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In partnership with
Best practice guidance for dietitians on
the nutritional
management of Parkinson’s
Introduction
3
Nutritional management at different stages of Parkinson’s
3
3
Dietetic assessment
3
Dietary intervention
4
Healthy eating
4
Weight maintenance
4
High fibre diet with good fluid intake
4
Antioxidants
5
Co-enzyme Q10
5
B Vitamins
6
Vitamin D
6
Monitoring
6
7
Dietetic assessment
7
Dietary intervention
9
Oral nutrition support (ONS)
9
Artificial Nutrition Support (ANS)
10
Bone health/Osteoporosis
11
Orthostatic hypotension (OH)
11
Dietary management of OH
12
PPH accompanied by weight loss
13
Weight gain post-deep brain stimulation
13
Dietary protein manipulation
14
Monitoring
15
15
Dietetic assessment
16
Dietary intervention
16
Monitoring
16
Summary
17
References
18
Acknowledgements
24
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Introduction
People living with Parkinson’s are particularly susceptible to weight loss and malnutrition.
Involuntary movements associated with Parkinson’s result in increased energy expenditure,
while disease symptoms and medication side effects can limit food intake and alter
metabolism. They may also choose to follow unconventional nutritional therapies that
consequently exacerbate malnutrition. Dietitians play a key role in helping people with
Parkinson’s to optimise their nutritional status and manage various nutrition-related
symptoms and medication side effects. To assume this role, dietitians need to have up-to-
date knowledge about the nutritional consequences of Parkinson’s, as well as strategies
for managing a variety of nutrition-related symptoms.
For an overview of Parkinson’s Disease, including symptoms and treatments, we
recommend accessing the Parkinson’s UK website
1
for up-to-date information, and
signposting to other learning content and programmes. In order to help establish any
learning needs you may have, it is recommended you utilise the AHP Competency
Framework for Progressive Neurological Conditions
2
, which also includes a section
dedicated to Parkinson’s Disease
Nutritional management at different stages of Parkinson’s
Diagnosis and early disease
Parkinson’s can be a challenging diagnosis to make in its early stages. It is a diagnosis based
on clinical observation and exclusion of other conditions
3
.
NICE recommend considering referring people with Parkinson’s Disease to a dietitian for specialist
advice
4
.
Dietetic assessment
The initial assessment could be facilitated by another healthcare professional as well as a
dietitian e.g. Parkinson’s Nurse, GP or practice nurse. Examples of assessments that could
be undertaken are: weight; height; body mass index (BMI); and/or using a validated nutrition
screening tool e.g. the Malnutrition Universal Screening Tool (MUST)
5, or the Patients
Association Nutrition Checklist
6
.
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Dietary intervention
Healthy eating
There is no specific diet required; however, people newly diagnosed with Parkinson’s
should be advised to eat a healthy and well-balanced diet. Good nutrition is essential to the
wellbeing of this client group. It is imperative to establish and maintain good eating habits
throughout the course of the condition
7
.
Written and verbal information should be provided on how to adopt the Healthy Eating
Guidelines set out by the Food Standards Agency (FSA) and are incorporated into the
Parkinson’s UK resource Diet and Parkinson’s
8
.
Weight maintenance
Being underweight, something commonly experienced by those living with Parkinson’s, as
well as being overweight can lead to adverse health effects. In overweight individuals, it is
advised that an agreed goal for ideal body weight should be established. This is especially
significant in those who have co-morbidities e.g. hypertriglyceridaemia, diabetes, CVD etc.
9
.
Unintentional weight loss is common; people with Parkinson’s are at increased risk of
malnutrition and nutritional status should be monitored routinely regularly throughout the
course of the disease
10
. Malnutrition in Parkinson’s is probably under-reported, and
several predictors of malnutrition have been found: older age at diagnosis, higher
levodopa equivalent daily dose/body weight, anxiety and depression and living alone
10
.
Dysphagia in also frequently seen, especially in the advanced phases of the disease,
although it can be present at any stage
10
.
Body weight should be monitored throughout the course of the disease, and steps taken to
ensure nutritional needs are met this may include a food first approach, supplementation
including individual vitamins and oral nutrition support when deemed appropriate, as well as
consideration of artificial nutrition support where indicated (i.e. Nasogastric feeding, gastrostomy
and in very rare cases, if the enteral route is ruled out, parenteral nutrition). However, it
should always be remembered, as with many neurological conditions, this client group is
particularly unique and must be treated as individuals; it is well known that this condition
does not affect one person in the same way as the next.
