European Heart Journal (2011) 32, 30813087 REVIEW

doi:10.1093/eurheartj/ehr379

Controversies in cardiovascular medicine

Beyond salt: lifestyle modifications and

blood pressure
Tiberio M. Frisoli 1, Roland E. Schmieder 2, Tomasz Grodzicki 3, and Franz H. Messerli 1*
1
St Lukes-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 1000 Tenth Avenue, New York, NY 10019, USA; 2Department of Nephrology
and Hypertension, University Hospital, Erlangen, Germany; and 3Department of Internal Medicine and Gerontology, Medical College, Jagiellonian University, Cracow, Poland

Received 22 April 2011; revised 26 August 2011; accepted 13 September 2011; online publish-ahead-of-print 11 October 2011

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Lifestyle changes have been shown to effect significant blood pressure (BP) reductions. Although there are several proposed neurohormonal
links between weight loss and BP, body mass index itself appears to be the most powerful mediator of the weightBP relationship. There
appears to be a mostly linear relationship between weight and BP; as weight is regained, the BP benefit is mostly lost. Physical activity, but
more so physical fitness (the physiological benefit obtained from physical activity), has a dose-dependent BP benefit but reaches a
plateau at which there is no further benefit. However, even just a modest physical activity can have a meaningful BP effect. A diet rich in
fruits and vegetables with low-fat dairy products and low in saturated and total fat (DASH) is independently effective in reducing BP. Of
the dietary mineral nutrients, the strongest data exist for increased potassium intake, which reduces BP and stroke risk. Vitamin D is associated
with BP benefit, but no causal relationship has been established. Flavonoids such as those found in cocoa and berries may have a modest BP
benefit. Neither caffeine nor nicotine has any significant, lasting BP effect. Biofeedback therapies such as those obtained with device-guided
breathing have a modest and safe BP benefit; more research is needed before such therapies move beyond those having an adjunctive treat-
ment role. There is a strong, linear relationship between alcohol intake and BP; however, the alcohol effects on BP and coronary heart disease
are divergent. The greatest BP benefit seems to be obtained with one drink per day for women and with two per day for men. This benefit is
lost or attenuated if the drinking occurs in a binge form or without food. Overall, the greatest and most sustained BP benefit is obtained
when multiple lifestyle interventions are incorporated simultaneously.
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Keywords Hypertension Lifestyle Blood pressure Weight loss Alcohol Obesity Physical activity

consequential mediators of BP, and to design and implement

Introduction
Pharmacological treatment for hypertension (HTN) is effective in
reducing both blood pressure (BP) and morbidity and mortality
from cardiovascular and renal diseases. However, long-term
pharmacological therapy can have adverse effects and requires
continuous medical supervision. Lifestyle changes effect real and
significant BP reductions. Salt intake reduction is supported
perhaps by the greatest strength and diversity of evidence. This
review attempts to help synthesize and clarify which of the many
non-salt lifestyle modalities intended to reduce BP actually work,
for whom, and to what extent.
The challenges are to substantiate in the minds of physicians and
patients that lifestyle interventions for BP reduction are neither
impractical nor ineffective, but rather simple, safe, and greatly
public health initiatives.
Weight loss
A study of cause-specific deaths for the US population in 2004
revealed that obesity [body mass index (BMI) more than 30] was
associated with 112 159 excess cardiovascular disease-related
deaths and with 13 839 excess deaths from cancers considered
obesity-related. Overweight (BMI 2530) and obesity combined
were associated with 61 248 excess deaths from diabetes and
kidney disease.1
Weight loss is recommended, in major guidelines, as an initial
intervention in the treatment of hypertensive patients.2 In the

* Corresponding author. Tel: +1 212 523 7373, Fax: +1 212 523 7765, Email: messerli.f@gmail.com
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2011. For permissions please email: journals.permissions@oup.com
3082
TOHP-I trial, weight loss yielded a greater BP reduction at 6
months than did sodium intake reduction.3
Weight loss and blood pressure
reduction: mechanism of action
It is hypothesized that visceral (as opposed to subcutaneous) adi-
posity and BP are linked through increased calorie, protein, and
carbohydrate intake, resulting in increased plasma catecholamines,
sympathetic nervous system activity, and insulin secretion.4 Conse-
quently, reninangiotensin aldosterone system (RAAS) activation
results in renal sodium retention through aldosterone synthesis,
yielding increased cardiac output in the setting of insufficient
adjustment in peripheral vascular resistance, all of which results
in HTN (Figure 1).5 7 Obese women had higher circulating levels
of angiotensinogen, renin, aldosterone, and angiotensin-converting
enzyme when compared with lean women.8 Decrease in BP fol-
lowing weight loss is associated with reduced sympathetic
nervous system and RAAS activity, as well as accelerated natriur-
esis.9 With 10 kg weight loss, there was lowering of total circulat-
ing blood volume without change in peripheral vascular resistance,
thus yielding decreased venous return and cardiac output.7
A possible link between weight and various physiological
changes is leptin, which when secreted by adipocytes binds to a
receptor on the hypothalamus and increases renal sodium and
water excretion and alters vasoactive substances such as nitric
oxide in the endothelium.10,11 In human adult populations,
among the studies that report a positive association between
leptin and BP, some report the association to be independent of
adiposity, whereas others do not. A recent study illustrates that
leptin accounts for a proportion of the variance in the association
between BMI and BP, but that the association of leptin and BP is
almost entirely explained by BMI.12
Figure 1 Hypothetical mechanisms by which obesity may con-
tribute to HTN. CNPS, cardiac natriuretic peptide system; OSA,
obstructive sleep apnoea; RAAS, renin angiotensin aldosterone
system; SNS, sympathetic nervous system.
