Microsoft Word - Assignment 2 Overview 2019.docx
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HSN 301 DIET AND DISEASE
ASSIGNMENT 2: RESEARCH ARTICLE
Very low ca
ohydrate ketogenic diets and type 2 diabetes
Overview: You are asked to construct a "mock” research article using the results
provided to you.
Your research team has conducted a single‐blinded, randomized
controlled clinical trial in people with type 2 diabetes. Participants
were randomized to either a very low ca
ohydrate, ketogenic diet
or a low fat diet. Both diets were hypoenergetic, and involved the
same degree of total dietary energy restriction. Patients were
followed up at 12 months to investigate the primary outcome
measure of long term glucose control (HbA1c). More details on the
specifics of the study are provided in the Methods section below.
The maximum word count for the assignment is 2000 words
(excluding references, tables, figures, figure legends and table
captions).
Note that a methods section is not required in this assignment,
ut is provided to you for your information.
Learning outcomes of this assignment:
The Unit Learning Outcomes associated with this assignment are:
ULO1: Explain the aetiology and pathophysiology of common nutrition‐related
diseases. In this research articles, you should demonstrate a good understanding of
the pathophysiology of type 2 diabetes; as well as the clinical biomarkers of the
disease. You should demonstrate a good understanding of how they may respond to
dietary interventions.
ULO3: Search, interpret and critically evaluate scientific publications on the
elationship between diets and nutrition‐related diseases. In this assignment, you
will be given details on the methods and key findings of a clinical trial. Using the given
information to write your research article, you will demonstrate good skills in:
searching for appropriate reference articles; accurately interpreting those identified
studies; and critically evaluating them in the context of relationships between diet and
disease.
ULO4: Synthesise cu
ent scientific knowledge on the prevention (treatment) of
nutrition‐related diseases and produce reports for a professional and lay audience
You will learn to synthesize information from cu
ent scientific publications to provide
strong background, rationale and discussion of results in this research article. You will
also learn to use language suitable for a research article.
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The following information describes the major requirements of each section of the
assignment. Use this in conjunction with the other support materials provided to
get the most out of this assignment.
Components of a research article
A. TITLE: Do not exceed two lines – 100 characters including spaces
Titles should include sufficient detail for indexing purposes (on databases such as
PubMed), but also be general enough for readers outside the field to appreciate what
the paper is about.
B. ABSTRACT (250 words)
Typically, an abstract provides one or two lines regarding the importance and context
of the cu
ent work, a statement of aims, a
ief description of the methods, the major
findings which include a summary of the data e.g. in an intervention study what factors
changed and degree of change and a conclusion. This is often difficult to fit into such a
ief number of words. You can however, assume a large amount of previous
knowledge in terms of background and methodology on behalf of the reader. This
allows you to focus more on what new information the cu
ent article is presenting.
The abstract should not contain any undefined a
eviations or unspecified references.
Use the conventional subheadings in your abstract:
INTRODUCTION/AIMS:
METHODS:
RESULTS:
CONCLUSION:
C. INTRODUCTION (500 WORDS)
Your introduction should provide a
ief but relevant literature review that places the
importance of this study within the context of the cu
ent literature. While the included
information will be specific to the topic, you can funnel your logical flow of ideas down
from a “more general” level to a “more specific” level relevant to your aims.
A suggested structure for your writing in this section is as follows:
• Include prevalence/statistical data to outline the burden of type 2 diabetes
• Describe the major clinical and pathophysiological aspects of type 2 diabetes
• Describe the importance of dietary management for type 2 diabetes
• What is the proposed benefits and/or mechanisms of very low
ca
ohydrate ketogenic diets in the management of type 2 diabetes?
• What biomarkers would be expected to be altered with reductions in the
ca
ohydrate content of the diet?
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• What previous research has been conducted on the topic and where does the focus
of this study fit into that research area (research gaps)?
• What are the aims of this study? (note: aims have been provided for you)
METHODS
There is no need to include this section in your assignment.
