SlideShare a Scribd company logo
1 of 27
Sugar intake and Pancreatic Cancer
1
University of Balamand
Faculty of Health Sciences
Research Methods
FHSC288
Increased sugar intake and the risk of developing pancreatic cancer in Lebanese adults
between the age of 50 and 80 years, a case-control study.
El Jalbout Ralph
Hamieh Cyma
Massaad Nadine
May 2015
Sugar intake and Pancreatic Cancer
2
Acknowledgment
We would like to thank our mentor Dr. Nivine Abbass for supporting and guiding
us during our research project. We also appreciate the explanations and advices provided
by our instructors Dr. Laurie Abi Habib and Miss Joumana Yeretzian which were very
beneficial. We are grateful to Miss Nadine Haddad for her help in the methods section and
developing the questionnaire. Finally, we would like to thank our University for the open
access to a rich database and to Miss Dolly Radi and Miss Sylvie Sleiman for the help in
obtaining articles from additional databases.
Sugar intake and Pancreatic Cancer
3
Table of content
Sugar intake and Pancreatic Cancer
4
I- Abstract
Ranked as the fourth leading cause of cancer-related deaths in the world, pancreatic cancer
is the causes of over 200 000 death yearly. In Lebanon as mentioned by the Ministry of
Public Health in 2005, 143 out of 7914 cancer patients reported having pancreatic cancer,
with comparable statistics in the years 2006, 2007 and 2008 for both genders in equal
proportions with a peek at the ages 62-63. Considering its low prognosis and 5% survival
rate after five years, preventing this disease is a necessity. Hyperglycemia is one of the
major underlying risk factors of pancreatic cancer considering most of its patients are
diagnosed with high glucose levels and diabetes. Therefore, decreasing sugar consumption
might help on decreasing the risk of developing the disease and preventing its occurrence.
In order to see the relation between sugar intake and pancreatic cancer, a case-control study
will be conducted for about five years. A questionnaire and a food frequency checklist will
be provided for the assessment of pancreatic cancer patients in several hospitals in
Lebanon. In parallel, four controls for each case will be matched. Based on the results, we
will try to deduce and find an association between cancer patients’ diet and the disease.
Key words: Sugar Intake, Pancreatic Cancer, Cancer Prevention
Table of contents
Sugar intake and Pancreatic Cancer
5
Increased sugar intake and the risk of developing pancreatic cancer, in Lebanese adults
between the age of 50 and 80 years, a case-control study.
Sugar intake and Pancreatic Cancer
6
II- Introduction:
Globally, pancreatic cancer causes the death of over 200 000 people in the world
yearly (Michaud, 2004) and it is ranked as the fourth leading cause of cancer-related deaths
in the world (Hariharan et al, 2008). It is the fourth leading cause of death in the United
States out of all cancer types and the sixth in Europe. In 2014 in the USA, Pancreatic cancer
was diagnosed in 46,420 patients out of 1,665,540 (23,530 males and 22,890 females) and
caused the death of 39,590 out of 585,720 (20,170 males and 19,420 females) (Siegel et al,
2014). This cancer is defined as the development and spread of cancerous and malignant
tumor cells in the pancreas affecting both the exocrine (which is the most common
function) and endocrine function of the organ (American Cancer Society, 2015). The
Exocrine function of the pancreas participates in the digestion mechanism; the organ
produces digestive enzymes used in the small intestine for neutralization and breakdown.
The Endocrine function is defined by the production of hormones (glucagon and insulin
mainly) for the regulation of glucose blood levels (Johns Hopkins University, 2012).
Based on that, prevention is essential since it is considered as the most fatal cancer
providing a maximum of 5% survival chances for no more than five years of duration
(Nöthlings et al, 2007). Due to its high fatality rates, the incidence of pancreatic cancer is
directly associated with mortality; a lack in the screening tests for this disease prevent the
diagnosis until after its progression (Michaud, 2004). The incidence of this lethal disease
is strongly associated with an increase with age especially between the ages 50 to 80 years;
in the UK for example, 96% of pancreatic cancer patients were diagnosed over the age of
50 years and 47% were diagnosed over the age of 75 between the years 2009 and 2011
(Office of National Statistics, 2011).
Sugar intake and Pancreatic Cancer
7
It has been evidenced that hyperglycemia is one of the underlying risk factors of pancreatic
cancer where “a large portion of pancreatic cancer patients suffer from either
hyperglycemia or diabetes, both of which are characterized by high blood glucose level.”
(Han et al, 2011). Moreover, there seems to be an association between increased sugar
consumption (including sweeteners, glucose, fructose, carbohydrate) and the increased risk
of becoming a pancreatic cancer patient as it has been demonstrated that hyperglycemia
aids in the proliferation and invasion capacity of pancreatic cells (Li et al, 2011). Sugar
intake is basically the consumption of items containing any sort of glucose or glucose
derivatives such as sugar-sweetened foods or beverages, carbohydrates, fructose (that is
transformed on the body to glucose during digestion). In a multiple of studies that
considered the Arab world, the prevalence of pancreatic cancer is significantly low but a
little bit higher in Lebanon and Syria (Salim et al, 2009). Based on the database of the
Ministry of Public Health in Lebanon, in 2005, 143 of the total 7914 cancer patients
reported had pancreatic cancer, in 2006 the values were 132 over 8491, in 2007 the values
were 118 over 9552, and in 2008 the values were 137 over 9499. In the National Cancer
Registry (NCR) report “Cancer in Lebanon: 2005-2007” the cases of pancreatic cancers
are equal among genders but occur mainly in people older than 50 years with a mean of
62-63 years. “The age-specific incidence rates showed an increase starting the 50-55 age-
group” according to the same report. In Lebanon, the adenocarcinoma is the most recurrent
type of pancreatic cancer notes the NCR.
Literature Review:
Sugar intake and Pancreatic Cancer
8
Based on that pancreatic cancer does not respond effectively to current cancer
treatment and has a low survival rate. Many studies worked on detecting risk factors in
order to prevent the tumor development. In their study, Nöthlings, Murphy, Wilkens,
Henderson, and Kolonel (2007) note that high glycemic load increased pancreatic cancer
onset. In their four years cohort study with 162,150 participants, 434 developed cancer.
The multiethnic study focused on African Americans, Japanese American, Latinos, Native
Hawaiians and whites (Nöthlings et al, 2007). Based on their follow up, dietary assessment
and results, Nöthlings et al (2007) pointed out that high sugar diet especially fructose, put
the individual at a higher risk of developing pancreatic cancer; foods like fruits and juices
are the key provider of fructose. Nöthlings et al (2007) mentioned that long study periods
are needed when working on pancreatic cancer because this malignancy has a low
occurrence rate. Overweight and obesity correlates with high sugar and fructose intake and
has to be taken into consideration.
In a prospective cohort study that has been done to investigate the relationship
between both dietary sugar and glycemic load and the risk for pancreatic cancer found that
any type of food that contribute to an increase in postprandial blood glucose levels may
have a great influence in a risk for pancreatic cancer (Michaud et al, 2002). In this study,
121 700 women were followed up for 18 years with examination of their dietary intake.
The results showed that high dietary sugar intakes along with a high glycemic load and
glycemic index were directly related to the increased risk of pancreatic cancer for sedentary
and overweight women. This a statistically significant increase in pancreatic cancer risk by
86% for inactive women who consumed high fructose compared to those who consumed a
Sugar intake and Pancreatic Cancer
9
low fructose diet with a P-value of 0.02. However, dietary intake did not reveal an
association with the risk of pancreatic cancer for active women (Michaud et al, 2002).
In another study done by Larsson, Bergkvist and Wolk (2006) diagnosed among 77
797 men and women between the ages 45 and 83 years adjusted for age, sex, smoking,
BMI, alcohol intake and energy 131 incident cases of pancreatic cancer, the participants
from Sweden were followed up from 1997 till June 2005 in a prospective study. Results
showed that a higher consumption of sugar-sweetened foods, soft drinks or sweetened
soups by participants, provided a greater risk of pancreatic cancer by 1.5 to 1.9 times than
in the group with the low consumption of these products (Larsson et al, 2006). However,
no association was found between the consumption of jam, marmalade or sweets and
pancreatic cancer considering that they contain a lot less sugar contents (30gr/serving) than
sweetened foods like soups (230gr/serving). Yet, it is important to note that the participants
handed a self-administered food frequency questionnaire, so misclassification may have
occurred between the sugar and the sweetened food consumption. Moreover, this study
correlates with another prospective cohort study done on nurses and health professionals
in the United States. It contributed to significant results were women who consumed more
than 3 sugar sweetened soft drinks per week had a greater risk of 57% of pancreatic cancer
than those who consumed less than 1 drink per week with a p-value of 0.05. On the other
hand, no association between the consumption of these items and pancreatic cancer was
found among men (Schernhammer et al, 2005). However, based on the work of Olson and
Kurtz (2013), gender plays a role and put men at a higher risk (13.5 for 100,000) of
developing this type of cancer compared to women (10.8 for 100,000). Thus, these studies
are based on the fact that a higher sugar intake causes elevated blood glucose levels which
Sugar intake and Pancreatic Cancer
10
affect the activity of pancreatic islet cells negatively causing glucose toxicity. Nevertheless,
glucose toxicity increases reactive oxygen that increases relatively the oxidative stress
along with the small presence of antioxidants in the islets cells, hence increasing the risk
of P.C.(Robertson,2004).
Further studies done by Ueno.Y, Makino.N, and Ito.M (2013) noted the importance
of early detection of pancreatic cancer to the scope of the treatment, they found that risk
factors can be associated with smoking, family history, age, sex, diabetes mellitus, chronic
pancreatitis, obesity and non-O blood group. In another study, done by Permuth-Wey et al,
results showed an increase in risk of pancreatic cancer if a relative was diagnosed with the
disease.
One major risk was obesity, according to a cohort study done in Japan by Lin.Y et
al, men and women with high BMI had risks 3.5 fold and 60% higher respectively, as
compared to those with normal BMI. Diabetes resulting from insufficient insulin
production by the pancreas, leading to high glucose levels in blood, has the highest
incidence among other diseases suspected to lead to pancreatic cancer, according to the
Committee for Pancreatic Cancer Registry in 2007.
These studies suggest that there is an association between diabetes and the onset of
pancreatic cancer, from which it is understandable to further investigate the role of
glycemia.
Consistently, Gapstur, Gann, Lowe, Liu, Colangelo, and Dyer (2000) highlight the
necessity to prevent pancreatic cancer because of its extreme malignancy, metastasis and
late detection. In those conditions, they worked on the effect of “abnormal glucose
metabolism on pancreatic cancer” (Gapstur et al, 2000). They worked on employees from
Sugar intake and Pancreatic Cancer
11
the Chicago Heart Association Detection Project in Industry (CHA) cohort study and
measured their post-load Glucose level. Among the 35,658 participants, 96 men and 43
women died from pancreatic cancer. The post-load glucose level is the amount of glucose
in the blood one hour after the 50g challenge test, and in this study, 11.1mmol/L or 200g/dL
was taken as cut off (Gapstur et al, 2000). The study concluded that participants with initial
post-load plasma glucose equal or higher than 11.1mmol/L are 2.2 times more at risk of
developing pancreatic cancer than participants with initial post-load plasma glucose equal
or lower than 6.6mmol/L (Gapstur et al, 2000). The abnormal glucose metabolism
associated with high insulin play a role in the development of pancreatic cancer; insulin at
high levels would act on promoting cellular growth especially pancreatic cells reaching
ultimately the cancer stage.
Hardey and Cowey concluded in a study on metabolic syndrome and its relation to
cancer, that hyperglycemia can directly damage the DNA of epithelium of pancreatic duct
