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How do high glycemic load diets influence coronary heart disease?

Mathews MJ, Liebenberg L, Mathews EH - Nutr Metab (Lond) (2015)

Bottom Line: However, LDL is not the only or even the most important biomarker for CHD risk.From this an integrated CHD pathogenetic pathway system was constructed.A focus primarily on the low density lipoprotein cholesterol biomarker for CHD risk has led to the traditional guidelines of CHD dietary recommendations.

View Article: PubMed Central - PubMed

Affiliation: CRCED, North-West University, and consultants to TEMM International (Pty) Ltd, P.O. Box 11207, Silver Lakes, 0054 South Africa.

ABSTRACT

Background: Diet has a significant relationship with the risk of coronary heart disease (CHD). Traditionally the effect of diet on CHD was measured with the biomarker for low-density lipoprotein (LDL) cholesterol. However, LDL is not the only or even the most important biomarker for CHD risk. A suitably integrated view of the mechanism by which diet influences the detailed CHD pathogenetic pathways is therefore needed in order to better understand CHD risk factors and help with better holistic CHD prevention and treatment decisions.

Methods: A systematic review of the existing literature was conducted. From this an integrated CHD pathogenetic pathway system was constructed. CHD biomarkers, which are found on these pathways, are the only measurable data to link diet with these CHD pathways. They were thus used to simplify the link between diet and the CHD mechanism. Data were systematically analysed from 294 cohort studies of CHD biomarkers constituting 1 187 350 patients.

Results and discussion: The resulting integrated analysis provides insight into the higher-order interactions underlying CHD and high-glycemic load (HGL) diets. A novel "connection graph" illustrates the measurable relationship between HGL diets and the relative risks attributed to the important CHD serological biomarkers. The "connection graph" vividly shows that HGL diets not only influence the lipid and metabolic biomarkers, but also the inflammation, coagulation and vascular function biomarkers in an important way.

Conclusion: A focus primarily on the low density lipoprotein cholesterol biomarker for CHD risk has led to the traditional guidelines of CHD dietary recommendations. This has however inadvertently led to HGL diets. The influence of HGL diets on the other CHD biomarkers is not always fully appreciated. Thus, new diets or other interventions which address the full integrated CHD impact, as shown in this paper, are required.

No MeSH data available.


Related in: MedlinePlus

Conceptual model of general lifestyle effects, salient CHD pathogenetic pathways and CHD hallmarks. The affective pathway of pharmacotherapeutics, blue boxes, is shown in Figure 1, and salient serological biomarkers are indicated by the  icon. The blunted blue arrows denote antagonise or inhibit and pointed blue arrows denote up-regulate or facilitate. HDL denotes high-density lipoprotein; LDL, low-density lipoprotein; oxLDL, oxidised LDL; FFA, free fatty acids; TMAO, an oxidation product of trimethylamine (TMA); NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; Hs, homocysteine; IGF-1, insulin-like growth factor-1; TNF-α , tumour necrosis factor-α; IL, interleukin; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; SSRI, serotonin reuptake inhibitors; ROS, reactive oxygen species; NFκβ, nuclear factor-κβ; SMC, smooth muscle cell; HbA1c, glycosylated haemoglobin A1c; P. gingivalis, Porphyromonas gingivalis; vWF, von Willebrand factor; PDGF, platelet-derived growth factor; MIF, macrophage migration inhibitory factor; SCD-40, recombinant human sCD40 ligand; MPO, myeloperoxidase; MMP, matrix metalloproteinase; VCAM, vascular cell adhesion molecule; ICAM, intracellular adhesion molecule; CRP, C-reactive protein; PAI, plasminogen activator inhibitor; TF, tissue factor, MCP, monocyte chemoattractant protein; BDNF, brain-derived neurotrophic factor; PI3K, phosphatidylinositol 3-kinase; MAPK, mitogen-activated protein (MAP) kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; OPG, osteoprotegerin; GCF, gingival crevicular fluid; D-dimer, fibrin degradation product D; BNP, B-type natriuretic peptide; ACE, angiotensin-converting-enzyme; COX, cyclooxygenase; β-blocker, beta-adrenergic antagonists.
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Fig1: Conceptual model of general lifestyle effects, salient CHD pathogenetic pathways and CHD hallmarks. The affective pathway of pharmacotherapeutics, blue boxes, is shown in Figure 1, and salient serological biomarkers are indicated by the icon. The blunted blue arrows denote antagonise or inhibit and pointed blue arrows denote up-regulate or facilitate. HDL denotes high-density lipoprotein; LDL, low-density lipoprotein; oxLDL, oxidised LDL; FFA, free fatty acids; TMAO, an oxidation product of trimethylamine (TMA); NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; Hs, homocysteine; IGF-1, insulin-like growth factor-1; TNF-α , tumour necrosis factor-α; IL, interleukin; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; SSRI, serotonin reuptake inhibitors; ROS, reactive oxygen species; NFκβ, nuclear factor-κβ; SMC, smooth muscle cell; HbA1c, glycosylated haemoglobin A1c; P. gingivalis, Porphyromonas gingivalis; vWF, von Willebrand factor; PDGF, platelet-derived growth factor; MIF, macrophage migration inhibitory factor; SCD-40, recombinant human sCD40 ligand; MPO, myeloperoxidase; MMP, matrix metalloproteinase; VCAM, vascular cell adhesion molecule; ICAM, intracellular adhesion molecule; CRP, C-reactive protein; PAI, plasminogen activator inhibitor; TF, tissue factor, MCP, monocyte chemoattractant protein; BDNF, brain-derived neurotrophic factor; PI3K, phosphatidylinositol 3-kinase; MAPK, mitogen-activated protein (MAP) kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; OPG, osteoprotegerin; GCF, gingival crevicular fluid; D-dimer, fibrin degradation product D; BNP, B-type natriuretic peptide; ACE, angiotensin-converting-enzyme; COX, cyclooxygenase; β-blocker, beta-adrenergic antagonists.

