“Within the next few
years, you will be able to have your entire genome sequenced for about $1000.
From the point of view of your future profession, leading on from your course
(medical science, clinical science, pharmacy, nutrition etc), review the literature
to find predictions or areas currently under research which rely on genetic
information and could affect your future practise (e.g. diagnosis, services,
treatment or advice). Explain, using examples of disease, how genetic
information facilitates these changes in practise”.
Word count: 1485
GENETIC
TESTING FOR INDIVIDUAL MTHFR POLYMORPHISMS: CLINCAL RELEVANCE AND ETHICAL
CONSIDERATIONS IN THE TOP 3 WORLDWIDE CAUSES OF MORBIDITY AND MORTALITY.
INTRODUCTION
According to the World Health Organization Cancer,
Type II Diabetes and Cardiovascular Disease represent the world’s leading
causes of morbidity and mortality. Cancer accounted for 7.6 billion, or 13% of
all deaths, 346 million people have diabetes with 3.4 million of those dying as
a direct result of high blood sugar, and 17.3 million people died from
Cardiovascular disease in 2008, representing 30% of all global deaths
(Worldwide death rates from cancer, 2014; Worldwide death rates from diabetes,
2014; Worldwide death rates from cardiovascular disease, 2014). Population-based
epidemiological evidence has clarified the role of diet in preventing and
controlling morbidity and mortality resulting from these NCDs (non-communicable
diseases) (WHO 2003, Hobbs et al. 2014; McMahon & Amaya, 2013; Hosking
& Danthiir, 2013; Annema et al., 2011). Stemming from the overwhelming
evidence regarding dietary intake and disease risk, International Government
bodies have focused on encouraging higher relative consumption of fruits,
vegetables and whole grains within the population’s daily food intake via
evidence-based macro and micronutrient recommendations (Rodriguez & Miller,
2015; Australian Dietary Guidelines, 2013). The Recommended Daily Intake (RDI)
value, for example, reflects the levels of essential nutrients considered
adequate to meet the nutritional needs of most
healthy people and are based on age, gender, level of physical activity,
and pregnancy/lactation status (Brownie, Muggleston & Oliver, 2015). Recent genetic research however. indicates that individual genetic polymorphisms, such as those on
the MTHFR gene may result in substantial relative risk changes for the
aforementioned diseases through epigenetic mechanisms (Kasapoglu et al, 2015;
Huemer et al., 2016), requiring a far more individualised approach to
recommended nutrient intake and overall dietary pattern. Despite these emerging
variations in individual vs population genetic responses to diet and nutrient
intake, the application of Nutrigenetics and Nutrigenomics to individual
nutrition consultation and dietary recommendation remains ethically
controversial (Paulidis, Patrinos & Katsila, 2015; Ferguson, 2014). This
paper elucidates the relationship between the aforementioned (NCDs ) and MTHFR
gene mutations and addresses both sides of the argument regarding current and
potential therapeutic applications, however, until definitive evidence is
presented supporting these therapeutic interventions, the usage is not recommended.
CURRENT DIAGNOSIS AND TREATMENT
Cancer, Type II Diabetes and Cardiovascular Disease
are all recognised as having both genetic and dietary/lifestyle aetiologies
(Eng, 2011; Printz, 2013; Nankervis, 2015; Dupas et al. 2016; Yu, 2016).
Hereditary breast and ovarian cancers are linked to BRCA1 and BRCA2 genes, while
MLH1 and MSH2 are linked to hereditary colon cancer (Eng, 2011). Type II
Diabetes is associated with 70 genomic regions that commonly involve mutations
in transcription factors HNF1á and HNF4á
that affect insulin secretion (Nankervis,
2015). Cardiovascular disease has been associated with alcohol dehydrogenase,
aP2, CCR2 and CCR5, PPARG2, lymphotoxin-a, ABCA1, a common variant at 9p21,
NFKB1 and ADRb1 (Yu et al., 2016). More recently, mutations on the MTHFR gene
have been linked to all of these diseases in both homozygotic and heterozygotic
individuals. Pathogenic mutations associated with an autosomal recessive error
of folate metabolism lead to increased homocysteine levels and alteration of
gene expression via methylation (Levin & Varga, 2016).
