ライフサイエンスコーパス: LDL cholesterol

1 ting plasma glucose, air pollution, and high LDL cholesterol).

2 adjustment for other risk factors (including LDL cholesterol).

3 ll as examples of trans-mediators (TAGAP for LDL cholesterol).

4 esterol, and 1.86 (95% CI: 1.62 to 2.14) for LDL cholesterol.

5 consumption, although there was no change in LDL cholesterol.

6 and may provide a target to modulate plasma LDL cholesterol.

7 nd obese (BMI: 30-45) subjects with elevated LDL cholesterol.

8 nd cholesterol intakes to reduce circulating LDL cholesterol.

9 mpedoic acid, and gemcabene primarily target LDL cholesterol.

10 ds to a greater effect on HbA1c, weight, and LDL cholesterol.

11 trategy to help manage total cholesterol and LDL cholesterol.

12 17-mmol/L (95% CI: 0.11-, 0.23-mmol/L) lower LDL cholesterol.

13 PUFAs, particularly in individuals with high LDL cholesterol.

14 ight, body mass index (BMI; in kg/m(2)), and LDL cholesterol.

15 nts in HbA1c, 5 mm Hg in SBP, or 10 mg/dL in LDL cholesterol.

16 crose and fructose with starch yielded lower LDL cholesterol.

17 revascularisation) per 1 mmol/L reduction in LDL cholesterol.

18 utation in LDLR causing a large reduction in LDL cholesterol.

19 ials of inclisiran in patients with elevated LDL cholesterol.

20 rated fats, full-fat dairy products increase LDL cholesterol.

21 ealth Questionnaire-9 score, HbA1c, SBP, and LDL cholesterol.

22 L) receptors and increasing the clearance of LDL-cholesterol.

23 A) content to raise low-density lipoprotein (LDL) cholesterol.

24 , reduces levels of low-density lipoprotein (LDL) cholesterol.

25 elevated levels of low-density lipoprotein (LDL) cholesterol.

26 unds its effects on low-density lipoprotein (LDL) cholesterol.

27 for the lowering of low-density lipoprotein (LDL) cholesterol.

28 viation decrease in low-density lipoprotein [LDL] cholesterol 0.76, 95% confidence interval [CI] 0.65

29 icant between group reduction in small dense LDL-cholesterol (0.2 mmol/L, p = 0.0241).

30 1.02-2.17), MI (OR 1.58, 95% CI 1.06-2.35), LDL-cholesterol (0.21 standard deviations, 95% CI 0.01-0

31 low-fat dairy was negatively associated with LDL cholesterol (-0.03 mmol/L; -0.05, -0.01 mmol/L), whe

32 PUFA diet compared with the SFA diet lowered LDL cholesterol (-0.31 mmol/L; 95% CI: -0.47, -0.15 mmol

33 o 0.09), p = 0.093; low-density lipoprotein (LDL) cholesterol, 0.06 mmol/L (-0.07 to 0.2), p = 0.37;

34 1.03-1.18]; p=0.0079), and concentrations of LDL cholesterol (1.14 [1.04-1.25]; p=0.0056), total chol

35 triglycerides (reductions of 33.2 to 63.1%), LDL cholesterol (1.3 to 32.9%), very-low-density lipopro

36 ment groups in mean changes from baseline in LDL cholesterol (-14.6 mg/dL, 95% CI -18.2 to -11.0) and

37 ependent SNPs associated at P < 5 x 10-8 for LDL cholesterol (220), apolipoprotein B (n = 255), trigl

38 VLDL cholesterol explained 50% and IDL + LDL cholesterol 29% of the risk of myocardial infarction

39 tandard deviation) lipid concentrations were LDL cholesterol 3.57 (0.87) mmol/L and HDL cholesterol 1

40 cal studies demonstrating that SFAs increase LDL cholesterol, a major causal factor in the developmen

41 ituting unsaturated fat for saturated fat on LDL cholesterol and apoB concentrations in normal-weight

42 LDL cholesterol and apoB were higher with red and white

43 r 12 wk showed beneficial effects on fasting LDL cholesterol and endothelial function compared with c

44 tic events in proportion to their effects on LDL cholesterol and have good safety profiles, though PC

45 and merged with available measures of serum LDL cholesterol and HDL cholesterol concentrations.

