The Melungeons

Melungeons and Arthritic-like disease

By:
Nancy Sparks Morrison
Roanoke, VA 24015
USA
Email nmorri3924@aol.com

December, 1998

The opinions in this post are strictly my own, but have been based upon my reading
and research of various materials noted herein. You may SHARE my work with anyone,
but it is not to be sold or used for profit in any way, without my permission.
Because there is so much information here, you may want to print out this material
for future reference.

Are you familiar with the term Melungeon? If you answer, “Who or what are
Melungeons,” you are like most people. If you have been researching your
family in the Cumberland Plateau of Virginia, Kentucky, North Carolina, West Virginia, and
Tennessee, during the early migration years, you may be able to find them through a
connection to this group of people who are only now being researched with unbiased eyes.
The Melungeons are a people of apparent Mediterranean descent who may have settled
in theAppalachian wilderness as early or possibly earlier than 1567. (The Melungeons: The
Resurrection of a Proud People; N. Brent Kennedy, Mercer University Press, Macon, GA,
USA, 1997; introduction, p. xiii) The Mediterrean includes areas of North Africa,
southern Europe and Central Asia.

According to Dr. Kennedy, the Melungeons were “a people who almost certainly
intermarried with Powhatans, Pamunkeys, Creeks, Catawbas, Yuchis, and Cherokees to
form what some have called, perhaps a bit FANCIFULLY, ‘a new race’.” Dr. Kennedy
does not believe that we can call the Melungeons a ‘race.’. No dictionary
definition of race fits with what we know of the Melungeons and recently, The American
Anthropological Association, declared that ‘race,’ was an inaccurate, artificial way of
defining a people and was no longer of any value.

Certain surnames are associated with this highly interesting group of people.
I am including a copy of those names. Be aware, however, that many people bearing
these surnames, even if they come from the Appalachian area, are NOT connected to
the Melungeons. The surnames are to be used as an INDICATOR of POSSIBLE Melungeon
ancestry. Also, note that many Melungeon women ‘out-married,’ carrying the
heritage with them, but not the names. Not having one of these names DOES NOT mean that
the family was not of Melungeon descent.

Finding out about the Melungeons and my possible connection to them is the MOST
fascinating thing I have EVER run into in my 20 years of genealogical research. The
‘so-called,’ Melungeons were ‘discovered’ in the Appalachian Mountains in 1654 by
English explorers and were described as being ‘dark-skinned, reddish-brown
complexioned people supposed to be of Moorish descent, who were neither Indian nor
Negro, but had fine European features, and claimed to be Portuguese.” (Louise Davis,
“The Mystery of the Melungeons.” Nashville Tennessean, 22 September, 1963,16.)

In April of 1673, James Needham, an Englishman and Gabriel Arthur, possibly an
indentured servant came with approximately eight Indians, as explorers to the
Tennessee Valley. There, Needham described finding “hairy people .... (who) have a bell
which is six foot over which they ring morning and evening and at that time a great number
of people congregrate together and talkes” in a language not English nor any Indian
dialect that the accompanying Indians knew. And yet these people seemingly looked European.
Needham described them as “hairy, white people which have long beards and whiskers and
weares clothing.” This bell seems to me to speak of a Latin influence among these
people. Other, later explorers, found people who lived in log cabins with peculiar arched
windows. Dr.Kennedy says that by the late 1700’s they were practicing the Christian
religion.

These people claimed that they were descended from a group of Portugese who
had been shipwrecked or abandoned on the Atlantic coast. (Byron Stinson, “The Melungeons,”
American History Illustrated, November, 1973:41) The term they used was ‘Portyghee.’
In other documents, some of these peoples were also described as having red hair and
others with VERY distinctive blue or blue/green eyes. This description leads me to believe
that these people were not Native American Indians. Altogether they must have been a
striking looking people.

