Final Poster Dissertation

1
Cardiovascular disease (CVD) is defined as a disorder relating to the heart or vasculature (World Health Organization, 2013). As of 2014, within the UK, CVD stands second only to cancer as the cause greatest cause of resident mortality, accounting for 28% of patient deaths (British Heart Foundation 2014) Diabetes mellitus type II (T2D) is characterised by hyperglycaemia, developing due to an inability to effectively utilize insulin – where cellular resistance to insulin is coupled with a reduction in pancreatic insulin secretion (World Health Organization, 1999). T2D stands as one of the leading causes of premature morbidity worldwide, due to associated CVD development (Ho et al., 1993; Grundy et al., 1999). T2D and CVD are associated with a plethora of risk factors/markers (such as high BMI and raised blood pressure), both of which are becoming increasingly prevalent worldwide, as more countries begin to adopt the ‘Western Lifestyle.’(Mente and Yusuf, 2012). This study aimed to identify correlations between bio-chemical markers and risk factors known to be associated with CVD and T2D development in the younger population, and determine whether these results were comparable to existing studies. Introduc tion Results Hypothesis The Relationship Between Metabolic Risk Markers and Other Relative Risk Factors for Diabetes Mellitus Type II and Cardiovascular Disease in those Under 40 The majority of the correlations between the bio-chemical markers (triglycerides, cholesterol and glucose) when correlated against each other and against known risk factors associated with CVD and T2D, will be found to express a significant positive correlation. This would support the role of triglycerides, cholesterol and glucose in the development of CVD and T2D as previously documented in past/ongoing studies. Discussion Results for triglycerides found 18 significant correlations against known risk factors for T2D/CVD when assessing the whole cohort plus males and females separately, many of which were similar to correlations found by larger studies –therefore reinforcing the fact that triglycerides concentration should be considered an independent CVD/T2D risk factor (Hokanson and Austin, 1996; Miller et al., 2011; Murad et al., 2012). However, our study failed to identify a correlation between triglycerides and weight in the total and female cohort, which has long since been identified as having a strong positive relationship (Sommariva et al., 1986). Cholesterol results identified correlations between systolic blood pressure and triglycerides, of which are supported by numerous studies which identify relationships between these findings and increased T2D and CVD risk (Eeg- Olofsson et al., 2014; Jiang et al., 2004; Thomas et al., 2002). When analysing the female cohort for glucose correlations, systolic and diastolic blood pressure, as well as triglycerides were found to be significantly correlated. These results are comparable to those found by published studies of a far larger cohort (Daboul, 2011; Filipovský et al., 1996). Interestingly, analysis of the male cohort found no statistical significance between glucose and the T2D/CDV risk factors – contradictory to extensive research by the Framingham study, which suggests that glucose is greatly linked with a potent risk of CVD and T2D development (Kannel & McGee, 1979; Mazzone, 2010; Buse, et al., 2007; Libby, et al., 2005). References: -Aspiring Bariatics Laproscopy and Endoscopy, 2005[WWW Document]. URL http://aspiringbariatrics.co.nz/about-us/ (accessed 4.30.15). -British Heart Foundation, 2014. Cardiovascular Disease Statistics 2014. Oxford. -Buse, J.B., Ginsberg, H.N., Bakris, G.L., Clark, N.G., Costa, F., Eckel, R., Fonseca, V., Gerstein, H.C., Grundy, S., Nesto, R.W., Pignone, M.P., Plutzky, J., Porte, D., Redberg, R., Stitzel, K.F., Stone, N.J., 2007. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Circulation 115, 114–26. -Daboul, M.W., 2011. A study measuring the effect of high serum triglyceride and cholesterol on glucose elevation in human serum. Oman Med. J. 26, 109–13. eg-Olofsson, K., Gudbjörnsdottir, S., Eliasson, B., Zethelius, B., Cederholm, J., 2014. The triglycerides-to-HDL-cholesterol ratio and cardiovascular disease risk in obese patients with type 2 diabetes: an observational study from the Swedish National Diabetes Register (NDR). Diabetes Res. Clin. Pract. 