4: Understanding diabetes Living a healthy lifestyle Understanding the medication Preventing complications The researchers reviewed a number of materials for group education and found the Conversation Map™ the most congruent with the design of the intervention [23-25]. The Conversation Map™ materials were piloted in a rural town to see which aspects were appropriate for the local context [26]. A number of the group activities, such as working with myths and facts cards, recommended in the Conversation Map™ material were adapted for the local context. The researchers also developed new graphic materials to help patients understand the pathophysiology of diabetes as well as the effect of medication and self-care activities. Pictures were developed to illustrate portion size and food choices. All these pictures were then designed and printed in the format of a flip chart. A comprehensive set of food cards illustrating local South African foods and which could be used in group activities were also purchased. Patient education materials on foot care, coping with stress, alcohol and smoking cessation were also developed or sourced locally. The sessions were designed to be congruent with a guiding communication style [10]. This style was intended to include the following characteristics: they are most interested in learning about with regard to a specific topic Provide the group with information in a neutral way that builds on what they already know or addresses what they are most interested in Elicit how group members will make sense of or apply this information personally The researchers recognized that health promoters were used to delivering health education in a directing style, often in quite difficult circumstances. This directing style was characterized by an authoritarian, expert role that told patients what they should be doing. Educational talks were often given to the whole reception area where health promoters had to shout over staff and patients waiting to be seen. The educational model developed in this study was therefore quite a shift from what health promoters were used to. The goals therefore in terms of communication skills were kept as simple as possible. The training manual with more detailed information on the sessions is available as a Additional file 1. Control group The control patients received usual education at the health centre. Usual education consisted of ad hoc educational talks in the reception area or club room as well as any individual counseling that providers might have time for in the consultation. Collaboration: Both health promoters and patients should contribute substantially to the group discussion Empathy: Health promoters should demonstrate active listening skills and their understanding of the patient’s perspective, particularly through the use of summaries. Support for autonomy: Health promoters should promote a sense of choice and control over behaviour change Evocation: Health promoters should elicit change talk and possible solutions from the group members Direction: Health promoters should manage time and keep aligned with the intended content and purpose of the sessions It was also recognized that diabetes education often involves a significant component of information and therefore strategies to exchange information rather than just transfer it were taught. In particular the use of Training of health promoters Health promoters were trained in an initial 4 day workshop which focused on the overall structure of the sessions, communication style and skills, diabetes knowledge and the first two sessions. Training was conducted in a similar small group educational process with the trainers modeling the same skills expected of the health promoters when they educated patients. Following the initial workshop health promoters began the education immediately and a further 2-day workshop was held 2 months later to reinforce the initial training and introduce the last 2 sessions. The researcher who evaluated their fidelity to the intervention visited each health centre at least twice and gave some feedback to the health promoters after the sessions. Implementation of intervention At the end of the HPO’s initial training a number of logistical issues were addressed. These included identifying Mash et al. BMC Family Practice 2012, 13:126 http://www.biomedcentral.com/1471-2296/13/126 the room where sessions could take place or if no space was available in the health centre a suitable local venue such as a library or community hall. Of the 17 randomly selected health centres only 13 had health promoters currently employed and therefore 4 of the health promoters agreed to offer the intervention at two sites. Following recruitment the patients at each health centre were grouped