Most Americans have been taught in school about the Lost Colony and Jamestown in
1607, Plymouth in 1620, with a few Spaniards and a smattering of Viking thrown in for
good measure. Where did these people come from? First of all, as the mixed-ancestry
descendents of native Americans as well as other ethnic identities, many
Melungeons will find this question to be offensive--many of their true ancestors were
ALREADY here, prior to contact with European and African in-migrants, the Official Voice of
the Second Union Planning Committee says. But recent research is giving an interesting
answer to that question. Again, from the Official Voice of the Second Union Planning
Committee comes the answer to this question. They “are a sizable mixed-ethnic
population spread throughout the southeastern United States and into southern Ohio and
Indiana. While the term ‘Melungeon’ is most commonly applied to those group members
living in eastern Kentucky, southwestern Virginia, eastern Tennessee, and southern West
Virginia, related mixed-ancestry populations also include the Carmel Indians of southern Ohio,
the Brown People of Kentucky, the Guineas of West Virginia, the We-Sorts of Maryland,
the Nanticoke-Moors of Delaware, the Cubans and Portuguese of North Carolina, the Turks
and Brass Ankles of South Carolina, and the Creoles and Redbones of Alabama,
Mississippi, and Louisiana.”

From the same source we find that “new evidence or rather old evidences re-examined
without prejudice, show a significant Spanish and Portuguese presence in
sixteenth-century America, including the large South Carolina coastal colony
of Santa Elena, as well as five outlying forts in what is now present day South
Carolina, North Carolina, north Georgia, and east Tennessee. Additionally men
of the Spanish and Portuguese newcomers were so-called ‘Conversos,’ -
that is, ethnic Jewish and Moorish people who had converted to Catholicism
prior to or during the Spanish Inquisition. Evidence is also strong
(see the work of English historian David Beers Quinn)
that in 1586 Sir Francis Drake deposited several hundred Turkish and Moorish sailors,
liberated from the Spanish, in present-day Central America, on the coast
of North Carolina at Roanoke Island. No trace was found of these people when
later English vessels dropped anchor for re-supplying.”

If you believe the Bering Strait migration of the Native American Indians and
you consider that most sixteenth century Turkish sailors were of central Asian
heritage, thus making them literal cousins to the Native Americans they would have
encountered, you will see that they would have had little trouble fitting in. There is more
evidence of Karachi, and Kavkaz Turkish, and Armenian, textile workers, artisans and
servants who were brought in by both the English and Spanish into sixteenth century
Virginia and other areas.This seems to lend support to previous claims of Melungeons to be
of Turkish origin. These people survived by blending into the surrounding groups of
peoples. Over time, they were put in to one of four permissable, inflexible and artificial
racial categories: White (northern European), black (African), Indian,
or mulatto, a mix of any of the first three.

By the time that the first U.S. census was conducted, there had been 200 years
of admixture and cultural fusing. This ensured that the story would remain
hidden and buried, and that no amount of the census research could ever tell the story
accurately. Traditional genealogy can not be used to find these people. There are are no
written records, no censuses, no marriage or death notices.

Dr. Kennedy’s interest in the Melungeons began with an illness that took him
to the emergency room in Atlanta, Georgia where he was diagnosed with erythema
nodosum sarcoidosis. In researching his own illness, Dr. Kennedy found that it is a
disease of primarily Middle Eastern and Mediterrean peoples, although it is not unknown
among the Irish and Scandanavians. He later discovered it was equally common among the
Portuguese immigrants of New England, and both southeastern Blacks and Caucasians of
seemingly unrelated backgrounds. He was told that he would just have to wait
to see if he lived or died. How could a southerner, of Appalachian roots, have a
Mediterrean disease? It was this question that Dr. Kennedy set out to answer,
by tracing his family background, and in the process he ‘rediscovered his heritage.’
His book, mentioned earlier, is not about historical research,
but his family’s genealogy and theoretical problem solving.

There are some physiological characteristics which are called ethnic markers,
that seem to be passed on through the lines of some Melungeon descendants. There is a bump
on the back of the HEAD of SOME descendants, that is located at mid-line, just ABOVE
the juncture with the neck. It is about the size and shape of half a golf ball or
smaller. If you cannot find the bump, check to see if you, like some descendants, including
myself, have a ridge, located at the base of the head where it joins the neck, rather than
the Anatolian bump. This ridge is an enlargement of the base of the skull, which is called a
Central Asian Cranial Ridge. My ridge is quite noticeable. It is larger than anyone else’s
that I have felt, except my father’s. I can lay one finger under it and the ridge
is as deep as my finger is thick. Other ridges are smaller.
To find a ridge, place your hand at the base of your neck where it joins your shoulders,
and on the center line of your spine. Run your fingers straight up your neck
toward your head. If you have a ridge, it will stop your fingers from going on up
and across your head. ONLY people who live/d in the Anatolian
region of Turkey or Central Asia also have this “bump/ridge.” See the following diagram
for the site of both the ridge and bump.

