基于China-PAR模型评估极低碳水化合物饮食对代谢相关脂肪性肝病患者心血管风险的影响
DOI: 10.12449/JCH251214
Impact of very-low-carbohydrate diet on cardiovascular risk in patients with metabolic associated fatty liver disease based on the China-PAR model
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摘要:
目的 通过观察极低碳水化合物饮食(VLCD)对代谢相关脂肪性肝病(MAFLD)患者各项指标的影响,分析其干预该病的有效性与安全性,为临床治疗提供依据。 方法 本研究为单中心、回顾性、单臂试验队列观察,选取2021年9月—2024年5月于北京中医药大学东直门医院确诊为MAFLD的103例患者为研究对象。所有患者均接受VLCD干预方案,干预时长为2~6周。对患者干预前后的体重、体重指数(BMI)、肝脏受控衰减参数(CAP)、空腹血糖(FPG)、空腹血清C肽(C-P)、空腹血清胰岛素(FINS)、稳态模型评估胰岛素抵抗指数(HOMA-IR)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)进行比较。最后运用中国心血管风险预测模型China-PAR计算干预前后的心血管事件风险,以评估该饮食干预方式对心血管的影响。计量资料的比较采用配对t检验或Wilcoxon符号秩检验。 结果 经VLCD干预后,患者的体重、BMI、CAP较干预前下降,差异均具有统计学意义(Z值分别为-8.515、-8.495、-8.204,P值均<0.001);经VLCD干预后,患者的FPG、FINS、C-P及HOMA-IR均较干预前改善(Z值分别为-4.215、-5.310、-4.482、-5.422,P值均<0.001)。经干预后患者TG水平下降(Z=-5.373,P<0.001)。采用China-PAR模型计算后显示,103例患者的心血管疾病10年风险和终身风险评估指数下降,差异均具有统计学意义(Z值分别为-5.406、-5.383,P值均<0.001)。性别亚组分析结果显示,男性亚组干预前后体重、BMI、CAP、FPG、FINS、C-P、HOMA-IR、TG、血压、腰围、心血管疾病风险评估比较差异均具有统计学意义(P值均<0.05)。女性亚组干预前后体重、BMI、CAP、FPG、FINS、C-P、HOMA-IR、TC、TG、LDL-C、血压、腰围、心血管疾病风险评估比较差异均具有统计学意义(P值均<0.05)。年龄亚组方面,青年组干预后其体重、BMI、CAP、FPG、FINS、C-P、HOMA-IR、TG、收缩压、腰围、心血管疾病风险评估均明显下降,差异均具有统计学意义(P值均<0.05)。中年组其体重、BMI、CAP、FPG、FINS、C-P、HOMA-IR、TG、收缩压、舒张压、腰围、心血管疾病风险评估均明显下降,差异均具有统计学意义(P值均<0.05)。老年干预组在体重、BMI、CAP、收缩压、腰围、心血管疾病风险评估水平均有明显下降,差异均具有统计学意义(P值均<0.05)。经干预后TC、TG、LDL-C升高患者分别有43例(41.7%)、24例(23.3%)、43例(41.7%);HDL-C降低患者有53例(51.5%);CAP升高9例(8.7%);HOMA-IR 升高26例(25.2%)。 结论 VLCD在干预MAFLD过程中,可有效改善患者MAFLD程度、降低胰岛素抵抗,且未观察到心血管疾病风险上升。 -
关键词:
- 代谢相关脂肪性肝病 /
- 膳食, 低碳水化合物 /
- 心血管疾病
Abstract:Objective To investigate the effectiveness and safety of very-low-carbohydrate diet (VLCD) in the treatment of metabolic associated fatty liver disease (MAFLD) by observing its impact on various indicators, and to provide a basis for clinical treatment. Methods This single-center retrospective single-arm cohort study was conducted among 103 patients who were diagnosed with MAFLD in Dongzhimen Hospital, Beijing University of Chinese Medicine, from September 2021 to May 2024, and all patients received the VLCD intervention regimen for 2 — 6 weeks. Related indicators were compared before and after treatment, including body weight, body mass index (BMI), liver controlled attenuation parameter (CAP), fasting plasma glucose (FPG), fasting serum C-peptide (C-P), fasting serum insulin (FINS), Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C). Finally, the China-PAR cardiovascular risk prediction model was used to calculate the risk of cardiovascular events