to time the educational sessions on the same date as their routine attendance for medication. Patients were sent bulk SMS reminders of the date and time of their educational sessions and health promoters were encouraged to call the patients prior to the meetings to remind and motivate them. A once off shopping voucher for a local supermarket was offered as an incentive to attend the sessions (this was equivalent to $2). Letters were sent to all those without a phone and to the pharmacist asking for medication to be handed out at or after the educational session. Attendance certificates were available for those who were working. Health promoters were also provided with glucometers so they could test patient’s glucose at the sessions in the hope that this would also encourage attendance. Data collection process Data was collected at baseline and 12 months later. Data collection teams were employed to visit the health centres over a period of 4 weeks and consisted of a nurse and field workers. Nurses were employed to collect blood and take physical measurements and all members completed the questionnaires with patients. Standard operating procedures were used in measuring weight (electronic scales), waist circumference (tape measure) and blood pressure (Omron digital blood pressure monitor). HbA1c and total cholesterol were measured by one laboratory under the National Health Laboratory Service where quality control measures were in place. The data collection teams received a 1-day training workshop prior to the data collection periods and were supervised daily by the project co-ordinator. It was not possible to blind the health promoters, patients or data collection teams as to whether the health centre was a control or intervention site. Data collection tools The following data was collected from participants and their medical records at baseline: Age, sex, duration of diabetes, medication used and medical history for concomitant diagnoses and complications. Medication use and new diagnoses were also recorded at follow up. Self-care activities were measured using a questionnaire that separately scores diet, exercise, foot care, smoking and medication use. This validated questionnaire had previously been used successfully in the South African context [27]. Page 5 of 7 Locus of control measures the patient’s belief in their ability to control their illness (internal locus of control) as opposed to a belief that their illness is outside their own control and primarily in the hands of others (external locus of control) or that control is a matter of luck (chance locus of control). Group education using a patient-centred approach has been shown to increase ones internal locus of control, which itself is linked to the likelihood of behaviour change. A specific questionnaire that measures diabetic locus of control has been developed and was used in this study [28]. Self-efficacy is a measure of the patient’s actual confidence in their ability to perform self-care activities. A simple measure of diabetic self-efficacy has been developed by Stanford University’s study on Diabetes SelfManagement [29]. Enhancing self-efficacy is one of the key principles of motivational interviewing and is linked to the likelihood of actual behaviour change [10]. The Stanford questionnaire was contextualized and used to measure self-efficacy. Diabetes quality of care was measured using a questionnaire that has previously been used in the South African context for Type 2 Diabetic patients [30]. Quality of life is an important health outcome that may be impacted by psychosocial factors, complications, duration of diabetes, demographic variables, gender, type of diabetes, glycaemic control and treatment regimes [31]. Process evaluation Fidelity to the planned educational programme and to the communication style was assessed by observing 36 randomly selected group sessions. Sessions were stratified to ensure that each site and session was sampled equally. The observer noted the extent to which the session followed the intended content and process and also made additional field notes. Sessions were recorded on audiotape and subsequently evaluated using the Motivational Interviewing Treatment Integrity Coding, which is a validated tool for assessing proficiency in MI [32]. This tool determines whether the counselor achieved beginning proficiency in MI. The health promoters experience was evaluated by means of three focus group interviews that were facilitated by an independent researcher. The initial focus group was held immediately after the training, the second was held mid-intervention and the third after all the education had been completed. The patient’s experience was evaluated by means of in depth interviews with one patient from