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Shamshirgardi E, Kazemi A, A. Ferns G, Sohrabi Z, Akbarzadeh M. The Association of Dietary Glycemic Index with the Prevention and Treatment of COVID-19: A Narrative Review. JNFS 2023; 8 (3) :486-492
URL: http://jnfs.ssu.ac.ir/article-1-612-en.html
URL: http://jnfs.ssu.ac.ir/article-1-612-en.html
Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Iran
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1 Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Iran; 2 Division of Medical Education, Brighton and Sussex Medical School, Brighton, England, UK.
Introduction
.PNG)
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Elahe Shamshirgardi; MSc*1, Asma Kazemi; PhD1, Gordon A. Ferns; PhD2, Zahra Sohrabi; PhD1 &
Marzieh Akbarzadeh; PhD*1
Marzieh Akbarzadeh; PhD*1
1 Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Iran; 2 Division of Medical Education, Brighton and Sussex Medical School, Brighton, England, UK.
| ARTICLE INFO | ABSTRACT | |
| REVIEW ARTICLE | In 2019, a new coronavirus causing a flu-like syndrome was discovered in Chinese province of Hubei and there was a subsequent outbreak in Wuhan in December 2019. The severity and mortality of COVID-19 are affected by several preexisting comorbidities such as type 2 diabetes mellitus (T2DM). A more severe complication of COVID-19 in patients with diabetes could be due to the fact that hyperglycemia and insulin resistance, as important features of diabetes mellitus, are associated with a higher expression rate of angiotensin-converting enzyme-2 (ACE-2). ACE-2 can act as the entry site for SARS-CoV-2 to lung cells. Furthermore, in diabetes mellitus, increased inflammatory responses and impaired immune function are often present. Glycemic index (GI) and glycemic load (GL) are the characteristics of the diet that can affect glycemic control and insulin resistance. These two characteristics could possibly affect infections through their effect on gut microbiota composition, free radical synthesis, and mitochondrial loading. Therefore, it can be proposed that dietary GI and GL might be important factors in the development of COVID-19. Keywords: COVID-19; Glycemic index; Glycemic load; Insulin resistance; Hyperglycemia |
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| Article history: Received: 5 Apr 2022 Revised: 12 Jun 2022 Accepted: 18 Jun 2022 |
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| *Corresponding author: m_akbarzadeh@sums.ac.ir Nutrition Research Center, School of Nutrition and Food Sciences, Shiraz University of Medical Sciences, Iran. Postal code: 7153675500 Tel: +98 917 3059840 |
Introduction
I
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n 2019, a new coronavirus causing a flu-like syndrome was discovered in Wuhan, China, in December 2019. Owing to its pulmonary symptoms, the virus was called “severe acute respiratory syndrome associated with coronavirus 2” (SARS-CoV-2) and which was the cause of COVID-19. The clinical symptoms of COVID-19 include fever, dry cough, muscle pain, and breath shortening, and in a few patients it could develop into acute respiratory distress syndrome (ARDS) and numerous organ failures (Liu et al., 2020). Severity and mortality rate of COVID-19 is affected by several preexisting factors such as old age, obesity, type 2 diabetes mellitus (T2DM), hypertension (HTN), dyslipidemia, and cardiovascular disease (CVD) (Rajpal et al., 2020). Diabetes is reported as frequent comorbidity in patients infected with COVID-19 (Orioli et al., 2020). Comparing patients with COVID-19 admitted to ICU and non-ICU wards, patients in the ICU are two times more likely to be diabetic than those in non-ICU wards (Shahwan et al., 2020). The mortality rate in diabetic COVID-19 patients was also reported to be three times higher than that of non-diabetic patients (Shahwan et al., 2020). Diabetes has been shown to be a risk factor for severe and critical types of influenza pneumonia (Zou et al., 2020), and coronavirus pneumonia in severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) epidemics (Hussain et al., 2020). More intense presentation of the illness in diabetic COVID-19 patients might be associated with hyperglycemia and the condition of insulin resistance in these patients. Hyperglycemia and insulin resistance are accompanied by enhanced production of glycosylation end products (GEP), pro-inflammatory cytokines, and the synthesis of inflammatory adhesive molecules in tissues. This inflammatory condition and cytokine storm can lead to more severe complications of COVID-19 in diabetic patients (Hussain et al., 2020). In COVID-19 patients, counter-regulatory hormones like cortisol, glucagon, and epinephrine are highly released and along with the cytokine storm, these could possibly lead to hyperglycemia in previously healthy or prediabetic patients (Orioli et al., 2020).