High fibre diet with good fluid intake
Constipation is one of the most common problems experienced by Parkinson’s patients.
5 of 24
About 60-80% of patients with Parkinson’s complain of constipation, which usually
appears about 10 to 20 years before motor symptoms become evident
11
.
It is thought to be caused by damage to the peripheral or central nervous system
11
.
Other causes of constipation in Parkinson’s patients are lack of fibre intake, a lack of fluid
intake often associated with dysphagia, decreased mobility and as a result of some
Parkinson’s medications.
Dietary advice on how to prevent constipation by following a high fibre/fluid intake should
be provided, and supporting written information is available in the Parkinson’s UK resource
Looking after your bladder and bowels when you have Parkinson’s
12
.
In addition to advising on a high fibre and fluid intake, ESPEN suggest people with
Parkinson’s experiencing constipation can benefit from the use of fermented milk
containing probiotics and prebiotic fibre
10
.
Antioxidants
There is no evidence to support that taking supplemental doses of antioxidants
slows the progression of the condition or enhances the effects of Parkinson’s drugs.
NICE explicitly state that Vitamin E should not be used as a neuroprotective therapy
4
, and
ESPEN state that supplementation of antioxidants are not recommended
10
.
For those who are concerned about their intake of antioxidants, they should be reassured
that a well-balanced diet will meet their antioxidant needs. Signposting them to the section
on Antioxidants in the Parkinsons UK ‘Diet and Parkinsons’ resource will help reinforce
your advice and guidance
8
.
Co-enzyme Q10
It was previously thought that taking supplementary co-enzyme Q10 could delay the
progression. However, evidence remains inconclusive and NICE guidance recommends
that co-enzyme Q10 should not be used as a
neuroprotective therapy, except in the context of clinical trials
4
. Co-enzyme Q10 can be
found naturally in offal, beef, soya oil, oily fish and small amounts in peanuts.
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B Vitamins
ESPEN states that during regular monitoring of nutrition and vitamin status, particular
attention should be focused on folic acid, vitamin B12 and vitamin D
10
.
Treatment with levodopa has shown an elevation of homocysteine. This is greater in
patients on higher doses of levodopa and is due to levodopa methylation by catechol-O-
methyltransferase (COMT). Concomitant use of COMT inhibitors may limit the raising of
plasma levels, although the regulation is closely linked to vitamin B12 and folate status.
Studies have shown that levodopa-treated Parkinson’s patients have also lower circulating
levels of folate and vitamin B12. Administration of these vitamins is effective in reducing
homocysteine levels and should be considered to prevent neuropathy and other
complications associated with hyper-homocysteinaemia
10
the indication for
supplementation should be considered and discussed with the multi-disciplinary team.
Vitamin D
NICE advises people with Parkinson’s to take a Vitamin D supplement
4
. See NICE
guidance on Vitamin D for recommendations on vitamin D testing
13
, and the NICE quality
standards on Falls in Older people
14
and Osteoporosis
15
.
All at risk groups are currently advised to take a supplement that meets 100% of the
reference nutrient intake (RNI) for their age group. At the time of publication, the RNI is 10
micrograms/day for all the general population over 4 years old, and in population groups at
increased risk of vitamin D deficiency
13
.
Monitoring
Dietitians that specialise in progressive neurological conditions agree that people
newly diagnosed with, or in the early stages of Parkinson’s, should have a nutritional
assessment and/or their nutritional status reviewed at least on an annual basis if there are
no indications for a more frequent review (e.g. clinical changes), or at the patients’ and/or
multidisciplinary team’s request (this may be by a dietitian, or another health/care
professional) - this is supported by ESPEN
10
.