before and after treatment and evaluate the impact of this dietary intervention on cardiovascular health. The paired t-test or the Wilcoxon signed-rank test was used for comparison of continuous data between groups. Results After VLCD treatment, there were significant reductions in body weight, BMI, and CAP (Z=-8.515, -8.495, and -8.204, all P <0.001), and there were significant improvements in FPG, FINS, C-P, and HOMA-IR (Z=-4.215, -5.310, -4.482, and -5.422, all P<0.001). There was a significant reduction in TG after treatment (Z=-5.373, P<0.001). The China-PAR model showed significant reductions in the 10-year and lifetime risk assessment indices of cardiovascular disease in 103 patients (Z=-5.406 and -5.383, both P<0.001). The subgroup analysis based on sex showed that in the male group, there were significant differences in body weight, BMI, CAP, FPG, FINS, C-P, HOMA-IR, TG, blood pressure, waist circumference, and the risk of cardiovascular disease before and after treatment (all P<0.05), while in the female group, there were significant reductions in body weight, BMI, CAP, FPG, FINS, C-P, HOMA-IR, TC, TG, LDL-C, blood pressure, waist circumference, and the risk assessment of cardiovascular disease (all P<0.05). The subgroup analysis based on age showed that in the youth group, there were significant reductions in body weight, BMI, CAP, FPG, FINS, C-P, HOMA-IR, TG, systolic blood pressure, waist circumference, and the risk assessment of cardiovascular disease (all P<0.05); in the middle-aged group, there were significant reductions in body weight, BMI, CAP, FPG, FINS, C-P, HOMA-IR, TG, systolic blood pressure, diastolic blood pressure, waist circumference, and the risk assessment of cardiovascular disease (all P<0.05); in the elderly group, there were significant reductions in body weight, BMI, CAP, systolic blood pressure, waist circumference, and the risk assessment of cardiovascular disease (all P <0.05). After treatment, there were 43 patients with an increase in TC (41.7%), 24 patients with an increase in TG (23.3%), and 43 patients with an increase in LDL-C (41.7%); 53 patients (51.5%) showed a reduction in HDL-C; 9 patients (8.7%) showed an increase in CAP; 26 patients (25.2%) had an increase in HOMA-IR. Conclusion VLCD can effectively alleviate fatty liver disease and reduce insulin resistance in the treatment of MAFLD, without increasing the risk of cardiovascular disease. -
表 1 体重、BMI及CAP干预前后差异
Table 1. Difference inbody weight, body mass index and controlled attenuation parameter values before and after treatment