via oxidative stress, hence leading to the onset of the cancer. Dominique.S,et al, conducted
a prospective study to find a relation between glycemic load and pancreatic cancer, they
controlled for several risk factors and observed a 53% increase in risk of P.C for women
with high glycemic load intake as compared to those with low intake, similar increase was
observed when studying fructose level, 57%. In a different study done by Suzuki et al, it
was noted that fructose directly contributes to oxidative stress in growing cells. On the
other hand, a case-control study done by Lyon JL et al (1993), strong association was found
between pancreatic cancer and carbohydrate intake or added sugars, but due to high
mortality rate, the study design was prone to several bias and errors.
Sugar intake and Pancreatic Cancer
12
In addition to many other studies that search for the presence of an association between
hyperglycemia and pancreatic cancer, Huxley et al (2005) saw in a meta-analysis of 36
studies on type II diabetes and pancreatic cancer, that there is an overestimate of the size
of the relationship between the two variables. This exaggeration also exists in other studies
due to bias, first since smaller studies reported the existence of the association and second
because the authors note the relationship obtained can be justified by the existence of
confounders such as smoking and obesity.
Rationale:
Based on the literature, pancreatic cancer is a rapidly fatal disease with a very low
survival rate (Michaud, 2004). Not to forget that this disease has a very poor prognosis
(Nöthlings et al, 2007). Moreover, the disease in its early stages, is asymptomatic and
silent; therefore, to decrease from its fatality rate it is critical to search for ways to prevent
its occurrence. Moving from this point, one of the most basic aspects eligible to control in
a healthy population is diet; that is why, looking at sugar intake and added sweeteners in
one’s diet, is beneficial to try and find an association. In addition, some studies suggested
that an increase in glucose blood levels provoke an increase in insulin; thus, insulin increase
promotes the secretion of growth factors, which later on provoke pancreatic cancer cell
growth (Schneider et al, 2001). Zhou, Liotta, and Petricoin (2015) noted in their work that
the glycolitic activity of a tumor mass affects its diagnosis; therefore, tumor with higher
glycolitic activity and dependency on glucose have the poorer prognosis. In the case of
pancreatic cancer, they identified that those cells have higher number of enzymes
implicated in glucose metabolism and cellular respiration.
Sugar intake and Pancreatic Cancer
13
In addition to that, it is interesting to note that Lebanon is among the six world-leaders’
Arabic speaking countries for Diabetes type II (Badran, M & Laher.I. 2012), with almost
53% of the Lebanese population living in Great Beirut diagnosed with Diabetes (Jacob.S
et al, 2005). In Lebanon, the Ministry of Public Health and the National Cancer Registry
defined that in the years 2005, 2006, 2007 and 2008, the occurrence of pancreatic cancer
was respectively 143 out of 7914 cancer patients, 132 out of 8491, 118 over 9552, and 137
over 9499. Unfortunately, the report lacked information concerning effect of sugar on
pancreatic cancer patients in Lebanon. This information is alarming and highlights the
importance of raising awareness among Lebanese population about the dangerous
consequences of uncontrolled sugar diet, one of which is pancreatic cancer.
Many underlying factors can increase the risk of pancreatic cancer (like: smoking, family
history, age, sex, diabetes mellitus, chronic pancreatitis, obesity and non-O blood group,
obesity, diabetes, etc…). We found that a focus on sugar intake would be more effic ient
than any other risk factor bearing in mind that family history, age, sex, non-O blood group
factors cannot be controlled resulting from genetic predisposition. Diabetes mellitus is
directly related to sugar intake, not to forget that inappropriate sugar intake and dietary
practices are the main causes for diabetes mellitus and pancreatic dysfunction.
Therefore, our study will use a case-control study design where the exposure will be sugar
intake and the outcome will be pancreatic cancer. The sample will consist of exposed and
non-exposed cases and controls based on their sugar intake recall. This might lead to the
discovery of a positive link between sugar and pancreatic cancer. Although most of the
literature used a cohort study, taking into consideration the low prevalence of pancreatic
Sugar intake and Pancreatic Cancer
14
cancer, the limit in cost and time, we found that it is most suitable to follow a case-control
study design.
Consequently, in our case-control study, we are going to collect dietary information from
participants at a one point in time using a food frequency checklists that will helps us
determine the most frequent food items consumed during their past daily life routine. Then,
we want to check if any of the participants represent pancreatic cancer and relate it to their
dietary intake to study the relationship under investigation. By this design, we are hoping
to find the desired correlation between high sugar intake and risk for pancreatic cancer.
ResearchQuestion:
Does sugar intake predispose Lebanese men and women between the age of 50 and 80
years living in Beirut to pancreatic cancer along five years of follow-up?
Hypothesis:
The higher the sugar intake is, the higher is the risk of developing pancreatic cancer.
Objectives:
The purpose of this study is to examine the effect of high sugar consumption on people
predisposing them to pancreatic cancer.
The objective is to find a true liaison between high sugar consumption and pancreatic
cancer. In order to do so, patients will be asked to recall their sugar intake in their diet
and associate it with their disease. The same will be done to the controls.
Methods:
Sugar intake and Pancreatic Cancer
15
The aim of our case control study design is to examine the Lebanese population
suffering from pancreatic cancer. Therefore we will be visiting several hospitals in
Lebanon to investigate the relationship between sugar intake(independent variable) and
risk of pancreatic cancer occurrence(dependent variable); such as Saint George Hospital
University Medical Center (SGHUMC), Hotel-Dieu de France, AUBMC, Rafic Hariri
Governmental Hospital in Beirut, Jabal Amel Hospital in Tyr, Nini Hospital and Al Mounla
Hospital in Tripoli, Khoury Hospital and Reyaa Hospital in the Bekaa, Sayidat Al
Ma’ounat in Byblos, Beshare Governmental Hospital in Bechare, Bhaniss Hospital in
Bhaniss in order to cover all regions. These hospitals were chosen based on their
geographical location, reputation and patients from different countries attend it and ask to
benefit from their services.
The attainable population will cover cases diagnosed with pancreatic cancer, in the
oncology department of hospitals. On the socio-demographical level, women and men
eligible for this study as cases will be those between 50 and 80 years of age. On the clinical
level, our cases are chosen based on their diagnosis with pancreatic cancer in the Lebanese
Hospitals. We will try to get in touch with medical doctors and ask them to collaborate
with us in order to collect data related to patients diagnosed with pancreatic cancer. An
ethical letter will be sent to both the hospital and the oncologist explaining to them our
topic and its significance in addition to asking them for permission to work and collaborate
with them. The medical doctor will become part of the investigation, and all he or she will
do is report to us the incidence of a pancreatic cancer patient in the oncology section.
The study will be based on the usage of questionnaires offering information about gender,
ager, weight in addition to occupation and habits such as smoking from which we will be
Sugar intake and Pancreatic Cancer
16
able to understand and collect information about dietary habits of our cases and controls.
Most importantly, a food frequency checklist will be given in order for the participants to
fill. This table provides us with food frequency intake and the amount of food eaten. All
the types of food sited contain molecules that the body will transform into glucose: such as
starch (in bread, pasta and rice), fructose (in fruits) and sucrose (in beverages and table
sugar). Each person will have two sheets with his ID, his/her answers will be reported
using the numbering underneath each category in a Likert Scale: going from “Never or less
than 1/month” (0) to “More than 5 a day” (7) and from “Very large amount/portion” (4) to
“Small amount/portion” (1) (Refer to Questionnaire sheet). The participant will indicate
the average food intake during the last 2 years, each year separately. Moreover, the person
will give an estimate of the quantity eaten. We found a similar case-control study
previously done which applied the same chronological demarche to assessing sugar intake
and pancreatic cancer.
For each case, four controls will be chosen and matched in order to make our control
sample as representative as possible and minimize bias and chance considering the high
number of exclusion factors for both parties; we will be excluding the non-Lebanese
responders, those who do not belong to the age range or have family history of pancreatic
cancer disease or any kind of pancreatic disease (pancreatitis, insulinoma…) in both
controls and cases (Refer to Questionnaire sheet). These exclusions are used to try and
remove any sort of confounders. Matching will be based on their residence, age, smoking
habits and additional factors (diabetes) provided by the case (Refer to Questionnaire sheet).
More specifically, controls in the sample will be selected based on random digit sampling
method. The means that will be use would be the Lebanese white pages book from which
Sugar intake and Pancreatic Cancer
17
we will randomly select addresses belonging to the same area of residency of the case or
we will ask the municipality to provide us with the village or city phone codes. The same
question asked for the cases will be given to the controls during the phone call. For both
the cases and controls the purpose of the study will be explained and information needed
is going to be provided to check if they accept to cooperate. To increase participation rate
and minimize non response, we will be clearing up that we are avoiding invasive and
uncomfortable tests and simply ask for general information.
Moreover, we are going to control for smoking habits and diabetes by calculating the odds
ratio. We will hide from the participant the real purpose of assessing sugar and pancreatic
cancer not to trigger any recall bias in addition to an ethical issue (to be discussed in the
Ethics part).
To study the consistency and validity of the questionnaire, it will be first given to a sample
of volunteers not at all related to the study sample in order to test its questions. This sample
of 10 to 20 people, contacting them via phone calls and explaining the aims and objectives
of the study, will provide us with feedback concerning the questions, time needed to
accomplish the task, difficulties and any comments concerning the questions. Two weeks
later, 5 people from this sample will be asked to fill the form again in order to examine the
consistency of the answers, whether the questions generate the same responses or different
ones. As a result, the questionnaire is finalized and used on the study sample. Directly when
a case is located, he or she will be given the questionnaire to fill it in addition to an ID so
that the privacy of the person would not be disturbed. After collecting the cases
information, the four controls will be matched based on the requirements already
Sugar intake and Pancreatic Cancer
18
mentioned. Each time a case is detected, the person will be given the questionnaires and
directly after that, the controls will be matched.
After a lap of time of two weeks, during which we would have entered the data and wanted
to revise them, the survey questions will be asked again to some randomly chosen controls
in order to test response accuracy. This will be done also to assess observer reproducibility,
compare the answers of the same person for consistency and control for any recall bias.
The study will start on June 1st 2015 and will last five years till June 1st 2020 and this in
order to obtain a high number of pancreatic cancer cases considering the rareness of the
disease. All the cases reported during this period will be registered and questioned. This is
done in order to maximize our sample, making it larger so it will be more representative
and reduce sampling error. Based on that, there is no maximum sample size.
Following this, data analysis will start. The results will be compared to check
consistency. Then, data will be entered to Excel Software, and then check the entered data
to control and fix probable mistakes and errors in copying to ensure validity post-data entry.
After that, the data will be transferred to the SPSS Software for further investigation in the
