You made my day gwa and I needed that!gwa wrote:He also told him basically what is presented in the article you posted.
> Most autoimmune researchers seem to be convinced that incidence of
> autoimmune disease is owed to genetic predisposition and then an
> environmental trigger(s) to set the autoimmunity ball in motion.
I would say that it is more balanced now with increasing numbers
considering the alternative view that infection might have hitherto
inhibited the development of some autoimmune conditions.
> The basis of research is comparison and all autoimmune disease
> research to my awareness has compared people with autoimmune disease
> in developed populations to people without autoimmune disease in
> developed populations. It seems that comparison might be akin to
> comparing someone with disease to someone with predisposition.
> Obviously not the most favorable research situation. Kind of like
> comparing an orange to an orange. You're not going to discover many
> differences by looking at basically the same thing.
> My question is....do you know of any autoimmunity research actually
> focusing on a comparison between the systems of those in undeveloped
> countries with situations which are seen in autoimmunity?
There is a research interest in doing just that. Some Scandinavian
researchers were proposing to look at two populations which are
genetically rather similar but living in different conditions-
Scandinavia versus Eastern European countries.
This is NOT meant to be negative but I think evidence is starting show that it's time to eliminate that MS "truism".gwa wrote:The doctor told him that UC is a Caucasian disease
The best measures of the geographic distribution of MS
come from prevalence studies, of which there are now over
300. These works indicate that, geographically, MS is distributed
throughout the world within three zones, of high,
medium, and low frequency. High-frequency areas, with
prevalence rates of 30 or more per 100,000 population, now
mostly 50 to 120 per 100,000, comprise northern and central
Europe into Italy and the former USSR, Canada, the northern
United States, New Zealand, and southeastern Australia.
These regions are bounded by areas of medium frequency,
with prevalence rates of 5 to 29 per 100,000
population and comprising much of Australia; the southern
United States; southwestern Norway; northernmost Scandinavia;
much of the northern Mediterranean basin and possibly
its eastern and southern shores as well; probably Russia
from the Urals into Siberia as well as the Ukraine; South
Africa (whites); and perhaps central South America. All
other studied areas of Asia, Africa, and the Caribbean
region, including Mexico and possibly northern South America,
are all of low frequency, with prevalence rates of less
than 5 per 100,000 population. A number of nationwide
prevalence studies in Europe provide evidence for geographic
clustering of the disease, which is stable over time,
but with, however, evidence of diffusion over time as well.
There is a female preponderance in incidence, prevalence,
and mortality rates of about 1.5:1 (female/male). Annual
incidence rates are about 3 to 5 per 100,000 population in
high-risk areas, about 1 per 100,000 in medium-risk areas,
and about 1 per 1,000,000 in low-risk areas. Age-specific
incidence rates rise from 0 in childhood through adolescence
to a peak close to age 27 and then return more slowly to 0 by
age 60. This pattern is what one might expect for an
infectious disease with a limited age range of susceptibility.
All high- and medium-risk areas are among predominantly
white populations: MS is a white female burden. In the
United States, blacks, Orientals, and possibly American
Indians have much lower rates of MS than do whites, but each group still demonstrates the geographic gradients found
Aside from geography, age, sex, and race, risk factors for
MS include high socioeconomic status and level of urbanization
of preillness residence, at least in the U.S. Army
series. No meteorologic correlate of geography is a risk
factor for MS when latitude is controlled. In the United
States, there is a strong correlation of MS risk with populations
with Scandinavian, particularly Swedish, ancestry.
There is an increased familial frequency in MS. Twin
studies are inconclusive in terms of a genetic component,
and I believe that the familial excess reflects common
environment more than common genes.
Migration studies indicate that, on the whole, migrants do
not retain all of the risk of their birthplace. MS risk is clearly
not defined at birth: MS death rates for migrants born in one
risk area and dying in another are intermediate between
those characteristic of their birthplace and their death residence,
regardless of the direction of the move. Prevalence
studies for migrants from high- to low-risk areas indicate age
of adolescence to be critical for risk retention; those migrating
above age 15 retain the MS risk of their birthplace, and
those migrating below age 15 acquire the lower risk of their
new residence. Thus, in high-risk areas of endemicity, MS is
acquired in early adolescence, and young children are not
susceptible to the disease. Several studies of migrants moving
from low- to high-risk areas show that those migrating in
childhood or older do in fact increase their risk of MS, with
age 10 or 11 apparently being the minimum age of susceptibility
and about ages 40 to 45 being the maximum. The
migrant data and the geographic distributions serve to define
MS as an acquired, exogenous, environmental disease with a
prolonged incubation period between acquisition and clinical
expression-a situation most compatible with an infectious
disease with prolonged latency.
MS on the Faroe Islands has occurred as four successive
epidemics beginning in 1943. The disease was introduced by
British troops who occupied the islands for 5 years from
1940. What they introduced must have been an infection,
which is called PMSA.
In this concept, PMSA is a single widespread systemic
infectious disease (perhaps asymptomatic) that only rarely
leads to CNMS after an incubation period averaging 6 years
for virgin populations (and 12 years for populations in areas
of endemicity). It requires 2 (for the former populations) or
possibly 4 (for the latter populations) years of exposure
before the disease is acquired. Susceptibility to PMSA is
limited to about ages 11 to 45 at the start of exposure;
transmissibility ends at about age 26.
If the PMSA agent has these characteristics of prolonged
exposure, limited age of susceptibility, prolonged incubation,
and rare clinical disease, then the geographic spread of
this disorder would also be prolonged. In this manner, one
could explain the current distribution of MS as the result of
slow diffusion from an origin in the lower Scandinavian
peninsula at or before the start of the 18th century, with
overseas spread by migrations: Scandinavians to America in
the mid-19th century and British to Australia, New Zealand,
and South Africa rather later.
Thus, I believe that clinical MS is the rare late outcome of
a specific but unknown infectious disease of adolescence and
young adulthood and that this infection could well be caused
by a thus-far-unidentified (retro)virus.
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