The potential role of nutrition in hyperglycemia, controlling diabetes as well as reducing the complications of COVID-19 disease is evident (Fernández-Quintela et al., 2020, Mirabelli et al., 2020, Zabetakis et al., 2020). Dietary glycemic index (GI) and glycemic load (GL), which are effective indicators in determining the quantitative and qualitative effect of dietary carbohydrates on postprandial blood sugar (Brouwer-Brolsma et al., 2019), are considered as two dietary factors affecting insulin resistance and serum blood sugar levels (Shahrdami et al., 2020). Studies have shown that high GI and GL diets can lead to reduced pulmonary function, poor consequences of chronic obstructive pulmonary disease, respiratory infection, as well as greater risk of mortality due to the respiratory diseases (Huang et al., 2021).
Hyperglycemia and COVID-19
Previous studies have reported the effects of hyperglycemia on worsening the complications in other critical coronavirus infections such as SARS and MERS (Liu et al., 2020). Similarly, in COVID-19, hyperglycemia is recognized as a significant risk factor for mortality in critically ill patients (Zabetakis et al., 2020). Therefore, glycemic control could possibly affect severe symptoms and complications of the disease and is a usual concern in COVID-19 patients (Hussain et al., 2020). Glycemic control might be also representative of reduced insulin resistance, which in turn has a key role in COVID-19 control (Rajpal et al., 2020). Several mechanisms can be suggested for the role of hyperglycemia in increasing the risk and severity of COVID-19. This association might be in part related to the angiotensin-converting enzyme-2 (ACE-2), which is a cell surface protein expressed in pulmonary epithelial and lung alveolar cells and also many other cells in the body. The SARS-CoV-2 virus binds to ACE2 using spike-like protein on its surface and the complex is internalized leading to the intracellular reproduction of the virus. Therefore, ACE2 serves as SARS-CoV-2 receptor and is the main site to get the virus into the body (Rajpal et al., 2020). The expression of ACE-2 was reported to be up-regulated in diabetic patients, and in response to hyperglycemia (Rajpal et al., 2020). Prolonged uncontrolled hyperglycemia played a role in the pathogenesis through linking SARS‐CoV‐2 to ACE-2 (Brufsky, 2020). ACE2 is also expressed in insulin producing β-cells and it was reported that in COVID-19, as the virus enters the cells, β-cells are predisposed to cell impairment and apoptosis which could lead to relative insulin inadequacy and urgent hyperglycemic condition (Rajpal et al., 2020). Moreover, the inflammatory responses are crucially involved in clinical manifestations of COVID-19 (Zabetakis et al., 2020). Hyperglycemia enhances the expression of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) as well as monocyte chemoattractant protein-1 (MCP-1) in mononuclear cells. On the other hand, high blood glucose has pro-inflammatory effects, but insulin secretion is an anti-inflammatory condition (Sun et al., 2014). Studies have also shown that insulin therapy in diabetic and even non-diabetic patients with COVID-19 hospitalized in the ICU, reduces the mortality rate (Orioli et al., 2020). Immune responses are also highly related to glycemic control. Hyperglycemia could affect the cellular immune reaction, causing the susceptibility to infection and infection-associated mortality (Liu et al., 2020). Activation of protein kinase C following hyperglycemia could restrain neutrophil migration, phagocytosis, superoxide formation, and microbial killing. In addition, it inhibits the function of neutrophils and apoptosis by inducing the expression of Toll receptors (Jafar et al., 2016). High concentrations of glucose reduce the production of neutrophil extracellular traps and reduce vascular expansion and enhance permeability in the course of primary inflammatory responses, maybe by the activation of protein kinase C (Jafar et al., 2016). Also, T2DM patients might have changes in their innate immune system which increase pro-inflammatory cytokines besides having an impaired host immune system in contact with viral infections through impeding IFN-1 formation and signaling (Rajpal et al., 2020). Inadequately controlled diabetes is related to impaired lymphocyte, monocyte, macrophage, and neutrophil roles and causes unusual deferment type hypersensitivity response and complement activation impairment (Hussain et al., 2020). Furthermore, hyperglycemia in COVID-19 patients can increase lung infection by reducing mucus clearance (Rajpal et al., 2020).
