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新研究挑战主流观点:限盐,错了吗?


西安交通大学医学院第一附属医院 牟建军、刘治全

  我们的祖先在2600多年前就认识到“多食咸,则脉凝泣而变色”,尽管近百年来有关盐与血压的大量流行病学、基础和临床研究结果基本肯定了盐是高血压重要易患因素,多数高血压患者限盐后血压降低。但“盐与血压及心血管健康”的关系一直是学界争论焦点,其争论核心仍是有无必要在全民提倡限盐,及减少盐摄入是否会降低人群总死亡率和心血管病发生率。近期发表的荟萃分析(Am J Hypertens 2011,24:843)及对列随访研究(JAMA 2011,305:1777)结果提示,摄盐量与心血管病死亡率呈负相关,激发了又一轮争论。

Am J Hypertens. 2011 Aug;24(8):843-53.

Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review).

Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Peninsula College of Medicine and Dentistry, University of Exeter, Exeter, UK.

BACKGROUND: Although meta-analyses of randomized controlled trials (RCTs) of salt reduction report a reduction in the level of blood pressure (BP), the effect of reduced dietary salt on cardiovascular disease (CVD) events remains unclear.

METHODS: We searched for RCTs with follow-up of at least 6 months that compared dietary salt reduction (restricted salt dietary intervention or advice to reduce salt intake) to control/no intervention in adults, and reported mortality or CVD morbidity data. Outcomes were pooled at end of trial or longest follow-up point.

RESULTS: Seven studies were identified: three in normotensives, two in hypertensives, one in a mixed population of normo- and hypertensives and one in heart failure. Salt reduction was associated with reductions in urinary salt excretion of between 27 and 39 mmol/24 h and reductions in systolic BP between 1 and 4 mm Hg. Relative risks (RRs) for all-cause mortality in normotensives (longest follow-up-RR: 0.90, 95% confidence interval (CI): 0.58-1.40, 79 deaths) and hypertensives (longest follow-up RR 0.96, 0.83-1.11, 565 deaths) showed no strong evidence of any effect of salt reduction CVD morbidity in people with normal BP (longest follow-up: RR 0.71, 0.42-1.20, 200 events) and raised BP at baseline (end of trial: RR 0.84, 0.57-1.23, 93 events) also showed no strong evidence of benefit. Salt restriction increased the risk of all-cause mortality in those with heart failure (end of trial RR 2.59, 1.04-6.44, 21 deaths).We found no information on participant's health-related quality of life.

CONCLUSIONS: Despite collating more event data than previous systematic reviews of RCTs (665 deaths in some 6,250 participants) there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or CVD morbidity. Our estimates of benefits from dietary salt restriction are consistent with the predicted small effects on clinical events attributable to the small BP reduction achieved.

JAMA. 2011 May 4;305(17):1777-85.

Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion.

Stolarz-Skrzypek K, Kuznetsova T, Thijs L, Tikhonoff V, Seidlerová J, Richart T, Jin Y, Olszanecka A, Malyutina S, Casiglia E, Filipovsky J, Kawecka-Jaszcz K, Nikitin Y, Staessen JA; European Project on Genes in Hypertension (EPOGH) Investigators.

Studies Coordinating Centre, Division of Hypertension and Cardiovascular Rehabilitation, Department of Cardiovascular Diseases, University of Leuven, Leuven, Belgium.

CONTEXT: Extrapolations from observational studies and short-term intervention trials suggest that population-wide moderation of salt intake might reduce cardiovascular events.

OBJECTIVE: To assess whether 24-hour urinary sodium excretion predicts blood pressure (BP) and health outcomes.

DESIGN, SETTING, AND PARTICIPANTS: Prospective population study, involving 3681 participants without cardiovascular disease (CVD) who are members of families that were randomly enrolled in the Flemish Study on Genes, Environment, and Health Outcomes (1985-2004) or in the European Project on Genes in Hypertension (1999-2001). Of 3681 participants without CVD, 2096 were normotensive at baseline and 1499 had BP and sodium excretion measured at baseline and last follow-up (2005-2008).

MAIN OUTCOME MEASURES: Incidence of mortality and morbidity and association between changes in BP and sodium excretion. Multivariable-adjusted hazard ratios (HRs) express the risk in tertiles of sodium excretion relative to average risk in the whole study population.

