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Dietary acid load and risk of type 2 diabetes among Malaysian
postmenopausal Chinese women
Presenter : Lim Sook Yee
The Global Prevalence of Diabetes
8
8.1
8.2
8.3
8.4
8.5
8.6
8.7
8.8
8.9
2013 2035
Total diabetes
Total diabetes
Guariguata L et al., 2014
around 55% of the world’s diabetes population is from Asia
%
Year
Trend of diabetes in Malaysia
11.6
15.2
17.5
14.9
20.8 22.5
0
5
10
15
20
25
NHMS III (2006) NHMS 2011 NHMS 2015
Total diabetes (≥ 18 years)
Total diabetes (≥ 30 years)
Prevalence (%)
Prevalence of people by age and sex, 2017
International Diabetes Federation
The identification of modifiable risk factors for diabetes is thus a
priority issue
What is dietary acid load?
• Acidic diet
– Diet that high in animal proteins such as derived from red meat and cheese.
• Alkaline diet
– Diet that high in potassium, magnesium and calcium such as derived from vegetables and fruits.
Historical of Acid-base Balance Theory
Sherman & Sinclair (1907) (Cations and
anions of the mineral)
Sherman and Gettler (1912)
(A list of acid-base elements in 47 different
kinds of food)
Shohl & Sato (1923)
(Experiment on two normal infant)
Gonick et al. (1968)
(H+ from organic sulfur and hydrolysis of phosphoesters)
Gonick & Goldberg (1966) (urinary acid
excretion due to invariably alkaline in
feces )
Remer (1994)
[potential renal acid load (PRAL)
Frassetto et al. (1998)
[net endogenous acid production (NEAP)]
Remer (2000)
(5 factors: food composition, bioavailability, sulfate production, grades of dissociation of phosphorus and
the valence ions of Cal and Mg
Remer (2000) How the 4 main organs interact in managing acid-base homeostasis?
• Figure 1 show how the 4 main organs interact in managing acid-base homeostasis. – At first, intestine is the initial organ to absorb nutrients and alters the blood bicarbonate level
base on the food composition consumed. – Intestine determines the absorbed amounts of sulfur-containing amino acids (AA-SH) and
alkali salts of nonmetabolizable organic acids (OA-) before they involve in the liver buffer system.
– In the liver system, it produces hydrogen ions (H+) and alkali ions (OH-) by oxidizing the absorbed AA-SH and OA.
– The H+ and OH- are finally excreted by kidney. – On the other hand, lungs are responsible to regulate the volatile acids, carbonic acid (H2CO3)
without adding or subtracting H+ into the blood
(Adapted from Remer, 2000)
Previous studies
a diet with high acid-forming potential might increase the risk of type 2 diabetes.
states that men with highest PRAL quartile had 61 % increased type 2 diabetes prevalence in over 5 years follow-up period
Problem statement
• Dietary acid load is associated with chronic diseases especially cardiovascular disease, diabetes, cancer and osteoporosis. However, the result is INCONSISTENT and the study is SCARCE in postmenopausal Asians population.
Objective
• to determine the association between dietary acid load and blood glucose level among postmenopausal Chinese women.
Methodology
Study design
• Analytical cross sectional study
Location • NACSCOM in Kuala Lumpur and
Selangor
Sampling design
• Two-stage sampling technique
• simple random sampling to select seven affiliates
• Participants were recruited based on the inclusion and exclusion criteria.
Ethical approval
The ethical clearance was obtained from
• Ethics Committee for Research Involving Human Subjects with project reference number was FPSK (FR16) P019.
Data collection instrument
Questionnaire sociodemographic background
Global Physical Activity Questionnaire (GPAQ)
Validated semi-quantitative food frequency questionnaire (FFQ)
Dietary acid load estimation
PRAL score (Remer, 1994):
+ 0.49 x protein (g/day)
+ 0.037 x phosphorus (mg/d)
-0.021 x potassium (mg/d)
-0.026 x magnesium (mg/d)
-0.013 x calcium (mg/d)
= PRAL (mEq/d)
NEAP score(Frassetto et al., 1998):
[54:5 x protein intake (g/d) / potassium intake (mEq/d]
- 10:2
-PRAL and -NEAP +PRAL and +NEAP
base-forming potential acid -forming potential
Results: characteristics of the participants
Results: characteristics of the participants Table 1. characteristics of women (n = 217) cont.