指标 干预前(n=103) 干预后(n=103) Z值 P值 BMI(kg/m2) 28.88(26.56~31.80) 27.34(25.20~30.09) -8.495 <0.001 体重(kg) 83.00(73.00~95.00) 78.00(69.50~90.50) -8.515 <0.001 CAP(dB/m) 318.00(291.00~345.00) 277.00(253.00~303.00) -8.204 <0.001 注: BMI,体重指数;CAP,肝脏受控衰减参数值。
表 2 血糖、血脂代谢指标干预前后差异
Table 2. Differences in glucose metabolism indicators and blood lipid before and after treatment
指标 干预前(n=103) 干预后(n=103) Z值 P值 FPG(mmol/L) 5.64(5.20~6.56) 5.36(4.86~5.86) -4.215 <0.001 FINS(μIU/mL) 16.33(11.92~20.77) 11.47(8.77~16.12) -5.310 <0.001 C-P(ng/mL) 3.21(2.63~4.32) 2.78(2.20~3.32) -4.482 <0.001 HOMA-IR 4.15(3.07~6.10) 2.80(1.92~3.93) -5.422 <0.001 TC(mmol/L) 5.35(4.42~6.09) 5.23(4.31~5.79) -1.689 0.091 TG(mmol/L) 1.80(1.27~2.69) 1.35(0.98~2.07) -5.373 <0.001 HDL-C(mmol/L) 1.18(1.00~1.35) 1.19(0.98~1.36) -0.389 0.697 LDL-C(mmol/L) 3.39(2.58~3.95) 3.31(2.59~3.87) -1.145 0.252 注:FPG,空腹血糖;FINS,空腹血清胰岛素;C-P,空腹血清C肽;HOMA-IR,稳态模型评估胰岛素抵抗指数;TC,总胆固醇;TG,甘油三酯;HDL-C,高密度脂蛋白胆固醇;LDL-C,低密度脂蛋白胆固醇。
表 3 心血管疾病基本风险评估因素及风险预测值
Table 3. Basic risk assessment factors and risk predictors for cardiovascular disease
指标 干预前(n=103) 干预后(n=103) Z值 P值 收缩压(mmHg) 120.00(115.00~125.00) 116.00(112.00~120.00) -6.085 <0.001 舒张压(mmHg) 82.00(78.00~87.00) 80.00(75.00~84.00) -3.407 <0.001 腰围(cm) 98.00(94.50~100.00) 88.50(85.50~90.00) -8.769 <0.001 心血管疾病10年风险评估(%)1) 1.80(0.70~5.10) 1.50(0.60~4.60) -5.406 <0.001 心血管疾病终身风险评估(%)1) 21.50(17.80~22.40) 19.20(16.50~22.40) -5.383 <0.001 注:1)China-PAR风险评估等级:10年风险:低危(<5%)、中危(5%~9.9%)、高危(≥10%);终身风险:低危(<32.8%)、高危(≥32.8%)。终身风险评估只在60岁以下人群计算[11]。
表 4 性别亚组干预前后各指标分析
Table 4. Analysis of indicators in the gender subgroups before and after treatment
指标 例数 干预前 干预后 统计值 P值 男性亚组 57 体重(kg) 90.00(83.00~102.00) 86.00(77.45~96.75) Z=-6.571 <0.001 BMI(kg/m2) 29.32(27.45~32.98) 28.20(25.50~30.99) Z=-6.567 <0.001 CAP(dB/m) 325.68±39.71 282.07±5.68 t=9.115 <0.001 FPG(mmol/L) 6.00(5.33~6.95) 5.41(4.87~6.25) Z=-3.496 <0.001 FINS(μIU/mL) 17.13(12.07~20.27) 11.11(8.04~15.94) Z=-4.096 <0.001 C-P(ng/mL) 3.70±0.19 3.00±1.21 t=3.692 <0.001 HOMA-IR 4.42(3.46~6.60) 2.93(1.91~3.97) Z=-4.422 <0.001 TC(mmol/L) 5.29(4.25~5.97) 5.42(4.33~5.76) Z=-0.012 0.990 TG(mmol/L) 1.98(1.16~3.15) 1.56(0.98~2.27) Z=-3.619 <0.001 HDL-C(mmol/L) 1.15(0.98~1.31) 1.13(0.91~1.26) Z=-1.667 0.096 LDL-C(mmol/L) 3.24±1.01 3.28±0.99 t=-0.515 0.608 收缩压(mmHg) 118.00(114.00~123.00) 115.00(110.00~119.00) Z=-4.685 <0.001 舒张压(mmHg) 83.00(79.00~87.00) 80.00(75.00~85.00) Z=-2.024 0.043 腰围(cm) 100.00(96.20~104.30) 89.00(86.50~90.00) Z=-6.568 <0.001 心血管疾病10年风险评估(%) 1.40(0.50~4.20) 1.20(0.40~4.10) Z=-2.136 0.033 心血管疾病终身风险评估(%) 19.00(15.80~22.60) 