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Advanced disease
Dietetic assessment
Assessment is similar to the early stages of the condition paying particular attention to:
unintentional weight-loss
decreased oral intake
swallowing difficulties
poor dentition, dry mouth
changes to taste and smell
increased frequency of dyskinesias (abnormal involuntary movements)
early satiety
gastrointestinal problems: Nausea, vomiting, gastroparesis, reflux, diarrhoea
constipation
side effects of medication (see Table 1 below)
physical difficulties impairing eating and drinking and preparing meals
bone health
weight-gain after deep brain stimulator (DBS) insertion
mental health problems, including impulse control disorders (e.g. binge eating)
frequency of ‘on’ (increased involuntary movements) and ‘off’ (increased muscle
tone) periods
orthostatic hypotension (OH) characterised by a sudden fall in blood
pressure that occurs when a person assumes a standing position
Name of drug
Mode of action
Side effects
Levodopa
(Co-beneldopa, co-
careldopa)
The most effective drug in the
treatment of Parkinson’s.
It is a larger neutral amino
acid tyrosine derivative
and is absorbed in the small
intestine. Once absorbed it
crosses the blood-brain
barrier where it is converted to
Prolonged use can result in
nausea, vomiting and
hypotension. Associated with
hyper-homocysteinaemia.
A decarboxylase inhibitor,
Benserazide, is combined
with levodopa to minimise
these side effects.
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dopamine.
Weight loss.
Dopamine
agonists
(pramipexole,
ropinirole)
These are a class of drugs
that provide antiparkinsonian
effects while avoiding some of
the problems associated with
levodopa.
Acute side effects of these
drugs include nausea,
vomiting, postural
hypotension and psychiatric
problems. Increased risk of
developing impulse control
disorders.
They tend to occur with the
initiation of treatment and as
intolerance develops over
several days to weeks.
MAO-B inhibitors
(rasagiline, selegiline,
safinamide)
This is used in the early
stages of Parkinson’s to delay
the use of levodopa. It
provides reduced motor
fluctuations and increased ‘on’
time.
It has amphetamine and
metamphetamine
metabolites which can cause
insomnia, therefore could
induce daytime sleeping.
Anticholinergics
(procyclidine,
trihexyphenidyl)
This is typically used in
younger Parkinson’s patients
(<60 years) in whom resting
tremor is the dominant clinical
feature and cognitive function
is preserved.
Side effects may include dry
mouth, constipation and
nausea
Amantidine
This is an antiviral agent that
is believed to increase
dopamine release by
blocking dopamine re-
Side effects include
confusion, hallucinations,
insomnia, nightmares and dry
mouth.
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uptake
by stimulating receptors and
possibly by anticholinergic
effects.
Table 1: Medication side effects: the following medications are commonly used in the
management of Parkinson’s
Antiemetics are usually used in conjunction with these medications to ease the
symptoms of nausea and vomiting.
Dietary intervention
Oral nutrition support (ONS)
ONS should be provided when the patient can no longer maintain their body weight
through oral diet/intake alone
16
.
A food first approach should be explored first, with suggestions such as food fortification,
high energy/protein advice, and regular small energy-dense meals.
The use of oral nutrition support products, including sip feeds, should be considered for
those who are unable to maintain an adequate intake with food alone, or are unable to
adhere to food fortification due to, for example, anxiety at meal times, early satiety or lack
of sufficient help to prepare the fortified meals and snacks.
Imaginative use of these products will help reduce taste fatigue and increase adherence
to recommendations.
Particular attention should be paid to those on a texture modified diet (TMD), especially
puree diets. Puree diets are known to provide varying nutritional adequacy and can be
unpalatable, if not prepared imaginatively. Some fortification techniques and suggestions
may need to be amended. All patients on texture modified diets should have their intake
assessed by a dietitian for nutritional adequacy
17
.
It is recommended that the dietitian and speech and language therapist work closely to
10 of 24
ensure the patient receives appropriate and optimal nutrition and hydration, and
consideration should be given to the use of pre-thickened ONS.
People with Parkinson's should be advised not to take over-the-counter dietary
supplements without first consulting their pharmacist or other healthcare professional
4
.
Artificial Nutrition Support (ANS)
In Parkinson’s it often helps to anticipate artificial feeding, or the placement of a feeding
tube to support hydration, at an early stage through discussions with the patient and/or
carer, supported by the multidisciplinary team
18
.
Swallowing difficulties need to be addressed promptly to prevent weight loss and
malnutrition. About 95% of Parkinson’s patients experience swallowing difficulties at
some stage of the condition
19
.
Silent aspiration can occur, and many people with Parkinson’s may be unaware they
have a problem. When assessing and monitoring, always look out for red flags that
indicate silent aspiration could be happening.