Results Table 2. Bivariate Pearson correlation coefficients for rate of Blood glucose level, NEAP, PRAL score and controls.
Blood glucose is weakly but significantly correlate with PRAL score, BMI and age
Result: regression Table 3. regression analysis of PRAL score and control variables predicting high blood glucose
Table 4. regression analysis of NEAP score and control variables predicting high blood glucose
Result: 4 quartiles of NEAP scores and blood glucose level
P value = ns, One-way ANOVA analysis.
Result: 4 quartiles of PRAL scores and blood glucose level
P value = ns, One-way ANOVA analysis.
Discussion
• Result revealed that PRAL score was positively associated with blood glucose level after adjusted for covariates, but not for NEAP score.
• PRAL is estimated based on intake of five nutrients including protein, potassium, phosphorous, magnesium and calcium, whereas NEAP only considers protein and potassium intake.
• The differences in equation used to estimate the PRAL and NEAP score, might explain inconsistent findings association with blood glucose level.
Discussion
• The underlying mechanism by which high dietary acid load increased the blood glucose level remains unclear, Rylander et al. (2009) suggested:
– acid-base balance may influence mineral homeostasis by regulating the absorption of calcium and magnesium in the kidneys, and studies in human have shown that calcium and magnesium are important minerals for insulin action.
Conclusion
Our findings suggest that a high dietary acid load PRAL score was associated with an increased blood glucose level in postmenopausal Chinese women.
Acknowledgement
• This research was funded by Fundamental Research Grant Scheme (FRGS), Ministry of Higher Education, Malaysia.
• Supervisors: A.P. Dr. Chan Yoke Mun, Prof. Zalilah Mohd Shariff, Dr. Chin Yit Siew and Dr. Vasudevan Ramachandran
• Research team members: Mr. Leiu Kok Hong and Mr. Chan Kai Sze
References
• Atlas, D. (2006). International diabetes federation. Press Release, Cape Town, South Africa, 4.
• Chan, J. C., Malik, V., Jia, W., Kadowaki, T., Yajnik, C. S., Yoon, K.-H., & Hu, F. B. (2009). Diabetes in Asia: epidemiology, risk factors, and pathophysiology. Jama, 301(20), 2129-2140.
• Fagherazzi, G., Vilier, A., Bonnet, F., Lajous, M., Balkau, B., Boutron-Ruault, M.-C., & Clavel-Chapelon, F. (2014). Dietary acid load and risk of type 2 diabetes: the E3N-EPIC cohort study. Diabetologia, 57(2), 313-320.
• Fenton, T. R., Tough, S. C., Lyon, A. W., Eliasziw, M., & Hanley, D. A. (2011). Causal assessment of dietary acid load and bone disease: a systematic review & meta-analysis applying Hill's epidemiologic criteria for causality. Nutrition journal, 10(1), 41.
• Guariguata, L., Whiting, D. R., Hambleton, I., Beagley, J., Linnenkamp, U., & Shaw, J. E. (2014). Global estimates of diabetes prevalence for 2013 and projections for 2035. Diabetes research and clinical practice, 103(2), 137-149.
• Rebolledo, O. R., Hernandez, R. E., Zanetta, A. C., & Gagliardino, J. (1978). Insulin secretion during acid-base alterations. American Journal of Physiology-Endocrinology and Metabolism, 234(4), E426.
References
• Remer, T. 2000. Acid‐Base in Renal Failure: Influence of Diet on Acid‐Base Balance. Seminars in dialysis, hlm. 221-226.
• Rylander, R., Tallheden, T., & Vormann, J. (2009). Acid-base conditions regulate calcium and magnesium homeostasis. Magnesium research, 22(4), 262-265.
• Shoichiro (2016). High Dietary Acid Load Score Is Associated with Increased Risk of Type 2 Diabetes in Japanese Men: The Japan Public Health Center–based Prospective Study–. The Journal of nutrition, 146(5), 1076-1083.
• Whittaker, J., Cuthbert, C., Hammond, V., & Alberti, K. (1982). The effects of metabolic acidosis in vivo on insulin binding to isolated rat adipocytes. Metabolism-Clinical and Experimental, 31(6), 553-557.
• Xu, H., Jia, T., Huang, X., Risérus, U., Cederholm, T., Ärnlöv, J., Carrero, J.J. (2014). Dietary acid load, insulin sensitivity and risk of type 2 diabetes in community-dwelling older men. Diabetologia, 57(8), 1561-1568.