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Feng J He

Publications and source records attributed to Feng J He.

17 recordsLinked to original sources
PubMed2006

Importance of salt in determining blood pressure in children: meta-analysis of controlled trials.

To assess the effect of reducing salt intake on blood pressure in children, we carried out a meta-analysis of controlled trials. Trials were included if participants were children (< or = 18 years), and duration of salt reduction must have been for > or = 2 weeks. Mean effect size was calculated using a fixed-effect model, because there was no significant heterogeneity. Ten trials of children and adolescents with 966 participants were included (median age: 13 years; range: 8 to 16 years; median duration: 4 weeks; range: 2 weeks to 3 years). Salt intake was reduced by 42% (interquartile range [IQR]: 7% to 58%). There were significant reductions in blood pressure: systolic: -1.17 mm Hg (95% CI: -1.78 to -0.56 mm Hg; P<0.001); diastolic: -1.29 mm Hg (95% CI: -1.94 to -0.65 mm Hg; P<0.0001). Three trials of infants with 551 participants were included (median duration: 20 weeks; range: 8 weeks to 6 months). Salt intake was reduced by 54% (IQR: 51% to 79%). There was a significant reduction in systolic blood pressure: -2.47 mm Hg (95% CI: -4.00 to -0.94 mm Hg; P<0.01). This is the first meta-analysis of salt reduction in children, and it demonstrates that a modest reduction in salt intake causes immediate falls in blood pressure and, if continued, may well lessen the subsequent rise in blood pressure with age. This would result in major reductions in cardiovascular disease. These results in conjunction with other evidence provide strong support for a reduction in salt intake in children.

Adolescent↗
PubMed2006

Fruit and vegetable consumption and stroke: meta-analysis of cohort studies.

BACKGROUND: Increased consumption of fruit and vegetables has been shown to be associated with a reduced risk of stroke in most epidemiological studies, although the extent of the association is uncertain. We quantitatively assessed the relation between fruit and vegetable intake and incidence of stroke in a meta-analysis of cohort studies. METHODS: We searched MEDLINE, EMBASE, the Cochrane Library, and bibliographies of retrieved articles. Studies were included if they reported relative risks and corresponding 95% CIs of stroke with respect to frequency of fruit and vegetable intake. FINDINGS: Eight studies, consisting of nine independent cohorts, met the inclusion criteria. These groups included 257,551 individuals (4917 stroke events) with an average follow-up of 13 years. Compared with individuals who had less than three servings of fruit and vegetables per day, the pooled relative risk of stroke was 0.89 (95% CI 0.83-0.97) for those with three to five servings per day, and 0.74 (0.69-0.79) for those with more than five servings per day. Subgroup analyses showed that fruit and vegetables had a significant protective effect on both ischaemic and haemorrhagic stroke. INTERPRETATION: Increased fruit and vegetable intake in the range commonly consumed is associated with a reduced risk of stroke. Our results provide strong support for the recommendations to consume more than five servings of fruit and vegetables per day, which is likely to cause a major reduction in strokes.

Cohort Studies↗
PubMed2006

The effect of sodium and angiotensin-converting enzyme inhibition on the classic circulating renin-angiotensin system in autosomal-dominant polycystic kidney disease patients.

BACKGROUND: It has been suggested that inappropriate stimulation of the renin-angiotensin system (RAS) is responsible for the increase in blood pressure that occurs in autosomal-dominant polycystic kidney disease (ADPKD) before the development of renal failure. However, the interpretation of previous studies in ADPKD patients is confounded by inadequate matching with control populations for blood pressure and renal function, or failure to control the sodium intake of participants. METHODS: A double-blind, placebo-controlled study of two different sodium intakes (350 and 50 mmol/day for 5 days) in a group of 11 hypertensive ADPKD patients and eight matched control subjects with essential hypertension. In addition, blood pressure and hormonal responses were measured after the administration of the angiotensin-converting enzyme inhibitor enalapril for 3 days. RESULTS: Blood pressure and hormonal responses of the RAS after a reduction in sodium intake and after the administration of enalapril were identical in ADPKD patients and controls. CONCLUSIONS: Activation of the classic circulating RAS is no greater in hypertensive ADPKD patients than in individuals with essential hypertension.

