Discovering your "Celtic Connection" & Do you have the "Celtic Curse"
Are you Irish!? Scottish? Celtic ancestry?
New research finds high frequency of HH gene mutations in the Irish community!
If you have a Celtic heritage, ancestors from Ireland, Wales, Scotland, or Great Britain, then you are at high risk for carrying the HFE mutations for hereditary hemochromatosis (HH), also known as iron overload disease or iron storage disease according to researchers on both sides of the Atlantic Ocean.
Hereditary hemochromatosis (HH) has been dubbed the "Celtic Curse" by Sandra Thomas, President and Founder of the American Hemochromatosis Society (AHS), based in Lake Mary, Florida. HH is the most common genetic disease in the USA according to the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia. HH is also the most common genetic disease in Ireland where a great deal of research and studies of this disease are being conducted.
Sandra's mother, Josephine Bogie Thomas, died on May 13, 1999 of primary liver cancer/hepatocellular carcinoma due to cirrhosis of the liver caused by hereditary hemochromatosis in Pittsburgh, Pennsylvania where she had gone for liver cancer treatments. Josephine Thomas had strong Irish, Scottish and British lines in her family tree and she carried the two major HH mutations known as cys282 gene mutations. Her daughter, Sandra, is a "silent carrier" of the same mutation. The family tree contains such names as Cooper, Bogie, Ball, Kavanaugh, and Tandy. Little did she know when she visited Ireland that she was visiting the area of the world where hemochromatosis is thought to have originated.
Researchers believe that HH originated at least 40,000 years ago in the area we now know as Ireland with a single ancestor whose genes mutated to over-absorb iron from what was then a very poor iron diet and famine conditions. This was nature's way of over-compensating for the lack of iron in the diet at that time. Today, the descendants of these ancient Celtic persons have iron fortified foods as well as an easy trip to the grocery for a steak, but their bodies still carry these ancient "survival" gene mutations which don't know when to stop absorbing iron from a normal diet. Therefore, those people who descended from this ancestor carry the mutations which absorb too much iron until it reaches toxic levels. Excess iron has no way to leave the body but by bleeding.
Unlike our ancestors, we have a plentiful supply of iron, enriched breakfast cereals, enriched breads, and iron pills which you can buy over the counter (OTC). Iron, therefore, is potentially dangerous to the unsuspecting person who carries these mutations and even though one in eight people of Northern European ancestry have this mutation (that's 32 million Americans), most of them do not know it. They may not know it, but they easily could know it through a simple genetic/DNA test that has been commercially available since 1997.
Geoffrey Block, MD, a hepatologist (liver specialist) and former director of the Hemochromatosis Center at the University of Pittsburgh Medical Center (UPMC) in Pittsburgh, Pennsylvania, states, "
the appearance of the HFE gene mutation occurred somewhere from 40,000-60,000 years ago. Human DNA goes back to somewhere between 120,000-200,000 years ago. T
he ethnogenetic source for the C282Y (HFE) mutation arose in the Celtic 'empire'. Most people think that Celtic means Ireland, however, the Celts of 40-60,000 years ago covered Ireland to just west of Moscow, north to the upper reaches of Scandinavia, south into Spain and Portugal, and south east across the Italian peninsula and north of Greece and Turkey/Iraq."
{In short, it could have "arrived" on this planet from elsewhere. A "bloodline trail" that leads off the planet???}
...
Other ethnic groups can also have the mutations but it is much more infrequent (i.e. Asian or Jewish). People with northern European ancestry are highest at risk with family bloodlines that go to France, Germany, and the Scandinavian countries.
The following abstract from Dublin, Ireland discusses hereditary hemochromatosis:
(note: In Ireland, England, and Australia, hemochromatosis is spelled haemochromatosis)
HAEMOCHROMATOSIS - AN IRISH DISEASE
E. Ryan, V. Byrnes, A-M Flanagan, J. Crowe
Department of Hepatology, Mater Misericordiae Hospital, Dublin Ireland
(Hepatology Vol. 28, No.4, pt.2, October 1998; page 527A, abstract nr.1459; this is a special edition!)
It has been hypothesized that the genetic mutation leading to iron overload occurred in a race of Celtic origin and that the HLA-A3 allele might represent a marker of their migratory patterns (1) This hypothesis has recently been substantiated by the observation that individuals of British/Irish ancestry may be at particular risk of developing genetic haemochromatosis (HG) (2).
Furthermore, preliminary data on the global prevalence of the C282Y mutation found the highest allele frequency in the Irish (45 Individuals) (3).
Aims: The purpose of this study was to estimate the frequencies of the C282Y and H63D mutations in an Irish population.
Methods: Eighty-seven individuals responded to a payroll request for voluntary participation in the study. DNA was extracted and subjected to PCD using primers encompassing the C282Y and H63D mutations sites.
Following amplification, the PCR products were digested with RsaI and MboI for C282Y and H63D respectively. Restriction digests were separated on Nusieve gels and viewed under UV light.
Results:
C282Y Homozygote: 0
C282Y Heterozygote: 26
C282Y normal: 61
H63D Homozygote: 4
H63D Heterozygote: 15
H63D normal: 68
Of 87 volunteers, 26 were heterozygous for C282Y indicating an allele frequency of 15%, and 19 were heterozygous for H63D indicating an allele frequency of 11%. (there were 4 compound heterozygotes i.e. were heterozygous for both mutations).
Conclusion; The allele frequency of 15% for C282Y indicates a prevalence of 1:45 for GH. This is the highest reported prevalence worldwide and suggests an Irish origin for GH. This prevalence is not observed clinically which may represent underdiagnosis or incomplete penetrance in the Irish.
References:
(1) Simon M, Fauchet R, Hespel, JP, et all; Gastroenterology 1980; 78: 703-708.
(2) Smith BN, Kantrowitz, W; et al; Hepatology 1997; 25: 1439-1446
(3) Merryweather-Clarke AT, Pointon JJ, Shearman JD, Robson KJ, J. Med Genetics 1997; 34: 275-278.
Another abstract illustrating frequency of this disease in patients of this heritage:
J Med Genet 1997 Apr;34(4):275-8
Global prevalence of putative haemochromatosis mutations.
Merryweather-Clarke AT, Pointon JJ, Shearman JD, Robson KJ
MRC Molecular, Haematology Unit, John Radcliffe Hospital, Headington, Oxford,UK.
Haemochromatosis is a genetic disease associated with progressive iron overload, and is common among populations of northern European origin. HLA-H is a recently reported candidate gene for this condition. Two mutations have been identified, a substitution of cysteine for tyrosine at amino acid 282 (C282Y, nucleotide 845) and of histidine for aspartate at amino acid 63 (H63D, nucleotide 187). Over 90% of UK haemochromatosis patients are homozygous for the C282Y mutation. We have examined 5956 chromosomes (2978 people) for the presence of HLA-H C282Y and H63D by PCR followed by restriction enzyme analysis. We have found world wide allele frequencies of 1.9% for C282Y and 8.1% for H63D. The highest frequencies were 10% for C282Y in 90 Irish chromosomes and 30.4% for H63D in 56 Basque chromosomes. C282Y was most frequent in northern European populations and absent from 1042 African chromosomes, 484 Asian chromosomes, and 644 Australian chromosomes. The distribution of the C282Y mutation coincides with that of populations in which haemochromatosis has been reported and is consistent with the theory of a north European origin for the mutation. The H63D polymorphism is more widely distributed and its connection with haemochromatosis remains unclear.
I have low body temp. The normal 98.6 is a fever for me. Psychic...well prophetic dreams, lots of little stuff that starts to add up and makes one wonder. 