biostatics and epidemiological field. Most importantly, the results will help on assessing
the sugar intake of this person. Each participant will obtain a score.
Based on the results of the control group, a cut off value will be deduced with a
score as an indicator for a low or high sugar intake by the cases. The relation between the
sugar diet and onset of pancreatic cancer will be established. The Odds ratio for all the
categories will be calculated in order to complete the investigation. To control for diabetic
patients and smokers, the Odds ratio will be calculated respectively and for non-smokers
Sugar intake and Pancreatic Cancer
19
or non-diabetics. According to our calculations, the role of smoking and diabetes in
developing pancreatic cancer will be deduced.
Limitations:
Sugar is not the only risk factor that has to be taken into consideration; other
elements can predispose a person to develop pancreatic cancer. Smoking is seen to increase
the risk by 75% (Olson & Kurtz, 2013). Obesity, diabetes, pancreatitis mainly, in addition
to alcohol and allergies are also predisposing agents. Most notably, family history and
genetic polymorphisms according to Olson and Kurtz (2013) increase the chances of
having many cases of cancer in the same family. Those mutations include BRCA1,
BRCA2, PALBA2 and many others. Therefore, as already mentioned, diabetes and
smoking will be controlled in addition of excluding other confounders.
When it comes to the selection of cases and controls, difficulties will be faced. We will
need cooperation from the medical sector and the medical doctors to locate the cases,
considering that not all new cases will be reported. To be noted that cases can refuse
participating because of delicate matters and this is an important issue considering the
rareness the disease. Moreover, recall bias is important for both the cases and controls
especially if they have preconceived knowledge about pancreatic cancer; a person
diagnosed with pancreatic cancer would falsely associate the disease and a past unexciting
high sugar intake. Concerning the controls, that will be contacted by phone calls; no
accurate phone lists exist in Lebanon and not all houses have phones, disposing us to
selection bias. In addition, people can hang up, refuse to answer, or answer inaccurately
with bias.
Sugar intake and Pancreatic Cancer
20
Ethics
The ethical concern in this study is mainly the privacy of the participants and their
wellbeing.
First of all, the identity of a person will not be asked and the person will be given an ID
number once he or she enrolls in the study. We will then explain to the person the aim of
our study as detecting sugar in diet. The part about pancreatic cancer will be hidden in
order to avoid bias in recall, but most importantly to preserve the wellbeing of the
participants, especially the cases because not always they are informed with their disease.
If we reach a patient who does not know his clinical case and ask for his sugar intake based
on his disease, the psychological and emotional aspects of the person will be disturbed. In
this spirit, the P.C. will not be mentioned. The wellbeing of any of the participant should
be the same after the survey as it was before it. The physician will inform us about the
case’s situation. An ethical letter will be sent to each health establishment and oncologist
in order to ask for permission and cooperation in localizing and communicating with the
case.
We will then explain to the participants that no follow up will be done and that all what is
asked is some basic information without any invasive intervention. No further disturbance
will be mad after. The participant will also know that we are students under the cover of
the UOB and SGHMC only, without further relation with the establishment. We will
explain the importance of diet and its assessment for one’s health and in understanding it
from a scientific point of view. Once all the explanation is completed and the participant
understood the situation, he or she will be asked to repeat what is asked from them (what
Sugar intake and Pancreatic Cancer
21
is the purpose, what will they do?). Following this, the case will be asked for written
consent on the questionnaire’s paper and the control will be asked by phone for a verbal
consent. No pressure of any kind will be applied on the participant, a case who wishes not
to enroll will reject the survey, and a control who wishes not answer will hang up. A patient
at the hospital may be seen as vulnerable because of his medical condition, especially when
faced to health workers. As mentioned, no pressure will be exerted, and a person will freely
decide what to do (this will be guaranteed by the consent signed). Any of the participants
can stop the survey when he or she decides to. All the time a person needs to acknowledge
the situation will be given, and all the time needed to fill the survey will be provided, no
one will be rushed.
Once a case in the hospital is declared, he or she will be added to the sample directly if he
or she accepts to participate. We will count on the reporter (medical doctors) to be fair in
our selection. When it come to the controls, as said they will be chosen randomly base on
the phone area. In this study, very low are the physical, social, legal, economic or
psychological harms. Only those who wish to participate in the study will be asked
questions so no one’s time is lost. A mild psychological harm is avoided by not includ ing
the P.C. assessment. The benefit to the participants will be moral as they help research
progress. Based on that, harms and benefit are balanced.
Moreover, our survey and questions will be tested by the university IRB to get feedback
and authorization to use it.
The data will be kept safe in a closed drawer, and only the three of us will have access to
it. At the end of the analysis, all the data will be burned and the results will be published.
Sugar intake and Pancreatic Cancer
22
Conclusion
Finally yet importantly, it is important to prevent P.C. because of its rapid onset, low
prognosis, and high mortality. Sugar was seen in the literature as being a predisposing
factor to develop P.C.. In this spirit, reducing sugar intake would help on reducing the fact
of developing P.C.. Our research will conduct a case-control study in order to assess the
relation between sugar intake and the development of P.C. in adults aged 50 to 80 in all
Lebanon. The study will be conducted using a survey and a sugar diet assessment grid.
This will allow us to effectively decide on the relation sugar and P.C. have in Lebanon. If
a positive association is found, future regulation of sugar diet should be done to all persons
with family history of P.C.. The aim of the study being to prevent P.C., awareness
campaigns should be done to share with the society the results obtained.
Sugar intake and Pancreatic Cancer
23
References
American Cancer Society (2015). Retrieved from:
http://www.cancer.org/cancer/pancreaticcancer/overviewguide/pancreatic-cancer-
overview-what-is-pancreatic-cancer
Dominique, M., Liu, S., Giovannucci, E., Willet, W., Graham, C., & Fuchs, C. (2002).
Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study.
Journal of the National Cancer Institute , 1293-1300.
Forsmark CE. Pancreatitis. In: Goldman L, Shafer AI, eds. Cecil Medicine. 24th ed.
Philadelphia, Pa: Saunders Elsevier; 2011:chap 46.
Gapstur, S., Gann, P., Lowe, W., Liu, K., Colangelo, L., & Dyer, A., (2000). Abnormal
Glucose Metabolism and Pancreatic Cancer Mortality. Journal of American
Medical Association, 283 (19), 252-258
Han L, Ma Q, Li J, Liu H, Li W, Ma G, et al, (2011). High glucose promotes pancreatic
cancer cell proliferation via the induction of EGF expression and transactivation of
EGFR. PLoS One 2011;6:8.
Hariharan, D., Saied, A., & Kocher, H. (2008). Analysis of mortality rates for pancreatic
cancer across the world. HPB: The Official Journal of the International Hepato
Pancreato Biliary Association. 10(1), 58–62. doi: 10.1080/13651820701883148
Sugar intake and Pancreatic Cancer
24
Hirbli,K; Jambeine,M; Slim, Barakat,W; Habis,R; Francis,M., (2005). Prevalence of
Diabetes in Greater Beirut, Diabetes Care;1262-1262, DOI:
10.2337/diacare.28.5.1262
Huxley R, Ansary-Moghaddam A, Berrington de González A, et al. (2005). Type-II
diabetes and pancreatic cancer: a meta-analysis of 36 studies. Br J Cancer 92:2076-
83
Ito, M., Naohiko, M., & Yoshiyuki, U. (2013). Glucose intolerance and the risk of
pancreatic cancer. Transl Gastrointest Cancer, 223-229.
Johns Hopkins University (2012). Retrieved from:
http://pathology.jhu.edu/pancreas/basicoverview3.php?area=ba
Larsson S., Bergkvist L., Wolk A., (2006). Consumption of sugar and sugar-sweetened
foods and the risk of pancreatic cancer in a prospective study. The American
Journal of Clinical Nutrition 2006; 84, 1171-1176
Li J, Ma Q, Liu H, Guo K, Li F, Li W, et al, (2011). Relationship between neural alteration
and perineural invasion in pancreatic cancer patients with hyperglycemia. PLoS
One 2011;6:0017385
Lin Y, Kikuchi S, Tamakoshi A, Yagyu K, et al., (2007).Obesity, physical activity and the
risk of pancreatic cancer in a large Japanese cohort. Int J Cancer 120:2665-71.
Lyon JL, Slattery ML, Mahoney AW, Robison LM., (1993). Dietary intake as a risk factor
for cancer of the exocrine pancreas. Cancer Epidemiol Biomarkers Prev;2:513–8
Sugar intake and Pancreatic Cancer
25
Michaud, DS. (2004, April). Epidemiology of pancreatic cancer. Retrieved from
http://www.ncbi.nlm.nih.gov/pubmed/15238885
Michaud DS. et al, (2011). Dietary sugar, glycemic load, and pancreatic cancer risk in a
prospective study. Journal of the National Cancer Institute 2002. 94(17). 1293-
1300
Office of National Statistics. Rterieved from:
http://www.ons.gov.uk/ons/rel/vsob1/cancer-statistics-registrations--england--
series-mb1-/index.html
Badran, M. & Laher, I., (2006). Type II Diabetes Mellitus in Arabic-Speaking Countries.
International Journal of Endocrinology. doi:10.1155/2012/902873
Nöthlings, U., Murphy, S., Wilkens, L., Henderson, B., & Kolonel, L., (2007). Dietary
glycemic load, added sugars, and carbohydrates as risk factors for pancreatic
cancer: the Multiethnic Cohort Study1–4. American Journal of Clinical Nutrition,
86 , 1495–501
OLSON, S., & KURTZ, R.C., (2013). Epidemiology of Pancreatic Cancer and the Role
of Family History. Journal of Surgical Oncology, 107, 1–7
Permuth-Wey J, Egan KM., (2009). Family history is a significant risk factor for
pancreatic cancer: results from a systematic review and meta-analysis. Fam
Cancer;8:109-17
Sugar intake and Pancreatic Cancer
26
Robertson R.P., (2004). Chronic oxidative stress as a central mechanism for glucose
toxicity in pancreatic islet beta cells in diabetes. Journal of Biological Chemistry;
279:42351– 4.
Salim et al., (2009). Cancer epidemiology and control in the Arab world - past, present and
future. Asian Pacific Journal of Cancer Prevention; 10; 3-16
Schernhammer ES, Hu FB, Giovannucci E, et al., (2005). Sugar-sweetened soft drink
consumption and risk of pancreatic cancer in two prospective cohorts. Cancer
Epidemiology Biomarkers & Prevention;14:2098 –105.
Siegel R, Ma J, Zou Z, & Jemal A., (2014). Cancer statistics, 2014. CA Cancer Journal
for Clinicians; 64:9-29
Suzuki K, Islam KN, Kaneto H, Ookawara T, Taniguchi N. (2000).The contribution of
fructose and nitric oxide to oxidative stress in hamster islet tumor (HIT) cells
through the inactivation of glutathione peroxidase. Electrophoresis;21:285–8
Zhou, W., Capello, M., Fredolini, C., Racanicchi L., Dugnani, E., Piemonti, L., Liotta,
L.A., Novelli, F., & Petricoin, E.F., (2013). Mass spectrometric analysis reveals
O-methylation of pyruvate kinase from pancreatic cancer cells. Anal Bioanal
Chem, 405, 4937–4943
Zhou, W., Liotta, L., & Petricoin, E., (2015). Cancer metabolism and mass spectrometry-
based proteomics. Cancer Letters, 356, 176–183
Sugar intake and Pancreatic Cancer
27
(2013). NCR 2008, Table B both gender: Frequency (nb) of incident cases by primary
site & age group. Lebanese Ministry of Public Health, National Cancer Registry.
Retrieved from
http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2008.htm
(2013). NCR 2007, Table B both gender: Frequency (nb) of incident cases by primary
site & age group. Lebanese Ministry of Public Health, National Cancer Registry.
Retrieved from
http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2007.htm
(2013). NCR 2006, Table B both gender: Frequency (nb) of incident cases by primary
site & age group. Lebanese Ministry of Public Health, National Cancer Registry.
Retrieved from
http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2006.htm
(2013). NCR 2005, Table B both gender: Frequency (nb) of incident cases by primary
site & age group. Lebanese Ministry of Public Health, National Cancer Registry.
Retrieved from
http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2005.htm
(2013). Cancer in Lebanon: 2005 – 2007. Lebanese Ministry of Public Health, National
Cancer Registry. Retrieved from
http://www.moph.gov.lb/Prevention/Surveillance/documents/leb_ncr_2005_7.pdf

