Dr Weeks’ Comment: Vitamin D from sunlight can protect against H1V1 influenza but the CDC and “experts” are not talking about it – too inexpensive for their consideration.
The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918–1919 influenza pandemic in the
[Dermato-Endocrinology 1:4, 1-5; July/August 2009];
©2009 Landes Bioscience
This manuscript has been published online, prior to printing. Once the issue is complete and page numbers have been assigned, the citation will change accordingly.
William B. Grant1,* and Edward Giovannucci2
1Sunlight, Nutrition and
Department of Medicine; Brigham and Women’s Hospital;
Deaths during the 1918–1919 influenza pandemic have been
linked to both the influenza virus and secondary bacterial lung
infections. Case fatality rates and percentage of influenza cases
complicated by pneumonia were available from survey data for
This study analyzes case fatality rates and cases complicated by
pneumonia with respect to estimated summertime and wintertime
solar ultraviolet-B (UVB) doses as indicators of population
mean vitamin D status. Substantial correlations were found for
associations of July UVB dose with case fatality rates (r = -0.72,
p = 0.009) and rates of pneumonia as a complication of influenza
(r = -0.77, p = 0.005). Similar results were found for wintertime
UVB. Vitamin D upregulates production of human cathelicidin,
LL-37, which has both antimicrobial and antiendotoxin activities.
Vitamin D also reduces the production of proinflammatory
cytokines, which could also explain some of the benefit of
vitamin D since H1N1 infection gives rise to a cytokine storm.
The potential role of vitamin D status in reducing secondary
bacterial infections and loss of life in pandemic influence requires
In the twentieth century, there were three influenza pandemics,
in 1918, 1957 and 1968, caused by H1N1 (Spanish flu), H2N2
(Asian flu) and H3N2 (
1918–1919 pandemic was different from the subsequent ones as
it was the only one caused by an H1N1 virus, and is the only one
considered in this work.
“In 1918, there was one distinct peak of excess death in
young adults aged between 20 and 40 years old; leukopenia and
hemorrhage were prominent features. Acute pulmonary edema and
hemorrhagic pneumonia contributed to rapidly lethal outcome in
young adults. Autopsies disclosed multiple-organ involvement,
including pericarditis, myocarditis, hepatitis and splenomegaly.
These findings are, in part, consistent with clinical manifestations
of human infection with avian influenza A H5N1 virus, in which
reactive hemophagocytic syndrome was a characteristic pathologic
finding that accounted for pancytopenia, abnormal liver function
and multiple organ failure.”1
The influenza pandemic of 1918–1919 claimed many lives.
While the influenza virus played an important role, there is
evidence that the primary influenza infection was not necessarily
the proximate cause of death. For example, the median time
to death was 7–10 days, and a substantial proportion of deaths
occurred greater than 2 weeks after onset of the initial symptoms.2
The delay in death has been attributed to the influenza infection
allowing bacteria to colonize the lower respiratory system and
produce lethal pneumonias.2,3 Bacterial pneumonia also was noted
as a serious complication of influenza during 1957–8 influenza
pandemic,4 and antibacterial approaches have previously been
proposed for reduction of the case-fatality rate during influenza
Vaccines are the first line of defence against epidemic influenza.
However, successful treatment or prophylaxis of complicating
bacterial pneumonias may be important, since a presently unknown
or poorly characterized virus might cause a pandemic before an
effective vaccine becomes universal.2,5,6 Several months to a year
are typically needed to develop and universally administer an effective
vaccine for a new strain of influenza.7
While vaccines are absolutely essential for control of influenza,
they are not always effective in eliminating influenza cases, and the
associated risk of secondary respiratory infections, especially among
older adults. It has been estimated that a recent influenza vaccine
produced only a 27% reduction in hospital admissions for acute
respiratory infections, such as pneumonia.8 Other epidemiological
approaches, such as limiting travel and case containment, could
be part of an overall plan to limit the intensity of an influenza
UVB, vitamin D and pandemic influenza followed by pneumonia
pandemic.9 However such concepts are rarely implemented
successfully. Targeted layered containment has also been proposed
for limiting pandemic influenza cases in the United States.10 Such
epidemiological measures would have serious economic impacts.
Since the fatal complications of influenza are due in part to
secondary bacterial infection,2-4 the degree of immunity to the
most common bacterial agents of pneumonia may be important.
