The impact of statins on psychological wellbeing: a systematic review and meta-analysis

General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms SummaryThis review is intended to help clinicians, patients and the public make informed decisions about statin therapy for the prevention of heart attacks and strokes. It explains how the evidence that is available from randomized controlled trials yields reliable information about both the efficacy and safety of statin therapy. In addition, it discusses how claims that statins commonly cause adverse effects reflect a failure to recognise the limitations of other sources of evidence about the effects of treatment.Large-scale randomized trial evidence shows that statin therapy reduces the risk of heart attacks, ischaemic strokes and coronary revascularization procedures ("major vascular events") by about one quarter for each mmol/L reduction in low density lipoprotein (LDL) cholesterol during each year (after the first) that it continues to be taken. The absolute benefits of statin therapy depend on an individual's absolute risk of occlusive vascular events and the absolute reduction in LDL cholesterol that is achieved. For example, lowering LDL cholesterol by 2 mmol/L (77 mg/dL) with an effective low-cost statin regimen (e.g. atorvastatin 40 mg daily, costing about £2 per

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“…Nor was there evidence for an adverse effect of statin therapy in a meta-analysis of randomized trials that assessed psychological outcomes. 267 …”

Section: Quality Of Life Related Measuresmentioning

confidence: 99%

Interpretation of the evidence for the efficacy and safety of statin therapy

et al. 2016

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“…Lowered blood pressure in psychopathology may be a consequence of shared risk factors, such as levels of neuropeptide Y, which is associated with suppressed parasympathetic activity and stress, depression and anxiety 45. The reason for the positive association between symptom severity and HDL‐C is unclear, particularly since HDL‐C has anti‐inflammatory properties 46 and recent evidence suggests that use of cholesterol improving medication is associated with improved mental health 47. Nevertheless, the findings are consistent with previous research demonstrating that depressive symptoms and suicidality are associated with lowered total cholesterol and higher HDL‐C,48, 49 although heterogeneity between studies is high and the effect is not always observed 50, 51.…”

Section: Discussionmentioning

confidence: 99%

Bidirectional Prospective Associations of Metabolic Syndrome Components With Depression, Anxiety, and Antidepressant Use

et al. 2016

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BackgroundMetabolic syndrome components—waist circumference, high‐density lipoprotein cholesterol (HDL‐C), triglycerides, systolic blood pressure and fasting glucose—are cross‐sectionally associated with depression and anxiety with differing strength. Few studies examine the relationships over time or whether antidepressants have independent effects.MethodsParticipants were from the Netherlands Study of Depression and Anxiety (NESDA; N = 2,776; 18–65 years; 66% female). At baseline, 2‐ and 6‐year follow‐up, participants completed diagnostic interviews, depression and anxiety symptom inventories, antidepressant use assessment, and measurements of the five metabolic syndrome components. Data were analyzed for the consistency of associations between psychopathology indicators and metabolic syndrome components across the three assessment waves, and whether psychopathology or antidepressant use at one assessment predicts metabolic dysregulation at the next and vice versa.ResultsConsistently across waves, psychopathology was associated with generally poorer values of metabolic syndrome components, particularly waist circumference and triglycerides. Stronger associations were observed for psychopathology symptom severity than diagnosis. Antidepressant use was independently associated with higher waist circumference, triglycerides and number of metabolic syndrome abnormalities, and lower HDL‐C. Symptom severity and antidepressant use were associated with subsequently increased number of abnormalities, waist circumference, and glucose after 2 but not 4 years. Conversely, there was little evidence that metabolic syndrome components were associated with subsequent psychopathology outcomes.ConclusionsSymptom severity and antidepressant use were independently associated with metabolic dysregulation consistently over time and also had negative consequences for short‐term metabolic health. This is of concern given the chronicity of depression and anxiety and prevalence of antidepressant treatment.

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“…These drugs are thought to have a potential anti-depressive effect related to their anti-inflammatory properties [8,64]. A number of epidemiological studies show that statin use reduces depression risk [65,66], and the only randomized controlled trial to date suggests that lovastatin reduced symptoms of depression [67].…”

Section: Gaps and Required Improvements: New Treatmentsmentioning

confidence: 99%

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

et al. 2015

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Meta-analyses confirm that depression is accompanied by signs of inflammation including increased levels of acute phase proteins, e.g. C-reactive protein, and pro-inflammatory cytokines, e.g. interleukin-6. Supporting the translational significance of this, a meta-analysis showed that anti-inflammatory drugs may have antidepressant effects. Here we argue that inflammation and depression research needs to get onto a new track. Firstly, the choice of inflammatory biomarkers in depression research was often too selective and did not consider the broader pathways.Secondly, although mild inflammatory responses are present in depression, other immune-related pathways cannot be disregarded as new drug targets, e.g. activation of cell-mediated immunity, oxidative and nitrosative stress (O&NS) pathways, autoimmune responses, bacterial translocation, activation of the Toll-like Receptor and neuroprogressive pathways. Thirdly, antiinflammatory treatments are sometimes used without full understanding of their effects on the broader pathways underpinning depression. Since many of the activated immune-inflammatory pathways in depression actually confer protection against an overzealous inflammatory response, targeting these pathways may result in unpredictable and unwanted results. Furthermore, this paper discusses the required improvements in research strategy, i.e. path and drug discovery processes, omics-based techniques and systems biomedicine methodologies. Firstly, novel methods should be employed to examine the intracellular networks that control and modulate the immune, O&NS and neuroprogressive pathways using omics-based assays, including genomics, transcriptomics, proteomics, metabolomics, epigenomics and microbiomics. Secondly, systems biomedicine analyses are essential to unravel the complex interactions between these cellular 4 networks, pathways and the multifactorial trigger factors and to delineate new drug targets in the cellular networks or pathways. Drug discovery processes should delineate new drugs targeting the intracellular networks and immune-related pathways.

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The impact of statins on psychological wellbeing: a systematic review and meta-analysis

Cited by 72 publications

References 33 publications

Interpretation of the evidence for the efficacy and safety of statin therapy

Interpretation of the evidence for the efficacy and safety of statin therapy

Bidirectional Prospective Associations of Metabolic Syndrome Components With Depression, Anxiety, and Antidepressant Use

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

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