Dysphagia occurs in the later stages of Parkinson’s compared to atypical
parkinsonian syndromes e.g. progressive supranuclear palsy (PSP) or multiple system
atrophy (MSA)
20
.
Significant problems with swallowing require expert assessment from a speech and
language therapist and guidance regarding appropriate food texture modification. Since
texture modified diets e.g. puree, may be nutritionally diluted and not energy
dense enough to prevent weight loss, additional supplementary enteral nutrition support
may be indicated.
Tube feeding may be given alongside oral intake, or as the main source of nutrition.
Short-term feeding via nasogastric tube is likely appropriate to manage an acute event
impacting swallow or nutritional intake. For longer term, a gastrostomy (for example a PEG
or RIG) should be considered
16
.
Gastrostomies are being used increasingly in the treatment of patients with neurogenic
dysphagia to prevent or reverse nutritional deficits
21
and this can improve fitness
and quality of life for those patients unable to take sufficient supplements orally.
Reassurance should be given that gastrostomies can be placed before food intake has
fallen or weight loss has occurred, in order to support optimal hydration.
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Bone health/Osteoporosis
People with Parkinson’s have been found to have a lower bone mineral density (BMD)
and increased risk of osteoporotic fracture
10
. The reasons are multi-factorial and include
low mobility, decreased muscle strength, low body weight, deficiency in Vitamin D, B12,
folic acid and hyperhomocysteinaemia
22
. As discussed earlier (page 4), Vitamin D
supplementation is recommended for a large proportion of the general population if a
person is not already on a Vitamin D supplement when they are diagnosed, then they
should be re-assessed as their risk level will be greater.
If BMD is lower, then in line with usual treatment for osteoporosis, calcium
requirements are likely to be increased, and greater than the 700mg/day reference
nutrient intake for the general population over 19yrs old. A supplement may be
required to meet requirements, and this should be discussed with the MDT.
Orthostatic hypotension (OH)
OH (also known as postural hypotension) is a sudden fall in blood pressure that occurs
when a person assumes a standing position.
The prevalence of symptomatic orthostatic hypotension (OH) may be as high as 60% in
people living with Parkinson’s
23
.
This could be caused by: a) dopaminergic drugs which induce or worsen orthostatic
hypotension and/or b) primary autonomic failure with an involvement of the peripheral
autonomic system caused by Parkinson’s.
OH sufferers may also experience post-prandial hypotension (PPH), resulting in blurred
vision and dizziness after meals. These symptoms can occur any time from ingestion to
90 minutes post meal. Studies from long-term care facilities have shown that 24-36%
were diagnosed with PPH
24,25
. It has been suggested that the nutrient composition of
meals affect the magnitude of the decrease in postprandial hypotension.
The intestines require a large amount of blood for digestion. When blood flows to the
intestines after a meal, the heart rate increases and blood vessels in other parts of the
body constrict to help maintain blood pressure. However, with this patient group, such
mechanisms may be inadequate. Blood flows normally to the intestines, but the heart
rate does not increase adequately and blood vessels do not constrict enough to
maintain blood pressure. As a result, blood pressure falls.
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Symptoms include:
feeling dizzy and light-headed
changes in vision such as blurring, greying or blacking vision
feeling vague or muddled
losing consciousness with or without warning a ‘blackout’ or ‘faint’ as a result of
hypotension
pain across the back of shoulders or neck ‘coat hanger’ pain
pain in lower back or buttocks
angina-type pain in the chest
weakness
fatigue
The symptoms are typically worse when standing and improve on lying down.
Dietary management of OH
The main aim of the dietary management is to assist in the alleviation of the symptoms of
hypotension, by focusing on the factors that affect blood pressure.
The goals of treatment are improving functional capacity and quality of life, and
preventing injury, rather than achieving a target blood pressure
26
. Dietary changes aim to
alleviate the symptoms of postural and postprandial hypotension and assist with fatigue
management.
The skills of the dietitian are required when advising on ways to manipulate the diet, to
ensure the nutritional adequacy of the diet is not compromised. It should also be ensured
that restrictive diets are not followed, which would lead to further risk of malnutrition in an
already nutritionally vulnerable group of patients.