Adult↗
PubMed2005

Modest salt reduction reduces blood pressure and urine protein excretion in black hypertensives: a randomized control trial.

High blood pressure and proteinuria are the major risk factors for cardiovascular and renal disease. In black individuals, there is an increased risk of hypertension, stroke, heart failure, and kidney disease. There are no controlled studies of the effects of reducing salt intake on blood pressure and urine protein excretion in black individuals. Therefore, the aim of our study was to determine the effects of modest salt restriction on blood pressure and urine protein excretion in nondiabetic black hypertensive subjects. The study was randomized, double blind, and placebo controlled. After run-in periods on their usual diet and on reduced salt, participants continued to restrict their salt intake and then received either slow sodium tablets, designed to bring their salt intake back to normal, or placebo tablets for 4 weeks in a randomized, double-blind, crossover study. In the 40 who completed the study, urinary sodium excretion fell on slow sodium to placebo from 169+/-73 to 89+/-52 mmol per 24 hours (P<0.001; approximately 10 to 5 g salt per day). Blood pressure fell from 159/101+/-13/8 to 151/98+/-13/8 mm Hg (P<0.01). Protein excretion fell from 93+/-48 mg to 75+/-30 mg per 24 hours (P<0.008). Thus, reducing salt intake from approximately 10 to 5 g per day reduced blood pressure and urine protein excretion in black hypertensives. In light of these findings, we would recommend that all black individuals with raised blood pressure reduce their salt intake to < or =5 g per day.

Adult↗
PubMed2005

Modest salt reduction lowers blood pressure in isolated systolic hypertension and combined hypertension.

Many randomized trials have shown that a reduction in salt intake lowers blood pressure in hypertensive individuals. However, few have looked at the effects according to hypertension category. A recent analysis of the third and fourth National Health and Nutrition Examination Survey suggests that salt intake may not be related to blood pressure in isolated systolic or combined hypertension. To look at this further, we reanalyzed the data of our previous salt reduction trials. Hypertensive individuals were studied in randomized double-blind crossover studies: 1 month of usual salt intake compared with 1 month of reduced salt intake. In isolated systolic hypertension (n=24), blood pressure was reduced from 166+/-19/86+/-7 to 156+/-20/85+/-7 mm Hg (systolic P<0.001; diastolic P=0.459) with a reduction in urinary sodium from 175+/-51 to 87+/-38 mmol per 24-hour period (10.3 to 5.1 g per day of salt). In combined hypertension (n=88), blood pressure was reduced from 161+/-16/100+/-9 to 154+/-17/96+/-9 mm Hg (P<0.001) with a reduction urinary sodium from 176+/-65 to 98+/-51 mmol per 24-hour period (10.4 to 5.8 g per day of salt). These results demonstrate that salt reduction has a significant effect on blood pressure in isolated systolic and combined hypertension. The fall in systolic observed in isolated systolic hypertension would be predicted to reduce stroke by approximately one third, ischemic heart disease by one quarter, and heart failure by one quarter in the population between 60 and 80 years of age, in whom isolated systolic hypertension is the predominate form of hypertension and carries the highest risk. These results provide strong support for universal salt reduction in all hypertensives.

Adult↗
PubMed2005

Systematic review of combined angiotensin-converting enzyme inhibition and angiotensin receptor blockade in hypertension.

