Foods Glycemic Index (GI) Affects the Important Inflammatory Biomarkers with Considerations: A Systematic Review

doi:10.21203/rs.3.rs-1558724/v1

PDF

Research Article

Foods Glycemic Index (GI) Affects the Important Inflammatory Biomarkers with Considerations: A Systematic Review

https://doi.org/10.21203/rs.3.rs-1558724/v1

This work is licensed under a CC BY 4.0 License

Version 1

posted 02 May, 2022

You are reading this latest preprint version

Introduction: The glycemic index (GI) and inflammations both were introduced as essential factors affecting the diseases, but the relation between GI and inflammation is still unclear. In this systematic review, the authors hypothesized GI has effects on inflammatory biomarkers but can be highly disturbed by statical unrecognized confounders.

Method: A comprehensive search was made in Science Direct, PubMed, Cochrane, UpToDate, and Google Scholar from 2010 to March 2021 using MESH and un-MESH keywords. Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) was used for the review of articles.

Result: From seven hundred and ninety-one articles, a total of 13 studies including one master thesis enrolled in this review, six studies were conducted on people with diabetes, cardiovascular diseases (CVD), and polycystic ovary syndrome (PCOS). Six studies were on healthy or obese people without any illnesses and one study was on pregnant women. IL-6 was in 8 studies, TNF-a was in 5 studies, TNF was in 2 studies, CRP was in 6 studies, and hs-CRP was in 2 studies. Seven studies including all well-designed studies confirmed GI can affect inflammation while 5 rejected the association. Several unconsidered confounders and limitations had been found in previous studies.

Conclusion: There is some strong evidence that supports a slight effect of GI on inflammatory biomarkers. However, bias risk in different studies according to diet patterns and the impact of various food components on GI remains. In this review, the authors provide some essential considerations for further studies.

Glycemic Index

Inflammation

Inflammatory biomarkers

CRP

IL-6

Inflammation is a protective biological response through the immunological system, tissues, and organs to different damaging situations, including pathogens, cell damage, and surgery [1-3]. As a whole, inflammation is a driving factor of many diseases [1, 2]. There are many different tools to assess the severity of inflammation. However, the essential factors are inflammatory blood biomarkers [1, 2, 4].

During recent studies, it is well established that nutritional intake and diet can significantly impact the pro-inflammatory and severity of chronic diseases [3, 5-8]. In the previous studies, a significant relationship between carbohydrate and sugar consumption, the insulin level, and the risk of inflammation and chronic diseases founded [9-11].

Glycemic index (GI), one of the most important factors to detect the quality of carbohydrates during the last four decades, was introduced as an efficient factor by Jenkins et al. [12] in the 1980s for the first time. In general, it is known as the degree and duration to which blood glucose is elevated following 12-hours of fasting in response to a specific carbohydrate consumption ratio to standard carbohydrate, which generally is glucose or white bread [12, 13]. It is scaled between 0 to 100 and separated into three categories: Low GI (<56), Medium GI 56-69, and High GI (<69) [12-14].

During the last years, many studies have shown the impact of GI on some chronic diseases, especially diabetes, cardiovascular diseases, and breast cancer [9, 10, 15-21]. Obesity is one of the other factors that elevate the risk of inflammation in individuals, and some studies also showed a significant effect of GI on weight management [22-25]. Also, a weak inflammatory effect of GI in a systematic and meta-analyses was reported [10]. Nevertheless, a meta-analysis in 2018, showed no significant relation between GI and inflammatory cytokines counting CRP, Leptin, IL-6, and TNF-a [26].

Despite the same finding that shows the pro-inflammatory effect of the GL [9, 10, 26], the effect of GI on inflammation is still unclear. In another word, scientists still do not know whether the quality of carbohydrates can lead to inflammation or only the quantity plays a role. Additionally, by considering the effect of carbohydrate quantity and weight on the inflammation that was established several times before [3, 5, 6, 27] and its importance in the calculation of GL [13], the authors believe GL cannot be an excellent factor to assess the quality of carbohydrates independently from the weight of carbohydrate consumption [13]. This is while GI is entirely independent of the carbohydrate’s weight [12-14].