106, 136–44. -Filipovský, J., Ducimetiére, P., Eschwége, E., Richard, J.L., Rosselin, G., Claude, J.R., 1996. The relationship of blood pressure with glucose, insulin, heart rate, free fatty acids and plasma cortisol levels according to degree of obesity in middle-aged men. J. Hypertens. 14, 229–35. -Grundy, S.M., Benjamin, I.J., Burke, G.L., Chait, A., Eckel, R.H., Howard, B. V., Mitch, W., Smith, S.C., Sowers, J.R., 1999. Diabetes and Cardiovascular Disease : A Statement for Healthcare Professionals From the American Heart Association. Circulation 100, 1134– 1146. -Ho, K.K., Pinsky, J.L., Kannel, W.B., Levy, D., 1993. The epidemiology of heart failure: the Framingham Study. J. Am. Coll. Cardiol. 22, 6A–13A. -Hokanson, J.E., Austin, M.A., 1996. Plasma Triglyceride Level is a Risk Factor for Cardiovascular Disease Independent of High-Density Lipoprotein Cholesterol Level: A Metaanalysis of Population-Based Prospective Studies. Eur. J. Cardiovasc. Prev. Rehabil. 3, 213–219. -Jiang, R., Schulze, M.B., Li, T., Rifai, N., Stampfer, M.J., Rimm, E.B., Hu, F.B., 2004. Non-HDL cholesterol and apolipoprotein B predict cardiovascular disease events among men with type 2 diabetes. Diabetes Care 27, 1991–7. -Kalofoutis, C., Piperi, C., Kalofoutis, A., Harris, F., Phoenix, D., Singh, J., 2007. Type II diabetes mellitus and cardiovascular risk factors: Current therapeutic approaches. Exp. Clin. Cardiol. 12, 17–28. -Kannel, W.B., McGee, D.L., 1979. Diabetes and Glucose Tolerance as Risk Factors for Cardiovascular Disease: The Framingham Study. Diabetes Care 2, 120–126. -Laakso, M., 1999. Benefits of Strict Glucose and Blood Pressure Control in Type 2 Diabetes : Lessons From the UK Prospective Diabetes Study. Circulation 99, 461–462. -Libby, P., Nathan, D.M., Abraham, K., Brunzell, J.D., Fradkin, J.E., Haffner, S.M., Hsueh, W., Rewers, M., Roberts, B.T., Savage, P.J., Skarlatos, S., Wassef, M., Rabadan-Diehl, C., 2005. Report of the National Heart, Lung, and Blood Institute-National Institute of Diabetes and Digestive and Kidney Diseases Working Group on Cardiovascular Complications of Type 1 Diabetes Mellitus. Circulation 111, 3489–93. -Mannucci, E., Dicembrini, I., Lauria, A., Pozzilli, P., 2013. Is glucose control important for prevention of cardiovascular disease in diabetes? Diabetes Care 36, 259–263. -Mazzone, T., 2010. Intensive glucose lowering and cardiovascular disease prevention in diabetes: reconciling the recent clinical trial data. Circulation 122, 2201–11. -Mente, A., Yusuf, S., 2012. Reducing cardiovascular mortality through lifestyle change in Japan. Eur. Heart J. 33, 428–9. -Miller, M., Stone, N.J., Ballantyne, C., Bittner, V., Criqui, M.H., Ginsberg, H.N., Goldberg, A.C., Howard, W.J., Jacobson, M.S., Kris-Etherton, P.M., Lennie, T.A., Levi, M., Mazzone, T., Pennathur, S., 2011. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation 123, 2292–333. -Murad, M.H., Hazem, A., Coto-Yglesias, F., Dzyubak, S., Gupta, S., Bancos, I., Lane, M.A., Erwin, P.J., Berglund, L., Elraiyah, T., Montori, V.M., 2012. The association of hypertriglyceridemia with cardiovascular events and pancreatitis: a systematic review and meta- analysis. BMC Endocr. Disord. 12, 2. -Sommariva, D., Tirrito, M., Bellintani, L., Bonfiglioli, D., Branchi, A., Pogliaghi, I., Ottomano, C., 1986. Interrelationships between body mass and lipid and lipoprotein triglycerides and cholesterol in obese women. Ric. Clin. e Lab. 16, 481–488. Luke Peter Halpin (10202324) Senior Supervisor- Dr. Carol Rea Life Sciences Research Project BGY3003M Statistical Analysis: Using software by Minitab, measurements from the blood analysis and physiological measurements underwent calculation to determine the means, standard deviations, Pearson’s correlation. ANCOVA analysis was performed on significant data frpm the total cohort and regression analysis were performed on significant correlations found in the separate male and female cohorts Physiological Measurements: Measurements for body composition including: height, weight, hip circumference and waist circumference were taken from each participant. Fat % (via bioelectrical impedance) and blood pressure