Advice for people with OH:
Avoid large meals
27
- aim for smaller, evenly distributed meals
Reduce carbohydrate intake, especially simple sugars
28,29
. It has been
hypothesised that carbohydrates induce hypotension in autonomic failure through
the vasodilating properties of insulin
30
Increase intake of salt
Increase fluid intake
31
Decrease or omit alcohol intake
32
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PPH accompanied by weight loss
As the OH progresses, many patients experience weight loss, the reason being
multifactorial. Patients may restrict intake as they associate meals or a certain food with
post-prandial symptoms, or as a consequence of dysphagia.
Deciding upon which oral supplement to use can become a challenge if you are trying
to get your patient to avoid/decrease glucose intake. Some patients can tolerate
energy-dense oral sip feeds without experiencing symptoms, especially if sipped slowly.
However, for those that do experience PPH symptoms, a lipid-based solution such as
Calogen/Procal shots, can be useful. The provision of innovative recipes and
suggestions on how to incorporate these supplements into meals will be helpful to the
person living with PPH.
It is important to liaise with the MDT regarding treatments, as it may be preferred to
manage OH/PPH pharmacologically, allowing nutritional intake to be maximised
If the patient’s autonomic failure is so severe, dietary intervention may not offer any
benefit.
Weight gain post-chronic bilateral subthalamic or deep brain stimulation (CDBS)
Deep Brain Stimulation (DBS) is a procedure in which stimulating electrodes are placed
stereo-tactically into the deep structures of the brain. DBS in selected patients has
provided significant therapeutic benefits. Successful DBS allows a decrease in medication
or makes a medication regimen more tolerable. There are gains in movement and control.
Consequently, the intervention is used for patients who cannot be adequately controlled
with medications or whose medications have severe side effects. Only a very small sub-
group of people (~1-10%) diagnosed with Parkinson’s are eligible for DBS
33
.
It has been shown that weight gain can occur in 87% of patient’s post DBS surgery.
Around 38% of these patients were found to be overweight (BMI>2629.9) six-months
post-operatively. This is thought to be due to improvement in motor fluctuations, rather
than an increase in oral intake
34
.
Dietary intervention (using ideal body weight to calculate energy requirements) at time
of surgery has been advocated by researchers in Portugal
35
to enhance the benefit of
the surgery and prevent metabolic disorders. It is thought that excessive weight gain
could exacerbate motor function impairment in Parkinson’s.
It is suggested that clinicians actively monitor weight changes in these patients
10
.
Discussion of, and encouraging adoption of the Healthy Eating Guidelines as set out
14 of 24
by the Food Standards Agency (FSA) and incorporated into the Diet and Parkinson’s
resources
8
available from Parkinson’s UK can be a useful to prevent rapid weight gain in
those who are undergoing or have undergone DBS surgery.
Dietary protein manipulation
Levodopa is the standard, and often initial, therapy for patients with this condition;
however, with continued treatment and as the condition progresses, up to 80% of patients
experiencewearing off’ symptoms, dyskinesias and other motor complications.
It was believed in the late 1980s and early 1990s that dietary protein manipulation would
help control motor fluctuations
36,37,38,39,40,41
. Levodopa (L-dopa) disappears from the blood
very quickly, usually about 6090 minutes after administering the drug.
Protein can delay gastric emptying and competes with the absorption of L-dopa, and the
manipulation of dietary protein may reduce fluctuations in some patients.
Current recommendations
4
are to advise people with Parkinson's disease on levodopa
who experience motor fluctuations, to;
avoid a reduction in their total daily protein consumption, and
discuss a diet in which most of the protein is eaten in the final main meal of the day
(a protein redistribution diet)
There is no evidence to support low protein diets
10
.
Do not offer creatine supplements to people with Parkinson's disease
4
.
Dietary management of any gastro-intestinal symptoms, e.g. delayed gastric emptying,
constipation, may also be beneficial, as these can impair L-dopa efficacy
10
.
People with Parkinson’s treated with continuous duodenal duodopa should follow similar
recommendations, and should be advised to distribute food intake throughout the day and
to divide the protein intake
10
.
In cases of continuous enteral tube feeding (low-infusion-rate), there are no restrictions
but it is advisable to concentrate feeding during the night hours if possible, in order to limit
interactions
10
.