According to the unclear overall effect of GI on inflammation as well as the great range of differences in the studies; this systematic review aims to evaluate the impact of the Glycemic Index on inflammatory biomarkers, especially IL-6, IL-1, TNF-a, TNF, CRP, and HS-CRP, independently from GL to understand the association of carbohydrates quality with inflammation, presenting biases that need to be considered, and offer some recommendations for further studies. The authors hypothesis suggested GI effect inflammatory biomarkers but several confounders in previous studies were not considered that required to be addressed.

Search strategy: For this study, Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA) were used as the guideline. Three independent researchers (MRSh, PZSh, AV) investigated through scientific databases including, Science Direct, PubMed, Cochrane, and UpToDate from 2010 to March 2021 (Table.1). The search timeline of the study was limited based on two factors: 1—the change that was made within the GI table in 2008 [28] and 2—A comprehensive discussion by Galland et al. [9] followed by Milajerdi et al. [26] study in 2010. Also, a comprehensive search was made in Google Scholar from 2010 to July 2021, and all articles in this database were considered in this study.

Search keywords: Search keywords of this study were MESH (Medical Subject Heading) and un-MESH keywords, including ("Glycemic index" OR "Glycemic indices" OR "Glycemic index number" OR "Glycaemic index" OR "Glycaemic indices" OR "GI") AND ("inflammation" OR "inflammatory biomarkers" OR "IL" or "TNF" OR "inflammation biomarkers" OR "inflammation markers" OR "inflammatory markers" OR "inflammatory indices" OR "Interleukin-10" OR "Interleukin" OR "Interleukin-8" OR "Interleukin-6" OR "Inflammation mediator" OR "Tumor necrosis factor" OR "C- reactive protein" OR "Transforming growth factor" OR "Cytokine" OR "Systematic Inflammation") AND ("RCT" OR "clinical trial" OR "Cohort" OR "cross-sectional" OR "cross-sectional" OR "original" OR "case-control" or "case" OR "control" OR "case-control" (table 1). Moreover, the related and systematic reviews were reviewed to ensure no study would be missed. As a judge of findings, a secondary search was made with a pretty simple search: "glycemic index" and "inflammatory biomarkers" by a fourth researcher (MR), and the findings were compared with the previous search method's conclusions. All the founded papers in each database were merged and duplicated articles were removed. Finally, documents of all databases are merged into one file.

Inclusion criteria: All human studies (paper and theses), including clinical trials, case-control, cohort, and cross-sectional studies included. All the studies that considered the effect of GI, Low GI, and High GI on inflammatory biomarkers or inflammation published during the last ten years were considered.

Exclusion criteria: All duplicated studies were excluded. Reviews, systematic reviews, meta-analyses, editorial letters, and short communications were excluded. Other exclusion criteria of the study were 1. studies conducted in children or animal studies because of biological and physiological differences. 2. Not considering GI as a separate factor from GL. 3. Not to report inflammatory biomarkers in value. 4. Any other intervention besides dietary pattern intervention includes medical, physical activity, and exercise or supplementary interventions. And, 5. Studies in languages that authors were not able to read. The main reason for excluding GL was the effect of carbohydrate intake on inflammation as a possible confounder of GI. All in all, only studies that directly evaluate GI on inflammatory biomarkers were enrolled for review.

Study selection: During the study selection process, researchers reviewed all papers separated, and the final findings were merged. From 892 articles, 381 articles were duplicated and removed. Two researchers (SJ and AV) read each article's title and general information for indicating animal studies, children's studies, and review articles. Meta-analyses, Reviews, letters, systematic reviews, animal studies, and studies conducted on children were removed. Abstract of 244 papers thoroughly reviewed by reviewers (MRSh, PZSh, and FK). Two hundred and three articles met the exclusion criteria, and 41 articles were eligible for full-body review, which was reviewed by three reviewers (PZSh, MR, and MRSh). The final number of relevant articles suitable for this systematic review was thirteen. In all the review processes, two-judge (FK and RR) was presented. Reviewing process was repeated one more time, and there was no significant difference between the process. For full detail of this process is reported in figure 1.

