SUNNAH INTERMITTENT FASTING (SIF)ON COGNITIVE AND AMELIORATES THE - - PowerPoint PPT Presentation

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SUNNAH INTERMITTENT FASTING (SIF)ON COGNITIVE AND AMELIORATES THE - - PowerPoint PPT Presentation

Nutrition Society of Malaysia , 33 rd Scientific Conference: Investing In Nutrition - Act Now ; 24-26 July 2018 SUNNAH INTERMITTENT FASTING (SIF)ON COGNITIVE AND AMELIORATES THE EFFECT OF OXIDATIVE DAMAGE AMONG MCI OLDER ADULTS Ms Asheila


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SUNNAH INTERMITTENT FASTING (SIF)ON COGNITIVE AND AMELIORATES THE EFFECT OF OXIDATIVE DAMAGE AMONG MCI OLDER ADULTS

Ms Asheila Meramat, UKM PhD candidates

Dr Razinah Sharif, Prof Suzana Shahar, Prof Dr Nor Fadilah Rajab

Nutrition Society of Malaysia, 33rd Scientific Conference: Investing In Nutrition - Act Now ; 24-26 July 2018

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CONTENTS

  • Introduction
  • Methodology of the study
  • Result & Discussion
  • Conclusion
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AGEING POPULATION

Department Statistic of Malaysia Report, 2014-2016

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Aging associated Diseases

OLDER ADULTS Physiological function  organ function  mental health  physical function  Metabolic syndromes, Cognitive Diseases, Psychological problem (1)

AGEING

PRIMARY (innate maturational processes) SECONDARY (the effects of environment and disease) caloric intake Overnutrition/overconsumption

  • f foods

 Physical activity Unhealthy lifestyle

  • smoking habits
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CALORIC REDUCTION & FASTING

Low caloric diet/ Fasting

Slow down the metabolism (10%) oxidative stress Less damage to biomolecules and organ Slow aging process Live longer Reduced production of chronic low grade inflammation Improved mental health

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Research questions Is regularly practicing Sunnah Intermittent Fasting has an effects on cognitive, oxidative pathway, endocrine and metabolites among older adults who had MCI in order to improve cognitive status after 36 months of follow-up? Ha: YES regularly practicing Sunnah Intermittent Fasting has an effects on cognitive, oxidative pathway, endocrine and metabolites among older adults who had MCI in order to improve cognitive status after 36 months of follow-up.

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RESULTS & DISCUSSIONS

Charact aracteris eristics tics r-SIF IF (n = 3 33) Num (%) i-SIF SIF (n = 3 33) Num (%) n-SIF IF (n = 3 33) Num (%) X P-Val Value Age (mea ean) 68.55 (4.51) 68.04 (6.02) 68.90 (5.09 0.19 0.82a Sex Male 21 (39.6) 14 (26.4) 18 (34.0) 3.0 0.22 Female 12 (26.1) 19 (41.3) 15 (32.6) Years ars of

  • f education

ation (year ear) ≥ 6 years 21 (46.7) 15 (33.3) 9 (20.0) 8.8 0.012* < 6 years 12 (22.2) 18 (33.3) 24 (44.4) Livin ving arr rrang angeme ement Alone 1 (8.3) 4 (33.3) 7 (58.3) 5.12 0.07 With others 32 (36.8) 29 (33.3) 26 (29.9) Histo istory ry of

  • f demen

menti tia No 32 (36.4) 29 (33.0) 27 (30.7) 3.89 0.14 Yes 1 (9.1) 4 (36.4) 6 (54.5) Smokin king habits bits Active smoker 4 (11.4) 13 (37.1) 18 (51.4) 17.36 0.002* Ex-smoker 9 (52.9) 2 (11.8) 6 (35.3) Passive smoker 20 (42.6) 18 (38.3) 9 (19.1)

aOne way ANOVA

Unless indicated otherwise, data are given as the number (percentage); Chi square test. *p<0.05.