Back of Head

VVVVVVVVV
/ \
ears @___xx___@ ears xx marks the
The ridge is the line __ shown \valley / bump’s location
\ / neck
/ \____shoulders

There is also a ridge on the back of the first four teeth - two front teeth
and the ones on either side (upper and lower) of some descendants. If you place your
fingernail at the gum line and gently draw (up or down) you can feel it and it makes a slight
clicking sound. The back of the teeth also curve outward rather than straight as the
descendants of anglo-saxon parentage do. Teeth like these are called Asian Shovel Teeth.
Many Indian descendants also have this type of teeth. The back of the first four teeth of
Northern European descendants are straight and flat.
An example of northern European teeth would be similar to this diagram: \|
Shovel teeth look like this diagram. Back of teeth )/ front of teeth, straight.

SOME Melungeon descendants have what is called an Asian eyefold. This is
rather difficult to describe. At the inner corner of the eye, the upper lid attaches
slightly lower than the lower lid. That is to say that, it overlaps the bottom lid. If you
place your finger just under the inner corner of the eye and gently pull down, a wrinkle will
form which makes the fold more visible. Some people call these eyes, “sleepy eyes,
dreamy eyes, bedroom eyes.” Many Indian descendants also have these kinds of eyes.

Some families may have members with fairly dark skin who suffer with vitiligo,
a loss of pigmentation, leaving the skin blotched with white patches. Some descendants
have had six fingers or toes. There is a family of people in Turkey whose surname
translated into English is “Six Fingered Ones.”

If your family has an Indian Grandmother(father) ‘myth’ which you have been unable to
prove, an adoption story that is unprovable, or an orphan myth, and they have been hard
to trace and they lived in NC, TN, KY, VA, WV areas in the early migration years or if
they seem to have moved back and forth in these areas and if they share any of the
mentioned surnames and characteristics, you MAY find a connection here. Some
descendants do not show the physical characteristics and of course, there are many people
with the surnames who are not connected to this group.

Now, if I have piqued your interest, here is a URL for the Melungeon Homepage,
designed and hosted by Darlene Wilson, that I have found which has a lot of information
on the Melungeons. There is also a guestbook/forum on this list where you can
place your queries and read those of others:

http://pluto.clinch.edu/appalachia/melungeon/

Be sure and read all the pages and connected links! This is NOT a genealogy page,
but carries Melungeon information and research. Darlene is NOT a genealogist and
she has not set up this site to handle queries to her. She is a researcher and a doctural
candidate with a very busy schedule. There is excellent documentation on this interesting
group and it will give you the necessary information so that you can more easily
understand the Melungeons, and their reasons for doing what they did. What I am giving
you summarizes some but NOT ALL the information.

Dr. N. Brent Kennedy’s book, ‘The Melungeons: The Resurrection of a Proud People,’
both a genealogy and theoretical search for answers, is a must read for anyone who is
connected to this group. Most bookstores can order this book in paperback for you.
From some information in Dr. Kennedy’s book and information from the SecondUnion
Planning Committee, you can see the necessity for these people to hide.