From the total of 13 studies [27, 29-40] including one MSc. full theses [39] that enrolled in this review; six studies [29-31, 33, 38, 40] were conducted on people with diabetes mellitus, cardiovascular diseases (CVD), and polycystic ovary syndrome (PCOS). Six studies [27, 32, 35-37, 39] investigated within healthy or obese people without any diseases and one study [34] was at pregnant women, which were reviewed. Nine of the studies [27, 31, 33-40] assessed GI, and 3 Studies [27, 29, 30, 38] assessed both GI and GL. IL-6 was in 8 studies [27, 29, 30, 32-34, 37, 39], TNF-a was in 5 studies [27, 31-34], TNF was in 2 studies [29, 39], CRP was in 6 studies [27, 35-39] and HS-CRP was in 2 studies [30, 40]. The full detailed description of findings can be reached in the table 2.

From studies that addressed the relevance of GI to inflammatory biomarkers; a total of 7 Studies [29, 30, 32, 33, 36, 39, 40] with overall and mean sample sizes of 933 and 133 respectively, found a significant relationship between GI with at least one of the inflammatory biomarkers. There were also 5 Studies [31, 34, 35, 37, 38] with an overall sample size of 1409 and a mean sample size of 281 that did not find any relation between GI and inflammation. Nevertheless, one study [27] did not perform any statistical analyses for the GI and biomarkers. The effect of dietary patterns on the inflammatory effect of GI, the importance of study design, and the sensitivity of GI are some considerations derived out from studies. However, the evidence supporting the slight effect of GI on inflammation was more than the evidence that rejected this effect.

The reviewed studies confirmed the hypothesis of the authors. The findings of the reviewed studies showed GI can have a slight effect on inflammation. However, the complication of GI and the lack of sufficient studies with the same findings prevent us from providing a firm answer to this question. In this review, as any study had its own considerations, the authors provided a possible link between GI and inflammation as well as described the main limitations that are better to be considered during GI studies.

In 2010, findings from a multicenter diet intervention reported no significant differences between groups for CRP before and after adjustment in this study [35]. However, more investigations within the study showed two completely different effects of GI on CRP, one positive and one negative, with two different diet patterns. The findings of this study made this hypothesis that diet patterns, especially fat values, can affect the effect of GI [35].

The impact of diet patterns on GI and inflammation was repeated several times in other studies. According to the reports of a cohort study, diet patterns with higher GI scores had a slightly higher reported level of TNF-a and CRP than lower GI groups [27]. Another finding that could drive out from this study was that GI might significantly change in different diet patterns. In this study, diet patterns with sweets and desserts group had a lower GI than refined grains and breakfast cereal group which were believed to have a higher GI [27]. This can be a significant limitation for GI and GL studies. According to the current study, considering the populations' diet pattern and the consumption of unhealthy foods with higher inflammatory index and lower GI as a confounder is recommended.

However, the main limitation of GI and inflammatory studies can be related to their small sample size along with short follow-up. The majority of studies fell in this category [31, 38]. Nevertheless, all three studies that had a well-controlled low biased risk protocol showed a significant direct relation between GI and inflammation despite a small sample size [33, 36, 39]. In all of these studies, all the participants followed a close diet pattern during the assessment that showed the priority of confounders over the sample size [33, 36, 39]. However, another study shown providing linear graphs for these small sample-sized studies can provide good information [32].

In another Study with a considerable population, a 137-item Food Frequency Questionnaire (FFQ) was used to determine the dietary intake and GI [29]. In this study, which was based on the Brand-Miller GI table [28], a significant relation was found between IL-6 (P-ANOVA = 0.050) and TNF (P-ANOVA = 0.046) with GI at the baseline [29]. However, after the one-year intervention, no significant differences between GI with both IL-6 and TNF resulted [29]. The main reason for this difference can be explained by the method of this study which used low inflammatory diet patterns in the groups [41–43]. In this study, two possible anti-inflammatory patterns were compared to each other that could impact the finding.

