適切な塩分摂取量

行き過ぎた減塩は動脈硬化を起こす。また認知症のリスクも上げる。

これは脳神経への血流を確保する手段として、高齢になってくると、次第に高血圧になっていくことは自然なことです。

健康な中高年者のうち、少しずつ体重が増えていく人達の方がむしろ、健康寿命が長い。

まず、ここに書き記すことは腎不全の進んだ患者では当て嵌まらないことで、Na+もK+も高値になると共に有害になることを断っておかねばなりません。

大量に汗をかくアスリートや肉体労働者は違った条件になります。

しかし、多くの人にとっては少なすぎる塩分量は、多すぎる塩分量よりも害が大きいということを示しています。

血圧を下げることを最終目標とせず、健康寿命が最大化することが幸せなのだと思います。

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高血圧の人にとって、増塩（この研究の場合、約17.5g以上）が疾患のリスクを高めるとともに、減塩（この研究の場合、約7.5g以下）もリスクを高める

正常な血圧の人にとって、増塩は疾患のリスクを高めないが、一方で減塩はリスクを高める

Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies

The Lancet Volume 388, No. 10043, p465–475, 30 July 2016

Summary

Background

Several studies reported a U-shaped association between urinary sodium excretion and cardiovascular disease events and mortality. Whether these associations vary between those individuals with and without hypertension is uncertain. We aimed to explore whether the association between sodium intake and cardiovascular disease events and all-cause mortality is modified by hypertension status.

Methods

In this pooled analysis, we studied 133 118 individuals (63 559 with hypertension and 69 559 without hypertension), median age of 55 years (IQR 45–63), from 49 countries in four large prospective studies and estimated 24-h urinary sodium excretion (as group-level measure of intake). We related this to the composite outcome of death and major cardiovascular disease events over a median of 4·2 years (IQR 3·0–5·0) and blood pressure.

Findings

Increased sodium intake was associated with greater increases in systolic blood pressure in individuals with hypertension (2·08 mm Hg change per g sodium increase) compared with individuals without hypertension (1·22 mm Hg change per g; p_interaction<0·0001). In those individuals with hypertension (6835 events), sodium excretion of 7 g/day or more (7060 [11%] of population with hypertension: hazard ratio [HR] 1·23 [95% CI 1·11–1·37]; p<0·0001) and less than 3 g/day (7006 [11%] of population with hypertension: 1·34 [1·23–1·47]; p<0·0001) were both associated with increased risk compared with sodium excretion of 4–5 g/day (reference 25% of the population with hypertension). In those individuals without hypertension (3021 events), compared with 4–5 g/day (18 508 [27%] of the population without hypertension), higher sodium excretion was not associated with risk of the primary composite outcome (≥7 g/day in 6271 [9%] of the population without hypertension; HR 0·90 [95% CI 0·76–1·08]; p=0·2547), whereas an excretion of less than 3 g/day was associated with a significantly increased risk (7547 [11%] of the population without hypertension; HR 1·26 [95% CI 1·10–1·45]; p=0·0009).

Interpretation

Compared with moderate sodium intake, high sodium intake is associated with an increased risk of cardiovascular events and death in hypertensive populations (no association in normotensive population), while the association of low sodium intake with increased risk of cardiovascular events and death is observed in those with or without hypertension. These data suggest that lowering sodium intake is best targeted at populations with hypertension who consume high sodium diets.

Funding

Full funding sources listed at end of paper (see Acknowledgments).

食塩摂取量が最も少ないグループが、心筋梗塞や脳卒中による死亡率が一番高く、摂取量の最も多かったグループが、一番死亡率が低かった

Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I)

The Lancet Volume 351, No. 9105, p781–785, 14 March 1998

Summary

Background

Population-wide restriction of dietary sodium has been recommended. However, little evidence directly links sodium intake to morbidity and mortality. The aim of this study was to assess the relation of sodium intake to subsequent all-cause and cardiovascular-disease (CVD) mortality in a general population.

Methods

The first National Health and Nutrition Examination Survey established baseline information during 1971–75 in a representative sample of 20 729 US adults (aged 25–75). 11 348 underwent medical examination and nutritional examination based on 24 h recall. Two had no data on sodium intake available. Vital status at June 30, 1992, was obtained for the 11 346 participants through interview, tracing, and searches of the national death index. Mortality was examined in sex-specific quartiles of sodium intake, calorie intake, and sodium/calorie ratio. Multiple regression analyses were done to assess the relations with mortality.