More Related Content

What's hot

Ueda2016 diabetes & cancer - mesbah kamel
Ueda2016 diabetes & cancer - mesbah kamelUeda2016 diabetes & cancer - mesbah kamel
Ueda2016 diabetes & cancer - mesbah kamelueda2015
 
LAPAROSCOPIC SURGERY FOR MORBID OBESITY
LAPAROSCOPIC SURGERY FOR MORBID OBESITYLAPAROSCOPIC SURGERY FOR MORBID OBESITY
LAPAROSCOPIC SURGERY FOR MORBID OBESITYApollo Hospitals
 
Diet and physical activity in preventing cancer
Diet and physical activity in preventing cancerDiet and physical activity in preventing cancer
Diet and physical activity in preventing cancermercifulcrook7974
 
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...asclepiuspdfs
 
1 s2.0-s1877593410000706-main
1 s2.0-s1877593410000706-main1 s2.0-s1877593410000706-main
1 s2.0-s1877593410000706-mainSatria Kino
 
Overall Cancer Incident
Overall Cancer Incident Overall Cancer Incident
Overall Cancer Incident UCSI University
 
Hrt meme exeltis dernek 2017 son (1)
Hrt   meme  exeltis   dernek 2017 son (1)Hrt   meme  exeltis   dernek 2017 son (1)
Hrt meme exeltis dernek 2017 son (1)TrkiyeMenopozVeOsteo
 
Genetic testing of breast and ovarian cancer patients: clinical characteristi...
Genetic testing of breast and ovarian cancer patients: clinical characteristi...Genetic testing of breast and ovarian cancer patients: clinical characteristi...
Genetic testing of breast and ovarian cancer patients: clinical characteristi...dewisetiyana52
 
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...Islam Saeed
 
The evolving epidemiology of stone disease
The evolving epidemiology of stone diseaseThe evolving epidemiology of stone disease
The evolving epidemiology of stone diseaseYounis I Munshi
 
Nutritiona status frederici Bozzeti Nutrition
Nutritiona status frederici Bozzeti NutritionNutritiona status frederici Bozzeti Nutrition
Nutritiona status frederici Bozzeti NutritionVladislava DJurasinovic
 
What is the epidemiological evidence linking early life events and cancer ris...
What is the epidemiological evidence linking early life events and cancer ris...What is the epidemiological evidence linking early life events and cancer ris...
What is the epidemiological evidence linking early life events and cancer ris...World Cancer Research Fund International
 
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...Mostafa Gouda
 
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...Crimsonpublishers-IGRWH
 

What's hot (20)

Cancer prevention aspec
Cancer prevention aspecCancer prevention aspec
Cancer prevention aspec
 
Final abstract - 128061
Final abstract - 128061Final abstract - 128061
Final abstract - 128061
 
Ueda2016 diabetes & cancer - mesbah kamel
Ueda2016 diabetes & cancer - mesbah kamelUeda2016 diabetes & cancer - mesbah kamel
Ueda2016 diabetes & cancer - mesbah kamel
 
LAPAROSCOPIC SURGERY FOR MORBID OBESITY
LAPAROSCOPIC SURGERY FOR MORBID OBESITYLAPAROSCOPIC SURGERY FOR MORBID OBESITY
LAPAROSCOPIC SURGERY FOR MORBID OBESITY
 
How we eat affects our health
How we eat affects our healthHow we eat affects our health
How we eat affects our health
 
Diet and physical activity in preventing cancer
Diet and physical activity in preventing cancerDiet and physical activity in preventing cancer
Diet and physical activity in preventing cancer
 
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...
Periodontal Disease Indices and Colorectal Cancer Risk in Greek Adults: A Cas...
 
1 s2.0-s1877593410000706-main
1 s2.0-s1877593410000706-main1 s2.0-s1877593410000706-main
1 s2.0-s1877593410000706-main
 
Overall Cancer Incident
Overall Cancer Incident Overall Cancer Incident
Overall Cancer Incident
 
nihms411798
nihms411798nihms411798
nihms411798
 
Hrt meme exeltis dernek 2017 son (1)
Hrt   meme  exeltis   dernek 2017 son (1)Hrt   meme  exeltis   dernek 2017 son (1)
Hrt meme exeltis dernek 2017 son (1)
 
Genetic testing of breast and ovarian cancer patients: clinical characteristi...
Genetic testing of breast and ovarian cancer patients: clinical characteristi...Genetic testing of breast and ovarian cancer patients: clinical characteristi...
Genetic testing of breast and ovarian cancer patients: clinical characteristi...
 
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...
Pattern of Obesity and Associated Factors among Hirat Adult Citizens in Afgha...
 
The evolving epidemiology of stone disease
The evolving epidemiology of stone diseaseThe evolving epidemiology of stone disease
The evolving epidemiology of stone disease
 
Nutritiona status frederici Bozzeti Nutrition
Nutritiona status frederici Bozzeti NutritionNutritiona status frederici Bozzeti Nutrition
Nutritiona status frederici Bozzeti Nutrition
 
Austin Medical Sciences
Austin Medical SciencesAustin Medical Sciences
Austin Medical Sciences
 
Nikisher Breast Cancer
Nikisher Breast CancerNikisher Breast Cancer
Nikisher Breast Cancer
 
What is the epidemiological evidence linking early life events and cancer ris...
What is the epidemiological evidence linking early life events and cancer ris...What is the epidemiological evidence linking early life events and cancer ris...
What is the epidemiological evidence linking early life events and cancer ris...
 
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...
Nutritional Epidemiological Study to Estimate Usual Intake and to Define Opti...
 
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...
Crimson Publishers-Knowledge of Obesity Risks and Women’s Health: What do we ...
 

