Hypertension. 1997;30:150-156
(Hypertension. 1997;30:150-156.)
© 1997 American Heart Association, Inc.
Ultraviolet Light May Contribute to Geographic and Racial Blood Pressure Differences
Stephen G. Rostand
From the Nephrology Research and Training Center, Division of Nephrology,
Department of Medicine, The University of Alabama at Birmingham.
Correspondence to Stephen G. Rostand, MD, Division of Nephrology, 604 Zeigler Building, The University of Alabama at Birmingham, Birmingham, AL 35294.
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Abstract
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Abstract Mean systolic and diastolic
pressures and the prevalence
of hypertension vary throughout the world.
Published data suggest
a linear rise in blood pressure at increasing
distances from
the equator. Similarly, blood pressure is higher in
winter than
summer. Blood pressure also is affected by variations in
skin
pigmentation. Altered calcium, vitamin D, and parathyroid hormone
status
is associated with hypertension and may vary with latitude and
season.
Since changes in UV light affect vitamin D and parathyroid
hormone
status and UV light intensity are influenced by seasonal change
and
latitude, these disparate observations suggest an association
between
blood pressure and ultraviolet light. This discussion
presents
the hypothesis that reduced epidermal vitamin
D
3 photosynthesis
associated with high skin melanin content
and/or decreased UV
light intensity at distances from the equator,
alone or when
coupled with decreased dietary calcium and vitamin D, may
be
associated with reduced vitamin D stores and increased parathyroid
hormone
secretion. These changes may stimulate growth of vascular
smooth
muscle and enhance its contractility by
affecting intracellular
calcium, adrenergic responsiveness, and/or
endothelial function.
Thus, UV light intensity and
efficiency of epidermal vitamin
D
3 photosynthesis may
contribute to geographic and racial variability
in blood pressure and
the prevalence of hypertension.
Key Words: parathyroid hormones vitamin D blood pressure geography race ultraviolet rays
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Introduction
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Mean systolic
and diastolic pressures and the prevalence of
hypertension
vary widely throughout the world. BP is higher
and the occurrence of
hypertension greater in more industrialized
or Westernized regions
(20% to 30%), whereas the opposite is
found in the least
industrialized regions (0% to 15%).
1 2 3 4 5 6 Data also suggest
that people of color living in the
United States
7 and
Great Britain
8 have more hypertension than
those of
European origin. Moreover, those living in their indigenous
regions
have lower mean BPs and frequencies of hypertension
and rarely have the
age-associated rise in BP seen often in
whites and African
Americans.
3 4 9
Explanations for these geographic and racial differences in BP and
prevalence of hypertension have mostly been related to dietary changes,
particularly sodium and potassium consumption1 10 11 12 ; to
intrinsic racial differences in renal hemodynamics
and sodium metabolism13 14 15 16 ; and to social and
economic stresses of industrialization, or
Westernization.4 17 18 However, other factors may be
involved. Alterations in calcium, vitamin D, and PTH status have been
observed in experimental19 20 21 and human22 23 24 25 26 27 28 29
hypertension, and although controversial,29 30 such
changes have been felt to contribute to its pathogenesis. As will be
discussed in more detail below, these findings, along with data from a
variety of sources showing seasonal and geographic differences in BP,
suggest that reduced epidermal vitamin D3 photosynthesis
caused by decrements in ambient UVB radiation at progressive distances
from the equator results in reduced vitamin D stores and increased PTH
secretion. This effect may be further accentuated by less efficient
vitamin D3 photosynthesis in deeply pigmented skin.
Together, these conditions may not only contribute to geographic
differences in BP but also may partially explain the greater prevalence
of hypertension in dark-skinned people living in temperate
climates.
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UV Light and BP
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In humans, ambient sunlight plays a major role in vitamin D
production
because high-energy UVB light enters the epidermis,
transforming
7-dehydrocholesterol (provitamin
D
3) to previtamin D
3,
31 32 with
subsequent conversion to the more stable vitamin D
3.