RESULTS: Among 3681 participants followed up for a median 7.9 years, CVD deaths decreased across increasing tertiles of 24-hour sodium excretion, from 50 deaths in the low (mean, 107 mmol), 24 in the medium (mean, 168 mmol), and 10 in the high excretion group (mean, 260 mmol; P < .001), resulting in respective death rates of 4.1% (95% confidence interval [CI], 3.5%-4.7%), 1.9% (95% CI, 1.5%-2.3%), and 0.8% (95% CI, 0.5%-1.1%). In multivariable-adjusted analyses, this inverse association retained significance (P = .02): the HR in the low tertile was 1.56 (95% CI, 1.02-2.36; P = .04). Baseline sodium excretion predicted neither total mortality (P = .10) nor fatal combined with nonfatal CVD events (P = .55). Among 2096 participants followed up for 6.5 years, the risk of hypertension did not increase across increasing tertiles (P = .93). Incident hypertension was 187 (27.0%; HR, 1.00; 95% CI, 0.87-1.16) in the low, 190 (26.6%; HR, 1.02; 95% CI, 0.89-1.16) in the medium, and 175 (25.4%; HR, 0.98; 95% CI, 0.86-1.12) in the high sodium excretion group. In 1499 participants followed up for 6.1 years, systolic blood pressure increased by 0.37 mm Hg per year (P < .001), whereas sodium excretion did not change (-0.45 mmol per year, P = .15). However, in multivariable-adjusted analyses, a 100-mmol increase in sodium excretion was associated with 1.71 mm Hg increase in systolic blood pressure (P.<001) but no change in diastolic BP.

CONCLUSIONS: In this population-based cohort, systolic blood pressure, but not diastolic pressure, changes over time aligned with change in sodium excretion, but this association did not translate into a higher risk of hypertension or CVD complications. Lower sodium excretion was associated with higher CVD mortality.

新研究:有瑕疵,恐误导

  这两项研究因其设计和方法学上的瑕疵,所得结果与学术界主流观点背道而驰,产生一定误导效应,给大众和社会造成不良影响,应引起关注。

  发表于JAMA的队列随访研究:设计和方法存在缺陷

  ①分组不均一,不具可比性。该研究中最低钠组在基线时已显示出较高的心血管风险,如年龄大、收缩压及胆固醇水平偏高、接受教育水平低等;②尿钠测量欠准。在通常情况下,收集24小时尿是反映钠盐摄入的标准方法,由于尿钠排泄量个体内差异较大,故仅收集一次24小时尿样本,很难反映真实情况;③低钠组平均尿钠水平仅为50 mmol/d,这与欧洲人群日常实际摄钠量相差甚远;④低钠组人群尿肌酐、尿钾和尿量均较低且不能用体重指数解释,说明其可能并存其他疾病或是尿液收集不足,而不是钠摄入量低;⑤该队列人群总体年龄较轻,心血管事件发生率偏低,进而影响到随访结果。

  发表于Am J Hypertens的荟萃分析:缺点颇多,其结果不具说服力

  该荟萃分析共纳入7项研究,其中1项是评估心力衰竭(心衰)患者钠盐摄入量与心血管健康的关系。结果显示,与每日摄入1.8g钠相比,每日摄入2.7g钠者死亡、住院次数及终点事件总体减少25%。显然,这一结果也仅限于此类特殊患者,无法推及到其他人群。其余6项研究评估了限盐对血压的影响,结果未发现限盐与心血管死亡和发病相关,而这些研究存在样本量过小、随访时间短、未排除钾摄入量干扰及资料收集不齐等缺点。除此之外,这些研究设计本身旨在探求限盐的降压作用,而非心血管健康。因此,不具说服力。

限盐:作用确切,不容置疑

  盐摄入过多既可引起血压升高,使心脑血管风险增加;亦可独立于血压直接导致血管内皮功能受损、氧化应激、激活肾素-血管紧张素-醛固酮系统(RAAS)、刺激炎症并产生胰岛素抵抗等,进而造成心、脑、肾靶器官损害。盐与高血压、心脑血管疾病的关系已被大量动物实验、移民调查、遗传学研究、荟萃分析、人群和临床干预试验及国家限盐措施效果评价所证实。可见,高盐摄入是高血压和心脑血管病的一大危险因素,限盐是降压、防治心脑血管病的重要措施。

