Low Salt Diet Found to Increase Mortality by Jeffrey Dach MD
The Low Salt Diet Revisited
This article is part one of a series, for part two click here,
A recent Lancet study on the effect of a low salt diet made headlines, finding that a low salt diet increases mortality for patients with congestive heart failure.(1-6) The study concluded there was not enough evidence to advise a low-salt diet for the rest of us. They doubted a low salt diet would benefit the population.(6) In this article we will re-examine the low salt diet, clear away the confusion, and make recommendations about salt intake, hypertension, and health.
Above left image, harvesting sea salt courtesy of wikimedia commons. (Salt Farmers – Pak Thale.jpg)
Health Benefits of Salt
We know from many years of published studies that increasing salt intake increases blood volume and also blood pressure. Salt is essential for maintaining blood volume, blood pressure, and overall health. The salt content of blood is similar to ocean water. Both have sodium chloride, also known as salt.
Importance of Salt
One example of the importance of salt is the common practice of starting an intravenous solution of salt and water as the first line treatment for the trauma patient upon arrival to the hospital Emergency Room.
Low Salt Diet to Reduce Blood Pressure
One of the central dogmas of mainstream medicine is the “low salt diet” as a treatment for reducing blood pressure in the hypertensive patient. Indeed, popular wisdom says that the “low salt diet” is also healthy for the rest of us “normal” people who don’t have hypertension.(25) Along with the rest of my medical school class, I was indoctrinated to believe this. Is this really true? Many studies have looked at this question. They show the “low salt diet” will in fact reduce blood pressure slightly. However, this effect is minimal, and is counteracted by compensatory mechanisms that release harmful substances into the bloodstream, hormones and chemical mediators that counteract the “low salt diet”. The released chemical mediators include insulin, epinephrine, norepinephrine, renin, aldosterone, etc. These are harmful and damaging to the vascular system. (7-11)
Low Salt Diet Increases Cardiovascular Mortality
In addition, a number of studies have found that a “low salt diet” increases cardiovascular mortality. (5) A study published in the 1995 Hypertension found 4.3 times greater mortality in hypertensive men on a low salt diet.(12) They also found higher plasma renin in these men, a hormone produced by the body which causes salt and water retention by the kidney to compensate for the low salt diet.(12-15)
A 2011 JAMA provides the reasons for this increased mortality and says … (16)
The underlying mechanisms explaining the inverse association between cardiovascular mortality and 24-hour urinary sodium excretion might be that a salt intake low enough to decrease blood pressure also increases sympathetic nerve activity, decreases insulin sensitivity, activates the renin-angiotensin system, and stimulates aldosterone secretion. (16)
A 1998 JAMA report found that a low salt diet increased plasma renin 3.6-fold and aldosterone by 3.2-fold, increases that were proportional to the degree of sodium restriction. (17) The authors also reported the “low salt diet” increased other harmful substances such as noradrenaline, cholesterol, and low-density lipoprotein cholesterol (LDL). (17) A 1999 report in American Journal of Hypertension found that “moderate salt restriction aggravates both systemic and vascular insulin resistance.” (18)
In 2018, Dr Graudal calls for a redesign of the Salt Guidelines in hi report, the “Conflicting Evidence on Health Effects Associated with Salt Reduction Calls for a Redesign of the Salt Dietary Guidelines.” He says:
“Ninety-five percent of the World’s populations have a mean salt intake between 6 and 12 g, which is much lower than the tolerated daily level of up to 55 g/d. In spite of this, the recommended upper level by many health institutions is as low as 5.8 g/day. When reviewing the evidence for an upper level of 5.8 g/day, it becomes apparent that neither the supporting studies selected by the health institutions, nor randomized controlled trials and prospective observational studies disregarded by the health institutions, document that a salt intake below this 5.8 g, has beneficial health effects. Although there is an association between salt intake and blood pressure, both in randomized controlled trials and in observational studies, this association is weak, especially in non-obese individuals with normal blood pressure. Furthermore a salt intake below 5.8 g is associated with the activation of the renin-angiotensin-aldosteron system, an increase in plasma lipids and increased mortality. A redesign of the salt dietary guidelines, therefore, seems to be needed.”endquote.