Findings

There were 3923 deaths, of which 1970 were due to CVD. All-cause mortality (per 1000 person-years; adjusted for age and sex) was inversely associated with sex-specific quartiles of sodium intake (lowest to highest quartile 23·18 to 19·01, p<0·0001) and total calorie intake (25·03 to 18·40, p<0·0001) and showed a weak positive association with quartiles of sodium/calorie ratio (20·27 to 21·71, p=0·14). The pattern for CVD mortality was similar (sodium 11·80 to 9·60, p<0·0019; calories 12·80 to 8·94, p<0·0002; sodium/calorie ratio 9·73 to 11·35, p=0·017). In Cox multiple regression analysis, sodium intake was inversely associated with all-cause (p=0·0069) and CVD mortality (p=0·086) and sodium/calorie ratio was directly associated with all-cause (p=0·0004) and CVD mortality (p=0·0056). By contrast, calorie intake in the presence of the two measures of sodium intake was not independently associated with mortality (all-cause p=0·86; CVD p=0·74). Analysis restricted to participants with no history of CVD at baseline gave similar results.

Interpretation

This observational study does not justify any particular dietary recommendation. Specifically, these results do not support current recommendations for routine reduction of sodium consumption, nor do they justify advice to increase salt intake or to decrease its concentration in the diet.

●【結果】

18か国で102,216人の成人を対象

回帰分析では1gナトリウム排泄が増えるたびに収縮期血圧が2.11mmHg、拡張期血圧が0.78mmHg増えた。この相関関係はNaの摂取量が増えるほど顕著になり尿中Na排泄が5g/日以上では2.58mmHg収縮期血圧が上昇し、3-5g/日では1.74mmHg、3g未満では0.74mmHgの上昇であった(P<0.001)であった。また高齢であるほどその相関関係は顕著であり、55歳以上では2.97mmHg、45-55歳では2.43mmHg、45歳では1.96mmHgの増加であった(P<0.001)。カリウム排泄は収縮期血圧と逆相関しており高血圧の患者及び高齢であればあるほど、その程度は非高血圧患者と比べて顕著であった(P<0.001)。

●【結論】

本研究では、(尿中排泄量から計算された)ナトリウム及びカリウムの摂取量と血圧の関係は非線形であり、治り生む摂取量が少ないほど、カリウム摂取量が多いほど血圧は低い傾向にあり、高Na摂取患者・高血圧患者・高齢者ではその関係は顕著であった。

Urinary Sodium and Potassium Excretion, Mortality, and Cardiovascular Events

NEJM 2014;371:612-623

長期味噌摂取が血圧および代謝に与える影響

〜二重盲検ヒト比較介入試験〜

味噌と一緒に摂った塩分の3割が自然排泄されるらしい。

Long Term Intake of Miso Soup Unaffected Blood Pressure in Subjects

with Normal or StageⅠ Hypertension

－Double Blind Comparative Intervention Trial－

Jpn Pharmacol Ther　2016　44（11）1601-12

http://www.lifescience.co.jp/yk/yk16/nov/ab5.html

Objective　The present study aimed at investigating the effects of newly developed Miso with potent ACE inhibition on blood pressure and its safety in 39 subjects aged 20-65 years with normotension or stageⅠ hypertension along with conventional Shinshu Miso.

Methods　A double-blind parallel-group study was conducted, and the subjects were allocated into newly developed Miso（N）or Shinshu Miso（C）. They were served two cups of Miso soup a day（32 g Miso; 3.7-3.8 g salt）. Blood pressure and the changes of metabolism were investigated.

Results　N group tended to decrease blood pressures throughout the study while consuming 3.8 g more salt due to the Miso soup. In N group, Ccr significantly decreased within the normal range. The Miso did not influence lipid and glucose metabolism. In C group blood pressure was unchanged with the Miso intake. Neither LDL-cholesterol nor triglyceride was changed. Interestingly, hANP was slightly increased in C Miso.

Conclusions 　This is the first intervention trial in humans suggesting that long-term Miso intake with salt intake does not increase blood pressures and that some antihypertensive constituents occur in Miso as reported in our previous animal studies. hANP increase might be related to natriuresis of Shinshu Miso reported.

（管理者注：これまでは血圧を下げることをOutcomeとしてきたが、健康寿命を延ばすことをOutcomeとするべきで、すでに日本人は8-10g/dayなので、問題が無いと思う。）