Insulin resistance and COVID-19
In addition to hyperglycemia, insulin resistance can also be one of the causes of more serious complications in diabetic COVID-19 patients. In postprandial state, insulin is secreted into the bloodstream from pancreatic beta cells in response to the rise in blood glucose. Binding of insulin to cell surface receptors increases cellular glucose uptake and thus decrease blood sugar. In diabetes, lack of insulin action leads to hyperglycemia and long-term damage to various tissues and organs (Berbudi et al., 2020). Insulin resistance is defined as an incomplete response of tissues to a certain amount of insulin. To compensate for this defect and for maintaining normal circulating glucose levels, insulin levels increase and hyperinsulinemia occurs (Bonakdaran and Barazandeh Ahmadabadi, 2014). Insulin resistance is common in T2DM and obese patients who are reported to be at greater risk for critical manifestations of COVID-19 (Bonakdaran and Barazandeh Ahmadabadi, 2014, Rajpal et al., 2020). The association between insulin resistance and COVID-19 can be explained through several mechanisms. Increased expression of ACE-2 protein was reported in insulin resistance and thus the entry of the virus into the body is facilitated (Finucane and Davenport, 2020). Moreover, hyperinsulinemia drives the production of mitochondrial reactive oxygen species (mtROS) and diminishes cellular anti-oxidative countermeasures, which could be associated with the severity of infection (Cooper et al., 2020). Insulin resistance also promotes the increased synthesis of pro-inflammatory cytokines including IL6, IL-8 and TNF-α. Furthermore, C-reactive protein (CRP), the inflammatory marker and a reactant of non-Exclusive acute phase, is usually increased in human insulin resistant state (De Luca and Olefsky, 2008). In general, insulin resistance and systemic inflammation cause oxidative stress and inflammatory reaction in the pulmonary system. It can also decrease respiratory muscle intensity leading to abnormal lung function (Rajpal et al., 2020). It should be noted that insulin resistance in obese people can be one of the causes of chronic inflammation and more severe complications of COVID-19 disease in these people (Rajpal et al., 2020).