T.M. Frisoli et al.
Relationship between weight loss and
blood pressure
The relationship between weight loss and BP reduction appears to
be linear (Figure 2).13 By and large, a reduction of 1 kg body weight
is associated with 2/1 mmHg BP reduction.14 Reduction in BP due
to weight loss is related to the decrease in visceral fat mass.15
Does it matter how one loses the weight?
The short answer is yes. Among the possible means of reducing
body weight are lifestyle modifications, pharmacological interven-
tions, and invasive or surgical interventions.
A 4 kg weight loss achieved with dietary treatment yielded a
6 mmHg systolic BP (SBP) reduction; the same 4 kg weight loss
achieved with orlistat (decreases dietary fat absorption by inhibit-
ing activity of pancreatic lipases) yields a lesser 2.5 mmHg
reduction in SBP.16 An 8.4 kg reduction in weight using orlistat
yielded a 4.0/3.0 mmHg reduction in BP, whereas an 8.3 kg
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weight reduction through the use of sibutramine (serotonin
norepinephrine reuptake inhibitor that acts as an appetite suppres-
sant) did not cause a change in BP. Sibutramine may actually have a
BP-raising effect that counteracts the BP reduction that comes with
its weight loss effects. In the SCOUT trial, sibutramine was
associated with a higher composite risk of heart attack, stroke,
resuscitated cardiac arrest, or death.17
Bariatric surgical methods allow for the greatest degree of
weight loss, ranging from 21 to 38%, 1-year post-operation
depending on the type of surgery.18 For a weight loss at 2- and
10-year post-surgery of 23.4 and 16.1%, respectively, BP change
was 24.4/25.2 and +0.5/22.6 mmHg. At 10-year post-surgery,
although weight loss was sustained (though somewhat diminished),
the BP-lowering effect was diminished.
Physical activity
A meta-analysis of randomized controlled trials found that aerobic
exercise reduced BP by roughly 5/3 mmHg.19 This effect appears
to be independent of the weight reduction associated with physical
activity.20 In a study of normotensives followed for a mean of 4
years, increased physical fitness (a physiological response to
regular physical activity) was significantly associated with decreased
risk of developing elevated BP.21
Fitness was determined based on the duration each person was
able to undergo a graded symptom-limited maximal exercise
test.22 The association of fitness with incident HTN and other car-
diovascular conditions is stronger than the association of physical
activity with those same cardiovascular diseases. In the Coronary
Artery Risk Development in Young Adults (CARDIA) Study,
both baseline fitness and physical activity were inversely associated
with incident HTN.23 The magnitude of association between phys-
ical activity and HTN was strongest and significantly inversely
related with HTN incidence only among participants in the high-
fitness category, whereas the magnitude of association between
fitness and HTN was similar across tertiles of physical activity.
The association of fitness or activity with incident HTN was mod-
estly attenuated when BMI and waist circumference were included.
Beyond salt: lifestyle modifications and BP
Figure 2 Weight and blood pressure appear to correlate in a linear relationship. The greatest blood pressure reduction was seen among
those who lost the most weight.
These findings may suggest that activity that does not raise fitness
levels may not lower the likelihood of developing HTN.
The association between physical activity and BP seems to be
dose-dependent, but only to a certain level of activity.24 Those
who exercised 61 90 min/week gained more benefit than the
3160 min/week group, but there was no further benefit beyond
6190 min/week. It seems, therefore, that one does not need to
train very aggressively to attain most of the fitness-related
BP-reduction benefits.
Further, physical activity need not be equated with formal phys-
ical training, as in a gym or on a playing field. In a Japanese study,
relative risk for HTN among middle-aged Japanese men decreased
from 1.0 to 0.84 to 0.75 to 0.54 moving up from the first to
fourth quartile of daily life energy expenditure.25 Daily life expen-
diture was calculated from the composite scores of such com-
monplace daily activities as sleeping, reading, driving, slow
walking, taking a bath, and climbing stairs. The most active in
this study, who incurred the greatest BP benefits, were doing
such basic activities such as walking and climbing stairs. This
study also showed that while exercise reduces the risk of HTN
for all three levels of normotension (low normal, normal, and
high normal), the benefit of activity in reducing HTN risk dimin-
ished with increasing baseline BP.
Exercise may diminish sympathoadrenergic activity and enhance
prostaglandin mechanisms26 and augment endothelium-dependent
vasodilatation through increasing production of nitric oxide.27
Exercise most effectively reduced BP in those with low-plasma
renin activity at baseline.
Older persons may be resistant to BP-lowering effects of exer-
cise. There was a lack of improvement in aortic stiffness with exer-
cise which likely explains why there was no reduction in SBP and
only modest reduction in diastolic BP (DBP) among elderly exerci-
sers compared with elderly controls.28
3083
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DASH diet
The landmark Dietary Approaches to Stop Hypertension (DASH)
showed that a diet rich in fruits and vegetables with fat content
typical for the US population lowered BP by 2.8/1.1 mmHg com-
pared with a control diet.29 When such a diet also incorporated
low-fat dairy products and low saturated and total fat (the
DASH diet), BP decreased by 5.5/3.0 mmHg. The findings were
even more pronounced in hypertensives (11.4/5.5 mmHg drop
in BP for the DASH diet). That dietary intervention lowered
BP in the normotensive participants implicates dietary intervention
in primary prevention of HTN. In those already with high BP,
dietary modification similar to the DASH diet has anti-hypertensive
efficacy comparable with drug monotherapy for mild HTN.30
Importantly, the reduction in BP began within 2 weeks and was
maintained for the duration of the dietary intervention (an
additional 6 weeks). The trial was not designed to assess the long-
term effects of the diets on BP or clinical cardiovascular events.