were also assessed. Blood Analysis: Each sample was centrifuged for 10 minutes at 3500 rpm , allowing the serum to be extracted and analysed by the ABX-Pentra 400 – concentrations for total triglycerides, cholesterol and glucose per sample were quantified. Phlebotomy: Blood samples were collected from each participant Participant Recruitment: Individuals < 40 years old were asked to participate in the study via social media, word-of-mouth and e-mail. The cohort consisted of 94 participants (32 males, 62 females) Information Leaflet: A leaflet outlining the purpose and procedures used in the study was produced. Background information on CVD and T2D was also included. Ethical and Risk Assessment: EA1 and EA2 forms and asCOSHH assessment were completed and approved by the Life Sciences ethical committee at the University of Lincoln. Methodology • Analysis of the total cohort identified 12 significant correlations out of 36 tested parameters for Pearson’s correlation analysis between triglycerides, glucose and cholesterol against each other and CVD/T2D associated risk factors (P=< 0.05, with 95% confidence). • ANCOVA analysis was performed on these significant correlations. 11 of these 12 parameters were found to be significant which suggested that there was significant difference between data collected between males and females (see table 1). Therefore, analysis of data was performed on male and female results separately. • Male cohort Pearson’s correlation identified 8 out of 36 tested parameters, with the following found to be significant to 95% confidence with a P-value < 0.05: Triglycerides against: weight, waist, waist:hip, body fat (% )and BMI Cholesterol against: waist:hip, body fat (%) and BMI • Female cohort Pearson’s correlation identified 8 out of 36 tested parameters, with the following found to be significant to 95% confidence with a P-value < 0.05: Triglycerides against: systolic blood pressure, glucose and cholesterol Cholesterol against: systolic blood pressure and triglycerides • Glucose against: systolic blood pressure, diastolic blood pressure and triglycerides Variable 1 Variable 2 Variable 3 F Value R 2 (adj) % P Value Triglycerides Waist Gender 11.99 13.47 0.001 Triglycerides Hip Gender 3.55 5.98 0.063 Triglycerides Waist:Hip Gender 6.15 8.63 0.015 Triglycerides Systolic Gender 4.84 13.35 0.030 Triglycerides Glucose Gender 5.03 11.20 0.027 Triglycerides Cholesterol Gender 14.20 19.23 <0.001 Triglycerides BMI Gender 10.70 12.36 0.002 Cholesterol Triglycerides Gender 15.49 15.96 <0.001 Glucose Hip Gender 4.83 3.17 0.031 Glucose Systolic Gender 6.86 8.42 0.010 Glucose Diastolic Gender 9.40 7.89 0.003 Glucose Triglycerides Gender 5.40 6.99 0.022 Table 1. ANCOVA results from statistically significant Pearson correlation results of the total cohort. 0 0.5 1 1.5 2 2.5 0 20 40 60 80 100 120 140 160 180 f(x) = 12.171377069943 x + 107 R² = 0.601097483087435 Regression between Triglycerides and Average Systolic Pressure in Females Triglycerides (mmol/L) Average Systolic Pressure (mm Hg) 0 0.5 1 1.5 2 2.5 0 5 10 15 20 25 30 35 40 f(x) = 3.33711208342772 x + 19.46 R² = 0.716760209427148 Regression between Triglycerides and BMI in Males Triglycerides (mmol/L) BMI (Kg/m2) Figure 2: A – Under 40 male cohort regression analysis for triglycerides against BMI (P= 0.005); B- Under 40 female cohort regression analysis for Triglycerides against systolic blood (P= < 0.001) A B Figure 1: Illustration of BMI classification (Aspiring Bariatics Laproscopy and Endoscopy, 2005) Conclusion Many significant correlations were identified between triglycerides, glucose and cholesterol and risk markers for T2D and CVD, the majority of which were correlative to previously existing studies – and therefore fulfilled the aim of this study. However, there were some discrepancies between some of the results and widely known correlations associated with glucose and cholesterol concentrations and risk factors. With CVD and T2D being amongst the main contributors for premature mortality in the UK, the continuation of research into the associated risk factors is required to fuel medical advances and disease understanding to effectively lower these statistics and improve the quality of life for CVD and T2D sufferers for generations to come.