Genetic predisposition is only one of many non-dietary
factors at play in the development and emergence of NCDs. Economic, social,
climatic, cultural, psychological and even polymorphisms in circadian genes
influence the hereditability of these diseases (Almon et al. 2012; Shanmugam et
al. 2013). As a result the global health community has recognised that social,
economic and political environments drive disease emergence just as, or more
strongly, than genetics, biology and individual choice. Combating the major
causes of chronic NCDs, rather than new symptom management in an acute care
setting is the major focus of the WHO’s Global Coordination Mechanism for NCDs.
Prevention is prioritized (Allen, 2016). It is precisely this focus on prevention
however that is driving frantic research into the MTHFR gene mutations
implicated in chronic NCDs. Identifying at-risk individuals and adjusting
specific nutrient values according to their individual polymorphism has been
strongly embraced by both the scientific research community and the allied
health internet communities as a potentially powerful prevention strategy (Kasapoglu
et al. 2015; Shiao et al. 2016; Clarke et al. 2016; Culson et al. 2015; Lynch
2016; Skeptical Raptor’s blog 2015). The multi-system effects of genetic
methylation variation due to MTHFR polymorphisms do suggest that a greater
understanding of these mutations and the epigenetic effects of diet and
lifestyle on the phenotype may be key to targeted prevention of NCDs, however
individual genetic testing and its application to disease prevention is still
mired in controversy.
MTHFR COMMON MUTATIONS AND PHENOTYPIC EXPRESSION
MTHFR, the methylenetetrahydrofolate reductase gene
has been widely investigated regarding epigenetics and human disease (Mcbride
& Koehly 2017; Wade, Mcbride, Kardia & Brody, 2010). Showing an
autosomal recessive inheritance pattern, the two most common loci exhibiting
polymorphism mutations
on the geneare
C677T and A1298C. These two single nucleotide polymorphisms are about 2,000
base-pairs apart (http://ghr.nlm.nih.gov/gene/MTHFR).
The MTHFR enzyme, coded by the MTHFR gene is responsible for homocysteine
remethylation to methionine. It catalyzes reduction of 5,10-
methylenetetrahydrofolate to 5-methylenetetrahydrofolate, the most common form
of folate in blood, tissues and cerebrospinal fluid. This folate formacts as a methyl donor for the methylation of homocysteine to methionine. In
those with MTHFR deficiency, this methylation is decreased so plasma levels of
homocysteine remain elevated while methionine levels are at low concentrations
(Burda et al. 2015). Low methionine then leads to a lack of
S-adenosylmethionine which is the primary donor for many important methylation
reactions including creatine synthesis and RNA and DNA methylation (Huemer et
al. 2016).
Enzyme function in affected individuals varies
according to hereditability patterns. With an MTHFR 677TT homozygous mutation,
70% of enzyme function is lost compared to 35% in a heterozygous mutation. In
MTHFR 1298CC mutations the respective loss of function is 30% (homozygous) and
15% (heterozygous). In rare cases, individuals can exhibit compound
polymorphisms or mutations at both loci and will be at increased risk of developing
health problems with both neurological and vascular symptoms (Shiao & Yu,
2016).
The resulting low plasma folate/high plasma
homocysteine levels associated with MTHFR mutation and their association with
Cancer, Cardiovascular disease, neurodevelopmental disease and Type II Diabetes
have been repeatedly researched, as folate, the MTHFR gene, and methylation
pathways are critical to basic biological processes involving DNA and protein
methylation as well as DNA replication
and mutation (Inoue-Choi et al. 2013; Jamaluddin, Young & Wang, 2007;
Crider et al. 2012). Additionally, individuals with gene mutations in
methylation pathways have been shown to be compromised in their ability to
process environmental pollutants, with air pollution causing as much damage as
that caused by cigarette smoking ( Kloog, Ridgeway, Koutrakis, Coull &
Schwartz, 2013).