Vitamin
D
3 is translocated into the circulation and
transported to the
liver where it is converted to 25(OH)D
3,
the major index of
total body vitamin D
3
stores,
31 32 before its final renal conversion
to
1,25(OH)
2D
3. Among the numerous factors
influencing cutaneous
production of vitamin D
3 are
seasonal changes, degree of skin
pigmentation, and latitude north or
south of the equator.
31 33 34 35
It has been observed that with each 10° distance from the equator,
there is a progressive fall in ambient UVB radiation,33
and BP rises at increasing distances from the equator. For example,
when mean BPs noted for the various centers in the INTERSALT study are
plotted in relation to their latitudes north or south of the equator, a
highly significant positive association is seen (Fig 1
).1 The prevalence of hypertension has a
similar relationship to latitude (Fig 2
).1
Moreover, had 95% predictive limits been used instead of confidence
limits, the eightnon-INTERSALT centers36 37 38 39 40 (Fig 2
, labeled open boxes) would be seen to fall well within these
predictive intervals. There is also an association between mean BP and
latitude for black men living in Nigeria, Barbados, and the United
States.41 However, a comparison of BPs of Cape Verdeans
and Cape Verde immigrants to New England showed only small
differences.42

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Figure 1. A, Relationship of mean systolic blood
pressure (SBP) and distance north or south of the equator. Symbols
represent north or latitudes of INTERSALT
Centers.3 B, Relationship of mean diastolic
blood pressure (DBP) to distance north or south of the equator. For
both figures, broken lines represent 95% confidence
limits.
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Figure 2. Relationship of prevalence of hypertension to
distance north or south of the equator. Labeled open boxes
represent non-INTERSALT centers36 37 38 39 40 ; solid boxes
are INTERSALT centers. Broken lines represent 95% confidence
limits. Regression line and confidence limits are derived from
INTERSALT centers only.
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Seasonal variations in BP also have been observed in temperate
climates,43 44 with BP highest in winter, when ambient UVB
radiation is least, and at a nadir in summer, during peak UVB light.
Although one study43 related seasonal changes in BP to
ambient temperature, another44 was more cautious in its
interpretation. Thus, it is possible that seasonal and geographic
changes in BP are inversely associated with ambient UVB light intensity
and with vitamin D stores producing increased PTH secretion. Support
for this viewpoint comes from two studies examining the direct effects
of UVB light on BP. Kokot et al45 found small reductions
in BP in 23 Polish subjects exposed to light of UVB wavelengths.
Similarly, Krause et al46 recently reported that BP and
PTH fell after UVB irradiation of eight hemodialysis patients. This was
associated with increases in 25(OH)D3 and
1,25(OH)2D3, unlike Kokot et al, who found no
changes in vitamin D metabolites from their elevated baselines.
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Race, PTH, Vitamin D, and BP
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Hyperparathyroidism is the most consistent change in
calcium/vitamin
D/PTH status in human
hypertension.
24 25 27 47 Increased plasma
PTH and
1,25(OH)
2D
3 have been found in low-renin and
other forms
of hypertension
24 26 27 ; in hypertensive
individuals after
salt loading
48 49 50 ; in African Americans,
who also have been
reported to have reduced plasma 25(OH)D
3
concentrations and
increased parathyroid mass
51 52 ; and in
Zairians living in
Europe compared with those living in
Zaire.
53 Although no large-scale
systematic studies of
geographic differences in vitamin D metabolites
have been conducted,
one study of Europeans living between 35°N
and 60°N showed small
increases in vitamin D stores at more
northern
latitudes.
54 Nevertheless, these observations, although
controversial
and derived from various sources, when taken together
suggest
an effect of UV radiation on BP, possibly mediated through
changes
in vitamin D stores and PTH secretion.