D: RESULTS AND DISCUSSION (1000 words in total)
RESULTS:
Results should be succinctly summarised. You should firstly provide a
ief description
of the final sample population. You should summarize you findings clearly and
concisely, regardless of whether your outcomes measures changed significantly or not
during the intervention. The results section is an important one to consider as it
provides you with a list and the structure of what you need to focus on within your
discussion.
DISCUSSION:
Your discussion needs to be succinct, providing a critique of work undertaken within
the cu
ent article, highlighting the major findings and the importance of the results in
terms of the intervention. You should discuss whether the results would be expected
when compared results of other relevant studies. You should provide a summary of the
possible physiological mechanisms that may explain the study results. Discuss the
significance of the work and how this information adds to the scientific body of
knowledge (i.e. why should other researchers and the general population care). You
should also consider the strengths and potential limitations of this study, the generalisability
of results, and the future research directions following on from this work.
A suggested structure for your writing which follows the overall theme and structure of
the article is:
Provide a succinct summary of the key results
How do these findings fit within the context of the cu
ent literature? What do
these findings add to the cu
ent literature?
Based on evidence and data, how do you think the intervention acted to change
the outcome measures? (if in fact it did; and if it didn’t, why might this be?)
Is the magnitude of effect observed consistent with a clinical benefit? Note that
statistical significance does not automatically equate to clinical importance. This
is an important point, as it will be an important consideration for whether or not
the dietary intervention is a candidate treatment to translate into practice.
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What were some strengths of the study design, methods and data found? What
might have been some potential limitations of the study?
Given possible limitations of the study and/or new questions raised in relation to
the findings, what future investigations might be useful to further explore this
topic?
E. CONCLUSIONS (100 words)
A final conclusion is different from that presented in the abstract. It should be a touch
wordier and is really your final say regarding the importance of the major outcome(s)
of this work and how this information can be used for the common good (e.g. as a
therapeutic aid to a particular pathology). Don’t overstate your achievements ‐ for
example, by claiming you have cured cancer (unless you have indeed done this!). A
conclusion should never present new ideas or results that have not been described
previously within the results and discussion.
F: RESEARCH TRANSLATION (150 words)
A very important part of scientific research (particularly health‐‐based research) is to
highlight the importance of your work in a simple, yet succinct manner that is
understandable to a non‐‐specific health professional audience. You should summarise the
main implications of your findings as they pertain to potential translatability to the clinic,
public health and/or policy (whichever is most relevant to your research). You should
provide your summary as a text box within your article. The use of bullet points is
ecommended: a maximum of 4 points should be included. No references are required.
You need to keep the language simple without losing the impact of your findings, or, on
the flip‐‐side, without over‐‐stating your findings. Note that this section may include
epeating some of the same information you have already included in your discussion
and/or conclusions.
An example of research translation in a text box is shown below:
Adapted from: Baojian Xue, Yang Yu, Zhongming Zhang, Fang Guo, Te
y G. Beltz, Robert L. Thunhorst,
Robert B. Felder and Alan Kim Johnson. Leptin Mediates High‐Fat Diet Sensitization of Angiotensin II–Elicited
Hypertension by Upregulating the Brain Renin–Angiotensin System and Inflammation. Hypertension.
2016;67:970‐976.
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G. REFERENCES/BIBLIOGRAPHY
IT IS STRONGLY SUGGESTED THAT YOU USE THIS ASSIGNMENT TO PRACTICE USING A
REFERENCING SOFTWARE PACKAGE SUCH AS ENDNOTE. The last thing authors
generally do when writing an article is format the references. Also, most students leave
assignments until the last minute. This means you will be looking for stray commas, full
stops and “ghost” references (references from slabs of text you deleted but forgot to
take out of the bibliography) at 11.55 pm on the due date. Let the referencing software
do the work for you!
Deakin Li
ary has an excellent online help and training site for endnote:
Endnote: https:
www.deakin.edu.au/li
ary
esearch/manage‐references
How to use Endnote: http:
clarivate.libguides.com/endnote_training/home
The referencing and bibliographical format for this assignment is Vancouver style.
Information about Vancouver referencing can be found at:
https:
www.deakin.edu.au/students/studying/study‐support
eferencing/vancouver
NOTE: Vancouver style is a format listed within EndNote.