Despite the effect of MTHFR mutations on the most
fundamental biological processes and the broader implications of these effects,
many recent studies have found inconclusive evidence for high plasma
homocysteine levels and resulting disease states (Marti-Carvajal et al. 2009; Greenland et
al. 2010). With conflicting results and uncertainty as to clinical
implications, most worldwide health authorities recommend against testing for MTHFR polymorphisms (Levin & Varga, 2016). Further,
high plasma homocysteine and low folate levels can be routinely and
inexpensively treated via dietary changes or supplementation with folate, B12
and B6 (Prachi et al. 2010) although the form of folate
supplementation (Folic acid vs. Folinic acid) is still hotly debated (Hyland et
al. 2010; Diekman et al. 2014). According to the Academy of Nutrition and
Dietetics:
"There is
insufficient evidence regarding C677T polymorphism in the MTHFR gene to modify
current folate recommendations from those provided in the Dietary Reference Intakes. "(Camp & Trujillo, 2014).
Despite this statement, pilot studies have been
undertaken to treat C677T polymorphisms via dietary intervention, with results
suggesting that personalized dietary recommendations based on individual
genetic makeup and nutritional status are not only effective, but may reduce
further somatic complications and the social costs of these diseases (Di Renzo
et al. 2014).
ETHICS
With over 10% of the Australian population homozygous
or compound heterozygous for these polymorphisms, it is perhaps not surprising
that referrals for MTHFR polymorphism testing and counselling are on the
increase (Long & Goldblatt, 2016), despite no clinically significant
interventions that can reasonably be offered to carrier of the polymorphism
(MTHFR Support Australia). Companies like 23andMe and Navigenics offer genetic
testing for as little as US $99 to absolutely anyone with internet access,
although as they are both American companies, GINA (the Genetic Information
Nondiscrimination Act) does not apply to Australian consumers of their
services. The Australian Law Reform Commission outlines that although insurance
companies, for example, cannot ask an
individual to undergo genetic testing, they have every right to pursue whatever
genetic information may be available for underwriting purposes (ALRC, 2016). It
could be argued that the ethics of genetic testing is at least as complex as
the genome itself. While genetic testing enables the detection of new diseases
and leads to improved clinical interventions, there remains a high level of
concern regarding its social implications (Alper et al. 2002).
Knowing about the intricacies of one’s genome affects
how people see themselves, their social identity, and even leads to new kinds
of individual risk behaviours ( Arribas-Ayllon, Sarangi & Clark, 2011). The
argument quickly boils down to the ‘the right to know’ vs ‘the right not to know’ and must focus on both
individual autonomy and societal mores simultaneously (Hunt, Castaneda &
Voog, 2006; Gross & Shwval, 2008). The increased anxiety, social stigma and
potential discrimination resulting from poorly interpreted or incomplete
genetic testing may actually end up opposing one of the oldest medical
principles of all: Primum non nocere (Domaradzki,
2015). A psychiatrist friend of mine suggested that I start this paper with “It
was a dark and stormy night on Wisteria Lane…” and although he was being as
facetious as is expected of a long-term friend and academic, his suggested
literary trope for this topic (‘mystery’) was not entirely misplaced. The
palpable public fear and mistrust of scientific method and genetic
manipulation, whether actual or simply the fear of one portion of humanity
holding greater power over the individual through advanced knowledge in
genetics, cannot be dismissed lightly. With every advance in epigenetics and
nutrigenomics comes a responsibility for balanced and ethical stewardship of
information accessibility and dissemination (Pinigree, 2008).
