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While on genetics this article on back pain may be interesting

 

The importance of genetic factors in degenerative diseases of the spine has been

appreciated only relatively recently. In 1999, Sambrook et al .[41] conducted a

classic study among adult female twins (172 monozygotic and 184 dizygotic) from

a UK national volunteer registry. Magnetic resonance images of the cervical and

lumbar spine were evaluated for features of disc bulge, loss of disc signal,

disc herniation, and osteophytes. In both the cervical and the lumbar spine,

approximately 75% of the variation in degenerative change could be accounted for

by genetic variation within the sample. Both the severity of the changes and

their extent (assessed through the number of levels that were involved) showed a

genetic basis. The result took into account the confounding influence of age,

body mass index, occupational manual labor, exercise, and smoking history. A

later analysis of the same group of twins has shown that the distribution of

Schmorl nodes is also predominantly explained by genetic factors, indicating

heritable contribution to the degenerative process at its earliest stages.[40]

 

The extent to which genetic susceptibility also might explain the experience of

back and pain itself is more difficult to resolve. The data are conflicting. In

the UK twin study, full pain histories were taken from a group of 1064 twins

(the sample included those who had undergone magnetic resonance imaging

examinations in the initial study).[42**] Using a set of increasingly stringent

definitions of pain, significant heritable influences were demonstrated for back

pain, ranging from 52-68%. Contrasting results are presented in an analysis of

data from the Danish National Twin Cohort, however.[43] The main finding in the

Danish study was a modest genetic effect on 1-month prevalence of back pain

among men older than 70 years, but interestingly, this was not found among

women. The differences between these two studies may reflect differences in

definition (the Danish study restricted the definition of pain to that

experienced in the preceding month, while the UK study took into account

lifetime prevalence), the differences in the age distribution of the two

samples, and the differences in geographical location representing different

background levels of genetic and environmental variation. In the full analysis

of the data from the UK twins,[42**] there was considerable genetic overlap

between the reporting of back pain and the genetic determinants of psychological

well-being. Thus, psychological and behavioral variables, past experiences of

pain, patterns of learning, and cultural factors may all need to be included to

develop an adequate genetic model of back pain.

 

Candidate Gene Studies

The pathophysiological mechanisms that underlie disc degeneration and pain

perception have provided the focus for several studies attempting to identify

the influence of individual candidate genes. Potential candidates include

aggrecan, the vitamin D receptor gene, and metalloproteinase 3. The last year

has seen particular attention focused on collagen IX gene and the interleukin-1

gene cluster, for which significant associations with degenerative change and

back pain have been identified.

 

Type IX collagen is found in the nucleus, annulus, and vertebral endplates. It

is believed to provide mechanical support for tissues by acting as a bridging

molecule. It is a hetero-trimeric protein consisting of three genetically

distinct chains. Sequence variation in the a-2 chain of collagen IX (identified

by the Trp 2 allele) has been associated with dominantly inherited lumbar disc

disease.[44] A similar sequence variation has been found in the COL9A3 gene

coding for the a-3 chain of type IX collagen ( Trp 3 allele).[45] The latter

allele has been shown to be associated with a three-fold increased risk of

sciatica and represents the first common genetic factor for lumbar disc

disease.[45] The Trp 3 allele has also been associated with radiographic

features of Scheuermann disease.[46]

 

Inflammatory cytokines have a well-recognized contribution to the generation of

back pain. Interleukin-1 in particular contributes to disc degeneration by

inducing enzymes that destroy proteoglycan and is involved in the mediation of

pain. In recent studies, Solovieva et al .[47,48] have demonstrated an

association between interleukin-1 polymorphisms and features of disc

degeneration on magnetic resonance imaging in male Finnish workers. The

polymorphisms were associated with a 2.5-fold increased risk of back pain, and

an association was also seen with the intensity and duration of pain together

with the degree of functional limitation.

 

Association studies in genetic epidemiology are notoriously difficult to

replicate, and the seemingly promising results of candidate gene studies that

have emerged in recent years must be interpreted with some caution.[49] For

collagen IX, it is noteworthy that the association with Trp 3 allele has not

been replicated in the Greek population.[50] Evidence also suggests that the

association may be mediated by obesity and thus confined to particular at-risk

groups.[51] Nevertheless, the fact that candidate genes can be identified at all

for a phenotype as complex as back pain provides support for the notion that the

genetic factors have a dominating role.

 

 

 

 

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Cullen:

 

http://www.geocities.com/claud71_2000/asoc0.htm

 

Asociaciones de Acupunctura de Mexico - Mexican

acupuncture associations, includes email addresses and

phone numbers.

 

Regards, Jack

>

> Can anyone direct me to information on international

> regulations

> specifically Mexico?

>

> Thanks in advance -

> Cullen

>

>

>

> Cullen

 

 

 

 

 

 

 

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Have we ever considered that genes divide and are susceptible to mutations

making other factors much more important as to the " why " of the genetic

theory in health?