Known diet-related determinants of BPsalt intake, weight, and
alcoholcould not have accounted for the reductions in BP
because differences in these were small and similar for all the
diets. Further, multiple components of the DASH diet appear inde-
pendently effective in reducing BP. Therefore, incorporating at
least some of the components of the DASH diet into ones own
diet confers advantageous BP effects. A dietary intervention as in
DASH is one the average person can realistically model. Adher-
ence to the assigned diet was over 90% and not lower for the
intervention arms compared with the control group.
Dietary minerals and nutrients
Significant inverse associations of BP with intake of magnesium,
potassium, calcium, fibre, and protein have also been reported.31
3084
However, in trials that tested these nutrients, often as dietary sup-
plements, the reduction in BP has typically been small and incon-
sistent.32,33 The effect of any individual nutrient in lowering BP
may be too small to detect in trials. When several nutrients with
small BP-lowering effects are consumed together, however, the
cumulative effect may be sufficient for detection. The most convin-
cing data for any single mineral in isolation exist for potassium.
Potassium
A meta-analysis found that for a 1.7 g increase in potassium intake,
there was a 3.5/2.5 mmHg drop in BP for hypertensives and a 1.0/
0.3 mmHg drop for normotensives.34 In a meta-analysis of 32 trials,
potassium supplementation was associated with a fall in BP of 3.1/
2.0 mmHg; the effect was more pronounced in patients who had
higher salt intake (potassium has a powerful inhibitory effect on
salt sensitivity).35 Increases in serum potassium hyperpolarize the
endothelial cell through stimulation of the sodium pump, which
results in decreased cytosolic calcium, which in turn promotes
vasodilatation.36
A recent analysis of the NHANES III study found that the
sodium potassium ratio in the highest (87.5) compared with
lowest (12.5) quartiles was associated with a hazard ratio of
1.46, 1.46, and 2.15 for all-cause, cardiovascular disease, and
ischaemic heart disease mortality, respectively.37
Several epidemiological studies show an association between
increased dietary potassium intake and reduced stroke rate.38 An
increase in potassium intake of 10 mmol/day led to a 40%
reduction in stroke mortality;39 increased intake of 1.64 g/day
showed a statistically significant 21% risk reduction in stroke and
trend towards lower cardiovascular disease.40 The relationship
appears to be partly, but not entirely, mediated by the higher pot-
assium intake effect on BP.
Magnesium
Magnesium deficiency raises BP in animals,41 and supplementation
seems to prevent HTN in these models.42 Among trials in humans,
although there are data linking low magnesium to incident coron-
ary heart disease,43 there are no convincing data that magnesium
deficiency is significantly related to increased BP; in a Framingham
study cohort, for example, there was no association between base-
line magnesium and incident HTN.44
Vitamin D (25(OH)D)
25(OH)D is implicated in a great variety of clinical condition.45
Adolescents in NHANES II with the lowest 25(OH)D values had
more than a two-fold greater odds of having elevated BP compared
with the group of adolescents with higher 25(OH)D levels.46
Plasma 25(OH)D levels are inversely and independently associated
with the risk of developing HTN.47 Women in the lowest com-
pared with highest quartile of plasma 25(OH)D had an adjusted
odds ratio for incident HTN of 1.66.
Nonetheless, a causal relationship between vitamin D and HTN
(or many of the other cardiometabolic disease states) has not been
established, and there are no convincing data as of yet that increas-
ing vitamin D levels (via supplementation or increased sunlight
T.M. Frisoli et al.
exposure) may be effective for the primary prevention or treat-
ment of HTN.
Flavonoids
Flavonoids, polyphenolic compounds found in high concentrations
in foods such as fruits, vegetables, grains, legumes, tea, beer, and
wines, are known for their antioxidant properties. Experimental
evidence suggests that flavonoids exert beneficial BP effects by
increasing endothelial-derived nitric oxide.48,49 One meta-analysis
showed that some subclasses of flavonoids are associated with sig-
nificant BP reductions; cocoa flavan-3-ols (found in cocao beans
and tea), for example, reduced BP by 5.9/3.3 mmHg. However,
the design of the studies was such that the effect seen may be
exaggerated and not exclusively attributable to the flavonoid com-
ponents.50 Also, the quantity of flavonoids consumed by partici-
pants in the study was beyond the range typically consumed.
One small study showed that eating a small amount of dark choco-
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late daily lowered BP 2.9/1.9 mmHg in those with pre-HTN or
Stage 1 HTN.51 Another recent large prospective study of habitual
intake of the various subclasses of flavonoids showed that a higher
total anthocyanin (predominantly from blueberries and strawber-
ries) intake decreased the rate of incident HTN after correcting
for physical activity, BMI, and dietary factors.52
Caffeine and nicotine
Caffeine has been shown to increase BP, but this effect resolves 4 h
after ingestion.53 These effects are attenuated in habitual drinkers,
suggesting tolerance to adrenergic effects.54 Habitual caffeine use
has been shown to have a minimal effect on long-term BP.55
Nicotine seems to have divergent effects on BP; acutely, BP
seems to rise while one is smoking a cigarette,56 but chronic
tobacco use seems to be associated with lower BP, with one
study showing an SBP reduction of 1.3 and 4.6 mmHg for light
and heavy smokers, respectively.57
Biofeedback therapies
Biofeedback training includes elements of cognitive therapy and
relaxation training. Meditation, yoga, and breathing exercises are
just three of the various types of relaxation therapy. A Cochrane
meta-analysis comparing relaxation therapy to no active treatment
among hypertensive individuals showed a 5.5/3.5 mmHg reduction
in BP at 8 weeks; however, there were only nine trials with
outcome assessment blinding and these trials yielded a non-
significant 3.2 mmHg reduction in SBP.58 The authors concluded
that the evidence favouring a causal relationship between relax-
ation therapy and BP reduction was weak.