GI and GL of the foods and COVID-19
Hyperinsulinemia and insulin resistance are highly associated with dietary composition (Mirabelli et al., 2020). Among the characteristics of diet that can affect the control of insulin resistance are GI and GL of the diet (Shahrdami et al., 2020). GI and GL of the food/diet are indicators that are used to determine the quantitative and qualitative effect of dietary carbohydrates on postprandial blood sugar (Brouwer-Brolsma et al., 2019). GI is used to classify foods based on their effect on postprandial blood glucose. Besides, GL considers the number of carbohydrates ingested and is obtained by multiplying the amount of carbohydrates available in food and the GI (Shahrdami et al., 2020). Dietary fiber and carbohydrates are associated with immune system function (Fernández-Quintela et al., 2020). In a study on adolescent football athletes, low GI diets were associated with higher increase in total leukocytes, compared to high GL diets (Setyarsih et al., 2021). No previous study discussed the association between GI/GL of the diets and COVID-19 infection, but in the dietary recommendations released for the nutritional treatment of COVID-19, it was suggested to consider low GI carbohydrates in the patients’ diets. This recommendation might be pertinent to the association between dietary GI and GL with insulin function and glycemic control (Brugliera et al., 2020, Fernández-Quintela et al., 2020). Besides, high GI foods have been proved to increase the mitochondrial load and free radical synthesis (Fernández-Quintela et al., 2020). In addition, the consumption of these foods has been associated with inflammatory responses via increasing circulating amounts of pro-inflammatory cytokines like CRP, TNF-alpha, and IL-6 (Fernández-Quintela et al., 2020). In COVID-19 infection, inflammation is a factor that complicates the patient’s status. Dietary GI and GL are related to serum concentrations of inflammatory biomarkers (Milajerdi et al., 2018, Rajpal et al., 2020) such as CRP, TNF-α, and IL-6 (Fernández-Quintela et al., 2020). According to a meta-analysis, Milajerdi et al. demonstrated that serum high-sensitivity C-reactive protein (hs-CRP) consistency reduced after consuming low GI and GL diets compared to high GI and GL diets (Milajerdi et al., 2018). Another mechanism that could be explained for the effect of high GI/GL carbohydrate on COVID-19 infection is related to gut microbiota. Based on recent studies, diet is so effective in forming the community of the gut microbiota, thereby influencing the host health status (Durganaudu et al., 2020). Consumption of whole grains, as a low GI food (Nagaraju et al., 2020), and complex non-digestible carbohydrates existing in whole grains can considerably alter the large bowel microbial community and is considered to have valuable impacts on the host. Some whole grains can elevate the Firmicutes: Bacteroidetes ratio. In addition, consuming whole-grain barley increases genera Roseburia, Bifidobacterium, and Dialister, and the species of Eubacterium rectale, Roseburia faecis, and Roseburia intestinalis (Keim and Martin, 2014).
Previous studies have reported the effects of hyperglycemia on worsening the complications in other critical coronavirus infections such as SARS and MERS (Liu et al., 2020). Similarly, in COVID-19, hyperglycemia is recognized as a significant risk factor for mortality in critically ill patients (Zabetakis et al., 2020). Therefore, glycemic control could possibly affect severe symptoms and complications of the disease and is a usual concern in COVID-19 patients (Hussain et al., 2020). Glycemic control might be also representative of reduced insulin resistance, which in turn has a key role in COVID-19 control (Rajpal et al., 2020). Several mechanisms can be suggested for the role of hyperglycemia in increasing the risk and severity of COVID-19. This association might be in part related to the angiotensin-converting enzyme-2 (ACE-2), which is a cell surface protein expressed in pulmonary epithelial and lung alveolar cells and also many other cells in the body. The SARS-CoV-2 virus binds to ACE2 using spike-like protein on its surface and the complex is internalized leading to the intracellular reproduction of the virus. Therefore, ACE2 serves as SARS-CoV-2 receptor and is the main site to get the virus into the body (Rajpal et al., 2020). The expression of ACE-2 was reported to be up-regulated in diabetic patients, and in response to hyperglycemia (Rajpal et al., 2020). Prolonged uncontrolled hyperglycemia played a role in the pathogenesis through linking SARS‐CoV‐2 to ACE-2 (Brufsky, 2020). ACE2 is also expressed in insulin producing β-cells and it was reported that in COVID-19, as the virus enters the cells, β-cells are predisposed to cell impairment and apoptosis which could lead to relative insulin inadequacy and urgent hyperglycemic condition (Rajpal et al., 2020). Moreover, the inflammatory responses are crucially involved in clinical manifestations of COVID-19 (Zabetakis et al., 2020). Hyperglycemia enhances the expression of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) as well as monocyte chemoattractant protein-1 (MCP-1) in mononuclear cells. On the other hand, high blood glucose has pro-inflammatory effects, but insulin secretion is an anti-inflammatory condition (Sun et al., 2014). Studies have also shown that insulin therapy in diabetic and even non-diabetic patients with COVID-19 hospitalized in the ICU, reduces the mortality rate (Orioli et al., 2020). Immune responses are also highly related to glycemic control. Hyperglycemia could affect the cellular immune reaction, causing the susceptibility to infection and infection-associated mortality (Liu et al., 2020). Activation of protein kinase C following hyperglycemia could restrain neutrophil migration, phagocytosis, superoxide formation, and microbial killing. In addition, it inhibits the function of neutrophils and apoptosis by inducing the expression of Toll receptors (Jafar et al., 2016). High concentrations of glucose reduce the production of neutrophil extracellular traps and reduce vascular expansion and enhance permeability in the course of primary inflammatory responses, maybe by the activation of protein kinase C (Jafar et al., 2016). Also, T2DM patients might have changes in their innate immune system which increase pro-inflammatory cytokines besides having an impaired host immune system in contact with viral infections through impeding IFN-1 formation and signaling (Rajpal et al., 2020). Inadequately controlled diabetes is related to impaired lymphocyte, monocyte, macrophage, and neutrophil roles and causes unusual deferment type hypersensitivity response and complement activation impairment (Hussain et al., 2020). Furthermore, hyperglycemia in COVID-19 patients can increase lung infection by reducing mucus clearance (Rajpal et al., 2020).