Refined Salt or Natural Sea Salt ?
Dr. David Brownstein’s book, ” Salt – Your Way To Health”, points out the difference between Refined Salt, commonly used in all processed foods, and Natural Sea Salt.(21) White refined salt is processed so that all the trace minerals are removed, and instead has chemicals added (up to 2% of weight). The added chemicals are ferrocyanide, aluminum, ammonium citrate, etc and are used for anti-caking, free-flowing, and to prolong shelf life. The final result is a lifeless, unnatural salt product which tends to acidify the body also called refined salt. Natural Sea Salt, on the other hand, retains all the trace minerals naturally found in the ocean. In addition it alkalinizes the body and has many health benefits. Natural Sea Salt is made by evaporating ocean water, and then collecting or harvesting the salt.
Popular brands of natural sea salt include:
Case Reports from Dr Brownstein’s Sea Salt Book
Case Number One- Food Allergies (from the Salt book) 61 year old female with numerous allergies. The patient switched from refined salt to natural sea salt, measured urine and saliva pH, which went up (alkaline) and noted allergies resolved.
Case Number Two-Male Hypertension on Meds, Jack 63 year old hypertensive on two BP meds, Dyazide and Lopressor causing fatigue and erectile dysfunction. He switched from a low salt diet to natural sea salt and two months later blood pressure was lower. Pt reduced BP meds to dyazide at half dose.
Case three, Barbara -Hypertension, 53 y/o went to primary care doctor for check up and was shocked to find her BP was 165/100. She had been on a low salt diet for years. Blood tests showed a low sodium level (137). She was then placed on natural sea salt, half tsp per day, and vitamin-mineral regimen, and eliminated refined foods. Two months later her blood pressure was 110/70, and she felt better.
Case Four Sandra, similar story to Barbara.
Case Five, Seizure Disorder. Jerry 12 years old with recurrent seizures on meds.Sodium was 138 on low salt diet. Switched to natural sea salt. Seizures decreased by 50%.
Case Six Migraines. Lisa 31 , three migraines per month, clinically dehydrated, low sodium 139. Instructed to take half tsp Celtic Sea Salt per day, and 2 liters of water per day. Migraine headaches disappeared.
Case Seven- Fibromyalgia . Judy 35 y/o , five years with fibromyalgia. BP drops upon standing. Adrenal Fatigue. RX adrenal hormones (DHEA, cortisol, pregnenolone, testosterone, progesterone ) , and natural sea salt., whole foods, plentiful water. Immediate improvement.
Clinical Uses of Natural Sea Salt
Adrenal Exhaustion: Sea Salt is essential for treatment of adrenal fatigue.
Diabetes, Elevated Blood Sugar- It is impossible to control blood sugar on a “low salt diet”. These do well on sea salt.
Muscle Cramps – often relieved by minerals in Sea Salt.
Osteoporosis Treatment requires minerals found in Sea Salt
Hypertension – Low salt diet causes increased mortality. Use natural sea salt, with reduction in blood pressure noted in any cases.