REFERENCES
Almon, R.R., DuBois, D.C., Sukumaran, S., Wang, X.,
Xue, B., Nie, J., Jusko, W. (2012). Effects of High Fat Feeding on Liver Gene
Epxression in Diabetic Goto-Kakizaki Rats. Gene
Regulation and Systems Biology, 6. 151-165’
Alper, J.S., Ard, C., Ash, A., Beckwith, J. et al.
(2002). The double-edged helix. Social
implications of genetics in a diverse society. Baltimore, Johns Hopkins
University Press, 2002.
Annema, N., Heyworth, J.S., McNaughton, S.A.,
Lacopetta, B., Fritschi, L. (2011). Fruit and Vegetable Consumption and the
Risk of Proximal Colon, Distal Colon, and Rectal Cancers in a Case-Control
Study in Western Australia. Journal of
the American Dietetic Association, 111(10). 1479-1490 doi: http://dx.doi.org.ezproxy.csu.edu.au/10.1016/j.jada.2011.07.008
Arribas-Ayllon, M., Sarangi, S., Clark, A. (2011). Genetic testing: Accounts of autonomy,
responsibility and blame. London, Routledge.
Australian Dietary Guidelines Introduction [online]
(2013). Journal of the Home Economics
Institute of Australia, 20(1). 8-17
Botto, L.D. & Yang, Q. (2000).
5,10-methylenetetrahydrofolate Reductase Gene Variants and Congenital
Anomalies: A HuGE Review. American
Journal of Epidemiology, 151(9). 862-877
Brownie, S., Muggleston, H. & Oliver, C. (2015).
The 2013 Australian dietary guidelines and recommendations for older
Australians. Australian Family Physician,
44(5). 311-315
Burda, P., Schäfer,
A., Suormala, T. et al. (2015). Insights into severe
5.10-methylenetetrahydrofolate reductase deficiency: Molecular genetic and
enzymatic characterization of 76 patients. Human
Mutation, 36(6). 611-621
Clarke, R., Halsey, J., Lewington, S., Lonn, E.,
Armitage, J., Manson, J.E. et al. (2010). Effects of lowering homocysteine
levels with B vitamins on cardiovascular disease, cancer and cause-specific
mortality: meta-analysis of 8 randomized trials involving 37, 485 individuals. Archives of Internal Medicine, 170(18).
1622-1631
Crider, K.S., Yang, T.P., Berry, R.J. & Bailey,
L.B. (2012). Folate and DNA Methylation: A Review of Molecular Mechanisms and
the Evidence for Folate’s role. Advances
in Nutrition, 3(1). 21-38
Culson, N.J., Naug, H.L., Nikbakht, E., Zhang, P.,
McConnack, J. (2015). The impact of MTHFR 677 C/T genotypes on folate status
markers: a meta-analysis of folic acid intervention studies. European Journal of Nutrition, 1-14.
Advanced online publication. Doi:
10.1007/s00394-015-1076-x.
Diekman, E.F., de Koning, T.J., Verhoeven-Duit, N.M.,
Rovers, M.M., van Hasselt, R.M. (2014). Survival and psychomotor development
with early betaine treatment in patients with severe methylenetetrahydrofolate
reductase deficiency. JAMA Neurologica,
71(2). 188-194
Di Renzo, L., Marsella, L.T., Sarlo, F., Soldati, L.,
Gratten, S., Abenavoli, L., De Lorenzo, A. (2014). C677T gene polymorphism of
MTHFR and metabolic syndrome: response to dietary intervention. Journal of Translational Medicine, 12. P
329. Doi: 10.1186/s12967-014-0329-4
Domaradzki, J. (2015). Patient rights, risks, and
responsibilities in the genetic era –a right to know, a right not to know, or a
duty to know? Annals of Agricultural and
Environmental medicine, 22(1). 156-162
Dupas, J., Goanvec, C., Feay, A., Guernec, A.,
Guerrero, F., Mansouriti, J. (2016). 0021: Type II diabetes induced by a
fructose enriched diet: benefits of exercise training. Archives of Cardiovascular Disease supplements, 8(3). P 265
Eng, C. (2011). Cancer Genetics. The Journal of the American medical Association, 305(22). P 2353
Ferguson, L.R. (2014). Nutrigenomics and nutrigenetics in functional foods and personalized
nutrition. Boca Raton, Florida: CRC Press/Taylor & Francis Group.