Insulin resistance and COVID-19
In addition to hyperglycemia, insulin resistance can also be one of the causes of more serious complications in diabetic COVID-19 patients. In postprandial state, insulin is secreted into the bloodstream from pancreatic beta cells in response to the rise in blood glucose. Binding of insulin to cell surface receptors increases cellular glucose uptake and thus decrease blood sugar. In diabetes, lack of insulin action leads to hyperglycemia and long-term damage to various tissues and organs (Berbudi et al., 2020). Insulin resistance is defined as an incomplete response of tissues to a certain amount of insulin. To compensate for this defect and for maintaining normal circulating glucose levels, insulin levels increase and hyperinsulinemia occurs (Bonakdaran and Barazandeh Ahmadabadi, 2014). Insulin resistance is common in T2DM and obese patients who are reported to be at greater risk for critical manifestations of COVID-19 (Bonakdaran and Barazandeh Ahmadabadi, 2014, Rajpal et al., 2020). The association between insulin resistance and COVID-19 can be explained through several mechanisms. Increased expression of ACE-2 protein was reported in insulin resistance and thus the entry of the virus into the body is facilitated (Finucane and Davenport, 2020). Moreover, hyperinsulinemia drives the production of mitochondrial reactive oxygen species (mtROS) and diminishes cellular anti-oxidative countermeasures, which could be associated with the severity of infection (Cooper et al., 2020). Insulin resistance also promotes the increased synthesis of pro-inflammatory cytokines including IL6, IL-8 and TNF-α. Furthermore, C-reactive protein (CRP), the inflammatory marker and a reactant of non-Exclusive acute phase, is usually increased in human insulin resistant state (De Luca and Olefsky, 2008). In general, insulin resistance and systemic inflammation cause oxidative stress and inflammatory reaction in the pulmonary system. It can also decrease respiratory muscle intensity leading to abnormal lung function (Rajpal et al., 2020). It should be noted that insulin resistance in obese people can be one of the causes of chronic inflammation and more severe complications of COVID-19 disease in these people (Rajpal et al., 2020).