Finally, in tube-fed patients still treated with oral formulations of levodopa-containing
medications it is suggested the pausing of feeding for at least 1 h before and 30-40 min
after drug administration
10
.
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Monitoring
Every four to six weeks if there have been any changes to medications or treatment
plan, with particular focus on the swallowing recommendations.
Every three months if the patient’s condition is stable.
For oral nutrition support, regular review of ONS prescriptions every three months
is advisable, to ensure the appropriateness of the intervention. Samples of ONS can be
trialed before any changes are requested to the GP prescription.
Some centres offer one-day holistic reviews to re-assess mobility, swallow, speech and
nutritional status; if you do not have access to these, it is important to liaise with other
members of the MDT to ensure you are keeping in line with the patient’s overall
management plan.
Palliative Care
Palliative care is about helping to keep quality of life through managing symptoms,
relieving pain and managing any other distressing aspects of advanced Parkinson's. The
management of Parkinson’s remains largely palliative, despite huge advances in the
medical field. As Parkinson's progresses, many people will need some element of care
and support alongside their treatment. Palliative care isn't just for 'end of life'. It relies on
healthcare professionals making people with Parkinson’s aware of, and directing them
towards, services and support at an early stage.
NICE recommend that consideration is given to referring people at any stage of
Parkinson's disease to the palliative care team to give them and their family members or
carers (as appropriate) the opportunity to discuss palliative care and care at the end of
life
4
.
There is no set time for how long the palliative phase lasts. It can potentially be a long
time, and Parkinson's can still change and develop further within this time
42
.
It has been documented that a patient can spend on average 2.2 years in the palliative
care stage
43
. During this stage there may be a need to withdraw dopaminergic
medications due to lack of drug efficiency. Decreased mobility and being bed-bound can
result in the risk of pressure ulcer development.
Decisions may need to be made about the nutritional management and treatment in the
future to give the person with Parkinson’s an opportunity to state their preferences in
16 of 24
case they lose capacity for making decisions in the future
44
.
Dietetic assessment
Assessment will be similar to the early stage taking into special consideration:
suitability of active +/- aggressive nutrition support
prognosis
palliative care team advice
multidisciplinary team opinion
patient's wishes
any advanced care planning
Dietary intervention
Artificial nutrition support may be withdrawn if it is causing discomfort or distress, or not
deemed to be in patient’s best interest. You may be asked to reduce the volume of enteral
feeds to prevent fluid overload.
Oral nutrition should always be offered but not forced upon those who decline it
or when there is risk of aspiration or choking. If a patient chooses to maintain an oral
intake despite being advised it is unsafe, it should be ensured that the patient is fully
informed of the consequence of their decision, and they should be continued to be
supported.
Monitoring
Monthly reviews may be more appropriate or as agreed with/at the request of the MDT
or palliative care team.
17 of 24
Summary
The risk of malnutrition and body weight must be routinely monitored from diagnosis, and
as the condition progresses
10,45,46
. Worsening motor symptoms e.g. dyskinesias should
also be monitored to prevent or reverse weight loss in people living with Parkinson’s
10,47
.
As highlighted throughout this document the nutritional management of a person living with
Parkinson’s may change and evolve throughout the progression of the condition.
Dietitians have the skills to help people living with Parkinson’s to optimise their
nutritional status and manage nutrition-related symptoms at all stages of the condition
48
.
