Parasitic worms and inflammatory diseases

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Parasitic worms and inflammatory diseases

Postby Lyon » Sat Jul 14, 2007 12:39 pm

Despite the fact that it must infuriate Ian, Cambridge is also one of the leading research centers investigating the relationship between the loss of evolutionary normal conditions and the subsequent rise in incidence of inflammatory diseases.

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Postby gwa » Sat Jul 14, 2007 4:10 pm

Good article, Lyon. I enjoyed reading it.

My younger son has ulcerative colitis and was recently hospitalized for a week. His specialist is a physician from India. The doctor told him that UC is a Caucasian disease and that it is rarely seen in India, Asia or Africa.

He also told him basically what is presented in the article you posted.

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Postby Lyon » Sat Jul 14, 2007 4:58 pm

gwa wrote:He also told him basically what is presented in the article you posted.
You made my day gwa and I needed that!

I recently contacted one of the writers of that article, Professor Anne Cooke, and this is an excerpt:
> 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 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.

gwa wrote:The doctor told him that UC is a Caucasian disease
This is NOT meant to be negative but I think evidence is starting show that it's time to eliminate that MS "truism".

Although (using blacks as an example) blacks in Africa ("undeveloped") rarely experience inflammatory disease and although incidence data does reflect that blacks in the US ("developed") experience lower MS rates than whites, it's important to consider that the "hygiene hypothesis" more accurately reflects financial status and living conditions than "hygiene" Per se.

It also seems necessary to dispose of the genetic MS "truisms" based on genetics in which lighter skinned people are more genetically inclined to MS and that darker skinned people closer to the equator are less genetically inclined to MS, when considering the locations and complexion color of the populations which "developed" first and in reality remain among the areas of the world which are "developed" ("developed"=common availability of electricity, running water and flush toilets).

It's not hard to determine that the populations of the developed countries are and have always been primarily white and that those locations in which they populate, are and have always been more distant from the equator.

Is MS geographic prevalence really attributable to the long held assumptions regarding genetics or did the researchers long ago overlook the fact that the MS geographic incidence data also depicts a world map of economic wealth/development?

Regarding the current lower MS rates among blacks (or any darker complexion in the US) who has always been on the bottom of the economic totem pole and has experienced the poorer living conditions? Obviously those of darker persuasion.

The incidence figures we are familiar with have always been general, non specific averages. I THINK if someone were to do an MS incidence study and included Montel, Richard Pryor and all the other wealthy black Americans, they would show exactly the same incidence rate as U.S. Caucasians.

I've been corresponding with Dr Kurtzke about the loss of evolutionary normal conditions as a precursor to immune dysfunction in the attempt to convince him to investigate and form his own opinion. I'm convinced a little effort and an open mind would lead any intelligent person to become convinced.

I won't lie, the involvement of a name like Dr Kurtzke's would accelerate serious consideration in the science community, but what caused me to initially contact him was my recently reading his 1993 paper "Epidemiologic Evidence for Multiple Sclerosis as an Infection" in which he had done an awesome job of weighing every possible considerable factor at that point in time and came to the conclusion that the British troops must have spread MS in the Faroes by an, as yet, unidentifiable infection.

What his arrived conclusion meant to me is that one of the last researchers to realize that we can't cure MS until we can label the cause and one of the best minds in MS research went over all the information in this very contained and specific situation (Faroe "outbreak") and came to the conclusion that everything pointed towards the British soldiers spreading some undefinable infection among the residents of the Faroes, which even in 1993 (and 2007) was beyond our ability to confirm or identify.

I simply wanted to point out to Dr Kurtzke that if the British presence "eliminated" something which had always been present in the Faroe population, it would present the EXACT same picture as the introduction of his "unidentifiable infection".

Might the thing which the British presence (and influence) eliminated from the periphial Faroe residents have been their historic parasite infestations?


(Final comments from "Epidemiologic Evidence for Multiple Sclerosis as an Infection")
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
for whites.
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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