each of the health centres in the intervention group who had attended at least 3 of the sessions. Interviews were also conducted by an independent researcher in the patient’s home after the educational sessions were completed. The qualitative data from these interviews was transcribed verbatim and analysed using the framework method and Atlas-ti software. Mash et al. BMC Family Practice 2012, 13:126 http://www.biomedcentral.com/1471-2296/13/126 Data analysis Intention-to-treat analysis will evaluate the primary and secondary outcomes. Any missing baseline data will be imputed using the Markov chain Monte Carlo approach. Missing status at follow-up will be modelled on baseline covariates and randomised group using logistic regression. Inverse probability weighting will be used for the final trial analysis. Models for comparing continuous outcomes will use linear regression and for categorical outcomes will use logistic regression with adjustment for baseline covariates and clustering. Timeline Baseline data collection took place in SeptemberDecember 2010. The intervention was delivered between October 2010 and April 2011. Follow up data collection took place in September-December 2011. Data capture and cleaning were completed by February 2012 and we are now busy with data analysis. Discussion Although group diabetes education has been shown in systematic reviews to be effective these studies are mostly from resource rich countries with more developed primary care systems [17]. The South African primary care system is struggling to develop in the post-Apartheid era while simultaneously battling with a quadruple burden of disease in the form of HIV/AIDS, injury and violence, high maternal and child mortality and a growing epidemic of non-communicable diseases [1]. The Western Cape probably has the best resourced primary care system in the country, but even there health workers complain of long hours, burnout and depression [33]. Nationally the government is committed to the re-vitalisation of primary care over the next few years [34]. In this context we need to develop approaches to diabetes education that can work in our resource constrained and pressurized environment. This trial intends to evaluate one such approach as suggested by the primary care providers involved in chronic care [7]. The trial is pragmatic in the sense that the intervention is conducted under the organizational and clinical strengths and weaknesses of the current primary care service. It is also innovative in developing a model of group motivational interviewing that is intended to be delivered by a mid level health worker who themselves may only have basic education. Nevertheless in our context task shifting is common and much is expected of such mid level health workers. Group motivational interviewing is a relatively new field and little has yet been published on the topic. The Department of Health was a partner in the development of the research proposal with the intention that, should the intervention be effective, it can be implemented throughout the Western Cape. The research team maintains Page 6 of 7 links with the Director for Public Health, Deputy Director for Chronic Diseases, Director of District Health Services and the Human Resource and Development Directorate. The intervention being studied is congruent with the newly developed Provincial Policy on Chronic Diseases in the Western Cape Department of Health. The Department of Health is also a partner in the Chronic Disease Initiative in Africa which is a supporting institution. The Western Cape Province has a track record of developing innovations that are later taken up by the National Department of Health. The intervention being tested is also congruent with national policy and we anticipate interest in further implementation if it is effective. The Chronic Disease Initiative in Africa has a more regional vision and if the intervention is effective will assist with the dissemination of the programme. The International Diabetes Foundation is also the key funder of the study and will disseminate any useful learning to the international community. Additional file Additional file 1: Group diabetic education. Training manual for health promoters. Abbreviations AIDS: Acquired Immune Deficiency Syndrome; CI: Confidence Interval; HbA1c: Glycosylated Haemoglobin; HIV: Human Immunodeficiency Virus; MI: Motivational Interviewing. Competing interests The authors declare that they have no competing interests. Authors’ contributions All authors contributed to the research proposal described in this article. BM is the principal investigator with particular expertise in primary care and motivational interviewing. DL has particular expertise in clinical diabetes and KS in non-communicable