46 eceptor gene (LDLR) cause elevated levels of LDL cholesterol and premature cardiovascular disease.

47 were available through day 210, and data on LDL cholesterol and proprotein convertase subtilisin-kex

48 nt association was observed between achieved LDL cholesterol and safety outcomes, either for all seri

49 anced the effect of free sugars on total and LDL cholesterol and triacylglycerols.

50 inacumab and IONIS-ANGPTL3-L(Rx) target both LDL cholesterol and triglyceride.

51 MR analysis demonstrates that LDL cholesterol and triglycerides are associated with ad

52 These findings suggest that LDL cholesterol and triglycerides may have a causal effe

53 diabetes) and an unfavorable profile (higher LDL cholesterol and triglycerides).Choline and its metab

54 onal clinical CVD biomarkers including serum LDL cholesterol and triglycerides.

55 n elevated level of low-density lipoprotein (LDL) cholesterol and an increased risk of premature athe

56 reduces the plasma low-density lipoprotein (LDL) cholesterol and subsequently the risk of cardiovasc

57 ated whether higher low-density lipoprotein (LDL) cholesterol and triglyceride levels and lower high-

58 . mansoni infection had lower triglycerides, LDL-cholesterol and diastolic blood pressure levels.

59 nd oleic acid had similar effects on fasting LDL-cholesterol and non-HDL-cholesterol concentrations a

60 Fasting LDL-cholesterol and non-HDL-cholesterol concentrations w

61 sitive associations of genetically predicted LDL-cholesterol and triglycerides with heart failure tha

62 ent score and lower serum total cholesterol, LDL cholesterol, and albumin concentrations.

63 tion were significant for total cholesterol, LDL cholesterol, and apoB ( P values <= 0.009).

64 cohorts in association with serum total and LDL cholesterol, and AT lipidomics.

65 ases in propionate with increases in leptin, LDL cholesterol, and blood pressure; and increases in bu

66 guideline-driven management of hypertension, LDL cholesterol, and diabetes is required.

67 condary outcomes included %SFA in purchases, LDL cholesterol, and feasibility outcomes.

68 ApoA-I, total cholesterol (TC), LDL cholesterol, and HDL cholesterol also did not change

69 iglycerides, baseline hypertension, baseline LDL cholesterol, and most recent HbA(1c) Major atheroscl

70 to derive from the capacity of SFAs to raise LDL cholesterol, and the evidence that LDL-cholesterol l

71 ide analyses of circulating HDL cholesterol, LDL cholesterol, and triglyceride levels in up to 120,97

72 accounts for the etiological basis of apoB, LDL cholesterol, and triglycerides in relation to ischem

73 In multivariable MR analysis including apoB, LDL cholesterol, and triglycerides in the same model, ap

74 Increased levels of apoB, LDL cholesterol, and triglycerides were associated with

75 were strongest for low-density lipoprotein (LDL)-cholesterol, and remained significant after adjusti

76 ce reduced total cholesterol, triglycerides, LDL-cholesterol, and the atherogenic index of plasma (AI

77 The primary outcomes were LDL cholesterol, apolipoprotein B (apoB), small + medium

78 they bind modified low-density-lipoprotein (LDL) cholesterol as normal.

79 n on SFA intake and low-density lipoprotein (LDL) cholesterol as well as the feasibility and acceptab

80 A genetic risk score based on LDL-cholesterol-associated loci has consistent effects o

81 LDL cholesterol associations were carried out in a sampl

82 rences across glycaemic categories in median LDL cholesterol at baseline (2.20-2.28 mmol/L), after 4

83 (95% CI: 0.01-0.12 mmol/l, p = 0.016) higher LDL-cholesterol at 5 years, respectively.

84 rable concentrations of blood lipids (higher LDL cholesterol: beta = 0.006 SD/allele; 95% CI: 0.001,

85 tion does not appear to affect size-specific LDL cholesterol but is likely to lower CHD risk by lower

86 onut oil consumption significantly increased LDL-cholesterol by 10.47 mg/dL (95% CI: 3.01, 17.94; I(2

87 Statins, which reduce LDL-cholesterol by inhibition of 3-hydroxy-3-methylgluta

88 (95% CI: 0.09, 11.9) of the variance in 1-y LDL cholesterol changes in the intervention arm but was

89 plasma total cholesterol, triglycerides and LDL cholesterol comparable to oral ATV.