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References
1. Parkinson’s UK (2018) https://parkinsons.org.uk Parkinson’s UK website
2. Parkinson’s UK (2018) ‘Allied Health Professionals’ competency framework for progressive
neurological conditions’ Parkinson’s UK website
https://www.parkinsons.org.uk/professionals/resources/allied-health-professionals-ahps-
competency-framework-progressive
3. Stacy M. et al (2009) ‘The Clinicians’ and Nurses’ Guide to Parkinson’s Disease’ Medscape
4. National Institute for Health and Care Excellence (NICE) (2017) ‘Parkinson’s disease in
adults’ NICE website https://www.nice.org.uk/guidance/ng71
5. BAPEN (2006) ‘Malnutrition Universal Screening Tool (MUST)’ BAPEN website
https://www.bapen.org.uk/screening-and-must/must/introducing-must
6. The Patients Association (2018) ‘The Patients Association Nutrition Checklist’ The Patients
Association website https://www.patients-association.org.uk/Blog/patients-association-
nutrition-checklist
7. Glynn K (2003) ‘Nutritional Issues in Parkinson’s Disease’ Complete Nutrition 3 (4): 13-16
8. Parkinson’s UK (2016) Diet and Parkinson’s’ Parkinson’s UK website
https://www.parkinsons.org.uk/information-and-support/diet
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9. Department of Health (2006) ‘Care Pathway for the management of overweight and obesity’
Department of Health Archives Care pathway for the management of overweight and obesity
(htmc.co.uk)
10. Burgos et al (2018) ‘ESPEN guideline clinical nutrition in neurology’ Clinical Nutrition 37:
354-396 https://www.espen.org/files/ESPEN-Guidelines/ESPEN-
guideline_clinical_nutrition_in_neurology.pdf
11. Ueki A (2004) ‘Life style risks of Parkinson’s disease: Association between decreased water
intake and constipation’ Journal of Neurology 251(suppl 7): vII 18-23
12. Parkinson’s UK (2020) ‘Looking after your bladder and bowels when you have Parkinson’s
Parkinson’s UK website https://www.parkinsons.org.uk/information-and-support/bladder-and-
bowel-problems
13. NICE (2017) ‘Vitamin D: supplement use in specific population groups’ Public health
guideline [PH56] https://www.nice.org.uk/guidance/ph56
14. NICE (2017) ‘Falls in Older People’ Quality standard [QS86]
https://www.nice.org.uk/guidance/qs86
15. NICE (2017) ‘Osteoporosis’ Quality standard [QS149]
https://www.nice.org.uk/guidance/qs149
16. NICE (2017) ‘Nutrition support in adults Oral nutrition support, enteral tube feeding and
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parenteral nutrition’ Clinical Guideline [CG32] https://www.nice.org.uk/guidance/cg32
17. Wright L et al (2005) Comparison of energy and protein intakes of older people consuming a
texture modified diet with a normal hospital diet’ Journal of Human Nutrition and Dietetics
18(3): 213-219
18. Park R H et al (1992) ‘Randomised comparison of Percutaneous Endoscopic Gastrostomy
and nasogastric tube feeding in patients with persisting neurological dysphagia’ British
Medical Journal 304: 1406-9
19. Rehman H U (2000) ‘Progressive supranuclear palsy’ Postgraduate Medical Journal 76: 333-
36
20. Logemann J A et al (1997) ‘Speech and Swallowing evaluation in the differential diagnosis of
neurological disease’ Neurologia-Neurocirugia-Psichustria 18: 71-8
21. Britton J E R et al (1997) ‘The use of Percutaneous Endoscopic Gastrostomy (PEG) feeding
tubes in patients with neurological disease’ Journal of Neurology 244: 431-434
22. Van den Bos et al (2013) ‘Parkinson's disease and osteoporosis’ Age and Ageing 42(2):156
162
23. NICE (2015) ‘Orthostatic hypotension due to autonomic dysfunction: midodrine Evidence
summary’ https://www.nice.org.uk/advice/esnm61/chapter/full-evidence-summary
21 of 24
24. Vaitkevicius PV et al (1991) ‘Frequency and importance of postprandial blood pressure
reduction in elderly nursing-home patients’ Ann Intern Med 115: 865-70
25. Staneczek O et al (2001) ‘A full stomach but an empty head’ J Am Geriatr Soc 49:1262-3
26. Lahrmann P et al (2011) ‘Orthostatic hypotension’ European handbook of neurological
management Volume 1. Oxford: Blackwell, 469−76
27. Sclater A et al (2004) ‘Orthostatic hypotension: a primary care primer for assessment and
treatment’ Geriatrics: 59: 22-7