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RESULTS & DISCUSSIONS

Table 2: Comparison of mean each cognitive test among three different SIF status groups based on time (time*treatment interaction effect)

Repeated measures ANCOVA between group analyses with regard to time was applied. Numerical covariate (age, level of education) was controlled using repeated measures ANCOVA. Assumptions

  • f normality, homogeneity of variances, compound symmetry and homogeneity of regression were checked and were fulfilled. *p<0.05
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  • 1. Better cognitive performance similar results with previous  IF diet exhibit less

neuronal dysfunction and degeneration on mice and rats [10]

  • 2. Mechanism contribute to the favorable effects of IF on the nervous systems

 accumulation of oxidatively damaged molecules  improved cellular bioenergetics  enhanced neurotrophic factor signaling  inflammation

  • 3. IF diets may aids to boost up levels of antioxidant defenses [11] and also promotes

restoration of new neurons from neural stem cells (neurogenesis) [12].

BETTER ER CO COGN GNITIVE E FUNC NCTION ON

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RESULTS & DISCUSSIONS

Table 3: Cognitive changes after 36 months follow-up

Unless indicated otherwise, data are given as the number (percentage); Chi square test. *p<0.05.

Characteristics r-SIF number (%) i-SIF number (%) n-SIF number (%) X P value Cognitive changes SA 8 (53.3) 6 (40.0) 1 (6.7) 46.12 0.001* UA 25 (43.9) 23 (40.4) 9 (15.8) MCI 1 (3.7) 3 (11.1) 23 (85.2)

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5 10 15 20 25

r-SIF i-SIF n-SIF

DNA in tail (%)

Consistency of SIF

Diagram 1: DNA in tail (%) among MCI older adults based on consistency of SIF

Baseline 36 months

*

0.2 0.4 0.6 0.8 1 1.2 1.4 1.6 1.8

r-SIF i-SIF n-SIF Tail moment (%)

Consistency of SIF

Diagram 2: Tail moment (%) among MCI older adults based on consistency of SIF

Baseline 36 months

Repeated measures ANCOVA between group analyses with regard to time was applied. Numerical covariate (age, level of education) was controlled using repeated measures ANCOVA. Assumptions

  • f normality, homogeneity of variances, compound symmetry and homogeneity of regression were checked and were fulfilled. *p<0.05

Diagram 1 and 2: Comparison of mean DNA Damage parameter among three different SIF status groups based on time (time*treatment interaction effect)

RESULTS & DISCUSSIONS

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Repeated measures ANCOVA between group analyses with regard to time was applied. Numerical covariate (age, level of education) was controlled using repeated measures ANCOVA. Assumptions

  • f normality, homogeneity of variances, compound symmetry and homogeneity of regression were checked and were fulfilled. *p<0.05

Diagram 3 and 4: Comparison of mean MDA & SOD levels among three different SIF status groups based on time (time*treatment interaction effect)

RESULTS & DISCUSSIONS

20 40 60 80 100 120 140 160 180 r-SIF i-SIF n-SIF MDA level (nmol/mg protein) Consistency of SIF

Diagram 3: MDA level among MCI older adults based on consistency of SIF

Baseline 36 months

* * *

10 20 30 40 50 60 70 80 90 r-SIF i-SIF n-SIF SOD level (u.e/min/mg protein) Consistency of SIF

SOD level among MCI older adults based on consistency of SIF

Baseline 36 months

* *

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Repeated measures ANCOVA between group analyses with regard to time was applied. Numerical covariate (age, level of education) was controlled using repeated measures ANCOVA. Assumptions

  • f normality, homogeneity of variances, compound symmetry and homogeneity of regression were checked and were fulfilled. *p<0.05

Diagram 5 and 6: Comparison of mean CRP & INS levels among three different SIF status groups based on time (time*treatment interaction effect)

RESULTS & DISCUSSIONS

0.5 1 1.5 2 2.5 r-SIF i-SIF n-SIF CRP level (mg/L) Consistency of SIF

Diagram 5: CRP level among MCI older adults based on consistency of SIF

Baseline 36 months

* * *

50 100 150 200 250 300 350 r-SIF i-SIF n-SIF INS level (pmol/L) Consistency of SIF

Diagram 6: INS level among MCI older adults based on consistency of SIF

Baseline 36 months

* * *

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  • 1. SIF protection against lipid peroxidation in plasma.