Transcript of Final Poster Dissertation

Page 1: Final Poster Dissertation

Cardiovascular disease (CVD) is defined as a disorder relating to the heart or vasculature (World Health Organization, 2013). As of 2014, within the UK, CVD stands second only to cancer as the cause greatest cause of resident mortality, accounting for 28% of patient deaths (British Heart Foundation 2014)

Diabetes mellitus type II (T2D) is characterised by hyperglycaemia, developing due to an inability to effectively utilize insulin – where cellular resistance to insulin is coupled with a reduction in pancreatic insulin secretion (World Health Organization, 1999). T2D stands as one of the leading causes of premature morbidity worldwide, due to associated CVD development (Ho et al., 1993; Grundy et al., 1999).

T2D and CVD are associated with a plethora of risk factors/markers (such as high BMI and raised blood pressure), both of which are becoming increasingly prevalent worldwide, as more countries begin to adopt the ‘Western Lifestyle.’(Mente and Yusuf, 2012).

This study aimed to identify correlations between bio-chemical markers and risk factors known to be associated with CVD and T2D development in the younger population, and determine whether these results were comparable to existing studies.

Introduction Results

Hypothesis

The Relationship Between Metabolic Risk Markers and Other Relative Risk Factors for Diabetes Mellitus Type II and Cardiovascular Disease in those

Under 40

The majority of the correlations between the bio-chemical markers (triglycerides, cholesterol and glucose) when correlated against each other and against known risk factors associated with CVD and T2D, will be found to express a significant positive correlation. This would support the role of triglycerides, cholesterol and glucose in the development of CVD and T2D as previously documented in past/ongoing studies.

DiscussionResults for triglycerides found 18 significant correlations against known risk factors for T2D/CVD when assessing the whole cohort plus males and females separately, many of which were similar to correlations found by larger studies –therefore reinforcing the fact that triglycerides concentration should be considered an independent CVD/T2D risk factor (Hokanson and Austin, 1996; Miller et al., 2011; Murad et al., 2012). However, our study failed to identify a correlation between triglycerides and weight in the total and female cohort, which has long since been identified as having a strong positive relationship (Sommariva et al., 1986).

Cholesterol results identified correlations between systolic blood pressure and triglycerides, of which are supported by numerous studies which identify relationships between these findings and increased T2D and CVD risk (Eeg-Olofsson et al., 2014; Jiang et al., 2004; Thomas et al., 2002).