Exposure to solar ultraviolet-B (UVB) starts a multi-step process,
starting with biosynthesis of vitamin D and its metabolites, followed
by upregulation of human cathelicidin (LL-37), by 1,25-dihydroxyvitamin
D.11 There are several recent reviews of the effects
of cathelicidin against bacterial infections such as Mycobacterium
tuberculosis.11-16 Cathelicidin appears to be effective in fighting
septicaemia, in part due to its antiendotoxin effects.12
The known benefit of cathelicidin is mainly limited to bacterial
or mycoplasmal infections. Cannell et al. hypothesized that
the annual seasonality of influenza was largely due to low solar
UVB irradiation and vitamin D biosynthesis in winter and
early spring.17 A post hoc analysis of self-reported incidence of
acute respiratory illnesses during a randomized controlled trial
of vitamin D for another purpose supported this hypothesis.18
Cannell et al. later extended their hypothesis.19 Regional solar
UVB irradiance is also inversely associated with incidence rates of
respiratory syncytial virus (RSV) infection.20 It is thought that the
higher incidence rates of RSV in darker-skinned infants may be
due to lower vitamin D production in them and their mothers.21
Vitamin D receptor polymorphisms were found correlated with
acute lower respiratory tract infection, primarily bronchiolitis, in
Canada.22 Vitamin D is also thought to reduce the risk of respiratory
infections that may lead to development of asthma.23
There are several aspects to incidence and death from influenza
including adaptive and innate immune response, exposure to the
influenza virus, season and development of complications from
other respiratory diseases. We analyzed data from the United
States during the 1918–1919 influenza pandemic to determine
whether solar UVB irradiance and vitamin D status might have
played a role in the development of pneumonia and in influenza-
pneumonia case fatality rates.24
The rates in each city, latitude and UVB irradiance are shown
in Table 1. The lowest case-fatality rates occurred in the area with
the highest solar UVB irradiance and lowest latitude,
TX, while the highest rates were in
the lowest UVB irradiance and highest latitude. The lowest rates of
pneumonia as a complication of influenza were in
between case-fatality rates for influenza and cases complicated
by pneumonia was r = 0.78 (p = 0.005).
The results for case fatality rates (CFR) with respect to solar
UVB are given in Table 2. Summer UVB irradiance had a slightly
higher correlation coefficient than latitude with CFR. The results
for influenza complicated by pneumonia are also given in Table 2.
The correlation coefficients were slightly higher than those for case
fatality rates. In the regression model, UVB accounted for 46% of
Cities included in the 1918–1919 influenza
pandemic study, case-fatality rates and
percentage of cases who developed
City and No. of No. of Influenza Pneumonia July Latitude
state influenza pneumonia case-complications* UVB (° N)
cases cases fatality (%) dose
Charles 6546 -2.25 -5.3 38.5
Minor MD 5060 322 1.66 6.4 5.1 39.2
Des Moines, 1353 138 1.63 10.2 4.8 41.6
Macon, 1681 103 1.49 6.1 7.5 32.8
Louisville, 1797 111 1.39 6.2 6.0 38.1
Spartanburg, 1126 35 0.89 3.1 7.0 35.0
San Antonio, 6701 303 0.78 4.5 8.2 31.6
Total 42,920 2290
*Incidence of pneumonia in influenza cases.
Association between UVB irradiance and
case-fatality rate of influenza or rate of
pneumonia as a complication of influenza
with respect to UVB indices, linear regressions
(from table 25 in Britten24)
UVB indicator r, adjusted r2, p
Case-fatality rate July UVB -0.72, 0.46, 0.009
Latitude 0.68, 0.42, 0.014
Pneumonia as a July UVB -0.77, 0.55, 0.005
complication of influenza
Latitude 0.81, 0.62, 0.003
UVB, vitamin D and pandemic influenza followed by pneumonia
the variation in case-fatality rates of pneumonia and 55% of the
variation in rates of pneumonia as a complication of influenza.
There was an inverse association between UVB irradiance
and case-fatality rate of influenza and rate of pneumonia as a
complication of influenza in the
similar results. According to data in Britten,24 the 1918 influenza
pandemic reached eastern
October to early December. Based on serum 25(OH)D measurements
of 45-year old British adults, levels would be intermediate
between summer and wintertime values.