Some evidence suggests that long-term angiotensin-converting enzyme (ACE) inhibition may become less effective, thereby increasing angiotensin II levels, which could be inhibited by the addition of an angiotensin receptor blocker. We conducted a meta-analysis of randomized trials with searches of MEDLINE, EMBASE, and Cochrane databases. Overall, the combination of an ACE inhibitor and an angiotensin receptor blocker reduced ambulatory blood pressure by 4.7/3.0 mm Hg (95% confidence interval [CI], 2.9 to 6.5/1.6 to 4.3) compared with ACE inhibitor monotherapy and 3.8/2.9 mm Hg (2.4 to 5.3/0.4 to 5.4) compared with angiotensin receptor blocker monotherapy. Clinic blood pressure was reduced by 3.8/2.7 mm Hg (0.9 to 6.7/0.8 to 4.6) and 3.7/2.3 mm Hg (0.4 to 6.9/0.2 to 4.4) compared with ACE inhibitor and angiotensin receptor blocker, respectively. However, the majority of these studies used submaximal doses or once-daily dosing of shorter-acting ACE inhibitors and, when a larger dose of shorter-acting ACE inhibitor was given or a longer-acting ACE inhibitor was used, there was generally no additive effect of the angiotensin receptor blocker on blood pressure. Proteinuria was reduced by the combination compared with ACE inhibitor and angiotensin receptor blocker monotherapy, an effect that was independent of blood pressure in several studies, suggesting that the combination could have benefits in proteinuric nephropathies. None of the studies was of sufficient size and duration to determine whether there may be safety concerns. In conclusion, although there is a small additive effect on blood pressure with an ACE inhibitor-angiotensin receptor blocker combination, the routine use of this combination in uncomplicated hypertension is not recommended until more carefully controlled studies are performed.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives.

Randomized trials have shown that increasing potassium intake lowers blood pressure. However, most previous trials used potassium chloride, whereas potassium in fruits and vegetables is not a chloride salt. It is unclear whether a nonchloride salt of potassium has a greater or lesser effect on blood pressure compared with potassium chloride. We performed a randomized crossover trial comparing potassium chloride with potassium citrate (96 mmol/d, each for 1 week) in 14 hypertensive individuals. At baseline, blood pressure was 151+/-16/93+/-7 mm Hg with a 24-hour urinary potassium of 81+/-24 mmol. During the randomized crossover part of the study, blood pressure was 140+/-12/88+/-7 mm Hg with potassium chloride (24-hour urinary potassium: 164+/-36 mmol) and 138+/-12/88+/-6 mm Hg with potassium citrate (24-hour urinary potassium: 160+/-33 mmol). These blood pressures were significantly lower compared with that at baseline; however, there was no significant difference in blood pressure between potassium chloride and potassium citrate, mean difference (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. Our results, in conjunction with the evidence from many previous trials that potassium chloride has a significant blood pressure-lowering effect, suggest that potassium citrate has a similar effect on blood pressure as potassium chloride. These results support other evidence for an increase in potassium intake and indicate that potassium does not need to be given in the form of chloride to lower blood pressure. Increasing the consumption of foods high in potassium is likely to have the same effect on blood pressure as potassium chloride.

Adult↗
PubMed2004

Plasma sodium: ignored and underestimated.

Salt intake is a major regulator of blood pressure. There is evidence that those who develop high blood pressure have an underlying defect in the ability of the kidney to excrete salt. It has been suggested that this results in a greater tendency to retain sodium and an increased compensatory response that is responsible for the rise in blood pressure. There is also evidence suggesting that small increases in plasma sodium may directly affect blood pressure, independent of the associated expansion in extracellular volume. We reanalyzed 3 types of studies of changing salt intake. (1) An acute and large reduction in salt intake from 350 mmol/d to 10 to 20 mmol/d for 5 days in hypertensives and normotensives was associated with a fall in plasma sodium of approximately 3 mmol/L (P<0.001). (2) Progressive increases in salt intake from 10 to 250 mmol/d by a daily amount of 50 mmol in normotensives caused increases in plasma sodium (P<0.001). (3) Longer-term modest reduction in salt intake in hypertensives was studied in double-blind randomized crossover studies; 1 month of usual salt intake ( approximately 170 mmol/d) compared with reduced salt intake ( approximately 100 mmol/d). There was a decrease in plasma sodium of 0.4+/-0.2 mmol/L (P<0.05), which was weakly but significantly correlated with the fall in systolic blood pressure (r=0.18; P<0.05). These studies demonstrate that an increase or a decrease in salt intake causes changes in plasma sodium. Small changes in plasma sodium alter extracellular volume, which may influence blood pressure. Changes in plasma sodium may also affect blood pressure directly.