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Methods and results of a randomized, controlled trial
Aim
The aim of this study is to assess the effects of a low ca
ohydrate ketogenic diet on
glycaemic control (HbA1c), insulin sensitivity, body weight, fat mass, and metabolic indicators
of inflammation and cardiovascular health in obese individuals with type 2 diabetes.
Methods
Study design:
This was a single‐blinded, randomized controlled, parallel‐arm study consisting of two study
groups.
Study population:
Male and female participants aged over 18 years were recruited from the community via
newspaper study advertisements. To be eligible for the study, the participants had to
have: (a) diagnosed type 2 diabetes; and (b) a BMI greater than 30 kg.m‐2. Participants
who were already diagnosed with cardiovascular diseases, renal diseases, neurological
diseases or musculoskeletal disorders were excluded from the study. Individuals who
had body weight fluctuations of >5 kg over the last 3 months or were following a weight
loss diet were also excluded. Volunteers who met all inclusion criteria were enrolled and
andomly assigned into one of the two study groups.
Study groups:
Following phone screening and clinical screening of potential participants, n=160
individuals were deemed eligible to participate. Participants were randomized to either
a VLCKD or a low fat diet for 12 months. Both diet groups consumed low‐energy diets that
were isoenergetic, but with differences in macronutrient percentages. Participants on the
VLCKD consumed a diet consisting of approximately 10% ca
ohydrate, 20% protein and
70% fat. Participants on the low fat diet consumed approximately 60% ca
ohydrate, 20%
protein and 20% fat. All participants were asked to maintain their usual physical activity
levels throughout the study to avoid potentially confounding effects. Physical activity recall
surveys were performed every 3 months to monitor activity. Participants from both groups
eceived dietary counselling from qualified dietitians every 4 weeks to ensure compliance
to the diets. Compliance with diet was assessed using: 1) 3‐monthly self‐reported 7‐day
weighed diet records; and 2) ketone concentrations in blood and urine taken every 3
months.
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Outcome measures:
All measurements were taken at baseline, 3 months, 6 months, 9 months and 12 months
of the study.
The primary outcome was glycated haemoglobin (HbA1c), which was measured from
whole blood samples using High Performance Liquid Chromatography.
Secondary outcomes included body weight, body mass index (BMI), and body
composition, including lean mass and fat mass measured using dual‐energy x‐ray
absorptiometry (DXA). Plasma outcome measures included markers of inflammation,
insulin sensitivity, and cardiovascular health. Fasting blood samples (after 10 hours of
overnight fasting) were collected from participants in EDTA blood tubes. Inflammation
markers included fasting plasma C‐reactive protein (CRP), tumor necrosis factor alpha
(TNF‐α), interleukin‐6 (IL‐6) and adiponectin were assessed. Fasting plasma glucose and
insulin were measured, from which homeostatic model assessment (HOMA‐IR) was
determined and used to estimate insulin sensitivity. Cardiovascular health indicators
measured were blood pressure, fasting plasma triglycerides, total cholesterol, LDL‐
cholesterol and HDL‐cholesterol levels.
Statistical Analysis:
The normality of data was confirmed using Shapiro‐Wilk tests. At baseline, study
outcomes of participants in the VLCKD and low fat groups were compared using
independent‐sample t‐tests and no significant differences were shown. Changes in
all study outcome measurements from baseline through to 12 months (baseline, 3‐
months, 6 months, 9 months, 12 months) were compared between the VLCKD and
low fat groups using repeated measures ANOVA with Bonfe
oni co
ections.
Statistical significance was determined at alpha of 5%, i.e. p<0.05, two‐sided.
Statistical analyses were performed using SPSS version 24.0 software. Data are
presented as mean ± SD.