Viewers also liked

Rekweb5 hilmi afifi-1512510213
Rekweb5 hilmi afifi-1512510213Rekweb5 hilmi afifi-1512510213
Rekweb5 hilmi afifi-1512510213helmy afifi
 
Haynes e week 11_final portfolio
Haynes e week 11_final portfolioHaynes e week 11_final portfolio
Haynes e week 11_final portfolioElisa Haynes
 
The Millennial Shift: Engaging the Redefined Millennials' Digital Behaviors
The Millennial Shift: Engaging the Redefined Millennials' Digital BehaviorsThe Millennial Shift: Engaging the Redefined Millennials' Digital Behaviors
The Millennial Shift: Engaging the Redefined Millennials' Digital BehaviorsMatt Doherty
 
Impacto del ser humano en el medio ambiente
Impacto del ser humano en el medio ambienteImpacto del ser humano en el medio ambiente
Impacto del ser humano en el medio ambienteLaura Arcila Gómez
 
Campus Drivers - Complete Campus Solution
Campus Drivers - Complete Campus SolutionCampus Drivers - Complete Campus Solution
Campus Drivers - Complete Campus SolutionCampus Drivers
 
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?UEFviestinta
 
Habilidades de pensamiento
Habilidades de pensamientoHabilidades de pensamiento
Habilidades de pensamientoCarolina Dusso
 

Viewers also liked (20)

CV ABDELHAMID Shawki Rwished 201600
CV ABDELHAMID Shawki Rwished 201600CV ABDELHAMID Shawki Rwished 201600
CV ABDELHAMID Shawki Rwished 201600
 
Resume
ResumeResume
Resume
 
Rekweb5 hilmi afifi-1512510213
Rekweb5 hilmi afifi-1512510213Rekweb5 hilmi afifi-1512510213
Rekweb5 hilmi afifi-1512510213
 
Las 70 alpacas.docx yarumi
Las 70 alpacas.docx yarumiLas 70 alpacas.docx yarumi
Las 70 alpacas.docx yarumi
 
Haynes e week 11_final portfolio
Haynes e week 11_final portfolioHaynes e week 11_final portfolio
Haynes e week 11_final portfolio
 
ANSYS Certificate
ANSYS CertificateANSYS Certificate
ANSYS Certificate
 
Diploma Business Studies
Diploma Business StudiesDiploma Business Studies
Diploma Business Studies
 
The Millennial Shift: Engaging the Redefined Millennials' Digital Behaviors
The Millennial Shift: Engaging the Redefined Millennials' Digital BehaviorsThe Millennial Shift: Engaging the Redefined Millennials' Digital Behaviors
The Millennial Shift: Engaging the Redefined Millennials' Digital Behaviors
 
Impacto del ser humano en el medio ambiente
Impacto del ser humano en el medio ambienteImpacto del ser humano en el medio ambiente
Impacto del ser humano en el medio ambiente
 
501 ilustraciones
501 ilustraciones501 ilustraciones
501 ilustraciones
 
Campus Drivers - Complete Campus Solution
Campus Drivers - Complete Campus SolutionCampus Drivers - Complete Campus Solution
Campus Drivers - Complete Campus Solution
 
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?
Tieteen päivät 2015: Anton Laakso - Ilmastoa voi muokata - miten ja miksi?
 
CIBERBULLYING
CIBERBULLYINGCIBERBULLYING
CIBERBULLYING
 
28921ip
28921ip28921ip
28921ip
 
A.Nassir CV new
A.Nassir CV newA.Nassir CV new
A.Nassir CV new
 
Sreekanth cv 12-7-15
Sreekanth cv 12-7-15Sreekanth cv 12-7-15
Sreekanth cv 12-7-15
 
Questionnaire Results
Questionnaire ResultsQuestionnaire Results
Questionnaire Results
 
Habilidades de pensamiento
Habilidades de pensamientoHabilidades de pensamiento
Habilidades de pensamiento
 
Mask Clean
Mask CleanMask Clean
Mask Clean
 
MUSAM
MUSAMMUSAM
MUSAM
 

Similar to FINAL Paper Research (2)

4 The Obesity Epidemic And Kidney Disease A Literature Review
4 The Obesity Epidemic And Kidney Disease  A Literature Review4 The Obesity Epidemic And Kidney Disease  A Literature Review
4 The Obesity Epidemic And Kidney Disease A Literature ReviewJanelle Martinez
 
Obesity & endometrial cancer
Obesity & endometrial cancerObesity & endometrial cancer
Obesity & endometrial cancerWafaa Benjamin
 
Diabetes and cancer 2015 march
Diabetes and cancer 2015 marchDiabetes and cancer 2015 march
Diabetes and cancer 2015 marchAnuradha Pandey
 
jnci.oxfordjournals.org JNCI Articles 1DOI 10.1093jn.docx
jnci.oxfordjournals.org   JNCI  Articles 1DOI 10.1093jn.docxjnci.oxfordjournals.org   JNCI  Articles 1DOI 10.1093jn.docx
jnci.oxfordjournals.org JNCI Articles 1DOI 10.1093jn.docxchristiandean12115
 
Robyn Toomath on obesity in New Zealand
Robyn Toomath on obesity in New ZealandRobyn Toomath on obesity in New Zealand
Robyn Toomath on obesity in New Zealandmhjbnz
 
RunningHead PICOT Question1RunningHead PICOT Question7.docx
RunningHead PICOT Question1RunningHead PICOT Question7.docxRunningHead PICOT Question1RunningHead PICOT Question7.docx
RunningHead PICOT Question1RunningHead PICOT Question7.docxrtodd599
 
Dyslipidemia and Fatty liver disease
Dyslipidemia and Fatty liver diseaseDyslipidemia and Fatty liver disease
Dyslipidemia and Fatty liver diseaseKeyarul Islam
 
Gynecological and Nutritional Risk Factors for Female Infertility
Gynecological and Nutritional Risk Factors for Female InfertilityGynecological and Nutritional Risk Factors for Female Infertility
Gynecological and Nutritional Risk Factors for Female Infertilityijtsrd
 
cancer prevention.pptx
cancer prevention.pptxcancer prevention.pptx
cancer prevention.pptxChijiokeNsofor
 
abc oncology . Colon session
abc oncology . Colon sessionabc oncology . Colon session
abc oncology . Colon sessionFadi Farhat
 

Similar to FINAL Paper Research (2) (20)

Cancer etiology
Cancer etiologyCancer etiology
Cancer etiology
 
4 The Obesity Epidemic And Kidney Disease A Literature Review
4 The Obesity Epidemic And Kidney Disease  A Literature Review4 The Obesity Epidemic And Kidney Disease  A Literature Review
4 The Obesity Epidemic And Kidney Disease A Literature Review
 
Cancer prevention
Cancer preventionCancer prevention
Cancer prevention
 
Obesity & endometrial cancer
Obesity & endometrial cancerObesity & endometrial cancer
Obesity & endometrial cancer
 
Diabetes and cancer 2015 march
Diabetes and cancer 2015 marchDiabetes and cancer 2015 march
Diabetes and cancer 2015 march
 
Weight loss 15
Weight loss 15Weight loss 15
Weight loss 15
 
jnci.oxfordjournals.org JNCI Articles 1DOI 10.1093jn.docx
jnci.oxfordjournals.org   JNCI  Articles 1DOI 10.1093jn.docxjnci.oxfordjournals.org   JNCI  Articles 1DOI 10.1093jn.docx
jnci.oxfordjournals.org JNCI Articles 1DOI 10.1093jn.docx
 
Robyn Toomath on obesity in New Zealand
Robyn Toomath on obesity in New ZealandRobyn Toomath on obesity in New Zealand
Robyn Toomath on obesity in New Zealand
 
RunningHead PICOT Question1RunningHead PICOT Question7.docx
RunningHead PICOT Question1RunningHead PICOT Question7.docxRunningHead PICOT Question1RunningHead PICOT Question7.docx
RunningHead PICOT Question1RunningHead PICOT Question7.docx
 
Dyslipidemia and Fatty liver disease
Dyslipidemia and Fatty liver diseaseDyslipidemia and Fatty liver disease
Dyslipidemia and Fatty liver disease
 
Metabolic_syndrome_among_obese_patients.pdf
Metabolic_syndrome_among_obese_patients.pdfMetabolic_syndrome_among_obese_patients.pdf
Metabolic_syndrome_among_obese_patients.pdf
 
Alcohol and Cancer
Alcohol and CancerAlcohol and Cancer
Alcohol and Cancer
 
Gynecological and Nutritional Risk Factors for Female Infertility
Gynecological and Nutritional Risk Factors for Female InfertilityGynecological and Nutritional Risk Factors for Female Infertility
Gynecological and Nutritional Risk Factors for Female Infertility
 
5.17.11.stones
5.17.11.stones5.17.11.stones
5.17.11.stones
 
5.17.11.stones
5.17.11.stones5.17.11.stones
5.17.11.stones
 
5.17.11.stones
5.17.11.stones5.17.11.stones
5.17.11.stones
 
cancer prevention.pptx
cancer prevention.pptxcancer prevention.pptx
cancer prevention.pptx
 
cancer.pdf
cancer.pdfcancer.pdf
cancer.pdf
 
Children's Health
Children's HealthChildren's Health
Children's Health
 
abc oncology . Colon session
abc oncology . Colon sessionabc oncology . Colon session
abc oncology . Colon session
 

FINAL Paper Research (2)