Device-guided breathing, through the use of commercially avail-
able FDA-approved electronic devices, is a form of biofeedback
therapy that guides users to slower respiratory rates, which
increases tidal volume, increases cardiopulmonary stretch receptor
stimulation, and reduces sympathetic efferent discharge, thus
resulting in vasodilatation.59,60 Such breathing has been shown to
achieve modest BP reduction effects without adverse effects in
observational61,62 and larger prospective-matched case control
Beyond salt: lifestyle modifications and BP
studies63,64 and prospective-randomized controlled trials.65,66
Studies, however, did not go beyond an 8-week follow-up
period. It is currently considered adjunctive treatment, and more
Table 1 Relative blood pressure impacts of some of
the major lifestyle modifications
Modification Recommendation2
................................................................................
Weight Maintain BMI 18.5 24.9
reduction
Adopt DASH Consume a diet rich in
eating plan fruits, vegetables, and
low-fat dairy products
with a reduced content
of saturated and total
fat
Dietary sodium Reduce dietary sodium
reduction intake to no more than
2.4 g sodium (or 6 g
salt)
Physical activity Engage in aerobic physical
activity 30 60 min/day,
3 5 days/week)
Moderation of Limit to no more than 2
alcohol drinks per day (men) or
consumption 1 drink/day (women)
Figure 3 Estimated decrease in blood pressure mediated by non-pharmacological intervention in hypertension (modified from Messerli
et al.).73
3085
evidence is needed before it can be widely recommended as a
treatment that provides predictable and meaningful BP reduction.
Alcohol
It has long been recognized that the problems with alcohol relate not
to the use of a bad thing, but to the abuse of a good thing. 67
Abraham Lincoln
Sixteen per cent of all hypertensive disease is attributed to
SBP reduction
alcohol.68 What makes the issue of alcohol and cardiovascular
4.4 mmHg14 (for risk intriguing and complicated is that unlike the effects on other
5.1 kg weight organ systems, the cardiovascular effects of alcohol consumption
loss) are a mixed bag: some advantageous and others deleterious.
5.511.4 mmHg29
(5.5 for
normotensives,
Magnitude and duration of effect
11.4 for Longitudinal studies have shown a strong, linear relationship
hypertensives) between alcohol consumption and BP. In one meta-analysis, an
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average 67% reduction in alcohol consumption yielded a net
4 7 mmHg85 (for decrease in BP of 3.31/2.04 mmHg.69 Importantly, alcohol intake
reduction by 6 g
in daily salt intake)
has paradoxically divergent effects on BP and coronary heart
disease. Heavy drinking is associated with a higher prevalence of
5 mmHg19 HTN, haemorrhagic stroke, and cardiomyopathy,70 whereas mod-
erate drinking is associated with lower prevalence of coronary
artery disease, ischaemic stroke, and sudden cardiac death.71,72
3 mmHg69 (for 67% Even in lower-risk individualsmen of mean age 57 who fol-
reduction from lowed all four of the major healthy lifestyle behaviours (abstinence
baseline of 3 6
drinks/day)
from smoking, maintaining a BMI 25 kg/m2, exercising at least
30 min daily, and eating a healthy diet)the consumption of one
or two drinks per day was associated with a 4050% decreased
3086 T.M. Frisoli et al.

risk of myocardial infarction.74 A meta-analysis of over 1 million
individuals showed that consumption of one drink (1.5 oz of
hard liquor, 5 oz of wine, or 12 oz of beer) daily by women and
one or two drinks daily by men was associated with a reduction
in total mortality of 18%.75 Intakes of two drinks daily in women
and three drinks daily in men, however, were associated with
increased mortality in a dose-dependent fashion.
Pattern and type of alcohol consumption
The frequency and setting of consumption was found consequen-
tial in more than one study. Data from the USA and Italy show that
after adjustment for average amount of alcohol consumed over 30
days, drinking without food was associated with a strong significant
increased risk of HTN, even in individuals with light-to-moderate
alcohol intake (less than two drinks per day).76 There were no
gender differences. The authors put forward possible explanations:
the effect of food on absorption and metabolism of ethanol leading
to lower peak of blood alcohol concentration; the effect of food
partial attainment of multiple lifestyle intervention goals. In fact,
the strongest evidence supporting non-drug interventions for BP
reduction is not for any single modality, but rather for the combin-
ing of several.
Comparing and combining
modalities
Patients who lost weight and reduced sodium intake delayed the
onset of HTN more than those who only lost weight or only
reduced sodium intake.80 Salt intake reduction confers a greater
BP reduction in obese than in non-obese individuals. Furthermore,
not only is BP more salt sensitive in the overweight,81 high-salt
intake is a stronger and independent risk factor for cardiovascular
disease and all-cause mortality in overweight people.82
Combining DASH diet with low-salt intake is another example

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of how effective combination lifestyle interventions can be
on increased alcohol elimination rates; alcohol intake with meals (Figure 3).83
represents a surrogate marker of health-related behaviours. The PREMIERE trial further assessed multifaceted behavioural
For predominant beverage preference, no consistent association interventions: an established behavioral intervention consisting
with HTN risk was found across the various types of beverages of weight loss, physical activity, and limitations in salt and alcohol
considered (beer, wine, and liquor). intake, established behavioral intervention plus DASH diet, and
The cardioprotective effects of mild moderate consumption one-time advice only. At 6 months, DASH plus established
are greatest when the consumption is spread out evenly over
the course of a week. Binge drinkinglinked to higher prevalence
of cerebral thrombosis, cerebral haemorrhage, and coronary
artery disease deathsattenuates completely the decrease in car-
diovascular mortality associated with moderate drinking.77

Why bother?