  限盐和血压

  流行病学调查研究(INTERSALT)采用标准化血压测量、尿液收集和钠集中测定的方法,对1万余名成人受试者的尿排钠量与血压的关系进行了分析。结果提示,24小时尿钠排泄量与收缩压的增龄性改变密切相关(P<0.001)。据推算,如每日减少100mmol钠的摄入,年龄25~55岁人群收缩压随年龄的增长亦会减少9mmHg。该结果提示,钠平均摄入量低会对血压随年龄的改变产生良性影响,利于降低心血管病患病率。

  上世纪70年代全球进行的一系列中度限盐试验(每日钠摄入量为70~100mmol)结果表明,中度限盐亦可降低血压正常和高血压患者的收缩压和舒张压水平。目前认为,长期限盐有助于降低血压正常人群的血压和减少高血压患者降压药的用量;长期限盐干预有助于预防或减缓血压随年龄上升,从而有利于减少心血管病的发生与死亡。

  限盐和心脑血管病

  斯特拉组洛(Strazzullo)等进行的迄今最大规模探讨盐与心脑血管关系的荟萃分析共纳入177025名受试者(平均随访3.5~19年),结果显示,高盐摄入明显增加卒中及心血管疾病风险。

  美国限盐干预试验(TOHPⅠ、TOHPⅡ)对限盐降低心血管事件风险更具说服力。TOHPⅠ研究限盐组通过18个月的干预,盐摄入量较对照组减少了44mmol/24h;TOHPⅡ研究限盐组通过36~48个月的干预,盐摄入量较对照组减少了33mmol/24h。两项研究队列分别随访15年、10年,将两组数据合并,总共有200例心血管事件发生。经校正种族、年龄、性别后,限盐组心血管事件发生危险较对照组低25%(7.5%对9.0%,相对危险(RR)=0.75,P=0.04);进一步校正基线尿钠水平及体重后,危险性降低达30%。研究结果提示,限盐能减少心血管事件发生的长期风险。

  全民限盐实践

  自上世纪50年代末以来,日本政府开展了全国性限盐运动,居民盐摄入量从平均13.5g/d降至12.1g/d,摄盐量较高的Akita地区从18.0g/d降至14.0g/d,结果卒中死亡率下降了近80%。

  据推测,在美国如每人每天减少3g盐摄入,则每年可减少新发冠心病6万~12万例,减少卒中3.2万~6.6万例,减少心梗5.4万~9.9万例,各种原因死亡可减少4.4万~9.2万例,总体可挽救19.4万~39.2万个生命年,每年可节省医疗花费100亿~240亿美元。

  英国数据显示,人群每天减少5~6g盐摄入,可使卒中风险降低24%,冠心病风险降低18%,每年可减少卒中和心脏死亡3.5万例,如全球实施这一措施每年可减少卒中和心脏死亡25万例。

  芬兰近30年通过政府干预使加工食品中盐的含量减少近1/3,降低了卒中和心血管病发病率75%~80%,居民平均寿命延长5~6年。

须考虑血压的盐敏感性问题

  研究表明,不同个体对盐负荷的反应呈离散性分布,存在盐敏感性问题。

  盐敏感性通常涉及人口、民族、社会因素及肾脏功能、激素和饮食习惯等,故盐敏感者在血压正常人群中的检出率为15%~42%,高血压人群中为28%~74%。不同种族和人群盐敏感性个体的检出率不同,血压的盐敏感性随年龄增长而增加,特别是在高血压患者中。人群中盐敏感者比例越大,则盐与血压的联系就越强。相反,比例越小联系越弱,甚至消失。有学者研究认为,当人群中盐敏感者的比例小于10%时,血压与盐的联系就可能被掩盖。因此,在一个日均摄盐量差别不大的人群中,很可能难以发现盐与血压的联系。

  研究发现,盐敏感者较早出现心、脑、肾、血管等靶器官损害。有研究发现,年龄25岁以上血压正常盐敏感者的远期(27年)累计生存率与高血压患者相当;而高血压盐敏感者的远期(18年)累计无心血管事件发生率和死亡率远低于高血压盐不敏感者。

  亦有研究结果提示,盐敏感性是心血管事件独立危险因素,被美国高血压学会(ASH)2005年高血压新定义确立为高血压早期损害标志。

  临床观察证明,在一个人群内个体间的血压对限盐亦呈现不同反应。米勒(Miller)等通过对血压正常个体进行饮食限盐试验发现,尽管限盐期血压明显降低,但年龄40岁以上与年龄40岁以下个体对限盐的反应明显不同,前者血压平均降低5.7mmHg,而后者不明显,有20%的人甚而表现为血压升高。后者可能有所谓反调节机制参与,即当盐的摄入量减少至一定程度时,会激活体内反调节激素,促使血压升高。

