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The mechanism by which moderate alcohol consumption influences coronary heart disease.

Mathews MJ, Liebenberg L, Mathews EH - Nutr J (2015)

Bottom Line: Moderate alcohol consumption is associated with a lower risk for coronary heart disease (CHD).The resulting integrated system now provides insight into the integrated higher-order interactions underlying CHD and moderate alcohol consumption.Thus, the possible reasons for the reduced RR for CHD with moderate alcohol consumption become clear at a glance.

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. mjmathews@rems2.com.

ABSTRACT

Background: Moderate alcohol consumption is associated with a lower risk for coronary heart disease (CHD). A suitably integrated view of the CHD pathogenesis pathway will help to elucidate how moderate alcohol consumption could reduce CHD risk.

Methods: A comprehensive literature review was conducted focusing on the pathogenesis of CHD. Biomarker data were further systematically analysed from 294 cohort studies, comprising 1 161 560 subjects. From the above a suitably integrated CHD pathogenetic system for the purpose of this study was developed.

Results: The resulting integrated system now provides insight into the integrated higher-order interactions underlying CHD and moderate alcohol consumption. A novel 'connection graph' further simplifies these interactions by illustrating the relationship between moderate alcohol consumption and the relative risks (RR) attributed to various measureable CHD serological biomarkers. Thus, the possible reasons for the reduced RR for CHD with moderate alcohol consumption become clear at a glance.

Conclusions: An integrated high-level model of CHD, its pathogenesis, biomarkers, and moderate alcohol consumption provides a summary of the evidence that a causal relationship between CHD risk and moderate alcohol consumption may exist. It also shows the importance of each CHD pathway that moderate alcohol consumption influences.

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Related in: MedlinePlus

Conceptual model of general lifestyle factors, salient CHD pathogenetic pathways and CHD hallmarks. From “How do high glycemic load diets influence coronary heart disease?” by Mathews MJ, Liebenberg L, Mathews EH. Nutr Metab. 2015:12:6 [14]. 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, glycated 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 factors, salient CHD pathogenetic pathways and CHD hallmarks. From “How do high glycemic load diets influence coronary heart disease?” by Mathews MJ, Liebenberg L, Mathews EH. Nutr Metab. 2015:12:6 [14]. 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, glycated 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: A suitably integrated CHD model of the pathogenesis and serological biomarkers of moderate alcohol consumption was not found in the literature. Such a model was thus developed and is presented in Figure 1, which schematically illustrates the complexity of CHD [14].Figure 1


The mechanism by which moderate alcohol consumption influences coronary heart disease.

Mathews MJ, Liebenberg L, Mathews EH - Nutr J (2015)

Conceptual model of general lifestyle factors, salient CHD pathogenetic pathways and CHD hallmarks. From “How do high glycemic load diets influence coronary heart disease?” by Mathews MJ, Liebenberg L, Mathews EH. Nutr Metab. 2015:12:6 [14]. 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, glycated 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=PMC4389579&req=5

Fig1: Conceptual model of general lifestyle factors, salient CHD pathogenetic pathways and CHD hallmarks. From “How do high glycemic load diets influence coronary heart disease?” by Mathews MJ, Liebenberg L, Mathews EH. Nutr Metab. 2015:12:6 [14]. 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, glycated 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: A suitably integrated CHD model of the pathogenesis and serological biomarkers of moderate alcohol consumption was not found in the literature. Such a model was thus developed and is presented in Figure 1, which schematically illustrates the complexity of CHD [14].Figure 1

Bottom Line: Moderate alcohol consumption is associated with a lower risk for coronary heart disease (CHD).The resulting integrated system now provides insight into the integrated higher-order interactions underlying CHD and moderate alcohol consumption.Thus, the possible reasons for the reduced RR for CHD with moderate alcohol consumption become clear at a glance.

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. mjmathews@rems2.com.

ABSTRACT

Background: Moderate alcohol consumption is associated with a lower risk for coronary heart disease (CHD). A suitably integrated view of the CHD pathogenesis pathway will help to elucidate how moderate alcohol consumption could reduce CHD risk.

Methods: A comprehensive literature review was conducted focusing on the pathogenesis of CHD. Biomarker data were further systematically analysed from 294 cohort studies, comprising 1 161 560 subjects. From the above a suitably integrated CHD pathogenetic system for the purpose of this study was developed.

Results: The resulting integrated system now provides insight into the integrated higher-order interactions underlying CHD and moderate alcohol consumption. A novel 'connection graph' further simplifies these interactions by illustrating the relationship between moderate alcohol consumption and the relative risks (RR) attributed to various measureable CHD serological biomarkers. Thus, the possible reasons for the reduced RR for CHD with moderate alcohol consumption become clear at a glance.

Conclusions: An integrated high-level model of CHD, its pathogenesis, biomarkers, and moderate alcohol consumption provides a summary of the evidence that a causal relationship between CHD risk and moderate alcohol consumption may exist. It also shows the importance of each CHD pathway that moderate alcohol consumption influences.

Show MeSH
Related in: MedlinePlus