GI and GL of the foods and COVID-19
Hyperinsulinemia and insulin resistance are highly associated with dietary composition (Mirabelli et al., 2020). Among the characteristics of diet that can affect the control of insulin resistance are GI and GL of the diet (Shahrdami et al., 2020). GI and GL of the food/diet are indicators that are used to determine the quantitative and qualitative effect of dietary carbohydrates on postprandial blood sugar (Brouwer-Brolsma et al., 2019). GI is used to classify foods based on their effect on postprandial blood glucose. Besides, GL considers the number of carbohydrates ingested and is obtained by multiplying the amount of carbohydrates available in food and the GI (Shahrdami et al., 2020). Dietary fiber and carbohydrates are associated with immune system function (Fernández-Quintela et al., 2020). In a study on adolescent football athletes, low GI diets were associated with higher increase in total leukocytes, compared to high GL diets (Setyarsih et al., 2021). No previous study discussed the association between GI/GL of the diets and COVID-19 infection, but in the dietary recommendations released for the nutritional treatment of COVID-19, it was suggested to consider low GI carbohydrates in the patients’ diets. This recommendation might be pertinent to the association between dietary GI and GL with insulin function and glycemic control (Brugliera et al., 2020, Fernández-Quintela et al., 2020). Besides, high GI foods have been proved to increase the mitochondrial load and free radical synthesis (Fernández-Quintela et al., 2020). In addition, the consumption of these foods has been associated with inflammatory responses via increasing circulating amounts of pro-inflammatory cytokines like CRP, TNF-alpha, and IL-6 (Fernández-Quintela et al., 2020). In COVID-19 infection, inflammation is a factor that complicates the patient’s status. Dietary GI and GL are related to serum concentrations of inflammatory biomarkers (Milajerdi et al., 2018, Rajpal et al., 2020) such as CRP, TNF-α, and IL-6 (Fernández-Quintela et al., 2020). According to a meta-analysis, Milajerdi et al. demonstrated that serum high-sensitivity C-reactive protein (hs-CRP) consistency reduced after consuming low GI and GL diets compared to high GI and GL diets (Milajerdi et al., 2018). Another mechanism that could be explained for the effect of high GI/GL carbohydrate on COVID-19 infection is related to gut microbiota. Based on recent studies, diet is so effective in forming the community of the gut microbiota, thereby influencing the host health status (Durganaudu et al., 2020). Consumption of whole grains, as a low GI food (Nagaraju et al., 2020), and complex non-digestible carbohydrates existing in whole grains can considerably alter the large bowel microbial community and is considered to have valuable impacts on the host. Some whole grains can elevate the Firmicutes: Bacteroidetes ratio. In addition, consuming whole-grain barley increases genera Roseburia, Bifidobacterium, and Dialister, and the species of Eubacterium rectale, Roseburia faecis, and Roseburia intestinalis (Keim and Martin, 2014).
Specific carbohydrates found in cereals could enhance colonic butyrate generation. Butyrate is a short-chain fatty acid with positive effects on maintaining the integrity of colonocytes and increasing the generation and release of glucagon-like peptide 1, which can improve insulin sensitivity and glucose homeostasis and decrease food intake by releasing satiety-related intestinal peptides (Keim and Martin, 2014). Resistant starch, as a part of low GI food (Afandi et al., 2021), alters the microbial ecology and enhances Lactobacillus, Bifidobacterium, and Akkermansia. This rearrangement in microbiota could reduce the release of inflammatory productions from the intestine to the bloodstream. The grain mixture produced in a study (containing whole-grain barley, brown rice, and the combination of these grains) could reduce peak postprandial glucose and plasma IL-6. These changes were related to the conversion in the markers of immunologic operation and improvements in blood glucose control (Keim and Martin, 2014). Exploration of a potential association between dietary GI and changes in the proportion of certain gut microbiota is relatively a new research area (Durganaudu et al., 2020). On the other hand, changes in the gastrointestinal microbiome are associated with lung health and respiratory infections (Dhar and Mohanty, 2020). Finally, low GI/GL carbohydrates also decrease the hazard of COVID-19 infection and severity indirectly by decreasing the risk of certain diseases such as CVD and diabetes, which enhance the risk and complications of COVID-19 disease (Augustin et al., 2002, Rajpal et al., 2020). The mechanisms of the association between high GI diet and COVID-19 are summarized in Figure 1.
Conclusion
Hyperglycemia and insulin resistance are important factors affecting immune system, inflammation, and infections. It is asserted that most critical dietary determinants of insulin function are dietary GI and GL. Dietary GI and GL might affect infections through their impacts on the composition of gut microbiota, free radical synthesis, and mitochondrial loading. Therefore, it is proposed that dietary GI and GL could be possibly important factors in the prevention and control of COVID-19 patients, especially in people with diabetes.