How to Reduce Blood Pressure Naturally – Salt Substitutes
The Low sodium, High potassium, High magnesium salt substitute (26)
A number of studies have looked at substituting table salt with a variant with reduced sodium, and increased potassium, and magnesium, which has shown to reduce blood pressure. (26) Magnesium alone is an excellent mineral supplement which may be effective for blood pressure control in hypertensive patients.(27)
Salt Substitute From Finland
Jonathan Wright’s clinic offers a salt substitute which contains potassium, magnesium, and lysine which was found beneficial in a Finland.(28)(29)
WrightSalt is available through the Tahoma Clinic Dispensary (www.tahomadispensary.com 888-893-6878 ), or Ayush Herbs (800-925-1371),
L- Arginine and the ADMA Connection
In 1998 the Nobel Prize in Medicine was awarded to Furchgott and colleagues for the discovery of the role of Nitric Oxide in blood pressure regulation (among other things). (29-31) Recently, a new test has been devised called the ADMA from Metametrix Labs which is useful in hypertensive patients, showing the ability (or inability) to manufacture Nitric Oxide. If ADMA is found to be high, indicating low Nitric Oxide production, then increases can be achieved with a simple amino acid supplement called L-Arginine. (29-31) The increased Nitric Oxide brings down and controls blood pressure.(32) The references for the ADMA test can be found here.
No Iodine Added to Natural Sea Salt
Remember, Natural Sea Salt does not contain added iodine, so it is important to test for iodine levels, and supplement with iodine if found low. Iodine supplementation is our most important means for breast cancer prevention.
Credit and thanks goes to the book, Salt – Your Way To Health by David Brownstein MD for much of the information in this article.
Articles with Related Interest
Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Florida 33314
Links and References
Posted at 12:01 AM ET, 07/06/2011 washington post
Salt-heart disease link questioned By Rob Stein. A major new scientific analysis is raising questions about the link between salt consumption and heart disease.
(2) Does Cutting Salt Really Improve Heart Health? By Meredith Melnick Thursday, July 7, 2011 Time Magazine
(3) UPDATE 1-Review raises questions over benefits of cutting salt. Wed Jul 6, 2011 Reuters.
(4) Interview with Dr Rod taylor author .The Impact of Dietary Salt on Mortality and Cardiovascular Disease: Cochrane Review
(5) www.thelancet.com/journals/lancet/article/PIIS0140-6736%2811%2960657-0/fulltext?rss%3Dyes Salt and cardiovascular disease mortality, The Lancet. The Lancet, Volume 377, Issue 9778, Page 1626, 14 May 2011
The debate over salt, blood pressure, and health has been ongoing since the US Government recommended salt reduction to treat hypertension in the 1970s. A May 4 study in the Journal of the American Medical Association, has rekindled controversy. Jan Staessen and colleagues found that systolic blood pressure positively correlated with 24-h urinary sodium excretion. Surprisingly, lower sodium excretion predicted higher cardiovascular disease (CVD) mortality. The researchers concluded that their findings did “not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level”.
Reduced Dietary Salt for the Prevention of Cardiovascular Disease: A Meta-Analysis of Randomized Controlled Trials (Cochrane Review). American Journal of Hypertension 24, 843-853 (August 2011). by Rod S. Taylor1, Kate E. Ashton2, Tiffany Moxham3, Lee Hooper4 and Shah Ebrahim5
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.
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).
Salt and Hypertension
(7) Salt saga continued, Salt has only small importance in hypertension, J. D. Swales BMJ 1988;297:307 (Published 30 July 1988) Swale Bmj
The Intersalt- Study Group conclude that for a reduction in sodium intake of 100 mmol a day (which is probably as great as can be achieved in a Western society) there would be a reduction in blood
pressure of 2 2 mm Hg (systolic) and 0 1 mm Hg (diastolic).
(8) www.ncbi.nlm.nih.gov/pubmed/1987008 Hypertension. 1991 Jan;17(1 Suppl):I27-33. An overview of randomized trials of sodium reduction and blood pressure. Cutler JA, Follmann D, Elliott P, Suh I.
To test for effects on systolic and diastolic blood pressure and to provide precise estimates of their magnitude, we conducted an overview of randomized clinical trials that aimed to reduce the intake of sodium in human subjects. We excluded from pooled analyses trials with confounded designs, those that compared intake levels beyond the usual range in the population, and those without published reports.
