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Van Bever, Lane and Common, in their Editorial, “Gene defects and
allergy”(1), highlight the role of the FLG gene in the allergic (or
atopic) disorders: atopic eczema, allergic rhinitis and asthma. Null
(loss of function) mutations of the FLG gene may be the most important
marker of the genotype that is susceptible to atopic disorders.
Intriguingly, the Editorial also draws attention to the increasing
worldwide prevalence of allergic disorders in recent decades.
In genetic terms, one or two generations is a very short time. It is
almost certainly too short a time to be able to allow a sufficient genetic
change to account for the massive rise in prevalence of the atopic
disorders over the last 30-40 years. The worldwide atopic epidemic is
more likely to have an environmental explanation.
The atopic disorders are common in westernised societies. In the
underdeveloped world, they remain uncommon. A paper from Zimbabwe (2)
compared the prevalence of atopic disorders in different communities. In
poor, traditional rural communities, they are rare; in shanty-town life
they are middling in prevalence; and in well-off town dwellers, living in
western conditions, prevalence is similar to that in western countries.
This African study, and similar studies from around the world, indicate
that environment determines whether latent atopy becomes clinical atopic
disease. Put another way, environment determines whether the atopic
genotype achieves phenotypic expression.
An environmental hypothesis – the humidity hypothesis (3) has been
proposed. The humidity hypothesis draws attention to the relationship
between improved economic circumstances and the increased availability of
central heating, air conditioning, washing and bathing. Each of these
better living standards disfavour humidity of the epidermis and of the
mucous membranes of upper and lower respiratory tracts. The humidity
hypothesis postulates that air dried by central heating or air
conditioning steals moisture from the ambient air and from skin and mucous
membranes and that in this dry environment, dust and other particles rise
and can tickle or irritate skin and mucous membranes precipitating eczema,
asthma and hay fever.
Further support for the humidity hypothesis exists in a number of
observations. Nebulisers and steam inhalations are standard treatments
for asthma and rhinitis. Emollients enhance skin
humidity and prevent attacks of atopic dermatitis. Humidification of
the indoor environment improves atopic dermatitis. Going on holiday from
London to the humid West Indies (so long as air conditioning is absolutely
avoided) will clear even the most severe forms of atopic dermatitis in
just a few days (much more swiftly than admission to hospital).
The humidity hypothesis may explain the key environmental change that
accounts for the worldwide atopic epidemic of the last 30 or 40 years.
Christopher Rowland Payne Consultant Dermatologist, The London
Clinic, 149 Harley Street, London W1G 6HL
1. Van Bever H, Lane B, Common J. Gene defects and allergy. Identifying
specific genotypes of allergy is a major breakthrough in patient care.
BMJ 2009;339:58-59.
2. Keeley DJ, Neill P, Gallivan S. Comparison of the prevalence of
reversible airways obstruction in rural and urban Zimbabwean children.
Thorax 1991;46:549-53.
3. Rowland Payne CME. The atopic epidemic: why are atopic diseases more
and more common? Diminished humidity may be the answer. Journal of
Cosmetic Dermatology 2004;2:117-118.
Competing interests:
None declared
Competing interests:
No competing interests
23 July 2009
Christopher ME Rowland Payne
Consultant Dermatologist
The London Clinic, 5 Devonshire Place, London W1G 6HL
Why have allergic diseases been increasing worldwide over several decades? The humidity hypothesis may be the answer
Van Bever, Lane and Common, in their Editorial, “Gene defects and
allergy”(1), highlight the role of the FLG gene in the allergic (or
atopic) disorders: atopic eczema, allergic rhinitis and asthma. Null
(loss of function) mutations of the FLG gene may be the most important
marker of the genotype that is susceptible to atopic disorders.
Intriguingly, the Editorial also draws attention to the increasing
worldwide prevalence of allergic disorders in recent decades.
In genetic terms, one or two generations is a very short time. It is
almost certainly too short a time to be able to allow a sufficient genetic
change to account for the massive rise in prevalence of the atopic
disorders over the last 30-40 years. The worldwide atopic epidemic is
more likely to have an environmental explanation.
The atopic disorders are common in westernised societies. In the
underdeveloped world, they remain uncommon. A paper from Zimbabwe (2)
compared the prevalence of atopic disorders in different communities. In
poor, traditional rural communities, they are rare; in shanty-town life
they are middling in prevalence; and in well-off town dwellers, living in
western conditions, prevalence is similar to that in western countries.
This African study, and similar studies from around the world, indicate
that environment determines whether latent atopy becomes clinical atopic
disease. Put another way, environment determines whether the atopic
genotype achieves phenotypic expression.
An environmental hypothesis – the humidity hypothesis (3) has been
proposed. The humidity hypothesis draws attention to the relationship
between improved economic circumstances and the increased availability of
central heating, air conditioning, washing and bathing. Each of these
better living standards disfavour humidity of the epidermis and of the
mucous membranes of upper and lower respiratory tracts. The humidity
hypothesis postulates that air dried by central heating or air
conditioning steals moisture from the ambient air and from skin and mucous
membranes and that in this dry environment, dust and other particles rise
and can tickle or irritate skin and mucous membranes precipitating eczema,
asthma and hay fever.
Further support for the humidity hypothesis exists in a number of
observations. Nebulisers and steam inhalations are standard treatments
for asthma and rhinitis. Emollients enhance skin
humidity and prevent attacks of atopic dermatitis. Humidification of
the indoor environment improves atopic dermatitis. Going on holiday from
London to the humid West Indies (so long as air conditioning is absolutely
avoided) will clear even the most severe forms of atopic dermatitis in
just a few days (much more swiftly than admission to hospital).
The humidity hypothesis may explain the key environmental change that
accounts for the worldwide atopic epidemic of the last 30 or 40 years.
Christopher Rowland Payne
Consultant Dermatologist, The London
Clinic, 149 Harley Street, London W1G 6HL
crp@thelondonclinic.co.uk
Competing interests: None declared.
1. Van Bever H, Lane B, Common J. Gene defects and allergy. Identifying
specific genotypes of allergy is a major breakthrough in patient care.
BMJ 2009;339:58-59.
2. Keeley DJ, Neill P, Gallivan S. Comparison of the prevalence of
reversible airways obstruction in rural and urban Zimbabwean children.
Thorax 1991;46:549-53.
3. Rowland Payne CME. The atopic epidemic: why are atopic diseases more
and more common? Diminished humidity may be the answer. Journal of
Cosmetic Dermatology 2004;2:117-118.
Competing interests:
None declared
Competing interests: No competing interests