18.20(15.50~21.30) Z=-1.994 0.046 女性亚组 46 体重(kg) 75.13±11.35 71.83±11.54 t=8.884 <0.001 BMI(kg/m2) 28.48±3.57 27.23±3.66 t=9.154 <0.001 CAP(dB/m) 303.00(287.00~329.00) 270.00(247.00~300.00) Z=-5.518 <0.001 FPG(mmol/L) 5.52(5.08~5.99) 5.34(4.84~5.66) Z=-2.500 0.012 FINS(μIU/mL) 14.86(10.75~20.91) 12.32(8.98~16.20) Z=-3.436 <0.001 C-P(ng/mL) 3.09(2.52~4.03) 2.60(2.24~3.31) Z=-3.799 <0.001 HOMA-IR 3.78(2.79~5.62) 2.77(1.90~3.97) Z=-3.381 <0.001 TC(mmol/L) 5.40(4.64~6.31) 5.14(4.07~5.89) Z=-2.409 0.016 TG(mmol/L) 1.71(1.31~2.04) 1.15(0.98~1.71) Z=-4.059 <0.001 HDL-C(mmol/L) 1.25(1.10~1.37) 1.31(1.10~1.46) Z=-1.276 0.202 LDL-C(mmol/L) 3.37(2.68~4.18) 3.17(2.45~3.91) Z=-2.156 0.031 收缩压(mmHg) 120.00(115.00~127.00) 117.00(113.00~121.00) Z=-3.912 <0.001 舒张压(mmHg) 82.00(78.00~87.00) 77.00(73.00~82.00) Z=-2.817 0.005 腰围(cm) 95.70±5.43 87.31±6.09 t=15.705 <0.001 心血管疾病10年风险评估(%) 2.40(1.20~7.60) 1.80(0.80~5.90) Z=-5.351 <0.001 心血管疾病终身风险评估(%) 23.50(19.60~28.10) 20.20(17.60~23.60) Z=-5.450 <0.001 注:BMI,体重指数;CAP,肝脏受控衰减参数;FPG,空腹血糖;FINS,空腹血清胰岛素;C-P,空腹血清C肽;HOMA-IR,稳态模型评估胰岛素抵抗指数;TC,总胆固醇;TG,甘油三酯;HDL-C,高密度脂蛋白胆固醇;LDL-C,低密度脂蛋白胆固醇。
表 5 年龄亚组干预前后各指标分析
Table 5. Analysis of indicators in the age subgroups before and after treatment
指标 例数 干预前 干预后 统计值 P值 青年组 57 体重(kg) 88.00(78.00~104.00) 83.00(73.30~98.30) Z=-6.249 <0.001 BMI(kg/m2) 29.39(27.39~32.98) 28.50(25.75~31.40) Z=-6.208 <0.001 CAP(dB/m) 322.67±37.76 281.32±41.67 t=9.278 <0.001 FPG(mmol/L) 5.54(5.13~6.22) 5.23(4.82~5.71) Z=-3.619 <0.001 FINS(μIU/mL) 16.95(12.07~23.35) 11.73(9.19~16.21) Z=-4.159 <0.001 C-P(ng/mL) 3.19(2.70~4.58) 2.88(2.24~3.31) Z=-3.402 <0.001 HOMA-IR 4.07(3.14~6.61) 2.80(2.15~3.96) Z=-4.382 <0.001 TC(mmol/L) 5.19±1.12 5.14±1.23 t=0.481 0.632 TG(mmol/L) 1.89(1.33~2.96) 1.43(1.02~2.20) Z=-4.164 <0.001 HDL-C(mmol/L) 1.17(1.00~1.30) 1.19(1.00~1.35) Z=-0.801 0.423 LDL-C(mmol/L) 3.31±0.98 3.31±1.00 t=0.047 0.963 收缩压(mmHg) 117.00(112.00~120.00) 115.00(110.00~118.00) Z=-3.463 <0.001 舒张压(mmHg) 80.00(75.00~85.00) 80.00(75.00~84.00) Z=-1.538 0.124 腰围(cm) 98.00(94.60~103.10) 87.90(85.50~90.00) Z=-6.510 <0.001 心血管疾病10年风险评估(%) 0.90(0.30~1.50) 0.70(0.30~1.20) Z=-3.402 <0.001 心血管疾病终身风险评估(%) 19.50(16.30~23.60) 18.20(16.00~20.60) Z=-3.276 0.001 中年组 34 体重(kg) 80.40±13.19 76.05±13.26 t=9.275 <0.001 BMI(kg/m2) 28.22±3.64 26.68±3.72 t=9.415 <0.001 CAP(dB/m) 302.00(287.00~334.00) 268.00(244.00~300.00) Z=-4.557 <0.001 FPG(mmol/L) 6.14±1.25 5.58±0.83 t=3.036 0.005 FINS(μIU/mL) 16.23(10.56~18.64) 10.42(8.04~15.89) Z=-3.052 0.002 C-P(ng/mL) 3.53±1.36 2.83±0.81 t=3.118 0.004 HOMA-IR 4.65±2.67 3.14±1.77 t=3.413 0.002 TC(mmol/L) 