Geographic variations in UV light, BP, PTH, and perhaps vitamin D
stores discussed above may be further accentuated by seasonal changes.
The least UVB radiation is available in winter and the most in
summer33 34 ; this may account for wintertime reductions of
25(OH)D3 in temperate climates.34 55 56 57 58 For
example, in winter, at 42°N and 52°N, skin samples exposed to
midday sunlight produced no previtamin D3, but at 18°N
and 34°N, previtamin D3 was formed.34
However, in the latter case, whether sunlight was sufficient to
maintain adequate vitamin D stores is uncertain since wintertime
reductions of "antirachitic factors" have been observed at
18°N.59 In winter, PTH increases
correspondingly.57 58 Since animal studies show that
decreases in 25(OH)D3 cause transient reductions in
1,25(OH)2D3,60 61 it is possible
that the wintertime fall in 25(OH)D3 results in decreases
in 1,25(OH)2D3 that stimulate PTH secretion.
Increased PTH secretion can augment 1,25(OH)D3
production,31 57 61 62 which may in part explain
the paradoxically normal serum 1,25(OH)2D3
levels seen with reduced vitamin D stores31 32 57 and the
elevated concentrations observed in some American and European
blacks.52 53
The above observations may have important implications for the BP of
dark-skinned people because the degree of skin pigmentation also alters
the effectiveness of vitamin D3 photosynthesis. Also, it
has been reported that within the African American community, greater
skin pigmentation, measured by UVB light reflectance, is associated
with higher BP.63 64 65 Holick31 reported that
20% to 30% of UVB radiation is transmitted through the epidermis of
white skin, but penetration is less than 5% in deeply pigmented skin
of African Americans. When skin specimens were exposed to simulated
sunlight under identical conditions, black skin required a longer
exposure than white skin to maximize previtamin D
production.31 Also, black subjects required
whole-body UVB radiation six times that of whites (enough to cause
severe second-degree sunburn in whites) to produce a similar increase
in circulating blood levels of 25(OH)D3.31
Such observations are not limited to people of African origin. Studies
of Pakistani and Indian children living in the United States suggest
that their capacity to produce vitamin D is the same as whites, but
like blacks, they require longer exposure to UV light because of
increased skin melanin content.31 Thus, a reduced
efficiency of vitamin D3 photosynthesis may partially
explain some of the interracial and intraracial differences in vitamin
D metabolites and PTH concentrations and the apparent direct
association between BP level and the degree of skin pigmentation in
African Americans.63 64 65
Although thus far a relationship of epidermal vitamin D3
photosynthesis to BP has been emphasized, vitamin D, PTH, and BP
interactions may also be linked to reduced concentrations of serum
ionized calcium noted in experimental hypertension and especially in
low-renin human hypertension.22 27 It has been suggested
that these changes in serum ionized calcium and PTH secretion are
caused by calciuresis either resulting from a primary renal calcium
leak or secondary to increased renal sodium
excretion,66 67 68 but increased urinary calcium excretion
has not been found in all subjects.27 47 68 69 However,
these differences may be due to the absence of a standardized dietary
calcium intake in several of the negative studies.68
Alternatively, changes in calcium homeostasis could relate to decreased
dietary calcium intake and/or calcium entry. In animal models,
particularly the spontaneously hypertensive rat, intestinal calcium
malabsorption and altered cellular calcium transport have been
demonstrated,20 70 71 72 but in human hypertension, no
disturbances of intestinal calcium absorption have been
noted.73 Nevertheless, a high prevalence of milk
intolerance, particularly in blacks, due to either lactase
deficiency74 or other factors75 might lead to
voluntary avoidance of milk products or to reduced calcium
absorption consequent to rapid gastrointestinal transit times.