However one of the most surprising findings was in the Bahado-Singh et al. study [40]. This study has shown a 38.24% decrease in HS-CRP level in the low-intermediate GI group in comparison with a 15.18% decrease in the low-intermediate GI group [40]. Despite the decrease in both groups, the decrease in the low-intermediate GI group was significantly lower than in the high GI group (p < 0.05), but there was no description of the reason for the anti-inflammatory effect of both high and low-intermediate GI diets in this study. However, despite both groups having the same diet during the assessment, this decrease can be affected by other anti-inflammatory components of both diets. Nevertheless, low GI had a higher anti-inflammatory impact.

Despite supporting data on the effect of GI on different diseases [7, 9, 10, 15–21, 44, 45], findings on inflammatory biomarkers are vastly ranged. A meta-analyzed study shows a significant difference between low and high GI groups in CRP for both models in obese people with and without diabetes [46]. A meta-analysis study by Milajerdi et al. rejected any inflammatory effect for GI that supported the Buyken et.al study [26, 47]. This is while another study showed GI is associated with oxidative stress [48].

Nevertheless, the most important finding regarding this relation was reported in Yeon-soo et al. study in 2018 [49]. In this study, an association had been found between GI and Dietary inflammatory Index (DII), which was developed by Dr. Shivapa and Dr. Hebert [50–53] to determine the dietary inflammatory potentials. This study and the effect of GI on CRP, which was reported by Schwingshackl et al. [46], suggests a reconsideration of the effect of GI on inflammation which was reported by Milajerdi et al. [26] recently.

Overall, the main weakness of GI is related to its nature which increases the bias risk (Fig. 2). Food processing, sugar-containing, other nutrients, food PH, speed of eating, blood glucose level, and insulin level are some factors that can affect the GI response of the body [12–14, 54–56]. The other critical weakness of GI is related to its pattern in food classification [12–14]. In this pattern, some pro-inflammatory foods like pizza (GI = 39), fructose (GI = 15), chocolate (GI = 40), ice cream (GI = 51), Soft drink/soda (GI = 59), potato crisps (GI = 56) have been classified as low-moderate GI foods while some fruits like pineapple (GI = 59), mango (51), watermelon (GI = 76) have higher GI [12–14]. Considering these issues, it may be possible that an unhealthy diet pattern has a lower GI than a healthy one; but research is needed to confirm this hypothesis.

Finally, by considering limitations, running a well-designed GI study has several complications that must be addressed first. Of all food components, it seems lipids have the most cofounding bias but still require more investigation. Continued follow-ups as a controlled clinical trial can be helpful too. In addition, a study to understand the association of diet patterns with GI is recommended. To understand the effect of GI on inflammation, using more homogenized populations as well as removing the effect of differences in diet patterns that can make biases has extra benefits. However, all in all, a dietary pattern high in fruit, vegetables, fish, poultry and legumes, whole grains, and low in red and processed meat, sweetened beverages, sweets, refined grains, and fried potatoes has been linked to a lower level of inflammatory biomarkers [3, 5, 6, 27].

The strength of this study is related to the point of view of the reviewers. In all steps, at least two researchers with two different opinions made the review of studies which provides a new point of view and hypotheses for further studies. Nevertheless, the main weaknesses of this study were related to the nature of GI and the lack of sufficient studies. The other limitation of this review is its close time to previous systematic studies, which is uncommon. The other limitation was the lack of any statistical analysis. Nevertheless, the authors understood current findings in GI are not suitable and homogenized for this purpose. As the effect of dietary patterns in the reviewed studies is unclear, any analysis can lead to a wrong but maybe statically specific answer on this subject.

Unfortunately, despite research in this field, the findings of studies are not homogenized and unexpected confounders that can affect the result of studies are too many. There is some strong evidence that supports a slight effect of GI on inflammatory biomarkers. Based on the evidence, the dietary lipid quality can significantly affect GI's relation to inflammation. However, for deciding on the link between GI and inflammation, first more research with a homogenized population with near the same diet pattern, and second continuous monitoring follow-up studies are suggested. Concerning the previous meta-analysis on this subject, the finding may have diet-related biases that statically are not recognized.