chronic diseases epidemiology. MZ has expertise in pragmatic clustered randomized trial design and contributed to the CONSORT statement in this area. SR is an international expert in motivational interviewing. All authors read and approved the final manuscript. Authors’ information BM co-ordinates a network of motivational interviewing practitioners, trainers and researchers in southern Africa. DL and KS are the directors of the Chronic Diseases Initiative in Africa which also supported this study. MZ is a South African and used to be head of the Health Systems Research Unit at the SA Medical Research Council prior to his current position at the University of Toronto. SR is also a South African and is one of the founding fathers of motivational interviewing as an approach to behavior change counseling. Acknowledgements We thank Ms Buyelwa Majikela-Dlangamandla and Dr Kathy Murphy for their assistance with the design of the educational intervention. Prof Carl Lombard, the head of biostatistics at the SA Medical Research Council, assisted with the sample size calculation and design of the analysis. Ms Unita van Vuuren and Ms Maureen McCrae provided essential support from the Department of Health. Apart from the international funding received from BRIDGES, additional funds were received from the Chronic Diseases Initiative in Africa of which Stellenbosch University is a member and directly from strategic research funds within Stellenbosch University. Mash et al. BMC Family Practice 2012, 13:126 http://www.biomedcentral.com/1471-2296/13/126 Funding This project is supported by a BRIDGES Grant from the International Diabetes Federation. BRIDGES, an International Diabetes Federation project, is supported by an educational grant from Lilly Diabetes (ST09-040). Author details 1 Family Medicine and Primary Care, Stellenbosch University, Box 19063, Tygerberg 7505, South Africa. 2Diabetic Medicine and Endocrinology, University of Cape Town and Chronic Diseases Initiative in Africa, Faculty of Health Sciences, University of Cape Town, P.Bag X3, Observatory 7935, Room J47 – 85, Old Groote Schuur Hospital Building, Cape Town, South Africa. 3 Chronic Diseases Initiative in Africa, Faculty of Health Sciences, University of Cape Town, P.Bag X3, Observatory, Room J47 – 85, Old Groote Schuur Hospital Building, Cape Town 7935, South Africa. 4Institute for Clinical Evaluative Sciences and Department of Health Policy, Management and Evaluation, University of Toronto, G1 06, 2075 Bayview Avenue, Toronto, ON M4N 3M5, Canada. 5Professor of Health Care Communication, Department of Primary Care and Public Health, Cardiff University, Neuadd Meirionnydd Heath Park, Cardiff, WALES CF14 4YS, UK. Received: 14 June 2012 Accepted: 6 December 2012 Published: 24 December 2012 References 1. Bradshaw D, Norman R, Schneider M: A clarion call for action based on refined DALY estimates for South Africa. SAMJ 2007, 97(6):438–440. 2. International Diabetes Foundation: Diabetes Atlas. 3rd edition. Brussels: International Diabetes Foundation; 2008. Available from Atlas: www.eatlas. idf.org. 3. Mollentze W, Levitt N: Diabetes Mellitus and Impaired Glucose Tolerance in South Africa. In Chronic Diseases of Lifestyle in South Africa: 1995–2005. Edited by Steyn K, Fourie J, Temple N. Cape Town: South African Medical Research Council; 2006:109–121. 4. Matsha TE, Hassan MS, Kidd M, Erasmus RT: The 30-year cardiovascular risk profile of South Africans with diagnosed diabetes, undiagnosed diabetes, pre-diabetes or normoglycaemia: The Bellville, South Africa pilot study. Cardiovasc J Afr. 2012, 23(1):5–11. doi:10.5830/CVJA-2010-087. 5. Levitt N, Bradshaw D, Zwarenstein M, Bawa A, Maphumolo S: Audit of public sector primary diabetes care in Cape Town. Diabet Med 1997, 14:1073–1077. 6. de Vries E, de Sa A, Murie M, Namane S, Govender S, Schlemmer A, et al: Auditing chronic disease care: does it make a difference? Presentation at the 15th National Family Practitioners Conference. Cape Town:; 2012. (Access 30th August 2012) Available from http://saafp.org/conferences. 7. Mash B, Levitt N, Van Vuuren U, Martell R: Improving the diabetic annual review in primary care: An appreciative inquiry in the Cape Town District Health Services. SA Fam Pract 2008, 50(5):50–50d. 8. Parker W: Lifestyle modification education in chronic disease of lifestyle: Insight into counselling provided by health professionals. Cape Town: University of Cape Town; 2008. 9. Stewart M: Effective physician-patient communication and health outcomes: A review. Can Med Assoc J 1995, 152(9):1423–1433. 10. Rollnick S, Miller W, Butler C: Motivational interviewing in health care: Helping patients change behaviour. London: The Guilford Press; 2008. 