Two reviewers abstracted information in duplicate and differences were reconciled. Twenty-three trials with outcome data from an aggregate of 1,536 subjects were included. Data were pooled both separately for hypertensive and normotensive subjects and for all trials combined. With the use of sample size weighting, blood pressure reductions (net of controls) were 4.9 +/- 1.3/2.6 +/- 0.8 mm Hg (systolic and diastolic, respectively, with 95% confidence limits) in hypertensive subjects and 1.7 +/- 1.0/1.0 +/- 0.7 mm Hg in normotensive subjects. The combined blood pressure reductions were 2.9 +/- 0.8/1.6 +/- 0.5 mm Hg. These changes were associated with mean reduction of urinary sodium excretion ranging from 16 to 171 mmol/24 hr for individual trials. A dose-response relation across trials was found, both in normotensive and in hypertensive subjects.
These results indicate that sodium reduction lowers mean blood pressure in both hypertensive and normotensive individuals for periods of at least several months. The findings are highly consistent with results of observational epidemiological studies and have implications for preventive strategies of blood pressure control.
Am J Clin Nutr. 1997 Feb;65(2 Suppl):643S-651S.
Randomized trials of sodium reduction: an overview. Cutler JA, Follmann D, Allender PS.
JAMA. 1996 May 22-29;275(20):1590-7. Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials. Midgley JP, Matthew AG, Greenwood CM, Logan AG.
DATA SYNTHESIS:The 56 trials The mean reduction (95% confidence interval) in daily urinary sodium excretion, a proxy measure of dietary sodium intake, was 95 mmol/d (71-119 mmol/d) in 28 trials with 1131 hypertensive subjects and 125 mmol/d (95-156 mmol/d) in 28 trials with 2374 normotensive subjects. After adjustment for measurement error of urinary sodium excretion, the decrease in blood pressure for a 100-mmol/d reduction in daily sodium excretion was 3.7 mm Hg (2.35-5.05 mm Hg) for systolic (P<.001) and 0.9 mm Hg (-0.13 to 1.85 mm Hg) for diastolic (P=.09) in the hypertensive trials, and 1.0 mm Hg (0.51-1.56 mm Hg) for systolic (P<.001) and 0.1 mm Hg (-0.32 to 0.51 mm Hg) for diastolic (P=.64) in the normotensive trials.
Dietary sodium restriction for older hypertensive individuals might be considered, but the evidence in the normotensive population does not support current recommendations for universal dietary sodium restriction.
Cochrane Database Syst Rev. 2003;(3):CD003656. Reduced dietary salt for prevention of cardiovascular disease. Hooper L, Bartlett C, Davey Smith G, Ebrahim S.
Systolic and diastolic blood pressures were reduced at 13 to 60 months in those given low sodium advice as compared with controls (systolic by 1.1 mm Hg, 95% CI 1.8 to 0.4, diastolic by 0.6 mm hg, 95% CI 1.5 to -0.3), as was urinary 24 hour sodium excretion (by 35.5 mmol/ 24 hours, 95% CI 47.2 to 23.9).
Hypertension. 1995 Jun;25(6):1144-52. Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men. Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH.
A sodium-reduced diet is frequently recommended for hypertensive individuals. To determine the relationship of sodium intake to subsequent cardiovascular disease, we assessed the experience of participants in a worksite-based cohort of hypertensive subjects.
The 24-hour urinary excretion of sodium (UNaV), potassium, creatinine, and plasma renin activity was measured in 2937 mildly and moderately hypertensive subjects who were unmedicated for at least 3-4 weeks.
Morbidity and mortality in these systematically treated subjects were ascertained. Men and women were stratified according to sex-specific quartiles of UNaV. Subjects in these strata were similar in race, cardiovascular status, and pretreatment and intreatment blood pressure. Subjects with lower UNaV were thinner, excreted less potassium, and had higher plasma renin activity.