Adult↗
PubMed2004

Plasma sodium and hypertension.

Dietary salt is the major cause of the rise in the blood pressure with age and the development of high blood pressure in populations. However, the mechanisms whereby salt intake raises the blood pressure are not clear. Existing concepts focus on the tendency for an increase in extracellular fluid volume (ECV), but an increased salt intake also induces a small rise in plasma sodium, which increases a transfer of fluid from the intracellular to the extracellular space, and stimulates the thirst center. Accordingly, the rise in plasma sodium is responsible for the tendency for an increase in ECV. Although the change in ECV may have a pressor effect, the associated rise in plasma sodium itself may also cause the blood pressure to rise. There is some evidence in patients with essential hypertension and the spontaneously hypertensive rat (SHR) that plasma sodium may be raised by 1 to 3 mmol/L. An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Such a rise can also induce changes in cultured vascular tissue similar to those that occur in the vessels of humans and animals on a high sodium diet, independent of the blood pressure. We suggest that a small increase in plasma sodium may be part of the mechanisms whereby dietary salt increases the blood pressure.

Animals↗
PubMed2003

How far should salt intake be reduced?

The current public health recommendations are to reduce salt intake from 9 to 12 g/d to 5 to 6 g/d. However, these values are based on what is feasible rather than the maximum effect of salt reduction. In a meta-analysis of longer-term trials, we looked at the dose response between salt reduction and fall in blood pressure and compared this with 2 well-controlled studies of 3 different salt intakes. All 3 studies demonstrated a consistent dose response to salt reduction within the range of 12 to 3 g/d. A reduction of 3 g/d predicts a fall in blood pressure of 3.6 to 5.6/1.9 to 3.2 mm Hg (systolic/diastolic) in hypertensives and 1.8 to 3.5/0.8 to 1.8 mm Hg in normotensives. The effect would be doubled with a 6 g/d reduction and tripled with a 9 g/d reduction. A conservative estimate indicates that a reduction of 3 g/d would reduce strokes by 13% and ischemic heart disease (IHD) by 10%. The effects would be almost doubled with a 6 g/d reduction and tripled with a 9 g/d reduction. Reducing salt intake by 9 g/d (eg, from 12 to 3 g/d) would reduce strokes by approximately one third and IHD by one quarter, and this would prevent approximately 20 500 stroke deaths and 31 400 IHD deaths a year in the United Kingdom. The current recommendations to reduce salt intake from 9 to 12 g/d to 5 to 6 g/d will have a major effect on blood pressure and cardiovascular disease but are not ideal. A further reduction to 3 g/d will have a much greater effect and should now become the long-term target for population salt intake worldwide.

Adult↗
PubMed2003

Salt, blood pressure and the renin-angiotensin system.

Much evidence from epidemiological, migration, intervention, animal and genetic studies suggests that salt intake plays an important role in regulating blood pressure (BP). At the same time, many clinical trials have shown that reducing salt intake lowers BP. However, the magnitude of the fall in BP for a given reduction in salt intake varies with age, ethnic group and BP levels. This difference has been suggested to be related to the responsiveness of the renin-angiotensin system (RAS). However, the sympathetic nervous system, the kallikrein-kinin system, the nitric oxide system, and many eicosanoids may also play a role. In this article, we address the important role of the RAS in determining the fall in BP with salt reduction.

Animals↗
PubMedDate not supplied

Salt in food.

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Cardiovascular Diseases↗