Interleukins-1: IL-1

Interleukins-6: IL-6

Interleukins-10: IL-10

Tumor Necrosis Factor: TNF

Tumor Necrosis Factor-α: TNF-α

C-Reactive Protein: CRP

High Sensitive C-Reactive Protein: HS-CRP

Glycemic Index: GI

Glycemic Load: GL

Food Frequency Questionnaire: FFQ

Preferred Reporting Items for Systematic Review and Meta-analysis: PRISMA

Ethics approval and consent to participate: not applicable.

Consent for publication: not applicable

Availability of data and materials: Data is available upon reasonable request.

Competing interests: Authors of this paper declare no conflict of interest.

Funding: This study received no fund

Authors' contributions: All authors participate in the search and reviewing of the papers as described within the method. MRSH, SJ, and AV drafted the paper, RR, and FK made the final revision, and RR accepts the responsibilities of the corresponding authorship. MRSH made to submission.

Acknowledgements: We thank all those who encouraged us to write this systematic review and review the manuscript. We also want to acknowledge the Varastegan Institute for Medical Sciences and Mashhad University of Medical Sciences for their support.

Hotamisligil GS: Inflammation, metaflammation and immunometabolic disorders. Nature 2017, 542(7640):177–185.
Netea MG, Balkwill F, Chonchol M, Cominelli F, Donath MY, Giamarellos-Bourboulis EJ, Golenbock D, Gresnigt MS, Heneka MT, Hoffman HM et al: A guiding map for inflammation. Nat Immunol 2017, 18(8):826–831.
Ricordi C, Garcia-Contreras M, Farnetti S: Diet and Inflammation: Possible Effects on Immunity, Chronic Diseases, and Life Span. Journal of the American College of Nutrition 2015, 34 Suppl 1(sup1):10–13.
Olson TP, Dengel DR, Leon AS, Schmitz KH: Changes in inflammatory biomarkers following one-year of moderate resistance training in overweight women. International journal of obesity (2005) 2007, 31(6):996–1003.
Sears B, Ricordi C: Anti-inflammatory nutrition as a pharmacological approach to treat obesity. Journal of Obesity 2011, 2011.
Sears B, Ricordi C: Role of fatty acids and polyphenols in inflammatory gene transcription and their impact on obesity, metabolic syndrome and diabetes. Eur Rev Med Pharmacol Sci 2012, 16(9):1137–1154.
Jenkins DJ, Dehghan M, Mente A, Bangdiwala SI, Rangarajan S, Srichaikul K, Mohan V, Avezum A, Díaz R, Rosengren A: Glycemic index, glycemic load, and cardiovascular disease and mortality. New England Journal of Medicine 2021, 384(14):1312–1322.
Bujtor M, Turner AI, Torres SJ, Esteban-Gonzalo L, Pariante CM, Borsini A: Associations of dietary intake on biological markers of inflammation in children and adolescents: a systematic review. Nutrients 2021, 13(2):356.
Galland L: Diet and inflammation. Nutrition in Clinical Practice 2010, 25(6):634–640.
Schlesinger S, Chan DS, Vingeliene S, Vieira AR, Abar L, Polemiti E, Stevens CA, Greenwood DC, Aune D, Norat T: Carbohydrates, glycemic index, glycemic load, and breast cancer risk: a systematic review and dose–response meta-analysis of prospective studies. Nutrition reviews 2017, 75(6):420–441.
Davis NJ, Crandall JP, Gajavelli S, Berman JW, Tomuta N, Wylie-Rosett J, Katz SD: Differential effects of low-carbohydrate and low-fat diets on inflammation and endothelial function in diabetes. J Diabetes Complications 2011, 25(6):371–376.
Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV: Glycemic index of foods: a physiological basis for carbohydrate exchange. The American journal of clinical nutrition 1981, 34(3):362–366.
Augustin LS, Kendall CW, Jenkins DJ, Willett WC, Astrup A, Barclay AW, Björck I, Brand-Miller JC, Brighenti F, Buyken AE: Glycemic index, glycemic load and glycemic response: an International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC). Nutrition, Metabolism and cardiovascular diseases 2015, 25(9):795–815.
Foster-Powell K, Holt SH, Brand-Miller JC: International table of glycemic index and glycemic load values: 2002. The American journal of clinical nutrition 2002, 76(1):5–56.
Pi-Sunyer FX: Glycemic index and disease. The American journal of clinical nutrition 2002, 76(1):290S-298S.
Willett W, Manson J, Liu S: Glycemic index, glycemic load, and risk of type 2 diabetes. The American journal of clinical nutrition 2002, 76(1):274S-280S.
Livesey G, Taylor R, Livesey HF, Buyken AE, Jenkins DJA, Augustin LSA, Sievenpiper JL, Barclay AW, Liu S, Wolever TMS et al: Dietary Glycemic Index and Load and the Risk of Type 2 Diabetes: A Systematic Review and Updated Meta-Analyses of Prospective Cohort Studies. Nutrients 2019, 11(6):1280.