There is other evidence for a role of vitamin D reducing the
risk of pneumonia. For example, pneumonia deaths in
2.7 with the peak in December and January and trough in JulySeptember.
of rickets among children with pneumonia than among controls
(odds ratio: 13.37 (95% CI 8.08–24.22), p < 0.001) in Ethiopia.32
Low serum 25(OH)D (<22.5 nmol/L) was associated with higher
risk of lower respiratory tract infection (odds ratio: 0.09; 95% CI
0.03–0.24; p < 0.001) in India.33
From inspection of the incidence and mortality rates from the
1918–1919 influenza pandemic at the total population level, it is
not possible to draw conclusions about vitamin D with respect to
pandemic influenza incidence.
As discussed above, the established role of vitamin D in upregulating
production of catheliciden, an endogenous anti-bacterial
peptide, may be a potential explanation of the association we
observed. An additional potential mechanism may be the role
of vitamin D in the reduction of pro-inflammatory cytokines.
One of the important observations of deaths during the 1918–19
influenza pandemic was that the death rate was high for young
adults.34 This is different than for seasonal influenza, during which
mortality rates are higher for the elderly and infants. The reason for
this difference seems to be that those in their 20s and 30s have a
more robust immune system which can mount a stronger attack on
microbial infections. From recent studies, it has been determined
that both H1N1 and H5N1 viruses induce a T-helper 1 (Th1)
type cytokine response to viral infection of macrophages.35 These
cytokines are proinflammatory and include IL-6 and TNFa.
Nuclear factor kappaB (NF.B) is also an important risk factor.36
Influenza A (H5N1) viruses induce production of proinflammatory
cytokines at a greater rate than do H1N1 viruses.37,38
1,25-dihydroxyvitamin D [1,25(OH)2D] reduces the production
of Th1 cells, thus shifting the Th1/Th2 balance towards Th2,
which is less inflammatory.39-41 1,25(OH)D has also been found
to reduce the production of NF.B42 and TNFa.43 Infection of
macrophages also induces a toll like receptor induction of human
cathelicidin, LL-37,44 which is effective in combating bacterial
infections such tuberculosis44 and others.45 Thus, an additional
mechanism whereby vitamin D could reduce the severity and likeliness
of death from H1N1 and H5N1 viral infections is reduced
production of proinflammatory cytokines and NF.B. However,
suppressing proinflammatory cytokines did not reduce the risk
of death for mice infected with H5N1 viruses.46,47 These results
may not apply to the H1N1 virus in humans because mice have
different immune responses than humans.
One strength of this study is that solar UVB was the primary
source of vitamin D since in 1919, vitamin D had not yet been
isolated or identified. The main limitation of this study is that
other confounding factors were not evaluated. For example, differences
in medical treatment or defensive measures48 in the twelve
cities were not considered. Also, differences in ethnic background
and skin pigmentation were not considered. The fraction of
African-Americans varied between locations. This was a study of
aggregates rather than individual subjects. Findings that apply to
aggregates may not apply to individuals. Another limitation is that
data presented in Britten24 were available for only twelve cities.
While the sampling was made under specific instructions and
careful supervision, “in 10 or more districts so situated geographically
as to give, presumably, a fair sample of the general population
of the city.”, the method of selecting the districts would probably
not meet today’s standards for random sampling. A further limitation
is that the fraction of the population surveyed varied from
the number of people surveyed in each region varied from 4,123
was at war then, the total populations of each region had some
Data and Methods
The approach taken in this work to investigate the role of
innate immune response is to examine case fatality rates for those
who contracted the H1N1 influenza virus. The body can have
both innate and adaptive immune responses; for respiratory infections,
the adaptive response is based on either prior exposure to the
same or similar virus, while the innate response is based on other
immune parameters such as T cell subsets and immunoglobulin
concentrations25 and LL-37. It is assumed that those who developed
H1N1 influenza had weaknesses in both the adaptive and
innate immune systems but that the strength of the innate immune
system is more important for survival.