5.57(4.83~6.14) 5.37(4.57~5.80) Z=-1.770 0.077 TG(mmol/L) 1.87(1.31~2.92) 1.24(1.14~1.83) Z=-3.240 0.001 HDL-C(mmol/L) 1.26(1.05~1.41) 1.19(1.00~1.38) Z=-1.179 0.238 LDL-C(mmol/L) 3.53(2.87~4.18) 3.48(2.63~3.84) Z=-1.483 0.138 收缩压(mmHg) 122.00(119.00~127.00) 119.00(114.00~121.00) Z=-4.164 <0.001 舒张压(mmHg) 82.00(79.00~89.00) 80.00(75.00~84.00) Z=-2.680 0.007 腰围(cm) 97.81±5.71 88.67±5.91 t=12.531 <0.001 心血管疾病10年风险评估(%) 3.90(2.90~6.10) 3.70(2.40~6.00) Z=-3.246 <0.001 心血管疾病终身风险评估(%) 22.20(18.30~25.80) 19.10(16.90~24.20) Z=-3.950 <0.001 老年组 12 体重(kg) 73.71±7.54 70.63±7.47 t=6.281 <0.001 BMI(kg/m2) 27.98±2.14 26.83±2.41 t=6.323 <0.001 CAP(dB/m) 318.58±33.42 275.92±32.82 t=3.763 0.003 FPG(mmol/L) 5.59(5.30~7.73) 5.76(5.01~6.10) Z=-0.118 0.906 FINS(μIU/mL) 14.69±6.38 12.58±7.18 t=0.944 0.366 C-P(ng/mL) 3.18(1.91~3.55) 2.52(1.41~3.15) Z=-1.295 0.195 HOMA-IR 3.78(2.03~6.40) 3.14(1.33~4.99) Z=-1.255 0.209 TC(mmol/L) 1.45(0.72~2.06) 0.96(0.66~1.59) Z=-1.805 0.071 TG(mmol/L) 1.45±0.69 1.28±0.90 t=0.952 0.362 HDL-C(mmol/L) 1.24±0.27 1.21±0.33 t=0.685 0.508 LDL-C(mmol/L) 2.80±1.03 2.75±1.09 t=0.532 0.605 收缩压(mmHg) 126.00(124.00~130.00) 118.00(113.00~124.00) Z=-2.983 0.003 舒张压(mmHg) 87.00(82.00~90.00) 80.00(77.00~85.00) Z=-1.930 0.054 腰围(cm) 96.62±7.14 87.20±8.25 t=10.252 <0.001 心血管疾病10年风险评估(%) 9.00(7.80~13.70) 6.90(6.10~9.40) Z=-2.847 0.004 注:BMI,体重指数;CAP,肝脏受控衰减参数值;FPG,空腹血糖;FINS,空腹血清胰岛素;C-P,空腹血清C肽;HOMA-IR,稳态模型评估胰岛素抵抗指数;TC,总胆固醇;TG,甘油三酯;HDL-C,高密度脂蛋白胆固醇;LDL-C,低密度脂蛋白胆固醇。
表 6 经干预后代谢相关的不良反应事件分析
Table 6. Analysis of metabolism-related adverse events after treatment
项目 例(%) 干预前后指标差值范围 TC升高 43(41.7) 0.03~2.65 mmol/L TG升高 24(23.3) 0.01~2.16 mmol/L HDL-C降低 53(51.5) 0.01~1.17 mmol/L LDL-C升高 43(41.7) 0.02~2.33 mmol/L CAP升高 9(8.7) 3.00~26.00 dB/m 体重升高 2(1.9) 1.00~4.50 kg/m2 HOMA-IR升高 26(25.2) 0.03~10.49 注:此表中提及的升高以及下降是以指标前后的绝对值进行定义。TC,总胆固醇;TG,甘油三酯;HDL-C,高密度脂蛋白胆固醇;LDL-C,低密度脂蛋白胆固醇;CAP,肝脏受控衰减参数;HOMA-IR,稳态模型评估胰岛素抵抗指数。
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[1] CHAN WK, CHUAH KH, RAJARAM RB, et al. Metabolic dysfunction-associated steatotic liver disease(MASLD): A state-of-the-art review[J]. J Obes Metab Syndr, 2023, 32( 3): 197- 213. DOI: 10.7570/jomes23052. [2] AU K, ZHENG MH, LEE WJ, et al. Resmetirom and metabolic dysfunction-associated steatohepatitis: Perspectives on multidisciplinary management from global healthcare professionals[J]. Curr Obes Rep, 2024, 13( 4): 818- 830. DOI: 10.1007/s13679-024-00582-z. [3] MIAO L, TARGHER G, BYRNE CD, et al. Current status and future trends of the global burden of MASLD[J]. Trends Endocrinol Metab, 2024, 35( 8): 