During an average 3.8 years of follow-up, a total of 55 myocardial infarctions occurred. Myocardial infarction and UNaV were inversely associated in the total population and in men but not in women, who sustained only nine events. In men, age- and race-adjusted myocardial infarction incidence in the lowest versus highest UNaV quartile was 11.5 versus 2.5 (relative risk, 4.3, 95% confidence interval,
Am J Clin Nutr. 1997 Feb;65 (2 Suppl):682S-686S.
Urinary sodium excretion and myocardial infarction in hypertensive patients: a prospective cohort study. Alderman M, Sealey J, Cohen H, Madhavan S, Laragh J.
rebuttal to ALderman
Commentary: Salt, blood pressure and health , G MacGregora and HE de Wardenerb
Int. J. Epidemiol. (2002) 31 (2): 320-327.
(15) Alderman, Michael H., Hillel Cohen, and Shantha Madhavan. “Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I).” The Lancet 351.9105 (1998): 781-785.
Recent JAMA article shows increased mortality on low salt diet.
Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. Katarzyna Stolarz-Skrzypek et al.JAMA. 2011;305(17):1777-1785.
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.
We studied the incidence of mortality and morbidity and the incidence of hypertension in relation to 24-hour urinary sodium excretion at baseline.
Our current observations on cardiovascular mortality are consistent with several other reports.33,38,39,40 The National Health and Nutrition Examination Surveys (NHANES) I38 and II39 demonstrated an inverse association of cardiovascular and total mortality with salt intake as assessed from dietary recall with a similar trend in NHANES III.40
Alderman and colleagues33 followed up for 3.5 years 2937 patients with mild to moderate hypertension. There was an inverse association between the incidence of myocardial infarction and 24-hour urinary sodium excretion at baseline for the total population and for men, but not women. For men, the race- and age-adjusted HR expressing the risk in the lowest vs the highest quartile of 24-hour urinary sodium was 4.3 (95% CI, 1.7-10.6).
Other investigators criticized Alderman’s findings, because he instructed his patients to avoid high-salt foods 4 to 5 days before sodium excretion measurements were taken, which might have led to distorted levels. In our epidemiological study, which was conducted outside a medical environment, participants did not receive any recommendations from the research team about moderating their salt consumption. The underlying mechanisms explaining the inverse association between cardiovascular mortality and 24-hour urinary sodium excretion might be that a salt intake low enough to decrease blood pressure also increases sympathetic nerve activity, decreases insulin sensitivity, activates the renin-angiotensin system, and stimulates aldosterone secretion.10
Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride. A Meta-analysis.
Niels A. Graudal, MD; Anders M. Galløe, MD; Peter Garred, DrMedSci.
JAMA. 1998; 279(17):1383-1391. doi: 10.1001/jama.279.17.1383
Data Synthesis.— In 58 trials of hypertensive persons, the effect of reduced sodium intake as measured by urinary sodium excretion (mean, 118 mmol/24 h) on SBP was 3.9 mm Hg (95% confidence interval [CI], 3.0-4.8 mm Hg) (P<.001) and on DBP was 1.9 mm Hg (95% CI, 1.3-2.5 mm Hg) (P<.001).
In 56 trials of normotensive persons, the effect of reduced sodium intake (mean, 160 mmol/24 h) on SBP was 1.2 mm Hg (95% CI, 0.6-1.8 mm Hg) (P<.001) and on DBP was 0.26 mm Hg (95% CI, −0.3-0.9 mm Hg) (P=.12).
The cumulative analysis showed that this effect size has been stable since 1985.
In plasma, the renin level increased 3.6-fold (P<.001), and the aldosterone level increased 3.2-fold (P<.001); the increases were proportional to the degree of sodium reduction for both renin (r=0.66; P<.001) and aldosterone (r=0.64; P<.001). Body weight decreased significantly, and noradrenaline, cholesterol, and low-density lipoprotein cholesterol levels increased. There was no effect on adrenaline, triglyceride, and high-density lipoprotein cholesterol.