To put lifestyle interventions into context, mean placebo-
subtracted SBP reduction for drug monotherapy is in the range
of 6.9 9.3 mmHg for four of the most common BP drug
classes.78 Estimated SBP reductions for some of the major lifestyle
modifications are in or near this range (Table 1).
Compliance with lifestyle modification can be difficult (of
course, compliance with medication is also not perfect). When
one sets out to lose weight or exercise, the goal is to succeed
and sustain that success. Losing weight to regain it a year later
would seem a failure to most. Why bother trying if one is unlikely
to succeed? The answer is that trying, even when ultimately failing,
may be better than not trying at all.
At 7-year follow-up of persons aged 3054 who lost 3.5 kg or
decreased salt intake by roughly 2 g/day, intervention effects on
body weight and urinary sodium excretion had disappeared but
the beneficial effect on HTN had not.79 In fact, the intervention
group was heavier by 4 kg than the control group at 7 years; yet,
average SBP and DBP were 1.8 and 1.3 mmHg lower, respectively.
It is likely that attempting to engage in one lifestyle modification
can have risk-reduction effects even when the intended interven-
tion is not fully achieved. The reason may be that it is hard to
Figure 4 Combining modalities for reducing BP can have addi-
pursue one lifestyle intervention in isolation; when one sets out
tive effects: DASH diet plus salt restriction reduced BP differen-
to lose weight, for example, one is likely to also pursue dietary tially for each level of salt intake. Reprinted with permission from
improvements and/or increased physical activity. If one does not Sacks et al.83 *P , 0.05, P , 0.01, P , 0.001.
achieve weight loss goals, one may incur overall benefit from
Beyond salt: lifestyle modifications and BP
behavioral intervention and established behavioral intervention
alone reduced BP 4.3/2.6 and 3.7/1.7 mmHg, respectively (Figure 4).
The kind of decrease in BP obtained with some non-drug mod-
alities would dramatically reduce incidence of and death from car-
diovascular disease in populations. Although it may be hard to get
40 people to lose 40 pounds or reduce salt intake by 6 g, it may be
less difficult to get 400 people to lose 4 pounds and reduce salt
intake by 2 g, especially if public health interventions create an
environment increasingly conducive to such efforts.
Intervening simultaneously to address smoking cessation,
reduced dietary salt intake, and increased physical activity, for
example, may be more effective than addressing each behaviour
sequentially.84 Individuals with the most physical activity and
dietary behaviour goals were the most likely to meet the most
goals; attempting to meet one physical activity or dietary goal
may actually enhance chances for attainment of a second such
goal.85 And just as a combination approach to lifestyle interven-
tions for BP reduction is greater than any single intervention, a
moderate but sustained intervention is better than a more signifi-
cant but short-lived one.
In conclusion, lifestyle changes safely and effectively delay or
prevent HTN in non-hypertensives, delay or prevent medical
therapy in Stage I hypertensives, and contribute to BP reduction
in hypertensives already on medical therapy.
Conflict of interest: none declared.
References
1. Flegal KM, Graubard BI, Williamson DF, Gail MH. Cause-specific excess deaths
associated with underweight, overweight, and obesity. JAMA 2007;298:
2028 2037.
2. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW,
Materson BJ, Oparil S, Wright JT, Roccella EJ. The Seventh Report of the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560 2572.
3. The Trials of Hypertension Prevention Collaborative Research Group. The
effects of nonpharmacologic interventions on blood pressure of persons with
high normal levels. Results of the trials of hypertension prevention, phase I.
JAMA 1992;267:1213 1220.
4. Lindmark S, Lonn L, Wiklund U, Tufvesson M, Olsson T, Eriksson JW. Dysregula-
tion of the autonomic nervous system can be a link between visceral adiposity and
insulin resistance. Obes Res 2005;13:717 728.
5. Sarzani R, Salvi F, Dessi-Fulgheri P, Rappelli A. Reninangiotensin system,
natriuretic peptides, obesity, metabolic syndrome, and hypertension: an inte-
grated view in humans. J Hypertens 2008;26:831 843.
6. Dornfield LP, Maxwell MH, Walk A, Tuck M. Mechanisms of hypertension in
obesity. Kidney Int Suppl 1987;22:S254S258.
7. Reisin E, Frohlich ED, Messerli FH, Dreslinski GR, Dunn FG, Jones MM,
Batson HM. Cardiovascular changes after weight reduction in obesity hyperten-
sion. Ann Intern Med 1983;98:315 319.
8. Engeli S, Bohnke J, Gorzelniak K, Janke J, Schling P, Bader M, Luft FC, Sharma AM.
Weight loss and the reninangiotensin aldosterone system. Hypertension 2005;
45:356 362.
9. Zhang R, Thakur V, Morse S, Reisin E. Renal and cardiovascular considerations for
the nonpharmacological and pharmacological therapies in obesity-hypertension.
J Hum Hypertens 2002;16:819827.
10. Villarreal D, Reams G, Samar H, Spear R, Freeman RH. Effects of chronic nitric
oxide inhibition on the renal excretory response to leptin. Obes Res 2004;12:
1006 1010; doi: 10.1038/oby.2004.123
11. Lembo G, Vecchione C, Fratta L, Marino G, Trimarco V, dAmati G. Leptin
induces direct vasodilation through distinct endothelial mechanisms. Diabetes
2000;49:293 297.
12. Grntved A, Steene-Johannessen J, Kynde I, Franks PW, Helge JW, Froberg K,
Anderssen SA, Andersen LB. J Hypertens 2011;29:1093 1100.