697- 707. DOI: 10.1016/j.tem.2024.02.007. [4] LE MH, LE DM, BAEZ TC, et al. Global incidence of non-alcoholic fatty liver disease: a systematic review and meta-analysis of 63 studies and 1 201 807 persons[J]. J Hepatol, 2023, 79( 2): 287- 295. DOI: 10.1016/j.jhep.2023.03.040. [5] ESLAM M, FAN JG, YU ML, et al. The Asian Pacific association for the study of the liver clinical practice guidelines for the diagnosis and management of metabolic dysfunction-associated fatty liver disease[J]. Hepatol Int, 2025, 19( 2): 261- 301. DOI: 10.1007/s12072-024-10774-3. [6] SETHI S, WAKEHAM D, KETTER T, et al. Ketogenic diet intervention on metabolic and psychiatric health in bipolar and schizophrenia: A pilot trial[J]. Psychiatry Res, 2024, 335: 115866. DOI: 10.1016/j.psychres.2024.115866. [7] KANWAL F, NEUSCHWANDER-TETRI BA, LOOMBA R, et al. Metabolic dysfunction-associated steatotic liver disease: Update and impact of new nomenclature on the American Association for the Study of Liver Diseases practice guidance on nonalcoholic fatty liver disease[J]. Hepatology, 2024, 79( 5): 1212- 1219. DOI: 10.1097/hep.00000000000-00670. [8] PAPADOPOULOU SK, NIKOLAIDIS PT. Low-carbohydrate diet and human health[J]. Nutrients, 2023, 15( 8): 2004. DOI: 10.3390/nu15082004. [9] CAREY RM, WHELTON PK. Prevention, detection, evaluation, and management of high blood pressure in adults: Synopsis of the 2017 American college of cardiology/American heart association hypertension guideline[J]. Ann Intern Med, 2018, 168( 5): 351- 358. DOI: 10.7326/m17-3203. [10] ROMERO-GÓMEZ M, CORTEZ-PINTO H. Detecting liver fat from viscoelasticity: How good is CAP in clinical practice? The need for universal cut-offs[J]. J Hepatol, 2017, 66( 5): 886- 887. DOI: 10.1016/j.jhep.2017.01.029. [11] YANG XL, LI JX, HU DS, et al. Predicting the 10-year risks of atherosclerotic cardiovascular disease in Chinese population: The China-PAR project(prediction for ASCVD risk in China)[J]. Circulation, 2016, 134( 19): 1430- 1440. DOI: 10.1161/circulationaha.116.022367. [12] YANAI H, YOSHIDA H. Beneficial effects of adiponectin on glucose and lipid metabolism and atherosclerotic progression: Mechanisms and perspectives[J]. Int J Mol Sci, 2019, 20( 5): 1190. DOI: 10.3390/ijms2005-1190. [13] AHMED B, SULTANA R, GREENE MW. Adipose tissue and insulin resistance in obese[J]. Biomed Pharmacother, 2021, 137: 111315. DOI: 10.1016/j.biopha.2021.111315. [14] KATTAMURI L, DUGGAL S, APARECE JP, et al. Cardiovascular risk factor and atherosclerosis in rheumatoid arthritis(RA)[J]. Curr Cardiol Rep, 2025, 27( 1): 31. DOI: 