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Results (summary of data, without a description)
Figure 1: Flow of participant recruitment during study
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Table 1. Dietary intake characteristics over 12 months (data are mean ± SD)
(*denotes sta s cally different between diets at the me point, p<0.05; †denotes sta s cally
different when compared to baseline [time=0], p<0.05)
Figure 2. Effect of diets on HbA1c over 12 months. Data are mean ± SD (*denotes statistically
different means between diets at the me point, p<0.05; †denotes sta s cally different mean
when compared to baseline [time=0], p<0.05)
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6
7
8
9
10
XXXXXXXXXX
H
A 1
c
(%
)
Time (months)
VLCKD Low Fat
* * *
†
†
†
†
†
†
†
†
Measure Baseline 3 months 6 months 9 months 12 months
Main
effect‐
ANOVA
VLCKD
(n=80)
Low
Fat
(n=80)
VLCKD
(n=77)
Low
Fat
(n=77)
VLCKD
(n=72)
Low
Fat
(n=73)
VLCKD
(n=66)
Low
Fat
(n=68)
VLCKD
(n=56)
Low
Fat
(n=62)
Energy
(kcal)
1998 ±
740
2034 ±
702
1258 ±
409†
1418 ±
468†
1324 ±
537†
1481 ±
483†
1448 ±
610†
1527 ±
522†
1501 ±
610†
1528 ±
503†
P=0.27
Ca
(g) 242 ±
92
242 ±
100
32 ±
15*†
212 ±
75
33 ±
26*†
222 ±
79
62 ±
29*†
224 ±
78
72 ±
29*†
220 ±
78
P<0.01
Ca
(% kcal)
48.1 ±
8.8
46.0 ±
7.8
10.2 ±
3.6*†
58.9 ±
10.7†
10.1 ±
4.1*†
57.9 ±
8.9†
16.2 ±
13.9*†
58.6 ±
9.6†
19.2 ±
6.9*†
57.6 ±
9.6†
P<0.01
Fat (g) 75.6 ±
36.4
80.7 ±
32.4
99.6 ±
28.6*†
35.3 ±
11.7†
103.2±
38.2*†
37.4 ±
13.9†
105.1±
36.8*†
39.7 ±
19.3†
106.8±
36.8*†
42.4 ±
18.3†
P<0.01
Fat
(% kcal)
32.5 ±
7.2
34.7 ±
6.6
71.1 ±
16.0*†
22.4 ±
8.8†
70.2 ±
15.8*†
22.7 ±
7.3†
66.2 ±
14.6*†
23.4 ±
8.8†
64.0 ±
14.6*†
25.0 ±
8.8†
P<0.01
Protein
(g)
86.4 ±
17.8
89.5 ±
16.6
59.5 ±
10.9
66.5 ±
15.7
63.9 ±
16.0
67.8 ±
18.9
63.0 ±
14.5
69.9 ±
18.2
63.4 ±
10.9
65.5 ±
9.1
P=0.19
Protein
(% kcal)
17.3 ±
5.0
17.6 ±
5.2
18.0 ±
7.7
19.0 ±
5.7
19.3 ±
5.6
18.5 ±
5.0
17.3 ±
7.4
18.9 ±
5.8
16.9 ±
7.4
17.2 ±
5.8
P=0.24
*
Main effect of ANOVA:
p=0.01 [VLCKD
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Table 2. Effect of different diets on secondary outcome measures (data are mean ± SD)
Measure Baseline 3‐months 6‐months 9‐months 12‐months
Main
effect‐
ANOVA
VLCKD