A study was found that reported data for influenza and pneumonia
case fatality rates for twelve cities in nine
the proportion of influenza cases complicated by pneumonia was
determined for eleven cities. The data reported (Table 1) are from
special surveys by the United States Public Health Service. These
surveys were conducted in ten cities “varying in population from
22,500 to 680,000 and certain small towns of
scattered, and generally in “localities in which the Public Health
Service was at the time maintaining established organizations
prepared to collect the requisite data reliably and efficiently.” The
surveys “were made as soon as possible after the subsidence of the
autumn (1918) wave of the epidemic in each locality” and generally,
started around December 2, 1918 and completed by the end
of December. However, second surveys were also conducted in
Dermato-Endocrinology 2009; Vol. 1 Issue 4
UVB, vitamin D and pandemic influenza followed by pneumonia
taken place in the interval. The
the epidemic had run its full course. “In the case of
SC some time after the completion of the canvass in the city itself,
an additional survey was made of adjacent mill villages. These
villages had a disproportionately large population of one selected
class-mill workers-and for this reason the
altogether comparable with those collected in other localities.” The
population canvassed ranged from 4,123 in
in Baltimore and represented 3.9% (
30% of the total population. There were 42,920 cases of influenza
and 2,290 cases of pneumonia in Table 1.24
“In making inquiry as to the type or nature of illness, the
enumerators were instructed to ask which members of a family
had “influenza,” “flu,” “grippe,” “pneumonia,” or “colds” since
September 1, 1918. Persons who were said to have been only
“feeling badly,” or as having a “cold” were recorded as “doubtful”
cases. If, however, the illness lasted not less than three days and
was of such severity as to confine the patient to bed for the whole
of one day, the case was classed as “influenza,” unless otherwise
diagnosed by the attending physician.”
Solar UVB indices. Summertime UVB irradiance for the
Ozone Mapping Spectrometer.26 This index has been used successfully
in ecologic studies of cancer mortality rates in the United
States.27,28 Winter UVB irradiance was estimated using a cosine
law that estimates solar irradiance based on season and latitude,
which are the determinants of solar zenith angle. Solar zenith angle
is the most important determinant of solar irradiance in winter.
This index has been found correlated with risk of multiple sclerosis,
29 for which the Epstein-Barr virus is a risk factor and vitamin
D a risk reduction factor,30 likely in part through combating the
virus through induction of LL-37.
Statistical analysis. Multiple linear regression was used to assess
the independent contributions of UVB irradiance and latitude to
case-fatality rates of pneumonia. All analyses were performed using
SPSS Grad Pack 13.0 (SPSS Inc.,
Summary and Conclusion
More research on this topic is needed. There is no question
that vaccine development and distribution is the most important
and reliable strategy for control of influenza epidemics and their
resulting mortality. On a far less well-established level of certainty
it should be determined whether higher serum 25(OH)D levels
might be associated with lower incidence of bacterial pneumonia
complicating influenza, particularly in older adults. Providing
vitamin D supplements or fortifying commonly consumed foods
with higher amounts of vitamin D should be evaluated further as a
possibly useful component of a comprehensive, vaccine-centered,
program to reduce influenza mortality rates, both in pandemics
and seasonal influenza, especially in the elderly.
WBG receives funding from the UV Foundation (McLean,
VA), the Vitamin D Society (
Hsieh YC, Wu TZ, Liu DP, Shao PL, Chang LY, Lu CY, et al. Influenza pandemics: past,
present and future. J Formos Med Assoc 2006; 105:1-6.
Brundage JF, Shanks GD. Deaths from bacterial pneumonia during 1918–19 influenza
pandemic. Emerg Infect Dis 2008; 14:1193-9.
Morens DM, Taubenberger JK,
cause of death in pandemic influenza: implications for pandemic influenza preparedness.
J Infect Dis 2008; 198:962-70.
McDonald JC. Asian influenza in Great Britain 1957–58. Proc Roy Soc Med 1958;
Gupta RK, George R, Nguyen-Van-Tam JS. Bacterial pneumonia and pandemic influenza
planning. Emerg Infect Dis 2008; 14:1187-92.
McCullers JA. Planning for an Influenza Pandemic: Thinking beyond the Virus. J Infect
Dis 2008; 198:945-7.
Cox RJ, Brokstad KA, Haaheim LR. Pandemic influenza vaccine development: time is
of the essence. Expert Rev Vaccines 2006; 5:603-6.
Nichol KL, Nordin JD, Nelson DB, Mullooly JP, Hak E. Effectiveness of influenza vaccine
in the community-dwelling elderly. N Engl J Med 2007; 357:1373-81.
mitigating an influenza pandemic. Nature 2006; 442:448-52.