11. Walters S, Ogle R, Martin J: Chapter 25: Perils and possibilities of group-based motivational interviewing in Miller W, Rollnick S (Eds) Motivational interviewing: Preparing people for change. London: Guilford Press; 2002. 12. Rubak S, Sandbæk A, Lauritzen T, Christensen B: Motivational interviewing: a systematic review and meta-analysis. Br J Gen Pract 2005, 55(513):305–312. 13. Mash B, Baldassini G, Mkhatshwa H, Sayeed I, Ndapeua S: Reflections on the training of counsellors in motivational interviewing for programmes for the prevention of mother to child transmission of HIV in sub-Saharan Africa. SA Fam Pract 2008 2008, 50(2):53–59. 14. Channon S, Smith V, Gregory J: A pilot study of motivational interviewing in adolescents with diabetes. Arch Dis Child 2003, 88:680–683. 15. Channon S, Huws-Thomas M, Rollnick S, Hood K, Cannings-John R, Gregory J: A Multicenter Randomized Controlled Trial of Motivational Interviewing in Teenagers With Diabetes. Diabetes Care 2006, 30(6):1390–1395. 16. Greaves C, Middlebrooke A, O’Loughline, et al: Motivational interviewing for modifying diabetes risk: a randomized controlled trial. Br J Gen Pract 2008, 58:535–540. Page 7 of 7 17. Deakin TA, McShane CE, Cade JE, Williams R: Group based training for selfmanagement strategies in people with type 2 diabetes mellitus. Cochrane Database of Systematic Reviews 2005, (2):CD003417. 18. Wagner C, Ingersoll K: The evidence for MI in groups (Chapter 5). In: C. Wagner & K. Ingersoll Motivational Interviewing in Groups. New York: Guilford Press; in press. 19. Velasquez M, Stephens N, Ingersoll K: Motivational Interviewing in Groups. Journal of Groups in Addiction and Recovery 2006, 1(1):27–50. 20. Knight KM, Bundy C, Morris R, Higgs JF, Jameson RA, et al: The effects of group motivational interviewing and externalizing conversations for adolescents with Type-1 diabetes. Psychology, Health and Medicine 2003, 6:149–157. 21. Zwarenstein M, Treweek S, Gagnier J, Altman D, Tunis S, and the CONSORT and Pragmatic Trials in Healthcare (Practihc) groups, et al: Improving the reporting of pragmatic trials: an extension of the CONSORT statement. BMJ 2008, 337:2390. 22. Steyn K, Levitt NS, Patel M, Fourie J, Gwebushe N, Lombard C, Everett K: Hypertension and diabetes: poor care for patients at community health centres. SAMJ 2008, 98(8):618–622. 23. Price C, Shandu D, Gill G: A practical diabetes education programme for rural Africa. African Journal of Diabetes Medicine 2008, 1(1):204–209. Available from http://www.africanjournalofdiabetesmedicine.com [Accessed 12th June 2012]. 24. Accu-Chek Education Programme: For people with type 2 diabetes on conventional insulin therapy. Pretoria: Roche; 2009. 25. International Diabetes Foundation: Conversation Maps.; 2012. Available from http://www.idf.org/diabetesatlas/5e/diabetes-conversations [Accessed on 29th May 2012]. 26. Beukes W: How to improve diabetic care in the Wesbank / Ilingu Lethu suburb of Malmesbury, Western Cape. Masters Thesis. Stellenbosch: Stellenbosch University; 2010. 27. Toobert D, Hampson S, Glasgow R: The summary of diabetes self-care activities measure. Diabetes Care 2000, 23(7):943–950. 28. Trento M, Passera P, Miselli V, et al: Evaluation of the locus of control in patients with type 2 diabetes after long-term management by group care. Diabetes Metab 2006, 32:77–81. 29. Diabetes Self-Management Study Group: Self-efficacy for diabetes.; . Available from http://patienteducation.stanford.edu [Accessed 14/6/09]. 30. Westaway M, Rheeder P, Gumede T: The effect of type 2 diabetes mellitus on health-related quality of life. Curationis 2001, 24(1):74–78. 31. Rubin R, Peyrot M: Quality of life and diabetes. Diabetes Metab Res Rev 1999, 15:205–218. 32. Moyers T, Martin T, Manuel J, Hendrickson S, Miller W: Assessing competence in the use of motivational interviewing. J Subst Abus Treat 2005, 28(19):26. 33. Rousseau L, Seedat S, Emsley R, Suliman S, Hagemeister D: The prevalence of burnout and depression among medical doctors working in the Cape Town metropole community health care clinics and district hospitals of the Provincial Government of the Western Cape: A Cross-Sectional Study [Masters thesis] Stellenbosch. Stellenbosch: Stellenbosch University; 2011. 34. Rispel L, Moorman J, Chersich M, Goudge J, Nxumalo N, et al: Re-vitalising primary health care in South Africa: Review of primary health care package, norms and standards. Johannesburg: Centre for Health Policy, University of Witwatersrand; 2010. doi:10.1186/1471-2296-13-126 Cite this article as: Mash et al.: Effectiveness of a group diabetes education programme in underserved communities in South Africa: pragmatic cluster randomized control trial. BMC Family Practice 2012 13:126. Purchase answer to see full attachment

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