90 resulted in near-identical associations with LDL cholesterol concentration estimated by the Friedewal

91 syndrome, alirocumab treatment targeting an LDL cholesterol concentration of 0.65-1.30 mmol/L produc

92 tatus, estimated glomerular filtration rate, LDL-cholesterol concentration, and use of lipid-lowering

93 was positively associated with the change in LDL-cholesterol concentration.

94 n in the stable low BMI trajectory had lower LDL cholesterol concentrations (0.14-0.17 mmol/L), HDL c

95 Plasma LDL cholesterol concentrations decreased in the almond g

96 Alirocumab was titrated to target LDL cholesterol concentrations of 0.65-1.30 mmol/L.

97 daily whole almond consumption lowers blood LDL cholesterol concentrations, but effects on other car

98 Mean +/- SEM LDL-cholesterol concentrations (109.9 +/- 4.5 compared w

99 ions were positively correlated with fasting LDL-cholesterol concentrations (r = 0.33; P = 0.011).

100 the relationship between progressively lower LDL-cholesterol concentrations achieved at 4 weeks and c

101 LDL-cholesterol concentrations after the cheese diet wer

102 The cheese diet increased serum LDL-cholesterol concentrations compared with the control

103 HDL cholesterol but differentially modifies LDL-cholesterol concentrations compared with the effects

104 there were no safety concerns with very low LDL-cholesterol concentrations over a median of 2.2 year

105 A reduction in LDL-cholesterol concentrations was shown for the exchang

106 The reduction in LDL-apoB and LDL-cholesterol concentrations was significantly greater

107 KJM), a viscous soluble fiber, for improving LDL-cholesterol concentrations.

108 mental impact of lifelong very low levels of LDL cholesterol due to del2.5 on health of the carriers.

109 y tested the hypothesis that genetically low LDL cholesterol due to PCSK9 variation is causally assoc

110 Genetically low LDL cholesterol due to PCSK9 variation was causally asso

111 Reduced low-density lipoprotein (LDL) cholesterol due to inhibition of proprotein convert

112 ith the APOE4 allele associated with greater LDL-cholesterol elevation in response to saturated fatty

113 Secondary outcomes were HbA1c, LDL cholesterol, estimated glomerular filtration rate (e

114 id profile, the principal target is lowering LDL cholesterol, firstly with lifestyle interventions an

115 Mean predicted changes in LDL cholesterol for an increase of 100 mg dietary choles

116 o 0.56 mmol/L (0.26-0.86) for clozapine; for LDL cholesterol from -0.13 mmol/L (-0.21 to -0.05) for c

117 Adults >=18 years with LDL cholesterol >3 mmol/L (n = 113) were recruited from

118 - SD age 64 +/- 7 y, BMI 26.4 +/- 3.4 kg/m2, LDL cholesterol >= 2.8 mmol/L) were provided with each o

119 cedure on the postintervention values of TC, LDL cholesterol, HDL cholesterol, TC:HDL cholesterol, tr

120 (BMI, systolic and diastolic blood pressure, LDL cholesterol, HDL cholesterol, total cholesterol, tri

121 nges in body weight, BMI, total cholesterol, LDL cholesterol, HDL cholesterol, triglyceride, and gluc

122 nse of 6 CRFs (BMI, systolic blood pressure, LDL cholesterol, HDL cholesterol, triglycerides, and fas

123 oncentrations and positively correlated with LDL cholesterol:HDL cholesterol (r = 0.37-0.54; P < 0.01

124 ncluded low-density lipoprotein cholesterol (LDL-cholesterol), high-density lipoprotein cholesterol (

125 with at least 1 of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholest

126 reporter and identify >100 genes involved in LDL-cholesterol import.

127 iding support for a potential causal role of LDL cholesterol in ICH.

128 is an effective additional option to reduce LDL cholesterol in patients with homozygous familial hyp

129 SK9 associated with low-density lipoprotein (LDL) cholesterol in a genome-wide association study (GWA

130 elevated levels of low-density lipoprotein (LDL) cholesterol in the blood.