Vega-López S, Venn BJ, Slavin JL: Relevance of the glycemic index and glycemic load for body weight, diabetes, and cardiovascular disease. Nutrients 2018, 10(10):1361.
Zazpe I, Santiago S, Gea A, Ruiz-Canela M, Carlos S, Bes-Rastrollo M, Martínez-González M: Association between a dietary carbohydrate index and cardiovascular disease in the SUN (Seguimiento Universidad de Navarra) Project. Nutrition, Metabolism and Cardiovascular Diseases 2016, 26(11):1048–1056.
Evans CE, Greenwood DC, Threapleton DE, Gale CP, Cleghorn CL, Burley VJ: Glycemic index, glycemic load, and blood pressure: a systematic review and meta-analysis of randomized controlled trials. The American journal of clinical nutrition 2017, 105(5):1176–1190.
Gao R, Duff W, Chizen D, Zello GA, Chilibeck PD: The Effect of a Low Glycemic Index Pulse-Based Diet on Insulin Sensitivity, Insulin Resistance, Bone Resorption and Cardiovascular Risk Factors during Bed Rest. Nutrients 2019, 11(9):2012.
Brand-Miller JC, Holt SH, Pawlak DB, McMillan J: Glycemic index and obesity. The American journal of clinical nutrition 2002, 76(1):281S-285S.
Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunesova M, Pihlsgard M et al: Diets with high or low protein content and glycemic index for weight-loss maintenance. N Engl J Med 2010, 363(22):2102–2113.
Lennerz B, Lennerz JK: Food Addiction, High-Glycemic-Index Carbohydrates, and Obesity. Clin Chem 2018, 64(1):64–71.
Petrella E, Tamborrino V, Di Cerbo L, Neri I, Facchinetti F: An early, customized low-glycemic-index diet prevents adverse pregnancy outcomes in overweight/obese women. Minerva Ginecol 2018, 70(3):254–260.
Milajerdi A, Saneei P, Larijani B, Esmaillzadeh A: The effect of dietary glycemic index and glycemic load on inflammatory biomarkers: a systematic review and meta-analysis of randomized clinical trials. The American journal of clinical nutrition 2018, 107(4):593–606.
Anderson AL, Harris TB, Tylavsky FA, Perry SE, Houston DK, Lee JS, Kanaya AM, Sahyoun NR: Dietary patterns, insulin sensitivity and inflammation in older adults. European journal of clinical nutrition 2012, 66(1):18–24.
Atkinson FS, Foster-Powell K, Brand-Miller JC: International tables of glycemic index and glycemic load values: 2008. Diabetes care 2008, 31(12):2281–2283.
Bulló M, Casas R, Portillo M, Basora J, Estruch R, García-Arellano A, Lasa A, Juanola-Falgarona M, Arós F, Salas-Salvadó J: Dietary glycemic index/load and peripheral adipokines and inflammatory markers in elderly subjects at high cardiovascular risk. Nutrition, Metabolism and Cardiovascular Diseases 2013, 23(5):443–450.
Argiana V, Kanellos P, Makrilakis K, Eleftheriadou I, Tsitsinakis G, Kokkinos A, Perrea D, Tentolouris N: The effect of consumption of low-glycemic-index and low-glycemic-load desserts on anthropometric parameters and inflammatory markers in patients with type 2 diabetes mellitus. European journal of nutrition 2015, 54(7):1173–1180.
Szczuko M, Zapalowska-Chwyc M, Drozd A, Maciejewska D, Starczewski A, Wysokinski P, Stachowska E: Changes in the IGF-1 and TNF-alpha synthesis pathways before and after three-month reduction diet with low glicemic index in women with PCOS. Ginekologia polska 2018, 89(6):295–303.
Priebe MG, Wang H, Weening D, Schepers M, Preston T, Vonk RJ: Factors related to colonic fermentation of nondigestible carbohydrates of a previous evening meal increase tissue glucose uptake and moderate glucose-associated inflammation. The American journal of clinical nutrition 2010, 91(1):90–97.
Campbell MD, Walker M, Trenell MI, Stevenson EJ, Turner D, Bracken RM, Shaw JA, West DJ: A low–glycemic index meal and bedtime snack prevents postprandial hyperglycemia and associated rises in inflammatory markers, providing protection from early but not late nocturnal hypoglycemia following evening exercise in type 1 diabetes. Diabetes care 2014, 37(7):1845–1853.
Walsh JM, Mahony RM, Culliton M, Foley ME, McAuliffe FM: Impact of a low glycemic index diet in pregnancy on markers of maternal and fetal metabolism and inflammation. Reproductive sciences (Thousand Oaks, Calif) 2014, 21(11):1378–1381.
AB RSGJSALJAGBAFGSMCSCMDBLJWCMST: Effect of changing the amount and type of fat and carbohydrate on insulin sensitivity and cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge, and Kings) trial. The American journal of clinical nutrition 2010, 92(4):748–758.
Ebbeling CB, Swain JF, Feldman HA, Wong WW, Hachey DL, Garcia-Lago E, Ludwig DS: Effects of dietary composition on energy expenditure during weight-loss maintenance. JAMA 2012, 307(24):2627–2634.