Conclusion.— These results do not support a general recommendation to reduce sodium intake. Reduced sodium intake may be used as a supplementary treatment in hypertension. Further long-term studies of the effects of high reduction of sodium intake on blood pressure and metabolic variables may clarify the disagreements as to the role of reduced sodium intake, but ideally trials with hard end points such as morbidity and survival should end the controversy.
Am J Hypertens. 1999 Jun;12(6):643-7. Moderate dietary salt restriction increases vascular and systemic insulin resistance. Feldman RD, Schmidt ND.
Our recent studies have indicated that severe salt restriction aggravates vascular insulin resistance in younger normotensive and hypertensive subjects. However, whether the extent of dietary salt restriction commonly advocated adversely affects vascular insulin resistance is unknown. To determine whether moderate dietary salt restriction might affect vascular and systemic sensitivity to insulin, we studied eight subjects after 1 week of a normal sodium diet (235 mEq/day) and 1 week of a moderate salt restriction (75 meq/day). Systemic insulin resistance as assessed by the fasting plasma glucose-to-insulin ratio was aggravated by dietary sodium restriction (normal sodium: 1.2 +/- 0.1 mmol/mIU; low sodium 0.6 +/- 0.1, P < .05). Salt restriction significantly reduced maximal insulin-mediated vasodilation (normal sodium: 51% +/- 5% of maximum nitroglycerin-mediated response; low sodium: 28% +/- 6%, P < .01). In contrast, no alterations in nitroglycerin-mediated vasodilation nor phenylephrine-mediated vasoconstriction were noted. These studies demonstrate that moderate salt restriction aggravates both systemic and vascular insulin resistance. This impairment of the vasodilating effect of insulin could be a factor attenuating the blood pressure lowering effect of a low sodium diet.
In Favor of salt restriction
Hypertension. 2005 Jul;46(1):66-70. Modest salt reduction lowers blood pressure in isolated systolic hypertension and combined hypertension. He FJ, Markandu ND, MacGregor GA.
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.
(20) Mente, A., et al. “Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies.” (2016): 465. 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.
1.Cutler, JA., et.al. An overview of randomized trials of sodium restriction and blood pressure. Hypertension. 1991;17(suppl 1): I-27 – I-33
2. Midgley, J., et al. Effect of reduced dietary sodium on blood pressure. JAMA, May 22/29, 1996. Vol. 275 No. 20
3. Smith, WCS, et al. Urinary electrolyte excretion, alcohol consumption, and blood pressure in the Scottish Heart Health Study. BMJ. 297:320-330,
4. Alderman, M., et al. Dietary sodium intake and mortality: The National Health and Nutrition Examination Survey (NHANES I). Lancet. Vol. 351, Issue 9105, March 14, 1998, 781-785
5. Swales, JD. Salt saga continued: Salt has only small importance in
hypertension. BMJ. 1988;297;307-8
6. Alderman, M. Low urinary sodium is associated with greater risk of
myocardial infarction among treated hypertensive men. Hypertension,
7. Rupert, M. et al. Short term dietary sodium restriction increases
serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Klin Wochenschr. 1991;69: (suppl. XXV):51-57
Note that 1 tsp of salt is 2400 milligrams of sodium, so that the equivalent of 1/2 tsp of salt is recommended for those over 70.
J Hum Hypertens. 1999 Nov;13(11):777-80. Effect of a mineral salt diet on 24-h blood pressure monitoring in elderly hypertensive patients. Katz A, Rosenthal T, Maoz C, Peleg E, Zeidenstein R, Levi Y.
The influence of a mineral salt on 24-h ambulatory blood pressure (BP) monitoring was studied in 20 elderly hypertensive subjects residing in an old peoples home. Ordinary table and cooking salt was substituted with a special Na-reduced, K-, Mg-, and l-lysine HCl-enriched mineral salt (Pansalt(R)) for 6 months. Antihypertensive therapy was uninterrupted. An ambulatory BP monitor (Suntech Accutracker) measured BP every 20 min during the day and every 30 min at night, before and 6 months after starting the diet.