131 86,1.07] p=0.42) but resulted in higher mean LDL-cholesterol in the intensive arm (2.86 vs 2.60 mmol/

132 hough SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due t

133 For LDL-cholesterol, in addition to the expected positive as

134 ASP1, LHX1, and SNTA1 loci and attenuate the LDL cholesterol-increasing effect of the CNTNAP2 locus.

135 iated by passage of low-density lipoprotein (LDL) cholesterol into the artery wall and its engulfment

136 LDL cholesterol is a well established risk factor for at

137 Elevated low-density lipoprotein (LDL) cholesterol is a major risk factor for cardiovascul

138 Lowering LDL-cholesterol is likely to prevent abdominal aortic an

139 re associated with low circulating levels of LDL cholesterol (LDL-C) and a reduced risk of coronary a

140 te gene investigations suggesting that lower LDL cholesterol (LDL-C) increases T2D risk.

141 e inferred that higher triglyceride (TG) and LDL cholesterol (LDL-C) levels caused elevated ACR.

142 all dense (sdLDL-C) low-density lipoprotein (LDL) cholesterol (LDL-C) on CVD events.

143 type 9 (PCSK9) is a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated targe

144 ural lipid lowering drug that reduces plasma LDL-cholesterol (LDL-C), total cholesterol (TC) and TG i

145 We report hypobetalipoproteinemia (LDL cholesterol [LDL-C] and apolipoprotein B below the f

146 esterol [HDL-C; 84 studies; 121,282 people], LDL-Cholesterol [LDL-C; 61 studies; 86,854 people], and

147 In PTDSS1-deficient cells where PS is low, LDL cholesterol leaves lysosomes but fails to reach the

148 hypercholesterolemia, evolocumab reduced the LDL cholesterol level and other lipid variables.

149 ry end point was the change from baseline in LDL cholesterol level at 180 days.

150 The mean (+/-SD) LDL cholesterol level at baseline was 103.2+/-29.4 mg pe

151 end point) was the percentage change in the LDL cholesterol level at week 12 of 52 weeks.

152 was the percent change from baseline in the LDL cholesterol level at week 16 with evinacumab as comp

153 was the percent change from baseline in the LDL cholesterol level at week 24.

154 the patients who received the regimen had an LDL cholesterol level below 50 mg per deciliter (1.3 mmo

155 The time-averaged percent change in the LDL cholesterol level between day 90 and day 540 was a r

156 adjusted percent change from baseline in the LDL cholesterol level between day 90 and day 540.

157 ast-squares mean change from baseline in the LDL cholesterol level between the groups assigned to rec

158 At week 12, bempedoic acid reduced the mean LDL cholesterol level by 19.2 mg per deciliter, represen

159 The mean LDL cholesterol level decreased by 15 mg per deciliter i

160 0 and the time-adjusted percentage change in LDL cholesterol level from baseline after day 90 and up

161 e the placebo-corrected percentage change in LDL cholesterol level from baseline to day 510 and the t

162 o weeks 22 and 24 and the absolute change in LDL cholesterol level from baseline to week 24.

163 primary end point was the percent change in LDL cholesterol level from baseline to week 24; key seco

164 y end points were the mean percent change in LDL cholesterol level from baseline to weeks 22 and 24 a

165 therapy, the reduction from baseline in the LDL cholesterol level in the evinacumab group, as compar

166 The mean LDL cholesterol level in the patients had decreased from

167 The mean baseline LDL cholesterol level in the two groups was 255.1 mg per

168 east 4 weeks before screening and who had an LDL cholesterol level of 130 mg per deciliter (3.4 mmol

169 ad a relative reduction from baseline in the LDL cholesterol level of 47.1%, as compared with an incr

170 sive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol

171 ctory hypercholesterolemia, with a screening LDL cholesterol level of 70 mg per deciliter or higher w

172 Patients had to have an LDL cholesterol level of at least 70 mg per deciliter wh

173 were the percent change from baseline in the LDL cholesterol level on day 510 and the time-adjusted p

174 er reductions in systolic blood pressure and LDL cholesterol level than were observed with usual care

175 east-squares mean absolute difference in the LDL cholesterol level was -132.1 mg per deciliter (95% C

176 24, the mean percent change from baseline in LDL cholesterol level was -44.5% in the evolocumab group

177 The absolute change in the LDL cholesterol level was -77.5 mg per deciliter (-2.0 m

178 pressure was 140/83 mm Hg, and the baseline LDL cholesterol level was 113 mg per deciliter.