Authors’ contributions
Shamshirgardi E, Kazemi A and Akbarzadeh M conceptualized the study. Shamshirgardi E, Kazemi A, Sohrabi Z, Akbarzadeh M prepared the manuscript draft. Feren GA critically revised the manuscript. Shamshirgardi E and Akbarzadeh M have primary responsibility for content; and all authors read and approved the final manuscript.
Conflict of interest
On behalf of all authors, the corresponding author states that there is no conflict of interest.
References
Afandi FA, Wijaya CH, Faridah DN, Suyatma NE & Jayanegara A 2021. Evaluation of various starchy foods: A systematic review and meta-analysis on chemical properties affecting the glycemic index values based on in vitro and in vivo experiments. Foods. 10 (2): 364.
Augustin L, Franceschi S, Jenkins D, Kendall C & La Vecchia C 2002. Glycemic index in chronic disease: a review. European journal of clinical nutrition. 56 (11): 1049-1071.
Berbudi A, Rahmadika N, Tjahjadi AI & Ruslami R 2020. Type 2 diabetes and its impact on the immune system. Current diabetes reviews. 16 (5): 442.
Bonakdaran S & Barazandeh Ahmadabadi F 2014. Assessment of insulin resistance in idiopathic hirsutism in comparison with Polycystic Ovary Syndrome (PCOS) patients and healthy individuals. Medical journal of mashhad university of medical sciences. 56 (6): 340-346.
Brouwer-Brolsma EM, et al. 2019. The Glycaemic Index-Food-Frequency Questionnaire: Development and validation of a food frequency questionnaire designed to estimate the dietary intake of glycaemic index and glycaemic load: An effort by the PREVIEW Consortium. Nutrients. 11 (1): 13.
Brufsky A 2020. Hyperglycemia, hydroxychloroquine, and the COVID‐19 pandemic. Journal of medical virology. 92 (7): 770-775.
Brugliera L, et al. 2020. Nutritional management of COVID-19 patients in a rehabilitation unit. European journal of clinical nutrition. 74 (6): 860--863.
Cooper ID, et al. 2020. Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management. Open heart. 7 (2): e001356.
De Luca C & Olefsky JM 2008. Inflammation and insulin resistance. FEBS letters. 582 (1): 97-105.
Dhar D & Mohanty A 2020. Gut microbiota and Covid-19-possible link and implications. Virus research. 285: 198018.
Durganaudu H, Kunasegaran T & Ramadas A 2020. Dietary glycaemic index and type 2 diabetes mellitus: Potential modulation of gut microbiota. Progress in microbes & molecular biology. 3 (1).
Fernández-Quintela A, et al. 2020. Key aspects in nutritional management of COVID-19 patients. Journal of clinical medicine. 9 (8): 2589.
Finucane FM & Davenport C 2020. Coronavirus and Obesity: Could Insulin Resistance Mediate the Severity of Covid-19 Infection? Frontiers in public health. 8: 174.
Huang H-L, et al. 2021. Dietary glycemic index, glycemic load and mortality: Japan Public Health Center-based prospective study. European journal of nutrition. 60 (8): 4607-4620.
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Keim NL & Martin RJ 2014. Dietary whole grain–microbiota interactions: insights into mechanisms for human health. Advances in nutrition. 5 (5): 556-557.
Liu L, et al. 2020. Glycemic control before admission is an important determinant of prognosis in patients with coronavirus disease 2019. Journal of diabetes investigation. 12 (6): 1064-1073.
Milajerdi A, Saneei P, Larijani B & Esmaillzadeh A 2018. The effect of dietary glycemic index and glycemic load on inflammatory biomarkers: a systematic review and meta-analysis of randomized clinical trials. American journal of clinical nutrition. 107 (4): 593-606.
Mirabelli M, Russo D & Brunetti A 2020. The Role of Diet on Insulin Sensitivity. Multidisciplinary Digital Publishing Institute.