Halloran ME, Ferguson NM, Eubank S, Longini IM Jr, Cummings DA, Lewis B, et al.
Modeling targeted layered containment of an influenza pandemic in the
Proc Natl Acad Sci USA 2008; 105:4639-44.
Liu PT, Stenger S, Tang DH, Modlin RL. Cutting Edge: Vitamin D-mediated human
antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction
of cathelicidin. J Immunol 2007; 179:2060-3.
Mookherjee N, Rehaume LM, Hancock RE. Cathelicidins and functional analogues as
antisepsis molecules. Expert Opin Ther Targets 2007; 11:993-1004.
Adams JS, Hewison M. Unexpected actions of vitamin D: new perspectives on the
regulation of innate and adaptive immunity. Nat Clin Pract Endocrinol Metab 2008;
14. Hewison M. Vitamin D and innate immunity. Curr Opin Investig Drugs 2008; 9:485-90.
Bikle DD. Vitamin D and the immune system: role in protection against bacterial infection.
Curr Opin Nephrol Hypertens 2008; 17:348-52.
White JH. Vitamin D signaling, infectious diseases, and regulation of innate immunity.
Infect Immun 2008; 76:3837-43.
Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, et al. Epidemic
influenza and vitamin D. Epidemiol Infect 2006; 134:1129-40.
Aloia JF, Li-Ng M. Re: epidemic influenza and vitamin D. Epidemiol Infect 2007;
Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. On the epidemiology of
influenza. Virol J 2008; 5:29.
Yusuf S, Piedimonte G, Auais A, Demmler G, Krishnan S, Van Caeseele P, et al. The
relationship of meteorological conditions to the epidemic activity of respiratory syncytial
virus. Epidemiol Infect 2007; 135:1077-90.
Grant WB. Variations in vitamin D production could possibly explain the seasonality of
childhood respiratory infections in
Roth DE, Jones AB, Prosser C, Robinson JL, Vohra S. Vitamin D status is not associated
with the risk of hospitalization for acute bronchiolitis in early childhood. Eur J Clin Nutr
Ginde AA, Mansbach JM, Camargo CA Jr. Vitamin D, respiratory infections and
asthma. Curr Allergy Asthma Rep 2009; 9:81-7.
Britten RH. The incidence of epidemic influenza, 1918–19. Pub Health Rep 1932;
Meyer KC. The role of immunity in susceptibility to respiratory infection in the aging
lung. Respir Physiol 2001; 128:23-31.
Leffell DJ, Brash DE. Sunlight and skin cancer. Sci Am 1996; 275:52-3. http://toms.
gsfc.nasa.gov/ery_uv/dna_exp.gif (accessed 2009).
Grant WB. An estimate of premature cancer mortality in the
doses of solar ultraviolet-B radiation. Cancer 2002; 94:1867-75.
Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk
of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer
mortality rates. Anticancer Res 2006; 26:2687-99.
Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a
review. Altern Med Rev 2005; 10:94-111.
Holmøy T. Vitamin D status modulates the immune response to Epstein Barr virus:
Synergistic effect of risk factors in multiple sclerosis. Med Hypotheses 2008; 70:66-9.
respiratory diseases in the
Muhe L, Lulseged S, Mason KE, Simoes EA. Case-control study of the role of nutritional
rickets in the risk of developing pneumonia in Ethiopian children. Lancet 1997;
Wayse V, Yousafzai A, Mogale K, Filteau S. Association of subclinical vitamin D deficiency
with severe acute lower respiratory infection in Indian children under 5 y. Eur J
Clin Nutr 2004; 58:563-7.
UVB, vitamin D and pandemic influenza followed by pneumonia
Richard SA, Sugaya N, Simonsen L, Miller MA, Viboud C. A comparative study of the
1918–1920 influenza pandemic in
for pandemic planning. Epidemiol Infect 2009; 12:1-11. [Epub ahead of print].
Kash JC, Tumpey TM, Proll SC, Carter V, Perwitasari O, Thomas MJ, et al. Genomic
analysis of increased host immune and cell death responses induced by 1918 influenza
virus. Nature 2006; 443:578-81.
Nimmerjahn F, Dudziak D, Dirmeier U, Hobom G, Riedel A, Schlee M, et al. Active
NFkappaB signalling is a prerequisite for influenza virus infection. J Gen Virol 2004;
Cheung CY, Poon LL, Lau AS, Luk W, Lau YL, Shortridge KF, et al. Induction of
proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a
mechanism for the unusual severity of human disease? Lancet 2002; 360:1831-7.