  • 1. Sugar intake and Pancreatic Cancer 1 University of Balamand Faculty of Health Sciences Research Methods FHSC288 Increased sugar intake and the risk of developing pancreatic cancer in Lebanese adults between the age of 50 and 80 years, a case-control study. El Jalbout Ralph Hamieh Cyma Massaad Nadine May 2015
  • 2. Sugar intake and Pancreatic Cancer 2 Acknowledgment We would like to thank our mentor Dr. Nivine Abbass for supporting and guiding us during our research project. We also appreciate the explanations and advices provided by our instructors Dr. Laurie Abi Habib and Miss Joumana Yeretzian which were very beneficial. We are grateful to Miss Nadine Haddad for her help in the methods section and developing the questionnaire. Finally, we would like to thank our University for the open access to a rich database and to Miss Dolly Radi and Miss Sylvie Sleiman for the help in obtaining articles from additional databases.
  • 3. Sugar intake and Pancreatic Cancer 3 Table of content
  • 4. Sugar intake and Pancreatic Cancer 4 I- Abstract Ranked as the fourth leading cause of cancer-related deaths in the world, pancreatic cancer is the causes of over 200 000 death yearly. In Lebanon as mentioned by the Ministry of Public Health in 2005, 143 out of 7914 cancer patients reported having pancreatic cancer, with comparable statistics in the years 2006, 2007 and 2008 for both genders in equal proportions with a peek at the ages 62-63. Considering its low prognosis and 5% survival rate after five years, preventing this disease is a necessity. Hyperglycemia is one of the major underlying risk factors of pancreatic cancer considering most of its patients are diagnosed with high glucose levels and diabetes. Therefore, decreasing sugar consumption might help on decreasing the risk of developing the disease and preventing its occurrence. In order to see the relation between sugar intake and pancreatic cancer, a case-control study will be conducted for about five years. A questionnaire and a food frequency checklist will be provided for the assessment of pancreatic cancer patients in several hospitals in Lebanon. In parallel, four controls for each case will be matched. Based on the results, we will try to deduce and find an association between cancer patients’ diet and the disease. Key words: Sugar Intake, Pancreatic Cancer, Cancer Prevention Table of contents
  • 5. Sugar intake and Pancreatic Cancer 5 Increased sugar intake and the risk of developing pancreatic cancer, in Lebanese adults between the age of 50 and 80 years, a case-control study.
  • 6. Sugar intake and Pancreatic Cancer 6 II- Introduction: Globally, pancreatic cancer causes the death of over 200 000 people in the world yearly (Michaud, 2004) and it is ranked as the fourth leading cause of cancer-related deaths in the world (Hariharan et al, 2008). It is the fourth leading cause of death in the United States out of all cancer types and the sixth in Europe. In 2014 in the USA, Pancreatic cancer was diagnosed in 46,420 patients out of 1,665,540 (23,530 males and 22,890 females) and caused the death of 39,590 out of 585,720 (20,170 males and 19,420 females) (Siegel et al, 2014). This cancer is defined as the development and spread of cancerous and malignant tumor cells in the pancreas affecting both the exocrine (which is the most common function) and endocrine function of the organ (American Cancer Society, 2015). The Exocrine function of the pancreas participates in the digestion mechanism; the organ produces digestive enzymes used in the small intestine for neutralization and breakdown. The Endocrine function is defined by the production of hormones (glucagon and insulin mainly) for the regulation of glucose blood levels (Johns Hopkins University, 2012). Based on that, prevention is essential since it is considered as the most fatal cancer providing a maximum of 5% survival chances for no more than five years of duration (Nöthlings et al, 2007). Due to its high fatality rates, the incidence of pancreatic cancer is directly associated with mortality; a lack in the screening tests for this disease prevent the diagnosis until after its progression (Michaud, 2004). The incidence of this lethal disease is strongly associated with an increase with age especially between the ages 50 to 80 years; in the UK for example, 96% of pancreatic cancer patients were diagnosed over the age of 50 years and 47% were diagnosed over the age of 75 between the years 2009 and 2011 (Office of National Statistics, 2011).
  • 7. Sugar intake and Pancreatic Cancer 7 It has been evidenced that hyperglycemia is one of the underlying risk factors of pancreatic cancer where “a large portion of pancreatic cancer patients suffer from either hyperglycemia or diabetes, both of which are characterized by high blood glucose level.” (Han et al, 2011). Moreover, there seems to be an association between increased sugar consumption (including sweeteners, glucose, fructose, carbohydrate) and the increased risk of becoming a pancreatic cancer patient as it has been demonstrated that hyperglycemia aids in the proliferation and invasion capacity of pancreatic cells (Li et al, 2011). Sugar intake is basically the consumption of items containing any sort of glucose or glucose derivatives such as sugar-sweetened foods or beverages, carbohydrates, fructose (that is transformed on the body to glucose during digestion). In a multiple of studies that considered the Arab world, the prevalence of pancreatic cancer is significantly low but a little bit higher in Lebanon and Syria (Salim et al, 2009). Based on the database of the Ministry of Public Health in Lebanon, in 2005, 143 of the total 7914 cancer patients reported had pancreatic cancer, in 2006 the values were 132 over 8491, in 2007 the values were 118 over 9552, and in 2008 the values were 137 over 9499. In the National Cancer Registry (NCR) report “Cancer in Lebanon: 2005-2007” the cases of pancreatic cancers are equal among genders but occur mainly in people older than 50 years with a mean of 62-63 years. “The age-specific incidence rates showed an increase starting the 50-55 age- group” according to the same report. In Lebanon, the adenocarcinoma is the most recurrent type of pancreatic cancer notes the NCR. Literature Review:
  • 8. Sugar intake and Pancreatic Cancer 8 Based on that pancreatic cancer does not respond effectively to current cancer treatment and has a low survival rate. Many studies worked on detecting risk factors in order to prevent the tumor development. In their study, Nöthlings, Murphy, Wilkens, Henderson, and Kolonel (2007) note that high glycemic load increased pancreatic cancer onset. In their four years cohort study with 162,150 participants, 434 developed cancer. The multiethnic study focused on African Americans, Japanese American, Latinos, Native Hawaiians and whites (Nöthlings et al, 2007). Based on their follow up, dietary assessment and results, Nöthlings et al (2007) pointed out that high sugar diet especially fructose, put the individual at a higher risk of developing pancreatic cancer; foods like fruits and juices are the key provider of fructose. Nöthlings et al (2007) mentioned that long study periods are needed when working on pancreatic cancer because this malignancy has a low occurrence rate. Overweight and obesity correlates with high sugar and fructose intake and has to be taken into consideration. In a prospective cohort study that has been done to investigate the relationship between both dietary sugar and glycemic load and the risk for pancreatic cancer found that any type of food that contribute to an increase in postprandial blood glucose levels may have a great influence in a risk for pancreatic cancer (Michaud et al, 2002). In this study, 121 700 women were followed up for 18 years with examination of their dietary intake. The results showed that high dietary sugar intakes along with a high glycemic load and glycemic index were directly related to the increased risk of pancreatic cancer for sedentary and overweight women. This a statistically significant increase in pancreatic cancer risk by 86% for inactive women who consumed high fructose compared to those who consumed a
  • 9. Sugar intake and Pancreatic Cancer 9 low fructose diet with a P-value of 0.02. However, dietary intake did not reveal an association with the risk of pancreatic cancer for active women (Michaud et al, 2002). In another study done by Larsson, Bergkvist and Wolk (2006) diagnosed among 77 797 men and women between the ages 45 and 83 years adjusted for age, sex, smoking, BMI, alcohol intake and energy 131 incident cases of pancreatic cancer, the participants from Sweden were followed up from 1997 till June 2005 in a prospective study. Results showed that a higher consumption of sugar-sweetened foods, soft drinks or sweetened soups by participants, provided a greater risk of pancreatic cancer by 1.5 to 1.9 times than in the group with the low consumption of these products (Larsson et al, 2006). However, no association was found between the consumption of jam, marmalade or sweets and pancreatic cancer considering that they contain a lot less sugar contents (30gr/serving) than sweetened foods like soups (230gr/serving). Yet, it is important to note that the participants handed a self-administered food frequency questionnaire, so misclassification may have occurred between the sugar and the sweetened food consumption. Moreover, this study correlates with another prospective cohort study done on nurses and health professionals in the United States. It contributed to significant results were women who consumed more than 3 sugar sweetened soft drinks per week had a greater risk of 57% of pancreatic cancer than those who consumed less than 1 drink per week with a p-value of 0.05. On the other hand, no association between the consumption of these items and pancreatic cancer was found among men (Schernhammer et al, 2005). However, based on the work of Olson and Kurtz (2013), gender plays a role and put men at a higher risk (13.5 for 100,000) of developing this type of cancer compared to women (10.8 for 100,000). Thus, these studies are based on the fact that a higher sugar intake causes elevated blood glucose levels which
  • 10. Sugar intake and Pancreatic Cancer 10 affect the activity of pancreatic islet cells negatively causing glucose toxicity. Nevertheless, glucose toxicity increases reactive oxygen that increases relatively the oxidative stress along with the small presence of antioxidants in the islets cells, hence increasing the risk of P.C.(Robertson,2004). Further studies done by Ueno.Y, Makino.N, and Ito.M (2013) noted the importance of early detection of pancreatic cancer to the scope of the treatment, they found that risk factors can be associated with smoking, family history, age, sex, diabetes mellitus, chronic pancreatitis, obesity and non-O blood group. In another study, done by Permuth-Wey et al, results showed an increase in risk of pancreatic cancer if a relative was diagnosed with the disease. One major risk was obesity, according to a cohort study done in Japan by Lin.Y et al, men and women with high BMI had risks 3.5 fold and 60% higher respectively, as compared to those with normal BMI. Diabetes resulting from insufficient insulin production by the pancreas, leading to high glucose levels in blood, has the highest incidence among other diseases suspected to lead to pancreatic cancer, according to the Committee for Pancreatic Cancer Registry in 2007. These studies suggest that there is an association between diabetes and the onset of pancreatic cancer, from which it is understandable to further investigate the role of glycemia. Consistently, Gapstur, Gann, Lowe, Liu, Colangelo, and Dyer (2000) highlight the necessity to prevent pancreatic cancer because of its extreme malignancy, metastasis and late detection. In those conditions, they worked on the effect of “abnormal glucose metabolism on pancreatic cancer” (Gapstur et al, 2000). They worked on employees from
  • 11. Sugar intake and Pancreatic Cancer 11 the Chicago Heart Association Detection Project in Industry (CHA) cohort study and measured their post-load Glucose level. Among the 35,658 participants, 96 men and 43 women died from pancreatic cancer. The post-load glucose level is the amount of glucose in the blood one hour after the 50g challenge test, and in this study, 11.1mmol/L or 200g/dL was taken as cut off (Gapstur et al, 2000). The study concluded that participants with initial post-load plasma glucose equal or higher than 11.1mmol/L are 2.2 times more at risk of developing pancreatic cancer than participants with initial post-load plasma glucose equal or lower than 6.6mmol/L (Gapstur et al, 2000). The abnormal glucose metabolism associated with high insulin play a role in the development of pancreatic cancer; insulin at high levels would act on promoting cellular growth especially pancreatic cells reaching ultimately the cancer stage. Hardey and Cowey concluded in a study on metabolic syndrome and its relation to cancer, that hyperglycemia can directly damage the DNA of epithelium of pancreatic duct via oxidative stress, hence leading to the onset of the cancer. Dominique.S,et al, conducted a prospective study to find a relation between glycemic load and pancreatic cancer, they controlled for several risk factors and observed a 53% increase in risk of P.C for women with high glycemic load intake as compared to those with low intake, similar increase was observed when studying fructose level, 57%. In a different study done by Suzuki et al, it was noted that fructose directly contributes to oxidative stress in growing cells. On the other hand, a case-control study done by Lyon JL et al (1993), strong association was found between pancreatic cancer and carbohydrate intake or added sugars, but due to high mortality rate, the study design was prone to several bias and errors.