 

 

Mike W. Bowser, L Ac

 

 

 

> " " <alonmarcus

>Chinese Medicine

><Chinese Medicine >

>Re: International Acupuncture Regulations

>Tue, 29 Mar 2005 18:16:15 -0600

>

>

>While on genetics this article on back pain may be interesting

>

>The importance of genetic factors in degenerative diseases of the spine has

>been appreciated only relatively recently. In 1999, Sambrook et al .[41]

>conducted a classic study among adult female twins (172 monozygotic and 184

>dizygotic) from a UK national volunteer registry. Magnetic resonance images

>of the cervical and lumbar spine were evaluated for features of disc bulge,

>loss of disc signal, disc herniation, and osteophytes. In both the cervical

>and the lumbar spine, approximately 75% of the variation in degenerative

>change could be accounted for by genetic variation within the sample. Both

>the severity of the changes and their extent (assessed through the number

>of levels that were involved) showed a genetic basis. The result took into

>account the confounding influence of age, body mass index, occupational

>manual labor, exercise, and smoking history. A later analysis of the same

>group of twins has shown that the distribution of Schmorl nodes is also

>predominantly explained by genetic factors, indicating heritable

>contribution to the degenerative process at its earliest stages.[40]

>

>The extent to which genetic susceptibility also might explain the

>experience of back and pain itself is more difficult to resolve. The data

>are conflicting. In the UK twin study, full pain histories were taken from

>a group of 1064 twins (the sample included those who had undergone magnetic

>resonance imaging examinations in the initial study).[42**] Using a set of

>increasingly stringent definitions of pain, significant heritable

>influences were demonstrated for back pain, ranging from 52-68%.

>Contrasting results are presented in an analysis of data from the Danish

>National Twin Cohort, however.[43] The main finding in the Danish study was

>a modest genetic effect on 1-month prevalence of back pain among men older

>than 70 years, but interestingly, this was not found among women. The

>differences between these two studies may reflect differences in definition

>(the Danish study restricted the definition of pain to that experienced in

>the preceding month, while the UK study took into account lifetime

>prevalence), the differences in the age distribution of the two samples,

>and the differences in geographical location representing different

>background levels of genetic and environmental variation. In the full

>analysis of the data from the UK twins,[42**] there was considerable

>genetic overlap between the reporting of back pain and the genetic

>determinants of psychological well-being. Thus, psychological and

>behavioral variables, past experiences of pain, patterns of learning, and

>cultural factors may all need to be included to develop an adequate genetic

>model of back pain.

>

>Candidate Gene Studies

>The pathophysiological mechanisms that underlie disc degeneration and pain

>perception have provided the focus for several studies attempting to

>identify the influence of individual candidate genes. Potential candidates

>include aggrecan, the vitamin D receptor gene, and metalloproteinase 3. The

>last year has seen particular attention focused on collagen IX gene and the

>interleukin-1 gene cluster, for which significant associations with

>degenerative change and back pain have been identified.

>

>Type IX collagen is found in the nucleus, annulus, and vertebral endplates.

>It is believed to provide mechanical support for tissues by acting as a

>bridging molecule. It is a hetero-trimeric protein consisting of three

>genetically distinct chains. Sequence variation in the a-2 chain of

>collagen IX (identified by the Trp 2 allele) has been associated with

>dominantly inherited lumbar disc disease.[44] A similar sequence variation

>has been found in the COL9A3 gene coding for the a-3 chain of type IX

>collagen ( Trp 3 allele).[45] The latter allele has been shown to be

>associated with a three-fold increased risk of sciatica and represents the

>first common genetic factor for lumbar disc disease.[45] The Trp 3 allele

>has also been associated with radiographic features of Scheuermann

>disease.[46]

>

>Inflammatory cytokines have a well-recognized contribution to the

>generation of back pain. Interleukin-1 in particular contributes to disc

>degeneration by inducing enzymes that destroy proteoglycan and is involved

>in the mediation of pain. In recent studies, Solovieva et al .[47,48] have

>demonstrated an association between interleukin-1 polymorphisms and

>features of disc degeneration on magnetic resonance imaging in male Finnish

>workers. The polymorphisms were associated with a 2.5-fold increased risk

>of back pain, and an association was also seen with the intensity and

>duration of pain together with the degree of functional limitation.

>

>Association studies in genetic epidemiology are notoriously difficult to

>replicate, and the seemingly promising results of candidate gene studies

>that have emerged in recent years must be interpreted with some

>caution.[49] For collagen IX, it is noteworthy that the association with

>Trp 3 allele has not been replicated in the Greek population.[50] Evidence

>also suggests that the association may be mediated by obesity and thus

>confined to particular at-risk groups.[51] Nevertheless, the fact that

>candidate genes can be identified at all for a phenotype as complex as back

>pain provides support for the notion that the genetic factors have a

>dominating role.

>

>

>

>

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