Chan MC, Cheung CY, Chui WH, Tsao SW, Nicholls JM, Chan YO, et al.
Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary
human alveolar and bronchial epithelial cells. Respir Res 2005; 6:135.
Cantorna MT, Mahon BD. D-hormone and the immune system. J Rheumatol Suppl
Schleithoff SS, Zittermann A, Tenderich G, Berthold HK, Stehle P, Koerfer R. Vitamin
D supplementation improves cytokine profiles in patients with congestive heart failure:
a double-blind, randomized, placebo-controlled trial. Am J Clin Nutr 2006; 83:754-9.
Ardizzone S, Cassinotti A, Trabattoni D, Manzionna G, Rainone V, Bevilacqua M, et al.
Immunomodulatory effects of 1,25-dihydroxyvitamin D3 on TH1/TH2 cytokines in
inflammatory bowel disease: an in vitro study. Int J Immunopathol Pharmacol 2009;
Talmor Y, Bernheim J, Klein O, Green J, Rashid G. Calcitriol blunts pro-atherosclerotic
parameters through NFkappaB and p38 in vitro. Eur J Clin Invest 2008; 38:548-54.
negatively correlated with serum 25(OH)D concentrations in healthy women. J Inflamm
(Lond) 2008; 5:10.
Liu PT, Stenger S, Li H, Wenzel L, Tan BH, Krutzik SR, et al. Toll-like receptor triggering
of a vitamin D-mediated human antimicrobial response. Science 2006; 311:1770-3.
White JH. Vitamin D signaling, infectious diseases and regulation of innate immunity.
Infect Immun 2008; 76:3837-43.
Salomon R, Hoffmann E, Webster RG. Inhibition of the cytokine response does not protect
against lethal H5N1 influenza infection. Proc Natl Acad Sci USA 2007; 104:12479-81.
Droebner K, Reiling SJ, Planz O. Role of hypercytokinemia in NFkappaB p50-deficient
mice after H5N1 influenza A virus infection. J Virol 2008; 82:11461-6.
Markel H, Lipman HB, Navarro JA, Sloan A, Michalsen JR, Stern AM, Cetron MS.
Nonpharmaceutical interventions implemented by US cities during the 1918–1919
influenza pandemic. JAMA 2007; 298:644-54.
2009; Vol. 1 Issue 4
Vitamin D may reduce the risk of incidence and death from the current A/H1N1 “swine flu” pandemic
William B. Grant, Ph.D.
Sunlight, Nutrition, and Health Research Center (SUNARC) P.O. Box 641603 San Francisco, CA 94164-1603, USA www.sunarc.org email@example.com 1-415-409-1980
Target journal: The Medical Journal of Australia
The current worldwide pandemic of A/H1N1 influenza “swine flu” has the potential to cause the infection and death of many people. This virus appears to have some seasonality, in common with epidemic influenza. There is good evidence that epidemic influenza is seasonal due to annual variations in solar ultraviolet-B (UVB) irradiance and vitamin D production.1 The beneficial role of vitamin D is thought to be induction of human cathelicidin, LL-37, which has antimicrobial and antiendotoxin effects and, thus, seems to explain the reduced risk of infection of epidemic influenza. However, vitamin D did not seem to reduce the risk of infection during the 1918-19 pandemic A/H1N1 influenza. However, there is evidence from an ecological study that solar UVB and vitamin D reduced case-fatality rates after infection by that virus: case-fatality rates were much lower in southern
I receive funding from the UV Foundation (
1. Cannell JJ, Zasloff M,
2. Grant WB, Giovannucci E. The possible roles of solar ultraviolet-B radiation and vitamin D in reducing case-fatality rates from the 1918-1919 influenza pandemic in the
3. Gracey M, King M. Indigenous health part 1: determinants and disease patterns. Lancet. 2009;374:65-75.
4. Nowson CA, Margerison C. Vitamin D intake and vitamin D status of Australians. Med J Aust. 2002;177:149-52.
5. Benson J, Wilson A, Stocks N, Moulding N. Muscle pain as an indicator of vitamin D deficiency in an urban Australian Aboriginal population. Med J Aust. 2006;185:76-7.