Mentions: The integrated model in Figure 1, which we developed, schematically illustrates the complexity of CHD. (A more detailed discussion of Figure 1 is given in Section “Pathogenetic effects of high glycemic load diets”). It is however important to realize that CHD involves inputs from hundreds of gene expressions and a number of tissues. Thus, analysing the individual components of the system would not be sufficient, as it is important to know how these components interact with each other [9]. For instance, genetic and lifestyle factors influence clinical traits by perturbing molecular networks [10]. A high-level systems-based view of CHD therefore has the potential to interrogate these molecular phenotypes and identify the patterns associated with the disease.Figure 1


How do high glycemic load diets influence coronary heart disease?

Mathews MJ, Liebenberg L, Mathews EH - Nutr Metab (Lond) (2015)

Conceptual model of general lifestyle effects, salient CHD pathogenetic pathways and CHD hallmarks. The affective pathway of pharmacotherapeutics, blue boxes, is shown in Figure 1, and salient serological biomarkers are indicated by the  icon. The blunted blue arrows denote antagonise or inhibit and pointed blue arrows denote up-regulate or facilitate. HDL denotes high-density lipoprotein; LDL, low-density lipoprotein; oxLDL, oxidised LDL; FFA, free fatty acids; TMAO, an oxidation product of trimethylamine (TMA); NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; Hs, homocysteine; IGF-1, insulin-like growth factor-1; TNF-α , tumour necrosis factor-α; IL, interleukin; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; SSRI, serotonin reuptake inhibitors; ROS, reactive oxygen species; NFκβ, nuclear factor-κβ; SMC, smooth muscle cell; HbA1c, glycosylated haemoglobin A1c; P. gingivalis, Porphyromonas gingivalis; vWF, von Willebrand factor; PDGF, platelet-derived growth factor; MIF, macrophage migration inhibitory factor; SCD-40, recombinant human sCD40 ligand; MPO, myeloperoxidase; MMP, matrix metalloproteinase; VCAM, vascular cell adhesion molecule; ICAM, intracellular adhesion molecule; CRP, C-reactive protein; PAI, plasminogen activator inhibitor; TF, tissue factor, MCP, monocyte chemoattractant protein; BDNF, brain-derived neurotrophic factor; PI3K, phosphatidylinositol 3-kinase; MAPK, mitogen-activated protein (MAP) kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; OPG, osteoprotegerin; GCF, gingival crevicular fluid; D-dimer, fibrin degradation product D; BNP, B-type natriuretic peptide; ACE, angiotensin-converting-enzyme; COX, cyclooxygenase; β-blocker, beta-adrenergic antagonists.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359552&req=5

