For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
53
views
116
references
 Top references
cited by
7
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      162
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The mechanism by which moderate alcohol consumption influences coronary heart disease

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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.

          Related collections

          Most cited references116

          • Record: found
          • Abstract: found
          • Article: not found

          Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators.

          Bruce McEwen (2008)
          Stress begins in the brain and affects the brain, as well as the rest of the body. Acute stress responses promote adaptation and survival via responses of neural, cardiovascular, autonomic, immune and metabolic systems. Chronic stress can promote and exacerbate pathophysiology through the same systems that are dysregulated. The burden of chronic stress and accompanying changes in personal behaviors (smoking, eating too much, drinking, poor quality sleep; otherwise referred to as "lifestyle") is called allostatic overload. Brain regions such as hippocampus, prefrontal cortex and amygdala respond to acute and chronic stress and show changes in morphology and chemistry that are largely reversible if the chronic stress lasts for weeks. However, it is not clear whether prolonged stress for many months or years may have irreversible effects on the brain. The adaptive plasticity of chronic stress involves many mediators, including glucocorticoids, excitatory amino acids, endogenous factors such as brain neurotrophic factor (BDNF), polysialated neural cell adhesion molecule (PSA-NCAM) and tissue plasminogen activator (tPA). The role of this stress-induced remodeling of neural circuitry is discussed in relation to psychiatric illnesses, as well as chronic stress and the concept of top-down regulation of cognitive, autonomic and neuroendocrine function. This concept leads to a different way of regarding more holistic manipulations, such as physical activity and social support as an important complement to pharmaceutical therapy in treatment of the common phenomenon of being "stressed out". Policies of government and the private sector play an important role in this top-down view of minimizing the burden of chronic stress and related lifestyle (i.e. allostatic overload).
          Article 0 comments Cited 382 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The metabolic consequences of sleep deprivation.

            Kristen Knutson, Karine Spiegel, Plamen Penev … (2007)
            The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.
            Article 0 comments Cited 334 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Molecular networks as sensors and drivers of common human diseases.

              Eric E. Schadt (2009)
              The molecular biology revolution led to an intense focus on the study of interactions between DNA, RNA and protein biosynthesis in order to develop a more comprehensive understanding of the cell. One consequence of this focus was a reduced attention to whole-system physiology, making it difficult to link molecular biology to clinical medicine. Equipped with the tools emerging from the genomics revolution, we are now in a position to link molecular states to physiological ones through the reverse engineering of molecular networks that sense DNA and environmental perturbations and, as a result, drive variations in physiological states associated with disease.
              Article 0 comments Cited 296 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Marc J Mathews: mjmathews@rems2.com
                Leon Liebenberg: lliebenberg@researchtoolbox.com
                Edward H Mathews: ehmathews@researchtoolbox.com
                Journal
                Journal ID (nlm-ta): Nutr J
                Journal ID (iso-abbrev): Nutr J
                Title: Nutrition Journal
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1475-2891
                Publication date (Electronic): 2 April 2015
                Publication date PMC-release: 2 April 2015
                Publication date Collection: 2015
                Volume: 14
                Electronic Location Identifier: 33
                Affiliations
                CRCED, North-West University, and Consultants to TEMM International (Pty) Ltd, P.O. Box 11207, Silver Lakes, 0054 South Africa
                Article
                Publisher ID: 11
                DOI: 10.1186/s12937-015-0011-6
                PMC ID: 4389579
                PubMed ID: 25889723
                SO-VID: cc5b2c83-5fce-403b-93e9-ad38dd17b774
                Copyright © © Mathews et al.; licensee BioMed Central. 2015
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 9 October 2014
                Date accepted : 13 February 2015
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2015

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: coronary heart disease,moderate alcohol consumption,biomarkers
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: coronary heart disease, moderate alcohol consumption, biomarkers

                Comments

                Comment on this article

                scite_

                Similar content162

                See all similar

                Cited by14

                See all cited by

                Most referenced authors3,511

                See all reference authors