When analysing the female cohort for glucose correlations, systolic and diastolic blood pressure, as well as triglycerides were found to be significantly correlated. These results are comparable to those found by published studies of a far larger cohort (Daboul, 2011; Filipovský et al., 1996). Interestingly, analysis of the male cohort found no statistical significance between glucose and the T2D/CDV risk factors – contradictory to extensive research by the Framingham study, which suggests that glucose is greatly linked with a potent risk of CVD and T2D development (Kannel & McGee, 1979; Mazzone, 2010; Buse, et al., 2007; Libby, et al., 2005).

References:-Aspiring Bariatics Laproscopy and Endoscopy, 2005[WWW Document]. URL http://aspiringbariatrics.co.nz/about-us/ (accessed 4.30.15).-British Heart Foundation, 2014. Cardiovascular Disease Statistics 2014. Oxford.-Buse, J.B., Ginsberg, H.N., Bakris, G.L., Clark, N.G., Costa, F., Eckel, R., Fonseca, V., Gerstein, H.C., Grundy, S., Nesto, R.W., Pignone, M.P., Plutzky, J., Porte, D., Redberg, R., Stitzel, K.F., Stone, N.J., 2007. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Circulation 115, 114–26.-Daboul, M.W., 2011. A study measuring the effect of high serum triglyceride and cholesterol on glucose elevation in human serum. Oman Med. J. 26, 109–13.eg-Olofsson, K., Gudbjörnsdottir, S., Eliasson, B., Zethelius, B., Cederholm, J., 2014. The triglycerides-to-HDL-cholesterol ratio and cardiovascular disease risk in obese patients with type 2 diabetes: an observational study from the Swedish National Diabetes Register (NDR). Diabetes Res. Clin. Pract. 106, 136–44.-Filipovský, J., Ducimetiére, P., Eschwége, E., Richard, J.L., Rosselin, G., Claude, J.R., 1996. The relationship of blood pressure with glucose, insulin, heart rate, free fatty acids and plasma cortisol levels according to degree of obesity in middle-aged men. J. Hypertens. 14, 229–35.-Grundy, S.M., Benjamin, I.J., Burke, G.L., Chait, A., Eckel, R.H., Howard, B. V., Mitch, W., Smith, S.C., Sowers, J.R., 1999. Diabetes and Cardiovascular Disease : A Statement for Healthcare Professionals From the American Heart Association. Circulation 100, 1134–1146.-Ho, K.K., Pinsky, J.L., Kannel, W.B., Levy, D., 1993. The epidemiology of heart failure: the Framingham Study. J. Am. Coll. Cardiol. 22, 6A–13A.-Hokanson, J.E., Austin, M.A., 1996. Plasma Triglyceride Level is a Risk Factor for Cardiovascular Disease Independent of High-Density Lipoprotein Cholesterol Level: A Metaanalysis of Population-Based Prospective Studies. Eur. J. Cardiovasc. Prev. Rehabil. 3, 213–219.-Jiang, R., Schulze, M.B., Li, T., Rifai, N., Stampfer, M.J., Rimm, E.B., Hu, F.B., 2004. Non-HDL cholesterol and apolipoprotein B predict cardiovascular disease events among men with type 2 diabetes. Diabetes Care 27, 1991–7.-Kalofoutis, C., Piperi, C., Kalofoutis, A., Harris, F., Phoenix, D., Singh, J., 2007. Type II diabetes mellitus and cardiovascular risk factors: Current therapeutic approaches. Exp. Clin. Cardiol. 12, 17–28.