  因此,不难解释为何米奇利(Midgley)等分析了全球56个限盐临床试验报告,胡普尔(Hooper)等对经严格筛选的全球11项对照试验进行荟萃分析,及最近美国高血压杂志对7项长期限盐干预预防心血管病发病研究的回顾分析来看,在血压正常人群限盐效果与预想的结果总是不一致。

  总之,限盐的降压效应及心血管保护作用与盐敏感性相关。限盐降压试验的效果在一定程度上取决于人群中盐敏感者所占比例,一些在正常人群中实施的限盐试验可能因盐敏感者比例太小,总体降压效应被掩盖。

补钾:为限钠加分

  有证据表明,钠与其他多种阳离子或阴离子(尤其是钾、钙、氯等)存在相互作用,在调控和维持血压稳定及心血管健康中发挥着重要作用。

  钾作为钠的“拮抗剂”,其摄入量的多少与盐敏感性高血压相关。因此,限盐对血压和心血管疾病的影响与钾的摄入量相关。

  国际上著名的高血压膳食疗法(DASH)研究给参与者提供了所有的食物,以期严格调整钠的摄入,并保证足够的钾和钙的摄入。研究结果显示,与对照正常钠(control normal sodium)摄入参与者相比,对照中间钠(control intermediate sodium)摄入者每日钠的排泄量减少了35mmol,收缩压下降2.1mmHg(95%置信区间[CI]:3.4~0.8mmHg),舒张压下降1.1mmHg(95%CI:1.9~0.2mmHg)。

  我国人群食盐摄入量普遍偏高,钾的摄入量较低,仅为欧美国家人群的1/2~1/3。这种高钠、低钾,钾/钠比值偏低的情况,是我国人群高血压及心脑血管发病的重要危险因素。

“J”型曲线:适当人群,适度限盐

  盐是维持人类身体机能的重要元素,目前的问题是,高盐摄入引起高血压,并对心血管系统造成损害。

  如同血压、血糖一样(降的过低会危害健康),过分地限制钠盐摄入也会影响身体健康。急性、过度限盐可能导致肾素-血管紧张素-醛固酮系统(RAAS)、交感神经激活,部分营养物质缺乏及应激能力减退等,对机体造成损害。

  分析既往限盐干预试验可发现,基于“高”摄盐量群体(>5g/d钠)的研究表明,盐与心血管疾病呈正相关;而基于“中低”摄盐量群体(2~4g/d钠)的研究结果显示,盐与心血管疾病不相关或呈负相关,即摄盐量越低者心血管死亡率越高。

  鉴于此,美国学者爱德曼(Alderman)提出,盐摄入量与心血管疾病存在“J”型曲线相关的假说(图)。


  图:饮食钠摄入与血压和心血管病事件的关系:与血压呈线性,与心血管事件呈“J”型。

  根据这一概念,即有一个与心血管健康相匹配的最适钠摄入范围,过高或过低都可能不利于身体健康。

  最近发表的3篇涉及尿排钠量低与死亡率增加或疾病恶化相关的研究报告,均提示了摄盐量较低人群的相关结果。

Diabetes Care. 2011 Mar;34(3):703-9.

Dietary salt intake and mortality in patients with type 2 diabetes.

Ekinci EI, Clarke S, Thomas MC, Moran JL, Cheong K, MacIsaac RJ, Jerums G.

Endocrine Centre, Austin Health and the University of Melbourne, Victoria, Australia.

OBJECTIVE: Many guidelines recommend that patients with type 2 diabetes should aim to reduce their intake of salt. However, the precise relationship between dietary salt intake and mortality in patients with type 2 diabetes has not been previously explored.

RESEARCH DESIGN AND METHODS: Six hundred and thirty-eight patients attending a single diabetes clinic were followed in a prospective cohort study. Baseline sodium excretion was estimated from 24-h urinary collections (24hU(Na)). The predictors of all-cause and cardiovascular mortality were determined by Cox regression and competing risk modeling, respectively.