Nine patients (45%) decreased both systolic and diastolic BP significantly: systolic BP fell from 154.92 +/- 33.67 mm Hg to 143. 45 +/- 53.1 mm Hg (P < or = 0.01) during the daytime from 6 am to midnight; and from 139.80 +/- 32.84 mm Hg to 137.87 +/- 31.17 mm Hg (P < or = 0.01) from midnight to 6 am.
Diastolic BP fell from 85.34 +/- 24.85 mm Hg to 70.29 +/- 18.31 mm Hg (P < or = 0.01) during the daytime from 6 am to midnight; and from 77.1 +/- 22.92 mm Hg to 67.76 +/- 15. 63 mm Hg (P < or = 0.01) at night.
It is concluded that decreased intake of Na and increased intake of both K and Mg can be useful in controlling high BP.
Note that 1 tsp of salt is 2400 milligrams o
American Journal of Clinical Nutrition, Vol. 83, No. 6, 1289-1296, June 2006. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men, Hsing-Yi Chang, Yu-Whuei Hu, Ching-Syang Jack Yue, Yu-Wen Wen, Wen-Ting Yeh, Li-San Hsu, Shin-Yin Tsai and Wen-Harn Pan
(24) Hypertens Res. 1998 Dec;21(4):235-43. Reduction in blood pressure with a sodium-reduced, potassium- and magnesium-enriched mineral salt in subjects with mild essential hypertension.Kawasaki T, Itoh K, Kawasaki M.
A parallel controlled clinical trial was carried out to investigate the effect on blood pressure (BP) of replacing normal salt with mineral salt in seasonings. After a 2-wk run-in period, 21 subjects (10 men and 11 women; age, 66.0+/-7.6 yr) were given mineral salt in seasonings instead of normal salt [mineral salt (MS) group], while 20 subjects (10 men and 10 women; age, 65.9+/-7.4 yr) continued to receive normal salt in seasonings [regular salt (RS) group] for the next 5 wk in the experimental (E) period. In the MS group, systolic (S) and diastolic (D) BP decreased significantly from 134.7+/-17.2/77.2+/-9.7 at baseline (week 0) to 127.3+/-12.0/73.5+/-8.9 mmHg at the end of the E period (week 5), and the reductions in both SBP and DBP were larger in hypertensive subjects than in normotensive subjects in the MS group. The serum sodium and chloride concentrations decreased significantly, while the serum potassium and HDL-cholesterol concentrations increased significantly at week 5. The 24-h urinary sodium excretion decreased, and the 24-h potassium and magnesium excretions increased significantly from week 0 to week 5 in the MS group. In contrast, SBP, DBP, serum chemistry, and urinary electrolyte excretion did not change significantly in the RS group. These findings suggest that the excessive salt content and insufficient potassium and magnesium content of the present Japanese diet could be easily and safely corrected by replacing seasonings prepared with regular salt with those prepared with mineral salt.
(25) Appel, Lawrence J., et al. “The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke a call to action from the american heart association.” Circulation 123.10 (2011): 1138-1143.
BMJ. 1994 August 13; 309(6952): 436–440. Reduction in blood pressure with a low sodium, high potassium, high magnesium salt in older subjects with mild to moderate hypertension. JM Geleijnse, J C MWitteman, A A A Bak, J H den Breeijen, D E Grobbee
(27) Sontia, Bruno, and Rhian M. Touyz. “Role of magnesium in hypertension.” (2006).Role of magnesium in hypertension Sontia Bruno and Rhian Touyz 2006
Magnesium affects blood pressure by modulating vascular tone and reactivity. It acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Magnesium deficiency has been implicated in the pathogenesis of hypertension with epidemiological and experimental studies demonstrating an inverse correlation between blood pressure and serum magnesium levels. Magnesium also influences glucose and insulin homeostasis, and hypomagnesemia is associated with metabolic syndrome. Although most epidemiological and experimental studies support a role for low magnesium in the pathophysiology of hypertension, data from clinical studies have been less convincing.