  • 12. Sugar intake and Pancreatic Cancer 12 In addition to many other studies that search for the presence of an association between hyperglycemia and pancreatic cancer, Huxley et al (2005) saw in a meta-analysis of 36 studies on type II diabetes and pancreatic cancer, that there is an overestimate of the size of the relationship between the two variables. This exaggeration also exists in other studies due to bias, first since smaller studies reported the existence of the association and second because the authors note the relationship obtained can be justified by the existence of confounders such as smoking and obesity. Rationale: Based on the literature, pancreatic cancer is a rapidly fatal disease with a very low survival rate (Michaud, 2004). Not to forget that this disease has a very poor prognosis (Nöthlings et al, 2007). Moreover, the disease in its early stages, is asymptomatic and silent; therefore, to decrease from its fatality rate it is critical to search for ways to prevent its occurrence. Moving from this point, one of the most basic aspects eligible to control in a healthy population is diet; that is why, looking at sugar intake and added sweeteners in one’s diet, is beneficial to try and find an association. In addition, some studies suggested that an increase in glucose blood levels provoke an increase in insulin; thus, insulin increase promotes the secretion of growth factors, which later on provoke pancreatic cancer cell growth (Schneider et al, 2001). Zhou, Liotta, and Petricoin (2015) noted in their work that the glycolitic activity of a tumor mass affects its diagnosis; therefore, tumor with higher glycolitic activity and dependency on glucose have the poorer prognosis. In the case of pancreatic cancer, they identified that those cells have higher number of enzymes implicated in glucose metabolism and cellular respiration.
  • 13. Sugar intake and Pancreatic Cancer 13 In addition to that, it is interesting to note that Lebanon is among the six world-leaders’ Arabic speaking countries for Diabetes type II (Badran, M & Laher.I. 2012), with almost 53% of the Lebanese population living in Great Beirut diagnosed with Diabetes (Jacob.S et al, 2005). In Lebanon, the Ministry of Public Health and the National Cancer Registry defined that in the years 2005, 2006, 2007 and 2008, the occurrence of pancreatic cancer was respectively 143 out of 7914 cancer patients, 132 out of 8491, 118 over 9552, and 137 over 9499. Unfortunately, the report lacked information concerning effect of sugar on pancreatic cancer patients in Lebanon. This information is alarming and highlights the importance of raising awareness among Lebanese population about the dangerous consequences of uncontrolled sugar diet, one of which is pancreatic cancer. Many underlying factors can increase the risk of pancreatic cancer (like: smoking, family history, age, sex, diabetes mellitus, chronic pancreatitis, obesity and non-O blood group, obesity, diabetes, etc…). We found that a focus on sugar intake would be more effic ient than any other risk factor bearing in mind that family history, age, sex, non-O blood group factors cannot be controlled resulting from genetic predisposition. Diabetes mellitus is directly related to sugar intake, not to forget that inappropriate sugar intake and dietary practices are the main causes for diabetes mellitus and pancreatic dysfunction. Therefore, our study will use a case-control study design where the exposure will be sugar intake and the outcome will be pancreatic cancer. The sample will consist of exposed and non-exposed cases and controls based on their sugar intake recall. This might lead to the discovery of a positive link between sugar and pancreatic cancer. Although most of the literature used a cohort study, taking into consideration the low prevalence of pancreatic
  • 14. Sugar intake and Pancreatic Cancer 14 cancer, the limit in cost and time, we found that it is most suitable to follow a case-control study design. Consequently, in our case-control study, we are going to collect dietary information from participants at a one point in time using a food frequency checklists that will helps us determine the most frequent food items consumed during their past daily life routine. Then, we want to check if any of the participants represent pancreatic cancer and relate it to their dietary intake to study the relationship under investigation. By this design, we are hoping to find the desired correlation between high sugar intake and risk for pancreatic cancer. ResearchQuestion: Does sugar intake predispose Lebanese men and women between the age of 50 and 80 years living in Beirut to pancreatic cancer along five years of follow-up? Hypothesis: The higher the sugar intake is, the higher is the risk of developing pancreatic cancer. Objectives: The purpose of this study is to examine the effect of high sugar consumption on people predisposing them to pancreatic cancer. The objective is to find a true liaison between high sugar consumption and pancreatic cancer. In order to do so, patients will be asked to recall their sugar intake in their diet and associate it with their disease. The same will be done to the controls. Methods:
  • 15. Sugar intake and Pancreatic Cancer 15 The aim of our case control study design is to examine the Lebanese population suffering from pancreatic cancer. Therefore we will be visiting several hospitals in Lebanon to investigate the relationship between sugar intake(independent variable) and risk of pancreatic cancer occurrence(dependent variable); such as Saint George Hospital University Medical Center (SGHUMC), Hotel-Dieu de France, AUBMC, Rafic Hariri Governmental Hospital in Beirut, Jabal Amel Hospital in Tyr, Nini Hospital and Al Mounla Hospital in Tripoli, Khoury Hospital and Reyaa Hospital in the Bekaa, Sayidat Al Ma’ounat in Byblos, Beshare Governmental Hospital in Bechare, Bhaniss Hospital in Bhaniss in order to cover all regions. These hospitals were chosen based on their geographical location, reputation and patients from different countries attend it and ask to benefit from their services. The attainable population will cover cases diagnosed with pancreatic cancer, in the oncology department of hospitals. On the socio-demographical level, women and men eligible for this study as cases will be those between 50 and 80 years of age. On the clinical level, our cases are chosen based on their diagnosis with pancreatic cancer in the Lebanese Hospitals. We will try to get in touch with medical doctors and ask them to collaborate with us in order to collect data related to patients diagnosed with pancreatic cancer. An ethical letter will be sent to both the hospital and the oncologist explaining to them our topic and its significance in addition to asking them for permission to work and collaborate with them. The medical doctor will become part of the investigation, and all he or she will do is report to us the incidence of a pancreatic cancer patient in the oncology section. The study will be based on the usage of questionnaires offering information about gender, ager, weight in addition to occupation and habits such as smoking from which we will be
  • 16. Sugar intake and Pancreatic Cancer 16 able to understand and collect information about dietary habits of our cases and controls. Most importantly, a food frequency checklist will be given in order for the participants to fill. This table provides us with food frequency intake and the amount of food eaten. All the types of food sited contain molecules that the body will transform into glucose: such as starch (in bread, pasta and rice), fructose (in fruits) and sucrose (in beverages and table sugar). Each person will have two sheets with his ID, his/her answers will be reported using the numbering underneath each category in a Likert Scale: going from “Never or less than 1/month” (0) to “More than 5 a day” (7) and from “Very large amount/portion” (4) to “Small amount/portion” (1) (Refer to Questionnaire sheet). The participant will indicate the average food intake during the last 2 years, each year separately. Moreover, the person will give an estimate of the quantity eaten. We found a similar case-control study previously done which applied the same chronological demarche to assessing sugar intake and pancreatic cancer. For each case, four controls will be chosen and matched in order to make our control sample as representative as possible and minimize bias and chance considering the high number of exclusion factors for both parties; we will be excluding the non-Lebanese responders, those who do not belong to the age range or have family history of pancreatic cancer disease or any kind of pancreatic disease (pancreatitis, insulinoma…) in both controls and cases (Refer to Questionnaire sheet). These exclusions are used to try and remove any sort of confounders. Matching will be based on their residence, age, smoking habits and additional factors (diabetes) provided by the case (Refer to Questionnaire sheet). More specifically, controls in the sample will be selected based on random digit sampling method. The means that will be use would be the Lebanese white pages book from which
  • 17. Sugar intake and Pancreatic Cancer 17 we will randomly select addresses belonging to the same area of residency of the case or we will ask the municipality to provide us with the village or city phone codes. The same question asked for the cases will be given to the controls during the phone call. For both the cases and controls the purpose of the study will be explained and information needed is going to be provided to check if they accept to cooperate. To increase participation rate and minimize non response, we will be clearing up that we are avoiding invasive and uncomfortable tests and simply ask for general information. Moreover, we are going to control for smoking habits and diabetes by calculating the odds ratio. We will hide from the participant the real purpose of assessing sugar and pancreatic cancer not to trigger any recall bias in addition to an ethical issue (to be discussed in the Ethics part). To study the consistency and validity of the questionnaire, it will be first given to a sample of volunteers not at all related to the study sample in order to test its questions. This sample of 10 to 20 people, contacting them via phone calls and explaining the aims and objectives of the study, will provide us with feedback concerning the questions, time needed to accomplish the task, difficulties and any comments concerning the questions. Two weeks later, 5 people from this sample will be asked to fill the form again in order to examine the consistency of the answers, whether the questions generate the same responses or different ones. As a result, the questionnaire is finalized and used on the study sample. Directly when a case is located, he or she will be given the questionnaire to fill it in addition to an ID so that the privacy of the person would not be disturbed. After collecting the cases information, the four controls will be matched based on the requirements already
  • 18. Sugar intake and Pancreatic Cancer 18 mentioned. Each time a case is detected, the person will be given the questionnaires and directly after that, the controls will be matched. After a lap of time of two weeks, during which we would have entered the data and wanted to revise them, the survey questions will be asked again to some randomly chosen controls in order to test response accuracy. This will be done also to assess observer reproducibility, compare the answers of the same person for consistency and control for any recall bias. The study will start on June 1st 2015 and will last five years till June 1st 2020 and this in order to obtain a high number of pancreatic cancer cases considering the rareness of the disease. All the cases reported during this period will be registered and questioned. This is done in order to maximize our sample, making it larger so it will be more representative and reduce sampling error. Based on that, there is no maximum sample size. Following this, data analysis will start. The results will be compared to check consistency. Then, data will be entered to Excel Software, and then check the entered data to control and fix probable mistakes and errors in copying to ensure validity post-data entry. After that, the data will be transferred to the SPSS Software for further investigation in the biostatics and epidemiological field. Most importantly, the results will help on assessing the sugar intake of this person. Each participant will obtain a score. Based on the results of the control group, a cut off value will be deduced with a score as an indicator for a low or high sugar intake by the cases. The relation between the sugar diet and onset of pancreatic cancer will be established. The Odds ratio for all the categories will be calculated in order to complete the investigation. To control for diabetic patients and smokers, the Odds ratio will be calculated respectively and for non-smokers