RESULTS: The mean baseline 24hU(Na) was 184 ± 73 mmol/24 h, which remained consistent throughout the follow-up (intraindividual coefficient of variation [CV] 23 ± 11%). Over a median of 9.9 years, there were 175 deaths, 75 (43%) of which were secondary to cardiovascular events. All-cause mortality was inversely associated with 24hU(Na), after adjusting for other baseline risk factors (P < 0.001). For every 100 mmol rise in 24hU(Na), all-cause mortality was 28% lower (95% CI 6-45%, P = 0.02). After adjusting for the competing risk of noncardiovascular death and other predictors, 24hU(Na) was also significantly associated with cardiovascular mortality (sub-hazard ratio 0.65 [95% CI 0.44-0.95]; P = 0.03).

CONCLUSIONS: In patients with type 2 diabetes, lower 24-h urinary sodium excretion was paradoxically associated with increased all-cause and cardiovascular mortality. Interventional studies are necessary to determine if dietary salt has a causative role in determining adverse outcomes in patients with type 2 diabetes and the appropriateness of guidelines advocating salt restriction in this setting.

Diabetes Care. 2011 Apr;34(4):861-6.

The association between dietary sodium intake, ESRD, and all-cause mortality in patients with type 1 diabetes.

Thomas MC, Moran J, Forsblom C, Harjutsalo V, Thorn L, Ahola A, Wadén J, Tolonen N, Saraheimo M, Gordin D, Groop PH; FinnDiane Study Group.

1Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.

OBJECTIVE: Many guidelines recommend reduced consumption of salt in patients with type 1 diabetes, but it is unclear whether dietary sodium intake is associated with mortality and end-stage renal disease (ESRD).

RESEARCH DESIGN AND METHODS: In a nationwide multicenter study (the FinnDiane Study) between 1998 and 2002, 2,807 enrolled adults with type 1 diabetes without ESRD were prospectively followed. Baseline urinary sodium excretion was estimated on a 24-h urine collection. The predictors of all-cause mortality and ESRD were determined by Cox regression and competing risk modeling, respectively.

RESULTS: The median follow-up for survival analyses was 10 years, during which 217 deaths were recorded (7.7%). Urinary sodium excretion was nonlinearly associated with all-cause mortality, such that individuals with the highest daily urinary sodium excretion, as well as the lowest excretion, had reduced survival. This association was independent age, sex, duration of diabetes, the presence and severity of chronic kidney disease (CKD) (estimated glomerular filtration rate [eGFR] and log albumin excretion rate), the presence of established cardiovascular disease, and systolic blood pressure. During follow-up, 126 patients developed ESRD (4.5%). Urinary sodium excretion was inversely associated with the cumulative incidence of ESRD, such that individuals with the lowest sodium excretion had the highest cumulative incidence of ESRD.

CONCLUSIONS: In patients with type 1 diabetes, sodium was independently associated with all-cause mortality and ESRD. Although we have not demonstrated causality, these findings support the calls for caution before applying salt restriction universally. Clinical trials must be performed in diabetic patients to formally test the utility/risk of sodium restriction in this setting.

  由此可见,并非“盐摄入越少越好”,适当人群、适度限盐才是预防心血管疾病有效的防治方法。

  对于摄盐量过高的人群,限盐不仅可降低血压,亦可降低心血管病风险。盐与心血管健康的“J”型曲线关系在一定程度上为今后探索不同人群、不同病理状况下,摄入多少盐量方有利于心血管健康提供了新思路。

  自阿马尔(Ambard)和博雅尔(Beaujard)于1904年首次报告盐摄入与血压相关,一个多世纪以来人类进行了大量限盐试验。总体上讲,限盐不仅能降低血压,还能降低心脑血管风险。有专家认为,限盐是自19世纪清洁水工程以来,人类最大的一项健康促进活动。国内外诸多专家委员会都将限盐列为防治高血压的一项重要措施,在人群中推广。2006年WHO 明确指出:“已有的科学证据足以证明在整个人群通过各种有效的公共卫生措施减少钠的摄入是正确的”,并建议盐(氯化钠)的每日摄入量应限于5 g(或2 g钠)。我国人群食盐量普遍偏高,尤其是居住在北方、寒冷地区的居民。因此, 提倡国人适当减少盐的摄入,有助于降低我国高血压和心脑血管病的发生和死亡率。

  当然,近一个世纪的探索与争论,盐与血压及心血管关系尚有许多问题有待解决。无论在国内还是国际上,对限盐特别是限盐是否有利于心血管健康的争议无疑还将继续下去。总结已取得的成绩、认识问题的复杂性,必将有利于拓宽我们的研究思路和视野,探索出科学有效的高血压预防和治疗措施。

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