Lipid trajectories as predictors of depressive symptoms: The Young Finns Study.

Elovainio, Marko; Pulkki-Råbäck, Laura; Kivimäki, Mika; Jokela, Markus; Viikari, Jorma; Raitakari, Olli T.; Telama, R.; Keltikangas‐Järvinen, Liisa

doi:10.1037/a0018875

Cited by 31 publications

(47 citation statements)

References 53 publications

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“…Antiinflammatory treatment that inhibits IL-6 also inhibits triglycerides [55]. Elevated IL-6 [9] and triglycerides [56] levels in childhood are associated with increased risk of depression in young adulthood. However, lowering of serum cholesterol in middle-aged subjects by diet, drugs, or both, leads to a decrease in CHD but an increase in deaths due to suicide or violence [57].…”

Section: Discussionmentioning

confidence: 99%

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

et al. 2019

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While comorbidity between coronary heart disease (CHD) and depression is evident, it is unclear whether the two diseases have shared underlying mechanisms. We performed a range of analyses in 367,703 unrelated middle-aged participants of European ancestry from UK Biobank, a population-based cohort study, to assess whether comorbidity is primarily due to genetic or environmental factors, and to test whether cardiovascular risk factors and CHD are likely to be causally related to depression using Mendelian randomization. We showed family history of heart disease was associated with a 20% increase in depression risk (95% confidence interval [CI] 16-24%, p < 0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of 1 standard deviation in the CHD genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0-3%; p = 0.11). Mendelian randomization analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal risk factors for depression. The odds ratio for depression per standard deviation increase in genetically-predicted triglycerides was 1.18 (95% CI 1.09-1.27; p = 2 × 10 −5); per unit increase in genetically-predicted log-transformed IL-6 was 1.35 (95% CI 1.12-1.62; p = 0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07-1.29; p = 0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. IL-6, CRP and triglycerides are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.

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Section: Discussionmentioning

confidence: 99%

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

et al. 2019

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“…Anti-inflammatory treatment that inhibits IL-6 also inhibits triglycerides 51 . Elevated IL-6 9 and triglycerides 52 levels in childhood are associated with increased risk of depression in young adulthood. However, lowering of serum cholesterol in middle-aged subjects by diet, drugs, or both, leads to a decrease in CHD but an increase in deaths due to suicide or violence 53 .…”

Section: Discussionmentioning

confidence: 99%

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

Khandaker

Zuber

Rees

et al. 2019

Preprint

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While comorbidity between coronary heart disease (CHD) and depression is evident, it is unclear whether the two diseases have shared underlying mechanisms. We performed a range of analyses in 367,703 unrelated middle-aged participants of European ancestry from UK Biobank, a population based cohort study, to assess whether comorbidity is primarily due to genetic or environmental factors, and to test whether cardiovascular risk factors and CHD are likely to be causally related to depression using Mendelian randomization. We showed family history of heart disease was associated with a 20% increase in depression risk (95% confidence interval [CI] 16% to 24%, p<0.0001), but a genetic risk score that is strongly associated with CHD risk was not associated with depression. An increase of one standard deviation in the CH D genetic risk score was associated with 71% higher CHD risk, but 1% higher depression risk (95% CI 0% to 3%; p=0.11). Mendelian randomization analyses suggested that triglycerides, interleukin-6 (IL-6), and C-reactive protein (CRP) are likely causal risk factors for depression. The odds ratio for depression per standard deviation increase in genetically-predicted triglycerides was 1.18 (95% CI 1.09 to 1.27; p=2×10-5); per unit increase in genetically-predicted log-transformed I L-6 was 0.74 (95% CI 0.62 to 0.89; p=0.0012); and per unit increase in genetically-predicted log-transformed CRP was 1.18 (95% CI 1.07 to 1.29; p=0.0009). Our analyses suggest that comorbidity between depression and CHD arises largely from shared environmental factors. I L-6, CRP and triglycerides, are likely to be causally linked with depression, so could be targets for treatment and prevention of depression.

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“…Some studies reported raised TG in depression(e.g. [42][43][44][45] ), but meta-analysis on the topic is lacking. Of note, a prospective study in Finnish young adults showed that steeply rising TG levels throughout childhood and adulthood was associated with increased DS in adulthood 43 , consistent with the present finding of a causal role of TG in the development of DS.…”

Section: Discussionmentioning

confidence: 99%

Causal relationships between blood lipids and depression phenotypes: A Mendelian randomization analysis

Cheng

Chau

2018

Preprint

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AbstractBackgroundThe etiology of depression remains poorly understood. Changes in blood lipid levels were reported to be associated with depression and suicide, however study findings were mixed.MethodsWe performed a two-sample Mendelian randomization (MR) analysis to investigate the causal relationship between blood lipids and depression phenotypes, based on large-scale GWAS summary statistics (N=188,577/480,359 for lipid/depression traits respectively). Five depression-related phenotypes were included, namely major depressive disorder (MDD; from PGC), depressive symptoms (DS; from SSGAC), longest duration and number of episodes of low mood, and history of deliberate self-harm (DSH)/suicide (from UK Biobank). MR was conducted with inverse-variance weighted (MR-IVW), Egger and Generalized Summary-data-based MR(GSMR) methods.ResultsThere was consistent evidence that triglyceride (TG) is causally associated with DS (MR-IVW beta for one-SD increase in TG=0.0346, 95% CI=0.0114-0.0578), supported by MR-IVW and GSMR and multiple r2 clumping thresholds. We also observed relatively consistent associations of TG with DSH/suicide (MR-Egger OR= 2.514, CI: 1.579-4.003). There was moderate evidence for positive associations of TG with MDD and the number of episodes of low mood. For HDL-c, we observed moderate evidence for causal associations with DS and MDD. LDL-c and TC did not show robust causal relationships with depression phenotypes, except for weak evidence that LDL-c is inversely related to DSH/suicide. We did not detect significant associations when depression phenotypes were treated as exposures.ConclusionsThis study provides evidence to a causal relationship between TG, and to a lesser extent, altered cholesterol levels with depression phenotypes. Further studies on its mechanistic basis and the effects of lipid-lowering therapies are warranted.

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Lipid trajectories as predictors of depressive symptoms: The Young Finns Study.

Cited by 31 publications

References 53 publications

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

Shared mechanisms between coronary heart disease and depression: findings from a large UK general population-based cohort

Causal relationships between blood lipids and depression phenotypes: A Mendelian randomization analysis

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