-Kannel, W.B., McGee, D.L., 1979. Diabetes and Glucose Tolerance as Risk Factors for Cardiovascular Disease: The Framingham Study. Diabetes Care 2, 120–126.-Laakso, M., 1999. Benefits of Strict Glucose and Blood Pressure Control in Type 2 Diabetes : Lessons From the UK Prospective Diabetes Study. Circulation 99, 461–462.-Libby, P., Nathan, D.M., Abraham, K., Brunzell, J.D., Fradkin, J.E., Haffner, S.M., Hsueh, W., Rewers, M., Roberts, B.T., Savage, P.J., Skarlatos, S., Wassef, M., Rabadan-Diehl, C., 2005. Report of the National Heart, Lung, and Blood Institute-National Institute of Diabetes and Digestive and Kidney Diseases Working Group on Cardiovascular Complications of Type 1 Diabetes Mellitus. Circulation 111, 3489–93.-Mannucci, E., Dicembrini, I., Lauria, A., Pozzilli, P., 2013. Is glucose control important for prevention of cardiovascular disease in diabetes? Diabetes Care 36, 259–263.-Mazzone, T., 2010. Intensive glucose lowering and cardiovascular disease prevention in diabetes: reconciling the recent clinical trial data. Circulation 122, 2201–11.-Mente, A., Yusuf, S., 2012. Reducing cardiovascular mortality through lifestyle change in Japan. Eur. Heart J. 33, 428–9.-Miller, M., Stone, N.J., Ballantyne, C., Bittner, V., Criqui, M.H., Ginsberg, H.N., Goldberg, A.C., Howard, W.J., Jacobson, M.S., Kris-Etherton, P.M., Lennie, T.A., Levi, M., Mazzone, T., Pennathur, S., 2011. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation 123, 2292–333.-Murad, M.H., Hazem, A., Coto-Yglesias, F., Dzyubak, S., Gupta, S., Bancos, I., Lane, M.A., Erwin, P.J., Berglund, L., Elraiyah, T., Montori, V.M., 2012. The association of hypertriglyceridemia with cardiovascular events and pancreatitis: a systematic review and meta-analysis. BMC Endocr. Disord. 12, 2.-Sommariva, D., Tirrito, M., Bellintani, L., Bonfiglioli, D., Branchi, A., Pogliaghi, I., Ottomano, C., 1986. Interrelationships between body mass and lipid and lipoprotein triglycerides and cholesterol in obese women. Ric. Clin. e Lab. 16, 481–488.-Thomas, F., Bean, K., Guize, L., Quentzel, S., Argyriadis, P., Benetos, A., 2002. Combined effects of systolic blood pressure and serum cholesterol on cardiovascular mortality in young (<55 years) men and women. Eur. Heart J. 23, 528–35.-West, K.M., Ahuja, M.M.S., Bennett, P.H., Czyzyk, A., De Acosta, O.M., Fuller, J.H., Grab, B., Grabauskas, V., Jarrett, R.J., Kosaka, K., Keen, H., Krolewski, A.S., Miki, E., Schliack, V., Teuscher, A., Watkins, P.J., Stober, J.A., 1983. The Role of Circulating Glucose and Triglyceride Concentrations and Their Interactions with Other “Risk Factors” as Determinants of Arterial Disease in Nine -Diabetic Population Samples from the WHO Multinational Study. Diabetes Care 6, 361–369.-World Health Organization, 1999. Diabetes Mellitus WHO, Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications.-World Health Organization, 2013. WHO | Cardiovascular diseases (CVDs) [WWW Document]. Cardiovasc. Dis. URL http://www.who.int/mediacentre/factsheets/fs317/en/ (accessed 1.15.15).