13. Stevens VJ, Obarzanke E, Cook NR, Lee IM, Appel LJ, Smith WD, Milas NC,
Mattfeldt-Beman M, Belden L, Bragg C, Millstone M, Raczynski J, Brewer A,
3087
Singh B, Cohen J. Long-term weight loss and changes in blood pressure: results
of the trials of hypertension prevention, phase II. Ann Intern Med 2001;134:1 11.
14. Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight
reduction on blood pressure: a meta-analysis of randomized controlled trials.
Hypertension 2003;42:878 884.
15. Kanai H, Tokunaga K, Fujioka S, Yamashita S, Kameda-Takemura KK,
Matsuzawa Y. Decrease in intra-abdominal visceral fat may reduce blood pressure
in obese hypertensive women. Hypertension 1996;27:125 129.
16. Horvath K, Jeitler K, Siering U, Soz D, Stich AK, Soz-Pad D, DrRerNat GS,
Gratzer TW, Siebenhofer A. Long term effects of weight-reducing interventions
in hypertensive patients. Arch Intern Med 2008;168:571 580.
17. Torp-Pedersen C, Caterson I, Coutinho W, Finer N, Van Gaal L, Maggioni A,
Sharma A, Brisco W, Deaton R, Shepherd G, James P. Cardiovascular responses
to weight management and sibutramine in high-risk subjects: an analysis from the
SCOUT trial. Eur Heart J 2007;28:2915 2923.
18. Sjostrom L, Lindroos AK, Peltonen M, Torgerson J, Bouchard C, Carlsson B,
Dahlgren S, Larsson B, Narbro K, Sjostrom CD, Sullivan M, Wedel H. Lifestyle,
diabetes and cardiovascular risk factors 10 years after bariatric surgery. N Engl J
Med 2004;351:2683 2693.
19. Dickinson HO, Mason JM, Nicolson DJ, Campbell F, Beyer FR, Cook JV,
Williams B, Ford GA. Lifestyle interventions to reduce raised blood pressure: a
systematic review of randomized controlled trials. J Hypertens 2006;24:215 233.
20. Whelton SP, Chin A, Xin X, He J. Effect of aerobic exercise on blood pressure: a
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on April 25, 2016
meta-analysis of randomized, controlled trials. Ann Intern Med 2002;136:493.
21. Blair SN, Goodyear NN, Gibbons LW, Cooper KH. Physical fitness and incidence
of hypertension in healthy normotensive men and women. JAMA 1984;252:487.
22. Carnethon MR, Gidding SS, Nehgme R, Sidney S, Jacobs DR Jr, Liu K. Cardiore-
spiratory fitness in young adulthood and the development of cardiovascular
disease risk factors. JAMA 2003;290:3092 3100.
23. Carnethon MR, Evans NS, Church TS, Lewis CE, Schreiner PJ, Jacobs DR,
Sternfeld B, Sidney S. Joint associations of physical activity and aerobic fitness
on the development of incident hypertension: coronary artery risk development
in young adults. Hypertension 2010;56:4955.
24. Ishikawa-Takata K, Ohta T, Tanaka H. How much exercise is required to reduce
blood pressure in essential hypertensives: a dose response study. Am J Hypertens
2003;16:629.
25. Nakanishi N, Suzuki K. Daily life activity and the risk of developing hypertension in
middle-aged Japanese men. Arch Intern Med 2005;165:214.
26. Kiyonaga A, Arakawa K, Tanaka H, Shindo M. Blood pressure and hormonal
responses to aerobic exercise. Hypertension 1985;7:125131.
27. Goto C, Higashi Y, Kimura M, Noma K, Hara K, Nakagawa K, Kawamura M,
Chayama K, Yoshizumi M, Nara I. Effect of difference intensities of exercise on
endothelium-dependent vasodilation in humans: role of endothelium-dependent
nitric oxide and oxidative stress. Circulation 2003;108:530.
28. Steward KJ, Bacher AC, Turner KL, Fleg JL, Hees PS, Shapiro EP, Tayback M,
Ouyang P. Effect of exercise on blood pressure in older persons: a randomized
controlled trial. Arch Intern Med 2005;165:756.
29. Appel L, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA,
Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N, Simons-Morton D,
McCullough M, Swain J, Steele P, Evans MA, Miller ER, Harsha DW. A clinical
trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997;
336:1117 1124.
30. The Treatment of Mild Hypertension Research Group. The treatment of mild
hypertension study: a randomized, placebo-controlled trial of a nutritional-
hygienic regimen along with various drug monotherapies. Arch Intern Med 1991;
151:1413 1423.
31. Stamler J, Caggiula A, Grandits GA, Kjelsberg M, Cutler JA. Relationship to blood
pressure of combinations of dietary macronutrients: findings of the Multiple Risk
Factor Intervention Trial (MRFIT). Circulation 1996;94:2417 2423.
32. Whelton PK. Potassium and blood pressure. In: Izzo JL, Black HR, eds. Hyperten-
sion Primer: The Essentials of Hypertension. Dallas: American Heart Association;
1993.
33. Allender PS, Cutler JA, Follmann D, Cappuccio FP, Pryer J, Elliott P. Dietary
calcium and blood pressure: a meta-analysis of randomized clinical trials. Ann
Intern Med 1996;124:825831.
34. Geleijnse JM, Kok FJ, Grobbee DE. Blood pressure response to changes in sodium
and potassium intake: a metaregression analysis of randomized trials. J Hum
Hypertens 2003;289:2083 2093.
35. Whelton PK, He J, Cutler JA, Brancati FL, Appel LJ, Follmann D, Klag MJ. Effects of
oral potassium on blood pressure. Meta-analysis of randomized controlled clinical
trials. JAMA 1997;277:1624 1632.