Decreased calcium absorption might also be due to dietary intake of
food rich in phytates that can bind calcium. Reduced calcium entry can
lead to decreased concentrations of 25(OH)D3. Both low
serum ionized calcium and 25(OH)D3 stimulate PTH
production.61 Low 25(OH)D3 plasma
concentrations can cause decreases in
1,25(OH)2D3, with subsequent augmentation of
PTH secretion. This will in turn stimulate 25(OH)D3
1
-hydroxylase activity to correct
1,25(OH)2D3
concentrations.60 62 76 Calcium depletion not only
augments PTH secretion, it also has been shown to increase BP in
experimental hypertension.77 78 Moreover, reduced dietary
calcium has been demonstrated in some studies of human
hypertension79 80 ; however, there is no agreement on its
prevalence.23 30 Nevertheless, calcium supplementation has
been shown to lower BP in experimental hypertension81 82 83
and in human hypertensive subjects.84 85
It has been reported that African Americans consume less calcium than
whites,79 perhaps because of voluntary avoidance of milk
products, for reasons mentioned above, but the evidence is not
strong. Only one phase of the National Health and Nutrition Examination
Surveys (NHANES) revealed an association between low calcium intake and
BP in African Americans86 ; another study showed no racial
differences in calcium intake.53 However, as suggested
above, an absence of racial differences in calcium intake might not
accurately indicate intergroup rates or degrees of calcium entry into
the circulation. Thus, it may be that in blacks, reduced calcium entry
contributes to their susceptibility to hypertension, particularly in
the presence of inefficient epidermal photosynthesis of vitamin
D3.
The mechanisms whereby changes in calcium/vitamin D/PTH status
affect BP and their relative contributions are uncertain. Intracellular
calcium concentration is elevated in erythrocytes and platelets of
most, but not all, patients with essential
hypertension.28 87 88 89 These changes are thought to be
related to transcellular sodium and calcium fluxes due to increased
sodium loads48 49 66 or to abnormal plasma PTH and/or
1,25(OH)2D3 concentrations87 90 91
and may in part mediate increased vascular smooth muscle tone.
1,25(OH)2D3 has been shown to enhance the
contractile properties of resistance vessels in animal models by
affecting intracellular calcium and by altering adrenergic
responsiveness.91 92 93 94 95 PTH may interact with the vascular
endothelium.96 97 98 At present, however,
there is no agreement that all hypertensive individuals have altered
vitamin D status69 99 100 or that Africans living in
America or elsewhere have increased intracellular calcium
concentrations.89 101 102 103 However, low-renin hypertension
occurs frequently in African Americans, and increased intracellular
calcium is found more often in this condition,26 27 28
suggesting that increased intracellular calcium might mediate BP
control in this population.
Alterations in vitamin D and PTH status can affect vascular growth and
structure. Vitamin D3 depletion has been associated with
increased myocardial collagen content,104 and high calcium
diets can prevent intramyocardial vascular wall
thickening,105 suggesting that in some tissues, cell
growth is modified by changes in PTH and vitamin D concentrations. In
this regard, a recent study showed that PTH had a permissive effect in
the genesis of vessel wall thickening,106 and another
observed that 1,25(OH)2D3 stimulated
proliferation of quiescent vascular smooth muscles in
culture,107 suggesting a possible role for this hormone in
vascular smooth muscle cell proliferation.
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Summary and Conclusions
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An hypothesis is summarized in Fig 3

which suggests
that reduced
photosynthesis of vitamin D
3 at increasing
distances from the
equator, in deeply pigmented peoples, and with
reduction of
skin surface exposure produces limited vitamin D stores,
resulting
in augmented PTH production. There may be an
additional effect
of reduced dietary calcium intake or absorption in
some people.