Gross,S.E. & Shwval, J.T. (2008). On knowing and
believing: prenatal genetic screening and resistance to ‘risk-medicine’. Health, Risk & Society, 10(6).
549-564 doi: 10.1080/13698570802533721
Hosking, D. & Danthiir, V. (2013). Retrospective
lifetime dietary patterns are associated with demographic and cardiovascular
health variables in an older community-dwelling Australian population. British Journal of Nutrition, 110(11).
2069-2083 doi: https://doi.org.ezproxy.csu.edu.au/10.1017/500711451300144X
Huemer, M., Mulder-Bleile, R., Burda, P. … Morris, A.
et al. (2016). Clinical pattern, mutation and in vitro residual activity in 33
patients with severe 5,10 methylenetetrahydrofolate reductase (MTHFR)
deficiency. Journal of Inherited
Metabolic Disease, 39(1). 115-124
Hunt, L.M., Castañeda,
H., de Voog, S. (2006). Do notions of risk inform patient choice? Lessons from
a study of prenatal genetic counselling. Medical
Anthropology, 25(3). 193-219
Hyland, K., Shoffner, J., Heales, S.J. (2010).
Cerebral folate deficiency. Journal of
Inherited Metabolic Disease, 33(5) 563-570
Inoue-Choi, M., Nelson, H.H., Robien, K., Arning, E.,
Bottiglieri, T., Koh, W., Yuan, J. (2013). Plasma S-adenosylmethionine, DNMT
polymorphisms, and peripheral blood LINE-1 methylation among healthy Chinese
adults in Singapore. BMC Cancer, 13.
389. Doi: 10.1186/1471-2407-13-389
Jamaluddin, M.S., Yang, X. & Wang, H. (2007).
Hyperhomocysteinemia, DNA methylation and vascular disease. Clinical Chemistry and Laboratory Medicine,
45(12). 1660-1666.
Kasapoglu, B., Turkay, C., Yakin, K.S., Kosov, A.,
Bozkurt, A. (2015).MTHFR 677C/T and 1298 A/C mutations and non-alcoholic fatty
liver disease. Clinical Medicine, 15(3).
248-251
Kloog, I., Ridgway. B., Koutrakis, P., Coull, B.A.,
Schwartz, J.D. (2013). Long- and short-term exposure to PM2.5 and mortality:
using novel exposure models. Epidemiology,
24(4). 555-561
Levin, D.L. & Varga, E.J. (2010). MTHFR.
Addressing Genetic Counselling Dilemmas Using Evidence-Based Literature. Journal of Genetic Counselling, 25. P
901. Doi: 10.1007/s10897-016-9956-7
Lang, S. & Goldblatt, J. (2016). MTHFR genetic
testing: Controversy and clinical implications. Australian Family Physician, 45(4). 237-240
Lynch, B. (2016). MTHFR.Net: your expert resource on
MTHFR Gene Mutations. Retrieved from http:///www.mthfr.net
Marti-Carvajal, A.J., Sola, I., Lathyris, D., Salanti,
G. (2009). Homocysteine lowering interventions for preventing cardiovascular
events. Cochrane Database System Reviews,
4: CD006612. Doi: 10.1002/12651858.CD006612.pub.2
McBride, C.M. & Koehly, L.M. (2017). Imagining
roles for epigenetics in health promotion research. Journal of Behavioural Medicine, 40(2). 229-238
McMahon, S. & Amaya, G. (2013). Obesity Prevention
in Urban Settings: Creating Healthy Environments. American Journal of Health Sciences, 4(1). 45-50
Nankervis, A. (2015). Genetics in Diabetes: Type 2
Diabetes and Related Traits. Australian
Family Physician, 44(5). P.333
Paulidis, C., Patrinos, G.P., Katsila, T. (2015).