(n=80)
Low
Fat
(n=80)
VLCKD
(n=77)
Low
Fat
(n=77)
VLCKD
(n=72)
Low
Fat
(n=73)
VLCKD
(n=66)
Low
Fat
(n=68)
VLCKD
(n=56)
Low
Fat
(n=62)
Age (years) 51 ± 7 52 ± 9 51 ± 7 52 ± 9 51 ± 7 52 ± 9 51 ± 7 52 ± 10 52 ± 8 53 ± 10 P=0.91
Height (cm) 172 ± 8 170 ±
10
172 ± 8 170 ±
10
172 ± 8 170 ±
10
172 ± 8 170 ±
10
172 ± 8 170 ±
10
P=0.89
Weight (kg) 102.1 ±
10.5
99.8 ±
11.1
93.1 ±
10.5†
95.8 ±
11.1†
89.5 ±
10.5*†
92.6 ±
11.1†
91.3 ±
10.5†
93.7 ±
11.1†
92.2 ±
10.5†
94.2 ±
11.1†
P=0.01
BMI
(kg.m‐2)
35.1 ±
4.4
34.9 ±
5.1
32.8 ±
4.4†
33.9 ±
5.1
30.1 ±
4.4*†
32.1 ±
5.1†
31.1 ±
4.4†
32.9 ±
5.1†
32.0 ±
4.4†
33.2 ±
5.1†
P=0.03
Body fat (kg) 45.2 ±
5.5
47.1 ±
7.4
41.6 ±
5.4†
44.5 ±
7.9†
38.4 ±
5.8*†
41.1 ±
7.2†
39.3 ±
5.4*†
42.0 ±
7.0†
40.4 ±
5.0†
42.2 ±
7†
P=0.01
Blood
pressure
(mmHg)
SBP:
150 ±
10
DBP:
88 ± 7
SBP:
148 ±
12
DBP:
90 ± 10
SBP:
140 ±
10†
DBP:
85 ± 8†
SBP:
139 ±
10†
DBP:
86 ± 9†
SBP:
138 ±
9†
DBP:
83 ± 7†
SBP:
138 ±
10†
DBP:
82 ± 8†
SBP:
138 ±
8†
DBP:
84 ± 8†
SBP:
137 ±
9†
DBP:
85 ± 7†
SBP:
139 ±
9†
DBP:
85 ± 8†
SBP:
138 ±
9†
DBP:
84 ± 8†
P=0.55
P=0.49
CRP (mg/dL) 0.45 ±
0.08
0.51 ±
0.07
0.42 ±
0.08
0.45 ±
0.07†
0.40 ±
0.08†
0.43 ±
0.07†
0.40 ±
0.08†
0.42 ±
0.07†
0.42 ±
0.08
0.42 ±
0.07†
P=0.41
TNF‐α (pg/L) 18.3 ±
6.0
19.7 ±
4.2
18.0 ±
6.0
19.0 ±
4.2
17.7 ±
5.1
17.8 ±
4.0
17.7 ±
6.0
17.7 ±
4.2†
18.0 ±
6.0
17.7 ±
4.2†
P=0.28
IL‐6 (pg/mL) 15.1 ±
0.3
14.7 ±
0.6
14.5 ±
0.3
14.1 ±
0.6
14.2 ±
0.3†
13.9 ±
0.6†
14.2 ±
0.3†
13.8 ±
0.6†
14.4 ±
0.3†
13.9 ±
0.6†
P=0.06
Adiponectin
(ng/ml)
7692 ±
4425
8203 ±
5442
9225 ±
5620†
8970 ±
5322†
9582 ±
5501†
9280 ±
4499†
10236±
5622*†
9450 ±
5444†
9831 ±
5398†
9421 ±
5223†
P=0.04
Glucose
(mmol/L)
10.1 ±
0.4
10.3 ±
0.5
9.1 ±
0.4*†
9.8 ±
0.5†
8.2 ±
0.4*†
9.3 ±
0.5†
8.1 ±
0.4*†
9.4 ±
0.5†
8.4 ±
0.4*†
9.5 ±
0.5†
P=0.01
Insulin
(mU/L)
18.3 ±
5.0
18.8 ±
5.2
16.3 ±
5.0†
17.3 ±
5.2†
15.3 ±
5.0*†
17.0 ±
5.2†
16.0 ±
5.0†
17.0 ±
5.2†
16.3 ±
5.0†
17.1 ±
5.2†
P=0.03
HOMA‐IR 8.2 ±
1.0
8.6 ±
1.2
6.6 ±
0.9†
7.5 ±
0.8†
5.7 ±
1.0*†
7.0 ±
0.9†
5.8 ±
0.9*†
7.0 ±
0.8†
6.2 ±
0.9*†
7.2 ±
1.0†
P=0.01
Trigs
(mmol/L)
3.8 ±
0.7
3.7 ±
1.0
3.3 ±
0.7†
3.7 ±
0.9
3.1 ±
0.7*†
3.6 ±
0.8
3.0 ±
0.7*†
3.5 ±
0.6
3.1 ±
0.7*†
3.6 ±
0.7
P=0.03
Total
cholesterol
(mmol/L)
5.6 ±
1.3
5.8
±1.1
5.4 ±
1