2. Possible mechanismSIF reduces the ROS production by macrophage or reduce oxidative stress on macrophage

  • 3. Growing evidence proposed that hypo- and hyper-nutrition are associated with a higher likelihood
  • f cellular oxidation, mediated by nutrient pathways
  • 4. Older adults who are not practicing SIF are more prone to gain weight after 36 months might be

due to accumulation of saturated fatty acids (SFAs) and polyunsaturated fatty acids (PUFAs).  SFAs are more toxic than unsaturated fats.  High SFA intake  pro-inflammatory status resulting from an imbalance in lipid signaling pathways and  production of inflammatory cytokines.

  • 5. SIF the oxidative stress level, antioxidant defense (SOD).
  • SIF oxidative stress level  reduce the incidence of DNA damage  cognitive

impairment.

  • SIF  insulin and glucose level  ketone body levels generate a protective environment

 DNA damage and enhancing the programmed cell death for damaged DNA [13, 10].

BETTER ER CO COGN GNITIVE E FUNC NCTION ON

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CONCLUSION

  • 1. SIF has an effect on  ROS,  inflammation markers ,  insulin levels   incidence of DNA

damage revert back MCI to SA or UA (better cognitive function)

  • 2. R-SIF   NAS, acetoacetic acid metabolites (ketogenic pathway) neuroprotective effects and

oxidative damage better cognitive status and health status

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YOUR PREFERENCE?

OR

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FUTURE DIRECTIONS

  • Large scale of the study population that involved different races and religion
  • Different target population (middle age)
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ACKNOWLEDGEMENT

  • We are grateful for the Longitudinal Research Grant Scheme

awarded by Ministry of Education (LRGS/BU/2012/UKM- UKM/K/01) and all the participants

  • Bioscience Institute (IBS, UPM)
  • Makmal Bioserasi UKM, Bangi
  • Special thanks to :

Supervisor: Dr Razinah Sharif Co-Supervisor: Prof Suzana Shahar & Prof Nor Fadilah Rajab

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REFERENCES

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Jaul E, Barron J (2017) Age-Related Diseases and Clinical and Public Health Implications for the 85 Years Old and Over Population. Frontiers in public health 5, 335.

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Lombard DB, Chua KF, Mostoslavsky R, Franco S, Gostissa M, Alt FW (2005) DNA repair, genome stability, and

  • aging. Cell 120, 497-512.
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Krabbe KS, Pedersen M, Bruunsgaard H (2004) Inflammatory mediators in the elderly. Experimental gerontology 39, 687-699.

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Basu R, Breda E, Oberg AL, Powell CC, Dalla Man C, Basu A, Vittone JL, Klee GG, Arora P, Jensen MD (2003) Mechanisms of the age-associated deterioration in glucose tolerance: contribution of alterations in insulin secretion, action, and clearance. Diabetes 52, 1738-1748.

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Smith RG, Betancourt L, Sun Y (2005) Molecular endocrinology and physiology of the aging central nervous

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Teng NI, Shahar S, Rajab NF, Manaf ZA, Johari MH, Ngah WZ (2013) Improvement of metabolic parameters in healthy older adult men following a fasting calorie restriction intervention. Aging Male 16, 177-183.

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Vanoh D, Shahar S, Din NC, Omar A, Vyrn CA, Razali R, Ibrahim R, Hamid TA (2017) Predictors of poor cognitive status among older Malaysian adults: baseline findings from the LRGS TUA cohort study. Aging clinical and experimental research 29, 173-182.

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REFERENCES

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Morabia A, Curtin F, Bernstein MS (1999) Effects of smoking and smoking cessation on dietary habits of a Swiss urban population. European journal of clinical nutrition 53, 239.

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Arumugam TV, Phillips TM, Cheng A, Morrell CH, Mattson MP, Wan R (2010) Age and energy intake interact to modify cell stress pathways and stroke outcome. Annals of neurology 67, 41-52.

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Brandhorst S, Choi IY, Wei M, Cheng CW, Sedrakyan S, Navarrete G, Dubeau L, Yap LP, Park R, Vinciguerra M (2015) A periodic diet that mimics fasting promotes multi-system regeneration, enhanced cognitive performance, and

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Guevara-Aguirre J, Balasubramanian P, Guevara-Aguirre M, Wei M, Madia F, Cheng C-W, Hwang D, Martin- Montalvo A, Saavedra J, Ingles S (2011) Growth hormone receptor deficiency is associated with a major reduction in pro- aging signaling, cancer, and diabetes in humans. Science translational medicine 3, 70ra13-70ra13.

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