  • 19. Sugar intake and Pancreatic Cancer 19 or non-diabetics. According to our calculations, the role of smoking and diabetes in developing pancreatic cancer will be deduced. Limitations: Sugar is not the only risk factor that has to be taken into consideration; other elements can predispose a person to develop pancreatic cancer. Smoking is seen to increase the risk by 75% (Olson & Kurtz, 2013). Obesity, diabetes, pancreatitis mainly, in addition to alcohol and allergies are also predisposing agents. Most notably, family history and genetic polymorphisms according to Olson and Kurtz (2013) increase the chances of having many cases of cancer in the same family. Those mutations include BRCA1, BRCA2, PALBA2 and many others. Therefore, as already mentioned, diabetes and smoking will be controlled in addition of excluding other confounders. When it comes to the selection of cases and controls, difficulties will be faced. We will need cooperation from the medical sector and the medical doctors to locate the cases, considering that not all new cases will be reported. To be noted that cases can refuse participating because of delicate matters and this is an important issue considering the rareness the disease. Moreover, recall bias is important for both the cases and controls especially if they have preconceived knowledge about pancreatic cancer; a person diagnosed with pancreatic cancer would falsely associate the disease and a past unexciting high sugar intake. Concerning the controls, that will be contacted by phone calls; no accurate phone lists exist in Lebanon and not all houses have phones, disposing us to selection bias. In addition, people can hang up, refuse to answer, or answer inaccurately with bias.
  • 20. Sugar intake and Pancreatic Cancer 20 Ethics The ethical concern in this study is mainly the privacy of the participants and their wellbeing. First of all, the identity of a person will not be asked and the person will be given an ID number once he or she enrolls in the study. We will then explain to the person the aim of our study as detecting sugar in diet. The part about pancreatic cancer will be hidden in order to avoid bias in recall, but most importantly to preserve the wellbeing of the participants, especially the cases because not always they are informed with their disease. If we reach a patient who does not know his clinical case and ask for his sugar intake based on his disease, the psychological and emotional aspects of the person will be disturbed. In this spirit, the P.C. will not be mentioned. The wellbeing of any of the participant should be the same after the survey as it was before it. The physician will inform us about the case’s situation. An ethical letter will be sent to each health establishment and oncologist in order to ask for permission and cooperation in localizing and communicating with the case. We will then explain to the participants that no follow up will be done and that all what is asked is some basic information without any invasive intervention. No further disturbance will be mad after. The participant will also know that we are students under the cover of the UOB and SGHMC only, without further relation with the establishment. We will explain the importance of diet and its assessment for one’s health and in understanding it from a scientific point of view. Once all the explanation is completed and the participant understood the situation, he or she will be asked to repeat what is asked from them (what
  • 21. Sugar intake and Pancreatic Cancer 21 is the purpose, what will they do?). Following this, the case will be asked for written consent on the questionnaire’s paper and the control will be asked by phone for a verbal consent. No pressure of any kind will be applied on the participant, a case who wishes not to enroll will reject the survey, and a control who wishes not answer will hang up. A patient at the hospital may be seen as vulnerable because of his medical condition, especially when faced to health workers. As mentioned, no pressure will be exerted, and a person will freely decide what to do (this will be guaranteed by the consent signed). Any of the participants can stop the survey when he or she decides to. All the time a person needs to acknowledge the situation will be given, and all the time needed to fill the survey will be provided, no one will be rushed. Once a case in the hospital is declared, he or she will be added to the sample directly if he or she accepts to participate. We will count on the reporter (medical doctors) to be fair in our selection. When it come to the controls, as said they will be chosen randomly base on the phone area. In this study, very low are the physical, social, legal, economic or psychological harms. Only those who wish to participate in the study will be asked questions so no one’s time is lost. A mild psychological harm is avoided by not includ ing the P.C. assessment. The benefit to the participants will be moral as they help research progress. Based on that, harms and benefit are balanced. Moreover, our survey and questions will be tested by the university IRB to get feedback and authorization to use it. The data will be kept safe in a closed drawer, and only the three of us will have access to it. At the end of the analysis, all the data will be burned and the results will be published.
  • 22. Sugar intake and Pancreatic Cancer 22 Conclusion Finally yet importantly, it is important to prevent P.C. because of its rapid onset, low prognosis, and high mortality. Sugar was seen in the literature as being a predisposing factor to develop P.C.. In this spirit, reducing sugar intake would help on reducing the fact of developing P.C.. Our research will conduct a case-control study in order to assess the relation between sugar intake and the development of P.C. in adults aged 50 to 80 in all Lebanon. The study will be conducted using a survey and a sugar diet assessment grid. This will allow us to effectively decide on the relation sugar and P.C. have in Lebanon. If a positive association is found, future regulation of sugar diet should be done to all persons with family history of P.C.. The aim of the study being to prevent P.C., awareness campaigns should be done to share with the society the results obtained.
  • 23. Sugar intake and Pancreatic Cancer 23 References American Cancer Society (2015). Retrieved from: http://www.cancer.org/cancer/pancreaticcancer/overviewguide/pancreatic-cancer- overview-what-is-pancreatic-cancer Dominique, M., Liu, S., Giovannucci, E., Willet, W., Graham, C., & Fuchs, C. (2002). Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study. Journal of the National Cancer Institute , 1293-1300. Forsmark CE. Pancreatitis. In: Goldman L, Shafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 46. Gapstur, S., Gann, P., Lowe, W., Liu, K., Colangelo, L., & Dyer, A., (2000). Abnormal Glucose Metabolism and Pancreatic Cancer Mortality. Journal of American Medical Association, 283 (19), 252-258 Han L, Ma Q, Li J, Liu H, Li W, Ma G, et al, (2011). High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR. PLoS One 2011;6:8. Hariharan, D., Saied, A., & Kocher, H. (2008). Analysis of mortality rates for pancreatic cancer across the world. HPB: The Official Journal of the International Hepato Pancreato Biliary Association. 10(1), 58–62. doi: 10.1080/13651820701883148
  • 24. Sugar intake and Pancreatic Cancer 24 Hirbli,K; Jambeine,M; Slim, Barakat,W; Habis,R; Francis,M., (2005). Prevalence of Diabetes in Greater Beirut, Diabetes Care;1262-1262, DOI: 10.2337/diacare.28.5.1262 Huxley R, Ansary-Moghaddam A, Berrington de González A, et al. (2005). Type-II diabetes and pancreatic cancer: a meta-analysis of 36 studies. Br J Cancer 92:2076- 83 Ito, M., Naohiko, M., & Yoshiyuki, U. (2013). Glucose intolerance and the risk of pancreatic cancer. Transl Gastrointest Cancer, 223-229. Johns Hopkins University (2012). Retrieved from: http://pathology.jhu.edu/pancreas/basicoverview3.php?area=ba Larsson S., Bergkvist L., Wolk A., (2006). Consumption of sugar and sugar-sweetened foods and the risk of pancreatic cancer in a prospective study. The American Journal of Clinical Nutrition 2006; 84, 1171-1176 Li J, Ma Q, Liu H, Guo K, Li F, Li W, et al, (2011). Relationship between neural alteration and perineural invasion in pancreatic cancer patients with hyperglycemia. PLoS One 2011;6:0017385 Lin Y, Kikuchi S, Tamakoshi A, Yagyu K, et al., (2007).Obesity, physical activity and the risk of pancreatic cancer in a large Japanese cohort. Int J Cancer 120:2665-71. Lyon JL, Slattery ML, Mahoney AW, Robison LM., (1993). Dietary intake as a risk factor for cancer of the exocrine pancreas. Cancer Epidemiol Biomarkers Prev;2:513–8
  • 25. Sugar intake and Pancreatic Cancer 25 Michaud, DS. (2004, April). Epidemiology of pancreatic cancer. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15238885 Michaud DS. et al, (2011). Dietary sugar, glycemic load, and pancreatic cancer risk in a prospective study. Journal of the National Cancer Institute 2002. 94(17). 1293- 1300 Office of National Statistics. Rterieved from: http://www.ons.gov.uk/ons/rel/vsob1/cancer-statistics-registrations--england-- series-mb1-/index.html Badran, M. & Laher, I., (2006). Type II Diabetes Mellitus in Arabic-Speaking Countries. International Journal of Endocrinology. doi:10.1155/2012/902873 Nöthlings, U., Murphy, S., Wilkens, L., Henderson, B., & Kolonel, L., (2007). Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study1–4. American Journal of Clinical Nutrition, 86 , 1495–501 OLSON, S., & KURTZ, R.C., (2013). Epidemiology of Pancreatic Cancer and the Role of Family History. Journal of Surgical Oncology, 107, 1–7 Permuth-Wey J, Egan KM., (2009). Family history is a significant risk factor for pancreatic cancer: results from a systematic review and meta-analysis. Fam Cancer;8:109-17
  • 26. Sugar intake and Pancreatic Cancer 26 Robertson R.P., (2004). Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. Journal of Biological Chemistry; 279:42351– 4. Salim et al., (2009). Cancer epidemiology and control in the Arab world - past, present and future. Asian Pacific Journal of Cancer Prevention; 10; 3-16 Schernhammer ES, Hu FB, Giovannucci E, et al., (2005). Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts. Cancer Epidemiology Biomarkers & Prevention;14:2098 –105. Siegel R, Ma J, Zou Z, & Jemal A., (2014). Cancer statistics, 2014. CA Cancer Journal for Clinicians; 64:9-29 Suzuki K, Islam KN, Kaneto H, Ookawara T, Taniguchi N. (2000).The contribution of fructose and nitric oxide to oxidative stress in hamster islet tumor (HIT) cells through the inactivation of glutathione peroxidase. Electrophoresis;21:285–8 Zhou, W., Capello, M., Fredolini, C., Racanicchi L., Dugnani, E., Piemonti, L., Liotta, L.A., Novelli, F., & Petricoin, E.F., (2013). Mass spectrometric analysis reveals O-methylation of pyruvate kinase from pancreatic cancer cells. Anal Bioanal Chem, 405, 4937–4943 Zhou, W., Liotta, L., & Petricoin, E., (2015). Cancer metabolism and mass spectrometry- based proteomics. Cancer Letters, 356, 176–183
  • 27. Sugar intake and Pancreatic Cancer 27 (2013). NCR 2008, Table B both gender: Frequency (nb) of incident cases by primary site & age group. Lebanese Ministry of Public Health, National Cancer Registry. Retrieved from http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2008.htm (2013). NCR 2007, Table B both gender: Frequency (nb) of incident cases by primary site & age group. Lebanese Ministry of Public Health, National Cancer Registry. Retrieved from http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2007.htm (2013). NCR 2006, Table B both gender: Frequency (nb) of incident cases by primary site & age group. Lebanese Ministry of Public Health, National Cancer Registry. Retrieved from http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2006.htm (2013). NCR 2005, Table B both gender: Frequency (nb) of incident cases by primary site & age group. Lebanese Ministry of Public Health, National Cancer Registry. Retrieved from http://www.moph.gov.lb/Prevention/Surveillance/documents/BA2005.htm (2013). Cancer in Lebanon: 2005 – 2007. Lebanese Ministry of Public Health, National Cancer Registry. Retrieved from http://www.moph.gov.lb/Prevention/Surveillance/documents/leb_ncr_2005_7.pdf