179 At day 510, the percent change in the LDL cholesterol level was a reduction of 39.7% (95% conf

180 The LDL cholesterol level was lower in the evinacumab group

181 use of evinacumab significantly reduced the LDL cholesterol level, by more than 50% at the maximum d

182 n cases with low HDL cholesterol level, high LDL cholesterol level, high VLDL cholesterol level, high

183 diovascular disease per unit decrease in the LDL cholesterol level.

184 s per decrease of 10 mg per deciliter in the LDL cholesterol level: odds ratio for cardiovascular eve

185 blood pressure and low-density lipoprotein (LDL) cholesterol level at 12 months.

186 nit decrease in the low-density lipoprotein (LDL) cholesterol level, as the genetic inhibition of HMG

187 esterol level, high low-density lipoprotein (LDL) cholesterol level, high very low-density lipoprotei

188 ce, reduced HDL-cholesterol level, increased LDL-cholesterol level, and decreased insulin sensitivity

189 th diabetes; median low-density lipoprotein [LDL] cholesterol level, 75.0 mg/dL; median triglycerides

190 analysis, there were no associations between LDL cholesterol levels and cognitive changes.

191 a critical determinant of circulating plasma LDL cholesterol levels and hence development of coronary

192 ansfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipopr

193 Mean (+/-SD) LDL cholesterol levels at baseline were 104.7+/-38.3 mg

194 At day 510, inclisiran reduced LDL cholesterol levels by 52.3% (95% confidence interval

195 xin type 9 (PCSK9) have been shown to reduce LDL cholesterol levels by more than 50% but require admi

196 ibitors and statins appeared to lower plasma LDL cholesterol levels by the same mechanism of action a

197 equivalent (ORION-11 trial) who had elevated LDL cholesterol levels despite receiving statin therapy

198 tion mutation in LDLR with a large effect on LDL cholesterol levels has not been described.

199 There were robust reductions in LDL cholesterol levels in all genotypes of familial hype

200 ed trials had a mean change from baseline in LDL cholesterol levels of -56.0% in the bococizumab grou

201 Reductions in LDL cholesterol levels of approximately 50% were obtaine

202 Their large estimated effects on LDL cholesterol levels suggest strong impacts on protein

203 ab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per decilite

204 ay 180, the least-squares mean reductions in LDL cholesterol levels were 27.9 to 41.9% after a single

205 nal trials with different entry criteria for LDL cholesterol levels, we randomly assigned the 27,438

206 than placebo and led to significantly lower LDL cholesterol levels.

207 steatosis on LDLR expression and circulating LDL cholesterol levels.

208 n had dose-dependent reductions in PCSK9 and LDL cholesterol levels.

209 for cardiovascular disease who had elevated LDL cholesterol levels.

210 and significantly attenuated the lowering of LDL cholesterol levels.

211 magnitude and durability of the reduction in LDL cholesterol levels.

212 variants in LDLR that have a large effect on LDL cholesterol levels.

213 nd PCSK9 and genetically proxied circulating LDL cholesterol levels.

214 n regimen produced the greatest reduction in LDL cholesterol levels: 48% of the patients who received

215 y severely elevated low-density lipoprotein (LDL) cholesterol levels and premature cardiovascular dis

216 correlation between low-density lipoprotein (LDL) cholesterol levels and risk of intracerebral hemorr

217 emia, who have high low-density lipoprotein (LDL) cholesterol levels despite treatment with lipid-low

218 l Trial by reducing low-density-lipoprotein (LDL) cholesterol levels more than statin therapy alone.

219 ained reductions in low-density lipoprotein (LDL) cholesterol levels with infrequent dosing.

220 ator of circulating low-density lipoprotein (LDL) cholesterol levels, a known driver of CVD, the mech

221 and associated with low-density lipoprotein (LDL) cholesterol levels.