Increased PTH secretion and, in some circumstances,
increased
1,25(OH)
2D
3 concentrations may in
turn affect vascular structure
and function, thus influencing BP in
blacks and in others living
at distances from the equator. The
hypothesis attempts to integrate
numerous clinical and experimental
observations regarding vitamin
D, calcium, and PTH gathered from many
disciplines in order
to gain further understanding of the geographical
differences
in BP and of the susceptibility of African Americans to
developing
hypertension. As in any synthesis of this type, there are
many
pitfalls. Numerous studies of seasonal or geographic BP
differences
were not accompanied by measurements of PTH or vitamin D
metabolites
and the converse. In fact, geographic differences in
vitamin
D metabolites have not been well described, and the available
data
seem contradictory. Others found opposite or no changes in vitamin
D
metabolites and did not categorize the hypertension
studied.
69 99 100 Much of the variability in PTH and
vitamin D metabolite
concentrations occurred because
physiological conditions and
assay methodologies
differed among studies. In many, seasonal
conditions, sunlight
exposure, dietary calcium, phosphorus,
and vitamin D, or other factors
influencing bone, calcium, vitamin
D, and PTH concentrations were not
reported. Many studies did
not specify the ethnic background of the
patients. In addition,
since most industrialized nations are distant
from the equator,
cross-cultural conflicts and the social, economic,
and psychological
stress related to them may be important contributors
to the
BP differences discussed here.

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Figure 3. Outline of proposed interrelationships between BP
regulation and UV light, vitamin D, PTH, and calcium
metabolism. Solid arrows are interactions established in
humans. Stippled arrows are interactions established in animal and in
vitro studies. Stimulatory and inhibitory effects are
denoted by plus and minus signs, respectively.
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Despite such pitfalls, the evidence presented suggests a role
for altered PTH and calcium status consequent to reduced skin
photosynthesis of vitamin D3 in geographic and racial
differences in BP. The proposed hypothesis does not detract from other
proposed mechanisms of hypertension and fits well with a role of sodium
in hypertension, since the strongest associations between alterations
of PTH, vitamin D, and calcium status have been noted in low-renin,
presumably volume-expanded, forms of hypertension. The coexistence of
less-efficient vitamin D3 photosynthesis in deeply
pigmented skin, reductions in renal sodium excretion rates, and salt
sensitivity11 16 in African Americans complements an
hypothesis proposing that African slave trade with the Americas
abruptly exposed a population uniquely adapted to low salt, high
potassium diets of West Africa to nontraditional European diets high in
sodium and low in potassium, causing attendant increases in
BP.108 Explanations for the evolutionary advantages of
highly pigmented skin have been discussed without
conclusion.109 110 Nevertheless, the migration away from
equatorial regions of salt-sensitive, dark-skinned populations also
well adapted to high UV light conditions may have had an additional
impact on BP by reducing ambient UV light, thus affecting calcium, PTH,
and vitamin D status and in turn BP. This hypothesis warrants further
investigation and could be tested by exposing salt-sensitive, low-renin
hypertensive Europeans and Africans to varying doses of UV light or
perhaps more easily by supplementing them orally with vitamin D.
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Selected Abbreviations and Acronyms
|
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| BP |
= |
blood pressure |
| 1,25(OH)2D3 |
= |
1,25-dihydroxyvitamin D3 |
| 25(OH)D3 |
= |
25-hydroxyvitamin D3 |
| PTH |
= |
parathyroid hormone |
| UVB |
= |
ultraviolet light, midrange sunbeam spectrum |
|
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Acknowledgments
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This work was in part supported by the Nephrology
Research and
Training Center, Division of Nephrology, The
University of Alabama
at Birmingham and a grant from the National
Institutes of Health
(NIDDK 1 UO1 DK 48669). I would like to thank Drs
Tilman Drüeke,
David Warnock, Murray Epstein, and Katherine
Rostand for their
helpful comments, suggestions, and encouragement and
the entire
faculty and staff of INSERM Unité 90, Hôpital
Necker,
Paris, France, for their kind hospitality, support, and
patience
during my sabbatical. Katharine A. Kirk, PhD, performed the
statistical
analyses.
Received September 30, 1996;
first decision October 25, 1996;
accepted January 24, 1997.
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