Nagaraju R, et al. 2020. Glycemic index and sensory evaluation of whole grain based multigrain indian breads (Rotis). Preventive nutrition and food science. 25 (2): 194.
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Shahrdami F, Alipour B, Roohelhami E & Rashidkhani B 2020. Association of dietary glycemic index and glycemic load with serum lipids level in women with polycystic ovary syndrome. Iranian journal of obstetrics, gynecology and infertility. 23 (4): 54-61.
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Hyperglycemia and insulin resistance are important factors affecting immune system, inflammation, and infections. It is asserted that most critical dietary determinants of insulin function are dietary GI and GL. Dietary GI and GL might affect infections through their impacts on the composition of gut microbiota, free radical synthesis, and mitochondrial loading. Therefore, it is proposed that dietary GI and GL could be possibly important factors in the prevention and control of COVID-19 patients, especially in people with diabetes.
Authors’ contributions
Shamshirgardi E, Kazemi A and Akbarzadeh M conceptualized the study. Shamshirgardi E, Kazemi A, Sohrabi Z, Akbarzadeh M prepared the manuscript draft. Feren GA critically revised the manuscript. Shamshirgardi E and Akbarzadeh M have primary responsibility for content; and all authors read and approved the final manuscript.
Conflict of interest
On behalf of all authors, the corresponding author states that there is no conflict of interest.
References
Afandi FA, Wijaya CH, Faridah DN, Suyatma NE & Jayanegara A 2021. Evaluation of various starchy foods: A systematic review and meta-analysis on chemical properties affecting the glycemic index values based on in vitro and in vivo experiments. Foods. 10 (2): 364.
Augustin L, Franceschi S, Jenkins D, Kendall C & La Vecchia C 2002. Glycemic index in chronic disease: a review. European journal of clinical nutrition. 56 (11): 1049-1071.
Berbudi A, Rahmadika N, Tjahjadi AI & Ruslami R 2020. Type 2 diabetes and its impact on the immune system. Current diabetes reviews. 16 (5): 442.
Bonakdaran S & Barazandeh Ahmadabadi F 2014. Assessment of insulin resistance in idiopathic hirsutism in comparison with Polycystic Ovary Syndrome (PCOS) patients and healthy individuals. Medical journal of mashhad university of medical sciences. 56 (6): 340-346.
Brouwer-Brolsma EM, et al. 2019. The Glycaemic Index-Food-Frequency Questionnaire: Development and validation of a food frequency questionnaire designed to estimate the dietary intake of glycaemic index and glycaemic load: An effort by the PREVIEW Consortium. Nutrients. 11 (1): 13.
Brufsky A 2020. Hyperglycemia, hydroxychloroquine, and the COVID‐19 pandemic. Journal of medical virology. 92 (7): 770-775.
Brugliera L, et al. 2020. Nutritional management of COVID-19 patients in a rehabilitation unit. European journal of clinical nutrition. 74 (6): 860--863.
Cooper ID, et al. 2020. Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management. Open heart. 7 (2): e001356.
De Luca C & Olefsky JM 2008. Inflammation and insulin resistance. FEBS letters. 582 (1): 97-105.
Dhar D & Mohanty A 2020. Gut microbiota and Covid-19-possible link and implications. Virus research. 285: 198018.
Durganaudu H, Kunasegaran T & Ramadas A 2020. Dietary glycaemic index and type 2 diabetes mellitus: Potential modulation of gut microbiota. Progress in microbes & molecular biology. 3 (1).
Fernández-Quintela A, et al. 2020. Key aspects in nutritional management of COVID-19 patients. Journal of clinical medicine. 9 (8): 2589.
Finucane FM & Davenport C 2020. Coronavirus and Obesity: Could Insulin Resistance Mediate the Severity of Covid-19 Infection? Frontiers in public health. 8: 174.
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Type of article: review article |
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Received: 2022/04/5 | Published: 2023/08/28 | ePublished: 2023/08/28
Received: 2022/04/5 | Published: 2023/08/28 | ePublished: 2023/08/28
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