222 t patients to lower low-density lipoprotein (LDL) cholesterol levels.

223 showed higher triglyceride (p = 0.012), and LDL-cholesterol levels (p = 0.44), and a greater adheren

224 (EVOlocumab for Early Reduction of LDL-cholesterol Levels in Patients With Acute Coronary S

225 Total- and LDL-cholesterol levels were causally associated with inc

226 Lower LDL-cholesterol levels were observed in S. mansoni (2.37

227 sk factors such as inflammation and elevated LDL-cholesterol levels.

228 vailable and emerging therapies for lowering LDL cholesterol, lipoprotein(a), and triglycerides for p

229 d accumulation and increased autophagy under LDL cholesterol loading.

230 The benefit of LDL cholesterol lowering in older patients was observed

231 LDL cholesterol lowering significantly reduced the risk

232 We aimed to summarise the evidence of LDL cholesterol lowering therapies in older patients.

233 The clinical benefit of LDL cholesterol lowering treatment in older patients rem

234 We found that LDL cholesterol lowering was dispensable, but statin-ind

235 raise LDL cholesterol, and the evidence that LDL-cholesterol lowering reduces CVD incidence.

236 Investigational LDL cholesterol-lowering agents currently being tested i

237 lled trials of cardiovascular outcomes of an LDL cholesterol-lowering drug recommended by the 2018 Am

238 Furthermore, AAT3 augments LDL cholesterol-lowering effects of ApoB-ASO.

239 iew describes key stages in the evolution of LDL cholesterol-lowering treatment.

240 nt isocalorically replaces SFA, the greatest LDL-cholesterol-lowering effect is seen with PUFA, follo

241 2% from the baseline level; treatment goals (LDL cholesterol <100 mg per deciliter [2.59 mmol per lit

242 atment targets (HbA1c <7.0%, SBP <130 mm Hg, LDL cholesterol <100 mg/dL [<70 mg/dL if prior cardiovas

243 (normal: n = 44; obese: n = 39) and elevated LDL cholesterol (mean +/- SD, normal weight 4.6 +/- 0.9

244 In addition to LDL cholesterol, mendelian randomisation studies support

245 f >/=3 wk that assessed the effect of KJM on LDL cholesterol, non-HDL cholesterol, or apolipoprotein

246 We conclude that LDL cholesterol normally moves from lysosomes to the PM.

247 modified diet attenuated the rise in fasting LDL cholesterol observed with the control diet (0.03 +/-

248 Assessed individually using MR, LDL cholesterol (odds ratio [OR] 1.66 per 1-standard-dev

249 alleles were associated with stepwise lower LDL cholesterol of up to 0.61 mmol/l (24 mg/dl; 18.2%; p

250 least 140 mm Hg, or low-density lipoprotein (LDL) cholesterol of at least 130 mg/dL.

251 ndividuals might require further lowering of LDL cholesterol or be unable to tolerate statins.

252 ained a robust effect, with the estimate for LDL cholesterol (OR 0.85; 95% CI: 0.57-1.27; P = 0.44) r

253 nce interval [CI] = 0.85-0.99; p = 0.03) and LDL cholesterol (OR = 0.88; 95% CI = 0.81-0.95; p = 0.00

254 95% CI, 0.85-1.13]; P = .80), or circulating LDL cholesterol (OR, 0.98 [95% CI, 0.91-1.05]; P = .55)

255 n without significant changes in apoA-I, TC, LDL cholesterol, or HDL cholesterol, supporting the idea

256 er cardiovascular risk factors, particularly LDL cholesterol, oxLDL-IC and MDA-LDL-IC remained indepe

257 source, high compared with low SFA increased LDL cholesterol (P = 0.0003), apoB (P = 0.0002), and lar

258 ated with decreased low-density-lipoprotein (LDL) cholesterol (P = 1.3 x 10(-8)) without being associ

259 ic risk factors, including change scores for LDL-cholesterol (p<0.0001), total cholesterol to HDL-cho

260 Even with statin treatment to lower LDL cholesterol, patients with diabetes have a high resi

261 Hg reduction in SBP, >=10-mg/dL reduction in LDL cholesterol); percentage of patients who met all HbA

262 droxyl and peroxyl radicals), copper-induced LDL-cholesterol peroxidation, as well as alpha-glucosida

263 Only 1 of these genetic scores, for LDL cholesterol, predicted changes in the associated CRF

264 1), total-cholesterol (r=0.31, p=0.047), and LDL cholesterol (r=0.42, p=0.013), and decreases in HDL

265 lization, provide mechanisms for the greater LDL-cholesterol raising effect.