Luke Peter Halpin (10202324)Senior Supervisor- Dr. Carol Rea Life Sciences Research Project BGY3003M

Statistical Analysis:Using software by Minitab, measurements from the blood analysis and physiological measurements underwent calculation to determine the means, standard deviations, Pearson’s correlation. ANCOVA analysis was performed on significant data frpm the total cohort and regression analysis were performed on significant correlations found in the separate male and female cohorts

Physiological Measurements:Measurements for body composition including: height, weight, hip circumference and waist circumference were taken from each participant. Fat % (via bioelectrical impedance) and blood pressure were also assessed.

Blood Analysis:Each sample was centrifuged for 10 minutes at 3500 rpm , allowing the serum to be extracted and analysed by the ABX-Pentra 400 – concentrations for total triglycerides, cholesterol and glucose per sample were quantified.

Phlebotomy:Blood samples were collected from each participant

Participant Recruitment:Individuals < 40 years old were asked to participate in the study via social media, word-of-mouth and e-mail. The cohort consisted of 94 participants (32 males, 62 females)

Information Leaflet:A leaflet outlining the purpose and procedures used in the study was produced. Background information on CVD and T2D was also included.

Ethical and Risk Assessment: EA1 and EA2 forms and asCOSHH assessment were completed and approved by the Life Sciences ethical committee at the University of Lincoln.

Methodology

• Analysis of the total cohort identified 12 significant correlations out of 36 tested parameters for Pearson’s correlation analysis between triglycerides, glucose and cholesterol against each other and CVD/T2D associated risk factors (P=< 0.05, with 95% confidence).

• ANCOVA analysis was performed on these significant correlations. 11 of these 12 parameters were found to be significant which suggested that there was significant difference between data collected between males and females (see table 1). Therefore, analysis of data was performed on male and female results separately.

• Male cohort Pearson’s correlation identified 8 out of 36 tested parameters, with the following found to be significant to 95% confidence with a P-value < 0.05:

• Triglycerides against: weight, waist, waist:hip, body fat (% )and BMI• Cholesterol against: waist:hip, body fat (%) and BMI

• Female cohort Pearson’s correlation identified 8 out of 36 tested parameters, with the following found to be significant to 95% confidence with a P-value < 0.05:

• Triglycerides against: systolic blood pressure, glucose and cholesterol• Cholesterol against: systolic blood pressure and triglycerides• Glucose against: systolic blood pressure, diastolic blood pressure and triglycerides

Variable 1 Variable 2 Variable 3 F Value R2 (adj) % P Value

Triglycerides Waist Gender 11.99 13.47 0.001

Triglycerides Hip Gender 3.55 5.98 0.063

Triglycerides Waist:Hip Gender 6.15 8.63 0.015

Triglycerides Systolic Gender 4.84 13.35 0.030

Triglycerides Glucose Gender 5.03 11.20 0.027

Triglycerides Cholesterol Gender 14.20 19.23 <0.001

Triglycerides BMI Gender 10.70 12.36 0.002

Cholesterol Triglycerides Gender 15.49 15.96 <0.001

Glucose Hip Gender 4.83 3.17 0.031

Glucose Systolic Gender 6.86 8.42 0.010

Glucose Diastolic Gender 9.40 7.89 0.003

Glucose Triglycerides Gender 5.40 6.99 0.022

Table 1. ANCOVA results from statistically significant Pearson correlation results of the total cohort.

0 0.5 1 1.5 2 2.50

20

40

60

80

100

120

140

160

180

f(x) = 12.171377069943 x + 107R² = 0.601097483087435

Regression between Triglycerides and Average Systolic Pressure in Females

Triglycerides (mmol/L)

Aver

age

Syst

olic

Pre

ssur

e (m

m H

g)

0 0.5 1 1.5 2 2.50

5

10

15

20

25

30

35

40

f(x) = 3.33711208342773 x + 19.46R² = 0.716760209427148

Regression between Triglycerides and BMI in Males

Triglycerides (mmol/L)

BMI (

Kg/m

2)

Figure 2: A – Under 40 male cohort regression analysis for triglycerides against BMI (P= 0.005); B- Under 40 female cohort regression analysis for Triglycerides against systolic blood (P= < 0.001)

A B

Figure 1: Illustration of BMI classification (Aspiring Bariatics Laproscopy and Endoscopy, 2005)

ConclusionMany significant correlations were identified between triglycerides, glucose and cholesterol and risk markers for T2D and CVD, the majority of which were correlative to previously existing studies – and therefore fulfilled the aim of this study. However, there were some discrepancies between some of the results and widely known correlations associated with glucose and cholesterol concentrations and risk factors. With CVD and T2D being amongst the main contributors for premature mortality in the UK, the continuation of research into the associated risk factors is required to fuel medical advances and disease understanding to effectively lower these statistics and improve the quality of life for CVD and T2D sufferers for generations to come.