Nutrigenomics: A controversy. Applied and
Translational Genomics, 4. 50-53
Prachi, K., Dattaray, B., Lubree, H., Otivi, S.,
Jushi, S. et al. (2010). Vitamin B12 and folic acid supplementation and plasma
total homocysteine concentrations in pregnant Indian women with low B12 and
high folate status. Clinical Nutrition,
19(3). 335-343
Printz, C. (2013). Researchers continue to explore
links between diet and cancer. Cancer,
119. 1447-1448
Rodriguez, N.R. & Millder, S.L. (2015). Effective
translation of current dietary guidelines: understanding and communicating the
concepts of minimal and optimal levels of dietary protein. American Journal of Clinical Nutrition, 101(6). 1353-1358
Shanmugam, V., Wati, A., Al-Taweel, N., Busselberg, D.
(2013). Disruption of circadian rhythm increases the risk of cancer, metabolic
syndrome and cardiovascular disease. Journal
of Local and Global Health Science, 3. Doi: 10.5339/jlghs.2013.3
Shiao, S.P.K. & Yu, C.H. (2016). Meta-prediction
of MTHFR Gene Polymorphism Mutations and Associated Risk for Colorectal Cancer.
Biological Research for Nursing, 18(4).
Doi: 10.1177/1099800415628054
Wade, C.H., McBride, C.M., Kardia, S.L., Brody, L.C.
(2010). Considerations for designing a prototype genetic test for use in
translational research. Public Health
Genomics, 13(3). 155-165
WHO (2003). Diet, Nutrition and the prevention of
diseases. Wolrd Health Organization, 20 Avenue Appia. Geneva Ch-1211.
Switzerland.
Yu, E., Rimm, E., Qi, L., Rexrode, K., Albert, C.M. et
al. (2016). Diet, Lifestyle, Biomarkers, Genetic Factors, and Risk of
Cardiovascular Disease in the Nurse’s Health Studies. American Journal of Public Health, 106(9). 1618-1623
|
HD (100-85)
|
DI (85-75)
|
CR (75-65)
|
PS (65-50)
|
FL (<50)
|
Mark
|
Title & Introduction
(/10)
|
Very focused & concise title & introduction,
leading to a completely clear & logical plan.
A few significant diseases relevant to the
students course are introduced
|
Focused & concise title & introduction,
leading to a logical plan.
A few diseases relevant to the students course are
introduced
|
Title & introduction are reasonably well focused
and concise.
A disease relevant to the students course is
introduced
|
Title & introduction are somewhat focused and
concise.
A few diseases which are irrelevant to the students
course are introduced
|
Significant information in title & introduction
is missing.
No diseases are introduced
|
10
|
Presentation of content relevant to the current
diagnosis and treatment of disease, how this will change with genetic testing
and description of ethical consequences
(/45)
|
Very appropriate & accurate presentation of the
literature throughout.
Current diagnoses and treatment based on genetic
information accurate. Common mutations identified. Concise changes to
diagnosis and treatment as a result of genetic testing identified. Sound
description of ethical issues as a result of DNA testing
|
Appropriate & mostly accurate presentation of
the literature throughout.
Current diagnoses and treatment based on genetic
information included. Some common mutations identified. Some changes to
diagnosis and treatment as a result of genetic testing identified.
Sound description of ethical issues as a
result of DNA testing
|
Some minor inaccuracies and presentation of the
literature throughout.
