DP 11 - THE CUT-OFF VALUE FOR SUGAR INTAKE IN RELATION TO COGNITIVE IMPAIRMENT AND THE UNDERLYING MECHANISM AMONG MULTI-ETHNIC MALAYSIAN OLDER ADULTS Chong Ching Phang

CHONG C.P.2, SHAHAR S.1 , RAJAB N. F.1, HARON H.1, SHARIF R.1

 

1 Centre for Healthy Aging and Wellness, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Pahang, 50588 Kuala Lumpur, Malaysia

2 Klinik Kesihatan Jinjang

No. 2, Jalan Jinjang Setia 3, Jinjang Utara Tambahan, 52000 Kuala Lumpur

 

Objective

The intake of excess sugar has been linked to an increased risk of cognitive impairment. This study aimed to investigate the optimum cut-off values of sugar intake in relation to cognitive impairment and the underlying biochemical mediators among older adults in Malaysia.

 

Methodology

A total of 1,209 respondents aged ≥60 years were recruited through multistage random sampling from selected states. Dietary intake was derived using a 7-day dietary history questionnaire (DHQ) and food frequency questionnaire (FFQ) for added sugar intake. Optimal cut-off values was determined using the receiver operating characteristic (ROC) curve. The possible underlying biochemical mediators were determined using mediation analysis.

 

Results & Discussion

The optimal cut-off value in predicting cognitive impairment was 83.1 g/day for total sugars, 44.3 g/day for free sugars, and 26.7 g/day for sucrose. The results from biomarkers analysis (n=120) indicated that higher sugar intake was associated with reduced brain-derived neurotrophic factor (BDNF) but increased in malondialdehyde (MDA), insulin, glucose and homeostatic model assessment-insulin resistance (HOMA-IR) (p < 0.05 for all parameters). MDA appeared to be the full mediator linking free sugars and sugar from sugar-sweetened beverages with the MMSE score, while BDNF was the full mediator linking sugar from fruits with the MMSE score.

 

Conclusion

In conclusion, excessive consumption of more than 83.1 g total sugars and 44.3 g free sugars per day showed a notable risk for cognitive impairment. MDA and BDNF were two possible biochemical mediators involved.