28. Vloet LCM et al (2001) ‘The influence of low, normal and high carbohydrate meals on blood
pressure in elderly patients with postprandial hypotension’ J Gerontol A Biol Sci Med Sci
56A:M744-8
29. Jansen RW et al (1995) ‘Postprandial hypotension: epidemiology, pathophysiology, and
clinical management’ Ann Intern Med 122(4): 286-95
30. Brown RT et al (1989) ‘Euglycaemic insulin-induced hypotension in autonomic failure’ Clin
Neuropharmacol 12(3), 227231
31. Young TM et al (2005) ‘The effects of water ingestion on orthostatic hypotension in two
groups of chronic autonomic failure: multiple system atrophy and pure autonomic failure’
Journal of Neurology Neurosurgery and Psychiatry 75(12):1737-1741
22 of 24
32. Alagiakrishnan K (2007) ‘Postural and Postprandial Hypotension: Approach to Management’
Geriatrics and Aging 10(5): 298-304
33. NHS Commissioning Board (2013) ‘Clinical Commissioning Policy: Deep Brain Stimulation
(DBS) In Movement Disorders (Parkinson’s Disease, Tremor and Dystonia)’ Reference:
NHSCB/D03/P/b d03-p-b.pdf (england.nhs.uk)
34. Sauleau P et al (2009) ‘Comparison of weight gain and energy intake after subthalamic
versus pallidal stimulation in Parkinson’s disease’ Mov Disorders 24(14) 2149-5215
35. Guimaraes J et al (2009) ‘Modulation of nutritional stat in Parkinsonian patients with bilateral
subthalamic nucleus stimulation’ J Neurol 256: article 2072
36. Frankel JP et al (1989) ‘The effects of oral protein on the absorption of intraduodenal
levodopa and motor performance’ J Neurol Neurosurg Psychiatry: 52:1063-1067
37. Pincus JH & Barry KM (1987) ‘Plasma levels of amino acids correlate with motor fluctuations
in Parkinsonism’ Arch Neurol 44(10):1006-1009
38. Juncos JL et al (1987) ‘Dietary influences on anti-parkinsonian response to L-dopa’ Arch
Neurol 44(10):1003-1005
39. Carter JH et al (1989) ‘Amount and distribution of dietary protein affects clinical response to
levodopa in Parkinson’s disease’ Neurology: 39:552-556
23 of 24
40. Kaerstadt PJ & Pincus JH (1992) ‘Protein redistribution diet remains effective in patients with
fluctuating Parkinsonism’ Arch Neurol 49(2):149-151
41. Pare S et al (1992) ‘Effect of daytime protein restriction on nutrient intakes of free-living
Parkinson’s disease patients’ Am J Clin Nutr 55:701-707
42. Parkinson’s UK (2021) ‘Advanced Parkinson's treatments and therapies: Palliative Care’
Parkinson’s UK website https://www.parkinsons.org.uk/information-and-support/advanced-
parkinsons-treatments-and-therapies
43. MacMahon DG et al. (1999) ‘Validation of pathways paradigm’ Parkinsonism & Related
Disorders 5(S53) Ref ID: 19912
44. Royal College of Physicians, London (2006) ‘Parkinson’s disease: national clinical guideline
for diagnosis and management in primary and secondary care’ National Collaborating
Centre for Chronic Conditions (UK)
45. Rascol, O.F.J.J et al (2001) ‘Dopamine agonists: their role in the management of Parkinson’s
disease’ Calne, D.B. & Calne, S.M. Ed. Parkinson’s disease, Advance in Neurology.
Philadelphia: Lippincott, Williams and Wilkins: 301-309
46. Beyer P et al. (1995) ‘Weight change and body composition in patients with Parkinson’s
disease’ Journal of American Dietetic Association 95(9): 979-983
47. Bachmann CG & Trenkwalder C (2006) ‘Body weight in patients with Parkinson’s disease’
Movement Disorders 21(11): 1824-30
24 of 24
48. Cushing ML et al (2002) ‘Parkinson’s Disease: Implications for Nutritional Care’ Canadian
Journal of Dietetic Practice and Research 63(2): 81-87
Acknowledgements
This resource was initiated by Parkinson’s UK supported by the British Dietetics
Association (BDA), and was originally published in 2015, authored by Karen Green, Senior
Specialist Dietitian, (Neurosciences), at The National Hospital for Neurology &
Neurosurgery.
The document was reviewed and updated in January 2021 by:
Karen Robinson, Consultant Dietitian, RD, MSc Adv HCP, Chair of the Neurosciences
Specialist Group of the BDA, incorporating feedback and comments from the following
members of the Neurosciences Specialist Group of the BDA:
- Rebecca Picton, Neuroscience Dietitian, University Hospitals Southampton NHS
Foundation Trust.
- Sophie Harries RD BSc
- Anna Bruce, RD