Juanola-Falgarona M, Salas-Salvado J, Ibarrola-Jurado N, Rabassa-Soler A, Diaz-Lopez A, Guasch-Ferre M, Hernandez-Alonso P, Balanza R, Bullo M: Effect of the glycemic index of the diet on weight loss, modulation of satiety, inflammation, and other metabolic risk factors: a randomized controlled trial. The American journal of clinical nutrition 2014, 100(1):27–35.
Marsh KA, Steinbeck KS, Atkinson FS, Petocz P, Brand-Miller JC: Effect of a low glycemic index compared with a conventional healthy diet on polycystic ovary syndrome. The American journal of clinical nutrition 2010, 92(1):83–92.
Inflammation, insulin, and glucose differences between high and low glycemic index diets following downhill running in overweight and obese women. Montana State University-Bozeman, College of Education, Health & Human …
Bahado-Singh PS, Riley CK, Wheatley AO, Boyne MS, Morrison EY, Asemota HN: High Fiber Caribbean Diets with Low-Intermediate GI Improve Glycemic Control, Cardiovascular and Inflammatory Indicators in Overweight Persons with Type 2 Diabetes: A Randomized Control Study. Current Research in Nutrition and Food Science 2015, 3(1):36.
Sears B: Anti-inflammatory Diets. Journal of the American College of Nutrition 2015, 34 Suppl 1(sup1):14–21.
Ricker MA, Haas WC: Anti-Inflammatory Diet in Clinical Practice: A Review. Nutrition in clinical practice: official publication of the American Society for Parenteral and Enteral Nutrition 2017, 32(3):318–325.
Tolkien K, Bradburn S, Murgatroyd C: An anti-inflammatory diet as a potential intervention for depressive disorders: A systematic review and meta-analysis. Clinical Nutrition 2019, 38(5):2045–2052.
Tracy RP: Emerging relationships of inflammation, cardiovascular disease and chronic diseases of aging. Int J Obes Relat Metab Disord 2003, 27 Suppl 3(3):S29-34.
Chiavaroli L, Lee D, Ahmed A, Cheung A, Khan T, Mejia SB, Mirrahimi A, Jenkins D, Livesey G, Wolever T: Low Glycemic Index/Load Dietary Patterns and Glycemia and Cardiometabolic Risk Factors in Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Current Developments in Nutrition 2021, 5(Supplement_2):1018–1018.
Schwingshackl L, Hoffmann G: Long-term effects of low glycemic index/load vs. high glycemic index/load diets on parameters of obesity and obesity-associated risks: a systematic review and meta-analysis. Nutrition, metabolism, and cardiovascular diseases: NMCD 2013, 23(8):699–706.
Buyken AE, Goletzke J, Joslowski G, Felbick A, Cheng G, Herder C, Brand-Miller JC: Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies. The American journal of clinical nutrition 2014, 99(4):813–833.
Papachristoforou E, Lambadiari V, Maratou E, Makrilakis K: Association of glycemic indices (hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress and diabetic complications. Journal of diabetes research 2020, 2020.
Kim Y, Chen J, Wirth MD, Shivappa N, Hebert JR: Lower dietary inflammatory index scores are associated with lower glycemic index scores among college students. Nutrients 2018, 10(2):182.
Shivappa N, Steck SE, Hurley TG, Hussey JR, Hebert JR: Designing and developing a literature-derived, population-based dietary inflammatory index. Public Health Nutr 2014, 17(8):1689–1696.
Shivappa N, Hébert JR, Rietzschel ER, De Buyzere ML, Langlois M, Debruyne E, Marcos A, Huybrechts I: Associations between dietary inflammatory index and inflammatory markers in the Asklepios Study. British Journal of Nutrition 2015, 113(4):665–671.
Wirth M, Burch J, Shivappa N, Violanti JM, Burchfiel CM, Fekedulegn D, Andrew ME, Hartley TA, Miller DB, Mnatsakanova A: Association of a dietary inflammatory index with inflammatory indices and the metabolic syndrome among police officers. Journal of occupational and environmental medicine/American College of Occupational and Environmental Medicine 2014, 56(9):986.
van Woudenbergh GJ, Theofylaktopoulou D, Kuijsten A, Ferreira I, van Greevenbroek MM, van der Kallen CJ, Schalkwijk CG, Stehouwer CD, Ocke MC, Nijpels G et al: Adapted dietary inflammatory index and its association with a summary score for low-grade inflammation and markers of glucose metabolism: the Cohort study on Diabetes and Atherosclerosis Maastricht (CODAM) and the Hoorn study. The American journal of clinical nutrition 2013, 98(6):1533–1542.
Brand JC, Nicholson PL, Thorburn AW, Truswell AS: Food processing and the glycemic index. The American journal of clinical nutrition 1985, 42(6):1192–1196.
Jenkins DJ, Wolever TM, Jenkins AL: Starchy foods and glycemic index. Diabetes care 1988, 11(2):149–159.
Livesey G, Taylor R, Hulshof T, Howlett J: Glycemic response and health—a systematic review and meta-analysis: relations between dietary glycemic properties and health outcomes. The American journal of clinical nutrition 2008, 87(1):258S-268S.