10.1007/s11886-025-02198-8. [15] ALLAN GM, GARRISON S, MCCORMACK J. Comparison of cardiovascular disease risk calculators[J]. Curr Opin Lipidol, 2014, 25( 4): 254- 265. DOI: 10.1097/mol.0000000000000095. [16] DYŃKA D, KOWALCZE K, CHARUTA A, et al. The ketogenic diet and cardiovascular diseases[J]. Nutrients, 2023, 15( 15): 3368. DOI: 10.3390/nu15153368. [17] CAO QF, LI H, PAN XY, et al. A systematic review and meta-analysis of the predictive power of China-PAR against cardiovascular disease[J]. Clin Med Res, 2024, 22( 1): 28- 36. DOI: 10.3121/cmr.2024.1846. [18] ATHINARAYANAN SJ, HALLBERG SJ, MCKENZIE AL, et al. Impact of a 2-year trial of nutritional ketosis on indices of cardiovascular disease risk in patients with type 2 diabetes[J]. Cardiovasc Diabetol, 2020, 19: 208. DOI: 10.1186/s12933-020-01178-2. [19] TAGGART AKP, KERO J, GAN XD, et al.(D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G[J]. J Biol Chem, 2005, 280( 29): 26649- 26652. DOI: 10.1074/jbc.C500213200. [20] GUO YZ, ZHANG C, SHANG FF, et al. Ketogenic diet ameliorates cardiac dysfunction via balancing mitochondrial dynamics and inhibiting apoptosis in type 2 diabetic mice[J]. Aging Dis, 2020, 11( 2): 229. DOI: 10.14336/ad.2019.0510. [21] CHONG DY, GU YY, ZHANG TY, et al. Neonatal ketone body elevation regulates postnatal heart development by promoting cardiomyocyte mitochondrial maturation and metabolic reprogramming[J]. Cell Discov, 2022, 8: 106. DOI: 10.1038/s41421-022-00447-6. [22] LOPEZ-LOPEZ JP, GARCIA-PENA AA, MARTINEZ-BELLO D, et al. External validation and comparison of six cardiovascular risk prediction models in the Prospective Urban Rural Epidemiology(PURE)-Colombia study[J]. Eur J Prev Cardiol, 2025, 32( 7): 564- 572. DOI: 10.1093/eurjpc/zwae242. [23] MAKI KC, DICKLIN MR, KIRKPATRICK CF. Saturated fats and cardiovascular health: Current evidence and controversies[J]. J Clin Lipidol, 2021, 15( 6): 765- 772. DOI: 10.1016/j.jacl.2021.09.049. [24] CALZOLARI I, FUMAGALLI S, MARCHIONNI N, et al. Polyunsaturated fatty acids and cardiovascular disease[J]. Curr Pharm Des, 2009, 15( 36): 4094- 4102. DOI: 10.2174/138161209789909755. [25] ROS E, MARTÍNEZ-GONZÁLEZ MA, ESTRUCH R, et al. Mediterranean diet and cardiovascular health: Teachings of the PREDIMED study[J]. Adv Nutr, 2014, 5( 3): 330S- 336S. DOI: 10.3945/an.113.005389. [26] FERHATBEGOVIĆ L, MRŠIĆ D, KUŠLJUGIĆ S, et al. LDL-C: The only causal risk factor for ASCVD. why is it still overlooked and underestimated?[J]. Curr Atheroscler Rep, 2022, 24( 8): 635- 642. 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