36. Adrogue HJ, Madias NE. Sodium and potassium in the pathogenesis of hyperten-
sion. N Engl J Med 2007;356:1966.
3087a
37. Yang Q, Tiebin L, Kuklina EV, Flanders WD, Hong Y, Gillespie C, Chang MH,
Gwinn M, Dowling N, Khoury MJ, Hu FB. Sodium and potassium intake and mor-
tality among US adults. Arch Intern Med 2011;171:1183 1191.
38. Bazzano LA, He J, Ogden LG, Loria C, Vupputuri S, Myers L, Whelton PK. Dietary
potassium intake and risk of stroke in US men and women: National Health and
Nutrition Examination Survey I epidemiologic follow-up study. Stroke 2001;32:
1473 1480.
39. Khaw KT, Barrett-Connor E. Dietary potassium and stroke-associated mortality.
A 12-year prospective population study. N Engl J Med 1987;316:235 240.
40. DElia L, Barba G, Cappuccio F, Strazzullo P. Potassium intake, stroke, and cardi-
ovascular disease. A meta-analysis of prospective studies. J Am Coll Cardiol 2011;
57:1210 1219.
41. Laurant P, Hayoz D, Brunner HR, Berthelot A. Effect of magnesium deficiency on
blood pressure and mechanical properties of rat carotid artery. Hypertension
1999;33:1105 1110.
42. Kh R, Khullar M, Kashyap M, Pandhi P, Uppal R. Effect of oral magnesium sup-
plementation on blood pressure, platelet aggregation and calcium handling in
deoxycorticosterone acetate induced hypertension in rats. J Hypertens 2000;18:
919 926.
43. Liao F, Fosom AR, Brancati FL. Is low magnesium concentration a risk factor for
coronary heart disease? The Atherosclerosis Risk in Communities (ARIC) Study.
Am Heart J 1998;136:480.
44. Khan AM, Sullivan L, McCabe E, Levy D, Vasan RS, Wang TJ. Lack of association
between serum magnesium and the risks of hypertension and cardiovascular
disease. Am Heart J 2010;160:715 720.
45. Thatcher T, Clarke B. Vitamin D insufficiency. Mayo Clin Proc 2011;86:50 60.
46. Reiss JP, von Muhlen D, Miller ER III, Michos ED, Appel LJ. Vitamin D status and
cardiometabolic risk factors in the United States adolescent population. Pediatrics
2009;124:e371 e379.
47. Forman JP, Giovannucci E, Holmes MD, Bischoff-Ferrari HA, Tworoger SS,
Willett WC, Curhan GC. Plasma 25-hydroxyvitamin D levels and risk of incident
hypertension. Hypertension 2007;49:1063 1069.
48. Steffen Y, Gruber C, Schewe T, Sies H. Mono-O-methylated flavanols and other
flavonoids as inhibitors of endothelial NADPH oxidase. Arch Biochem Biophys
2008;469:209 219.
49. Schroeter H, Heiss C, Balzer J, Kleinbongard P, Keen CL, Hollenberg NK, Sies H,
Kwik-Uribe C, Schmitz HH, Kelm M. ( )-Epicatechin mediates beneficial effects
of flavanol-rich cocoa on vascular function in humans. Proc Natl Acad Sci USA
2006;103:1024 1029.
50. Hooper L, Kroon PA, Rimm EB, Cohn JS, Harvery I, Le Cornu KA, Ryder JJ,
Hall WL, Cassidy A. Flavonoids, flavonoid-rich foods, and cardiovascular risk: a
meta-analysis of randomized controlled trials. Am J Clin Nutr 2008;88:3850.
51. Taubert D, Roesen R, Lehmann C, Jung N, Schomig E. Effects of low habitual
cocoa intake on blood pressure and bioactive nitric oxide. JAMA 2007;298:
49 60.
52. Cassidy A, OReilly EJ, Kay C, Sampson L, Franz M, Forman JP, Curhan G,
Grimm EB. Habitual intake of flavonoid subclasses and incident hypertension in
adults. Am J Clin Nutr 2011;93:338 347.
53. Conrad KA, Blanchard J, Trang JM. Cardiovascular effects of caffeine in elderly
men. J Am Geriatr Soc 1982;30:267 272.
54. Corti R, Binggeli C, Sudano I, Spieker L, Hanseler E, Ruschitzka F, Chaplin WF,
Luscher TF, Noll G. Coffee acutely increases sympathetic nerve activity and
blood pressure independently of caffeine content: role of habitual versus nonha-
bitual drinking. Circulation 2002;106:2935 2940.
55. Birkett NJ, Logan AG. Caffeine-containing beverages and the prevalence of hyper-
tension. J Hypertens Suppl 1988;6:S620 S622.
56. Hill P, Wynder EL. Smoking and cardiovascular disease. Effect of nicotine on the
serum epinephrine and corticoids. Am Heart J 1974;87:491 496.
57. Hughes K, Leong WP, Sothy SP, Lun KC, Yeo PPB. Relationships between ciga-
rette smoking, blood pressure and serum lipids in the Singapore general popu-
lation. Int J Epidemiol 1993;22:637 643.
58. Dickinson HO, Beyer FR, Ford GA, Nicolson D, Campbell F, Cook JV, Mason J.
Relaxation therapies for the management of primary hypertension in adults.
Cochrane Database Syst Rev 2008. doi: 10.1002/14651858.CD004935.pub2.
59. Parati G, Izzo JL Jr, Gavish B. Respiration and blood pressure. In: Izzo JL Jr, Sica D,
Black HR, eds. Hypertension Primer. 4th ed. Dallas, TX: American Heart Associ-
ation; 2008. p136 138.