Fig1: Conceptual model of general lifestyle effects, salient CHD pathogenetic pathways and CHD hallmarks. The affective pathway of pharmacotherapeutics, blue boxes, is shown in Figure 1, and salient serological biomarkers are indicated by the icon. The blunted blue arrows denote antagonise or inhibit and pointed blue arrows denote up-regulate or facilitate. HDL denotes high-density lipoprotein; LDL, low-density lipoprotein; oxLDL, oxidised LDL; FFA, free fatty acids; TMAO, an oxidation product of trimethylamine (TMA); NLRP3, Inflammasome responsible for activation of inflammatory processes as well as epithelial cell regeneration and microflora; Hs, homocysteine; IGF-1, insulin-like growth factor-1; TNF-α , tumour necrosis factor-α; IL, interleukin; NO, nitric oxide; NO-NSAIDs, combinational NO-non-steroidal anti-inflammatory drug; SSRI, serotonin reuptake inhibitors; ROS, reactive oxygen species; NFκβ, nuclear factor-κβ; SMC, smooth muscle cell; HbA1c, glycosylated haemoglobin A1c; P. gingivalis, Porphyromonas gingivalis; vWF, von Willebrand factor; PDGF, platelet-derived growth factor; MIF, macrophage migration inhibitory factor; SCD-40, recombinant human sCD40 ligand; MPO, myeloperoxidase; MMP, matrix metalloproteinase; VCAM, vascular cell adhesion molecule; ICAM, intracellular adhesion molecule; CRP, C-reactive protein; PAI, plasminogen activator inhibitor; TF, tissue factor, MCP, monocyte chemoattractant protein; BDNF, brain-derived neurotrophic factor; PI3K, phosphatidylinositol 3-kinase; MAPK, mitogen-activated protein (MAP) kinase; RANKL, receptor activator of nuclear factor kappa-beta ligand; OPG, osteoprotegerin; GCF, gingival crevicular fluid; D-dimer, fibrin degradation product D; BNP, B-type natriuretic peptide; ACE, angiotensin-converting-enzyme; COX, cyclooxygenase; β-blocker, beta-adrenergic antagonists.
Mentions: The integrated model in Figure 1, which we developed, schematically illustrates the complexity of CHD. (A more detailed discussion of Figure 1 is given in Section “Pathogenetic effects of high glycemic load diets”). It is however important to realize that CHD involves inputs from hundreds of gene expressions and a number of tissues. Thus, analysing the individual components of the system would not be sufficient, as it is important to know how these components interact with each other [9]. For instance, genetic and lifestyle factors influence clinical traits by perturbing molecular networks [10]. A high-level systems-based view of CHD therefore has the potential to interrogate these molecular phenotypes and identify the patterns associated with the disease.Figure 1

Bottom Line: However, LDL is not the only or even the most important biomarker for CHD risk.From this an integrated CHD pathogenetic pathway system was constructed.A focus primarily on the low density lipoprotein cholesterol biomarker for CHD risk has led to the traditional guidelines of CHD dietary recommendations.

View Article: PubMed Central - PubMed

Affiliation: CRCED, North-West University, and consultants to TEMM International (Pty) Ltd, P.O. Box 11207, Silver Lakes, 0054 South Africa.

ABSTRACT

Background: Diet has a significant relationship with the risk of coronary heart disease (CHD). Traditionally the effect of diet on CHD was measured with the biomarker for low-density lipoprotein (LDL) cholesterol. However, LDL is not the only or even the most important biomarker for CHD risk. A suitably integrated view of the mechanism by which diet influences the detailed CHD pathogenetic pathways is therefore needed in order to better understand CHD risk factors and help with better holistic CHD prevention and treatment decisions.

Methods: A systematic review of the existing literature was conducted. From this an integrated CHD pathogenetic pathway system was constructed. CHD biomarkers, which are found on these pathways, are the only measurable data to link diet with these CHD pathways. They were thus used to simplify the link between diet and the CHD mechanism. Data were systematically analysed from 294 cohort studies of CHD biomarkers constituting 1 187 350 patients.

Results and discussion: The resulting integrated analysis provides insight into the higher-order interactions underlying CHD and high-glycemic load (HGL) diets. A novel "connection graph" illustrates the measurable relationship between HGL diets and the relative risks attributed to the important CHD serological biomarkers. The "connection graph" vividly shows that HGL diets not only influence the lipid and metabolic biomarkers, but also the inflammation, coagulation and vascular function biomarkers in an important way.

Conclusion: A focus primarily on the low density lipoprotein cholesterol biomarker for CHD risk has led to the traditional guidelines of CHD dietary recommendations. This has however inadvertently led to HGL diets. The influence of HGL diets on the other CHD biomarkers is not always fully appreciated. Thus, new diets or other interventions which address the full integrated CHD impact, as shown in this paper, are required.

No MeSH data available.


Related in: MedlinePlus