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Review
. 2018 May 12;10(5):606.
doi: 10.3390/nu10050606.

Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies

Karen W Della Corte  1 , Ines Perrar  2 , Katharina J Penczynski  3 , Lukas Schwingshackl  4 , Christian Herder  5   6 , Anette E Buyken  7
Affiliations
Review

Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies

Karen W Della Corte et al. Nutrients. .

Abstract

It has been postulated that dietary sugar consumption contributes to increased inflammatory processes in humans, and that this may be specific to fructose (alone, in sucrose or in high-fructose corn syrup (HFCS)). Therefore, we conducted a meta-analysis and systematic literature review to evaluate the relevance of fructose, sucrose, HFCS, and glucose consumption for systemic levels of biomarkers of subclinical inflammation. MEDLINE, EMBASE, and Cochrane libraries were searched for controlled intervention studies that report the effects of dietary sugar intake on (hs)CRP, IL-6, IL-18, IL-1RA, TNF-α, MCP-1, sICAM-1, sE-selectin, or adiponectin. Included studies were conducted on adults or adolescents with ≥20 participants and ≥2 weeks duration. Thirteen studies investigating 1141 participants were included in the meta-analysis. Sufficient studies (≥3) to pool were only available for (hs)CRP. Using a random effects model, pooled effects of the interventions (investigated as mean difference (MD)) revealed no differences in (hs)CRP between fructose intervention and glucose control groups (MD: −0.03 mg/L (95% CI: −0.52, 0.46), I² = 44%). Similarly, no differences were observed between HFCS and sucrose interventions (MD: 0.21 mg/L (−0.11, 0.53), I² = 0%). The quality of evidence was evaluated using Nutrigrade, and was rated low for these two comparisons. The limited evidence available to date does not support the hypothesis that dietary fructose, as found alone or in HFCS, contributes more to subclinical inflammation than other dietary sugars.

Keywords: dietary fructose; dietary glucose; dietary sucrose; high fructose corn syrup; inflammatory markers.

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Conflict of interest statement

A.E. Buyken is a member of the International Carbohydrate Quality Consortium and a member of an expert group convened by ILSI Europe which prepared a scientific review entitled “Dietary carbohydrates: A review of international recommendations and the methods used to derive them”[66]. K. Della Corte, K.J. Penczynski, I. Perrar, C. Herder, and L. Schwingshackl have no conflicts of interest.

Figures

Figure A1
Figure A1
Study selection process. 1 Of the 14 studies, two reports from one original study by Stanhope et al. [32] and each study (Cox et al. [33] Rezvani et al. [34]) report on different inflammatory markers measured in the original study. Therefore, there are technically 13 studies included in the review.
Figure A2
Figure A2
Risk of bias table.
Figure A3
Figure A3
Forest plot for fructose vs glucose and (hs)CRP as an outcome. Pooled estimates of effect sizes (95% confidence intervals) for the comparison of fructose and glucose expressed as mean differences (MD). Effect size units expressed in mg/L. MD = mean of intervention group – mean of control group. Fructose = intervention group and glucose = control group. No difference in effects on (hs)CRP between fructose and glucose groups. Tau2 value represents degree of heterogeneity within comparison groups. I2 represents the extent to which studies are statistically inconsistent. “Hypercaloric” refers to those trials that administered extra-physiological doses of sugars and “eucaloric” to trials in which daily energy requirements were not exceeded or restricted by administered doses of sugars.
Figure A4
Figure A4
Forest plot for HFCS vs sucrose and (hs)CRP as an outcome. Pooled estimates of effect sizes (95% confidence intervals) for the comparison of HFCS and sucrose expressed as mean differences (MD). Effect size units expressed in mg/L. MD = mean of intervention group − mean of control group. HFCS = intervention group and sucrose=control group. The increase in (hs)CRP was greater in HFCS groups vs sucrose groups but not significant. Tau2 value represents degree of heterogeneity within comparison groups. I2 represents the extent to which studies are statistically inconsistent. “Hypercaloric” refers to those trials that administered extra-physiological doses of sugars and “eucaloric” to trials in which daily energy requirements were not exceeded or restricted by administered doses of sugars.
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References

    1. Hotamisligil G.S. Inflammation and metabolic disorders. Nature. 2006;444:860–867. doi: 10.1038/nature05485. - DOI - PubMed
    1. Donath M.Y., Shoelson S.E. Type 2 diabetes as an inflammatory disease. Nat. Rev. Immunol. 2011;11:98–107. doi: 10.1038/nri2925. - DOI - PubMed
    1. Shoelson S.E., Lee J., Goldfine A.B. Inflammation and insulin resistance. J. Clin. Investig. 2006;116:1793–1801. doi: 10.1172/JCI29069. - DOI - PMC - PubMed
    1. Xu G., Zhou Z., Zhu W., Fan X., Liu X. Plasma C-reactive protein is related to cognitive deterioration and dementia in patients with mild cognitive impairment. J. Neurol. Sci. 2009;284:77–80. doi: 10.1016/j.jns.2009.04.018. - DOI - PubMed
    1. Howren M.B., Lamkin D.M., Suls J. Associations of depression with C-reactive protein, IL-1, and IL-6: A meta-analysis. Psychosom. Med. 2009;71:171–186. doi: 10.1097/PSY.0b013e3181907c1b. - DOI - PubMed

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