266 LDL cholesterol reached statistical significance only in

267 sorder characterised by substantially raised LDL cholesterol, reduced LDL receptor function, xanthoma

268 LDL cholesterol reduction was 31.1% with pitavastatin an

269 y SFAs lower the incidence of CVD, 2) is the LDL-cholesterol reduction with lower SFA intake predicti

270 nstrated that lower low-density lipoprotein (LDL) cholesterol results in fewer cardiovascular events.

271 er patients by 26% per 1 mmol/L reduction in LDL cholesterol (RR 0.74 [95% CI 0.61-0.89]; p=0.0019),

272 vel non-coding rare variants associated with LDL cholesterol (rs17242388 in LDLR) and HDL cholesterol

273 09, and rs11206510) scaled to 1 mmol/L lower LDL cholesterol showed associations with increased fasti

274 tage of patients who met all HbA1c, SBP, and LDL cholesterol targets; and mean reductions in SCL-20 s

275 inclisiran had significantly lower levels of LDL cholesterol than those who received placebo, with an

276 consumption results in significantly higher LDL-cholesterol than nontropical vegetable oils.

277 3) do dietary SFAs affect factors other than LDL cholesterol that may impact CVD risk, and 4) is ther

278 A reduction in mean LDL cholesterol to 1.4-1.8 mmol/L with ezetimibe or stat

279 c testing; risk restratification strategies; LDL-cholesterol treatment targets; management protocols

280 h on cardiometabolic risk markers, including LDL cholesterol, triacylglycerol (TG), fasting glucose (

281 Biobank (UKBB) for low-density lipoprotein (LDL) cholesterol, triglycerides, and apolipoprotein B to

282 5.89 mmol/L; CB: 6.11 mmol/L; P = 0.006) and LDL cholesterol (WA: 3.72 mmol/L; CB: 3.86 mmol/L; P = 0

283 and 47% were men; the mean baseline level of LDL cholesterol was 153 mg per deciliter.

284 Mean level of LDL cholesterol was 74% lower in del2.5 carriers than in

285 lent to a 1-mmol/L (38.7-mg/dL) reduction in LDL cholesterol was associated with lower odds of epithe

286 ic analyses, a 0.5-mmol/l (19.4-mg/dl) lower LDL cholesterol was associated with risk ratios for card

287 In 1-sample MR analysis, higher LDL cholesterol was causally associated with higher LV e

288 ntrast, a main-effect genetic risk score for LDL cholesterol was not useful for predicting dietary fa

289 effect (p < 0.05), whereas the estimate for LDL cholesterol was reversed, and that for triglycerides

290 Genetically predicted LDL-cholesterol was not associated with overall cancer r

291 However, beyond changes in LDL cholesterol, we lack a complete understanding of the

292 arisons found that the respective changes in LDL cholesterol were 9.7% (95% CI: 5.3%, 14.2%) compared

293 TATION: PCSK9 variants associated with lower LDL cholesterol were also associated with circulating hi

294 crease of genetically instrumented total and LDL cholesterol were associated with 23% (OR = 0.77; 95%

295 Reductions in the levels of PCSK9 and LDL cholesterol were maintained at day 180 for doses of

296 SFA intake increases LDL cholesterol whereas PUFA intake lowers it.

297 systolic blood pressure, smoking, and IDL + LDL cholesterol, whereas VLDL triglycerides did not ente

298 efficacy and safety of further reduction in LDL cholesterol with an inhibitor of proprotein converta

299 endent associations of genetically predicted LDL-cholesterol with abdominal aortic aneurysm (OR, 1.75

300 t 22% per 38.7 mg/dl (1 mmol/l) reduction in LDL cholesterol, with similar benefit across patient sub