Introducing Wright Salt, The international salt secret that could save your heart—and your life, By Jonathan V. Wright, M.D. sodium-reduced salt had been enriched not only with potassium, but also with magnesium and L-lysine-hydrochloride. After waiting 13 years since for someone to market an American version of the “novel, sodiumreduced, potassium-, magnesium-, and l-lysine-enriched salt” used nationwide in Finland, I’ve finally gotten together with Ayush Botanicals of Mercer Island, Washington, to introduce a very similar version. Holly and I are using it as our only salt at home already.
J Hum Hypertens. 1996 Feb;10 Suppl 1:S57-61.
Adherence to and population impact of non-pharmacological and pharmacological antihypertensive therapy.
Efforts in Finland to implement the recommended non-pharmacological and pharmacological principles for the control of hypertension, stroke and ischaemic heart disease have been accompanied by an approximately 10 mm Hg fall in the population average of diastolic blood pressure, and about 60% decrease in deaths from both stroke and ischaemic heart disease among 30-59-year-old men and women from 1972 to 1992. Adherence to antihypertensive drug therapy has been quite good. However, the drug treatment does not seem to account for more than 5-6% of the observed fall of blood pressure, and 10-15% of the decrease in deaths from strokes and ischaemic heart disease. There has been no overall adherence to several non-pharmacological recommendations, and marked increases in the intake of alcohol, obesity among men, and smoking among women have been observed. However, the population adherence to recommendations to decrease the intakes of sodium and saturated fats, and to reduce the sodium-to-potassium ratio and the saturated-to-unsaturated fat ratio, has been good. These dietary changes appear to account for a major part of the fall of blood pressure and the decrease in the cardiovascular diseases. Currently a rapid further population-wide decrease in the dietary sodium-to-potassium ratio is taking place, due to a decrease in the use of salt and replacement of common salt by a novel sodium-reduced, potassium-, magnesium-, and l-lysine HCI-enriched salt, both in home kitchens and in the food industry.
L-Arginine- Nitric Oxide- Assymetric -Di Methyl Arginine (ADMA)
The endothelium-derived relaxation factor, nitric oxide, provides a unifying mechanism for the action of many cardiovascular disease risk factors. Nitric oxide cannot easily be directly measured, but the inhibitor of its formation, asymmetric dimethylarginine (ADMA) can be. The function of ADMA in modulating nitric oxide production has a significant impact on cardiovascular endothelial function. There are inexpensive and safe ways to improve endothelial nitric oxide responses that can be monitored by following ADMA responses. These interventions promise to significantly reduce the mortality and morbidity statistics for heart disease. Plasma ADMA is now available as a routine laboratory evaluation.
Elevated ADMA is associated with Increase in blood pressure, coronary vasospasm, hypertension, Endothelium dysfunction, increased risk for stroke, Acute coronary events. Essential hypertension,Congestive heart failure. All of the effects are reversed by intravenous L-arginine.
The Nobel Prize in Physiology or Medicine 1998 was awarded jointly to Robert F. Furchgott, Louis J. Ignarro and Ferid Murad “for their discoveries concerning nitric oxide as a signalling molecule in the cardiovascular system”.
J. Nutr. 134:2842S-2847S, October 2004 Supplement: Arginine Metabolism: Enzymology, Nutrition, and Clinical Significance. Asymmetric Dimethylarginine, an Endogenous Inhibitor of Nitric Oxide Synthase, Explains the “L-Arginine Paradox” and Acts as a Novel Cardiovascular Risk Factor1,2 Rainer H. Böger3
Jeffrey Dach MD
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