60. Sharma M, Frishman WH, Gandhi K. RESPeRATE: nonpharmacologic treatment
for hypertension. Cardiol Rev 2011;19:4751.
61. Rosenthal T, Alter A, Peleg E, Gavish B. Device-guided breathing exercises reduce
blood pressure: ambulatory and home measurements. Am J Hypertens 2001;14:
74 76.
T.M. Frisoli et al.
62. Viskoper R, Shapira I, Priluck R, Mindlin R, Chornia L, Laszt A, Dicker D, Gavish B,
Alter A. Nonpharmacologic treatment of resistant hypertensives by device-
guided slow breathing exercises. Am J Hypertens 2003;16:484 487.
63. Meles E, Giannattasio C, Failla M, Gentile G, Capra A, Mancia G. Nonpharmaco-
logic treatment of hypertension by respiratory exercise in the home setting. Am J
Hypertens 2004;17:370 374.
64. Grossman E, Grossman A, Schein MH. Breathing-control lowers blood pressure.
J Hum Hypertens 2001;15:263 269.
65. Schein MH, Gavish B, Herz M, Rosner-Kahana D, Naveh P, Knishkowy B,
Zlotnikov E, Ben-Zvi N, Melmed RN. Treating hypertension with a device that
slows and regularizes breathing: a randomized, double-blind controlled study.
J Hum Hypertens 2001;15:271 278.
66. Elliot WJ, Izzo JL Jr, White WB, Rosing DR, Snyder CS, Alter A, Gavish B,
Black HR. Graded blood pressure reduction in hypertensive outpatients associ-
ated with use of a device to assist with slow breathing. J Clin Hypertens (Greenwich)
2004;6:553 559.
67. Ellison RC. Continuing reluctance to accept emerging scientific data on alcohol
and health. AIM Digest 2002;11:6 9.
68. Beilin LJ, Puddey IB. Alcohol and hypertension. Hypertension 2006;47:1035.
69. Xin X, He J, Frontini MG, Ogden LG, Motsamai OI, Whelton PK. Effects of
alcohol reduction on blood pressure: a meta-analysis of randomized controlled
trials. Hypertension 2001;38:1112 1117.
70. Klatsky AL. Alcohol and stroke: an epidemiological labyrinth. Stroke 2005;36:
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on April 25, 2016
1835 1836.
71. Klatsky AL. Drink to your health? Sci Am 2003;288:7481.
72. Ronksley P, Brien S, Turner B, Mukamal KJ, Gali WA. Association of alcohol con-
sumption with selected cardiovascular disease outcomes: a systematic review and
meta-analysis. BMJ 2011;342:d671.
73. Messerli FH, Williams B, Ritz E. Essential hypertension. Lancet 2007;370:591 603.
74. Mukamal KJ, Chiuve SE, Rimm EB. Alcohol consumption and risk for coronary
heart disease in men with healthy lifestyles. Arch Intern Med 2006;166:2145 2150.
75. DiCastelnuovo A, Castanzo S, Bagnardi V, Donati MB, Iacoviello L, de Gaetano G.
Alcohol dosing and total mortality in men and women. Arch Intern Med 2006;166:
2437 2445.
76. Stranges S, Wu T, Dorn JM, Freudenheim JL, Muti P, Farinaro E, Russell M,
Nochajski TH, Trevisan M. Relationship of alcohol drinking pattern to risk of
hypertension. Hypertension 2004;44:813 819.
77. Puddey IB, Beilin LJ. Alcohol is bad for blood pressure. Clin Exp Pharmacol Physiol
2006;33:847 852.
78. Wald DS, Law M, Morris JK, Bestwick JP, Wald NJ. Combination therapy versus
monotherapy in reducing blood pressure: meta-analysis on 11,000 participants
from 42 trials. Am J Med 2009;122:290 300.
79. He J, Whelton P, Appel LJ, Charleston J, Klag M. Long term effects of weight loss
and dietary sodium reduction on incidence of hypertension. Hypertension 2000;35:
544.
80. Whelton PK, Appel LJ, Espeland MA, Applegate WB, Wttinger WH, Kostis JB,
Kumanyika S, Lacy CR, Johnson KC, Folmar S, Cutler JA. Sodium reduction and
weight loss in the treatment of hypertension in the older persons: a randomized
controlled trial of nonpharmacologic interventions in the elderly (TONE). JAMA
1998;279:839 846.
81. Rocchini AP, Key J, Bondie D, Chico R, Moorehead C, Katch V, Martin M. The
effect of weight loss on the sensitivity of blood pressure to sodium in obese ado-
lescents. N Engl J Med 1989;321:580 585.
82. He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary sodium
intake and subsequent risk of cardiovascular disease in overweight adults. JAMA
1999;282:2027 2034.
83. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E,
Conlin PR, Miller ER, Simons-Morton DG, Karanja N, Lin PH. Effects on blood
pressure of reduced dietary sodium and the Dietary Approaches to Stop Hyper-
tension (DASH) Diet. DASH-Sodium Collaborative Research Group. N Engl J
Med 2001;344:3 10.
84. Hyman DJ, Pavlik VN, Taylor WC, Goodrick GK, Moye L. Simultaneous vs
sequential counseling for multiple behaviour change. Arch Intern Med 2007;167:
1152 1158.
85. Young DR, Vollmer WM, King AC, Brown AJ, Stevens VJ, Elmer PJ, Craddick S,
Sturtevant DL, Harsha DW, Appel LJ. Can Individuals meet multiple physical
activity and dietary behavior goals? Am J Health Behav 2009;33:277 286.
86. Feng FJ, MacGregor GA. Effect of modest salt reductions on blood pressure: a
meta-analysis of randomized trials. Implications for public health. J Hum Hypertens
2002;16:761 770.