Table 2 is available in the Supplementary Files section

TABLE 1. PICOS criteria for inclusion of studies in the systematic review

PICOS component	Description
Population	people of above 18 years, in any country
Intervention	With low GI or high GI diet pattern or report the GI score of diet (GL studies excluded)
Comparators	N/A
Outcomes	Reported any changes in IL-6, IL-1, TNF-a, TNF, CRP, and HS-CRP related to GI food consumption
Study design	Case-Control Studies, Intervention Studies, Cross-sectional studies, cohort studies
Language	English, Farsi

GI: Glycemic Index, GL: Glycemic Load, IL-6: Interleukin-6, IL-1: Interleukin-1, TNF-a: Tumor Necrosis Factor Alfa, TNF: Tumor Necrosis Factor, CRP: C-Reactive Protein, HS-CRP: High Sensitive C-Reactive Protein, N/A: Not applied

No competing interests reported.

TABLE2.docx

PDF

Version 1

posted 02 May, 2022

You are reading this latest preprint version

Foods Glycemic Index (GI) Affects the Important Inflammatory Biomarkers with Considerations: A Systematic Review

Status:

Version 1

Abstract

Figures

Introduction:

Methods:

Results:

Discussion:

Conclusion:

Abbreviations:

Declarations:

References:

Tables

Competing Interests

Supplementary Files

Status:

Version 1