Figures and tables
Inaccurate current diagnoses and treatment based on
genetic information included. Some common mutations identified. Some changes
to diagnosis and treatment as a result of genetic testing identified. Brief
description of ethical issues as a result of DNA testing
|
Some information presented which is inaccurate. Data
not described in appropriate detai. Current diagnoses and treatment based on genetic
information inaccurate. Common mutations identified. Minor changes to
diagnosis and treatment as a result of genetic testing identified.
Some description of ethical issues as a result
of DNA testing
|
No interpretation of relevant literature and inaccuracies
present.
Current diagnoses and treatment not based on genetic
information. Common mutations not identified. Minor changes to diagnosis and
treatment as a result of genetic testing identified.
No description of ethical issues as a result
of DNA testing
|
45
|
Evidence of linking of information from various
sources and critical analysis (/20)
|
Information from various sources and concepts is
linked throughout the assignment. There is evidence of critical analysis of
various sources. The balance of references is very good throughout the
assignment
|
Information from various sources and concepts is
linked throughout the assignment. There is limited critical analysis of
various sources. The balance of references is very good throughout the
assignment
|
There is some linkage of various sources and
concepts throughout the assignment. There is very limited critical analysis
The balance of references is very good throughout the assignment
|
There is some linkage of various sources and
concepts throughout the assignment. There is no critical analysis the
references are unbalanced.
|
No linking of concepts across the various parts of
the assignment.
Normal and abnormal situation are not clearly
separated and information is presented under the wrong headings. No balance of
references in the assignment (i.e.many references used for only one
paragraph, one reference used for the rest of the assignment
|
20
|
Clarity of expression
and logical flow of
information (/10)
|
No grammatical or spelling errors.
Professional expression & style used
consistently. Sections distinct & literature review logically organised.
|
No more than 4 grammatical and spelling errors.
Professional expression & style used consistently. Sections distinct
& literature review logically organised
|
No more than 4 grammatical and spelling errors.
Minor flaws in professional expression & style. Most of the literature
review logically organised.
|
No more than 4 grammatical and spelling errors.
Occasional flaws in professional expression & style and literature review
not logically organised.
|
More than 4 grammatical and spelling errors.
|
10
|
References (/10)
|
More than 80% of the references used are from
international peer reviewed journals and published after 2008.
No errors in reference list and no more than 5
errors in citation style list (APA format).
|
More than 70% of the references used are from
international peer reviewed journals and published after 2008.
No errors in reference list and no more than 5
errors in citation style list (APA format).
|
More than 50% of the references used is from
international peer reviewed journals and published after 2008.
No errors in reference list and no more than 10
errors in citation style list (APA format).
|
Less than 50% of the references used is from
international peer reviewed journals and published after 2008.
No more than 2 errors in reference list and no more
than 10 errors in citation style list (APA format).
|
Use of literature limited to a few articles &
reviews. Poor attempt to explore literature. Major errors in citations &
reference list.
|
|
Presentation (/5)
|
Word count clearly indicated. Full adherence to word
limit and presentation guidelines in subject outline (3cm margin, double or
1.5 line spacing, 12pt font, numbered
pages, header and footer, title page. Turnitin
report included.
|
Word count clearly indicated. Full adherence to word
limit and presentation guidelines in subject outline (3cm margin, double or
1.5 line spacing, 12pt font, numbered
pages, header and footer, title page Turnitin report
included.
|
Word count not indicated.Full adherence to word
limit and presentation guidelines in subject outline (3cm margin, double or
1.5 line spacing, 12pt font, numbered
pages, header and footer, title page. Turnitin
report included.
|
Word count not indicated.No adherence to word limit
and presentation guidelines in subject outline (3cm margin, double or 1.5
line spacing, 12pt font, numbered
pages, header and footer, title page. Turnitin
report not included.
|
Word count not indicated. No adherence to word limit
and presentation guidelines in subject outline not adhered to (3cm margin,
double or 1.5 line spacing,12pt font, numbered pages, header
and footer, title page). Turnitin report not
included.
|
5
|
Total = 98