These proud, strong, courageous, people were discriminated against by their Scots-Irish
and English neighbors as they moved into the areas where the Melungeons lived. They
wanted the rich valley lands occupied by the Melungeons they found residing there. They
practiced RACIAL discrimination against the Melungeons because they were darker
skinned than their own anglo-saxon ancestors and because this helped them obtain the
lands they coveted. In a society where slavery was an accepted way of life, where
genocide against the American Indian was government policy, hiding was sometimes the
only way to survive. This discrimination carried into the 1940’s-50’s and perhaps even
longer, because of the work of a man named Walter A. Plecker, who was the state of
Virginia’s first Director of Vital Statistics and an avowed racist. Some Germans say that
it was he, who first gave them the idea of eugenics, that was used during WWII to help
exterminate 6 million Jews. Plecker labeled the Melungeons, calling them ‘mongrels’ and
other worse terms - some were labeled FPC - Free Person of Color in Virginia. This in
turn led to their children being labeled as Mulatto (M) and both of those terms came to
mean “BLACK.” (There is information on Plecker and the letters he wrote to all the
counties in VA and the surrounding states to marginalize and discriminate against the
Melungeons on the Melungeon Homepage. Check under the Archives section.) Some
Melungeon families married white, some black, some Indian, some a combination. But for
all of them, the terms led to rulings in which they couldn’t own property, they couldn’t
vote, and they couldn’t school their children. Is it any wonder that they became
ANYTHING else in order to do these things? They hid their backgrounds with the Indian
myth, with the orphan myth (my family are all dead, and the adopted myth, and they
changed either the spelling of their surnames or they picked an entirely new name, moving
many times, anything to distance themselves from their Melungeon heritage. They became
‘Black Dutch,’ ‘Black Irish,’ ‘Black Scot or Swede,’ or some other combination to hide
their “otherness.” Is it any wonder they are so hard to find? They deliberately made it so,
in order for their descendants to have a better life than they had had.

I have a Ramey family that I have traced to France where they were the Remy family. This
Ramey family is also considered to be Melungeon. I will be glad to share the information I
have on them. I also have some one name lines that married into some of my other lines.
The names considered to be Melungeon are Thompson, Wood, and possibly Smith. I
would love to talk with anyone who shares these surnames and locations.

The closest Melungeon family, for whom I have searched the longest, were Collinses that
were connected with the Cunningham family. It took me twenty years of searching to find
only this little bit of information on them. I have this:

1. William Cunningham m. Susan Wood abt 1770
2. John Cunningham m Nancy Crump in 1794 in Washington Co., VA
2. Mary Ann Cunningham m. John Hutton in 1791 in Washington Co., VA
2. Elizabeth Cunningham m. John Dickenson in 1796 in Washington Co., Va.
2. William Cunningham, Jr. b. abt 1777, d. aft 1850, prob. in Johnson Co.,KY m. 1810,
Washington Co., VA, Rachel Ann Elizabeth Countiss, b. May 05, 1791 in MD, dtr
of Peter G. Countiss and Mary Burrt.
3. Maca/Macha Cunningham b. abt 1826 m WILL COLLINS, d. 1848-1850
4. MARY COLLINS b. abt 1843 in the Scott, Russell, Lee Co.,VA area
that is now Wise Co., VA, was a partner of Abraham Musick b. abt 1836 in VA, d. bef
May 15, 1914, son of James Musick and Mariah Shell.
5. Mary Arminta Musick
4. RACHEL COLLINS b. Jan. 01, 1844 inKY, d. May 15, 1914 m. Abraham
Musick of above.
4. CHARLES COLLINS b. abt 1848
4. CHRISTOPHER COLLINS b. abt 1850
I have information on other Cunningham siblings, the Countiss family, as well as the
Musick line back to the immigrant founding father.

I don’t have all that information up on my family’s webpage, which was set up
by my cousin Harold Sparks, yet, but I do have some information on my
greatgrandmother Mary Arminta Musick Hager whose mother was Mary Collins.
The address is:

http://www.awod.com/gallery/rwav/sparky

On the first page, click ‘continue’ and on the second page, scroll down until you come to
the words Nancy’s Corner, Click and my picture will come up. Further down that page
is a listing of all the surnames that I am researching. Please be sure to contact me if you
see any common surnames.

If you feel that any of this information applies to you, then please join a group of us,
searching our Melungeon roots on a mailing list that began when MaryK Goodyear
learned that she might have Melungeon heritage and wanted to find out more. We will be
forever grateful to MaryK for starting this list.

We share genealogy, folklore, cultural likenesses, even a recipe now and then. We are a
friendly group who has come to feel like family. We have a lot to offer. To join, send an
e-mail to:

Melungeon-L-request@rootsweb.com or Melungeon-D-request@rootsweb.com

In both the subject and body boxes put: subscribe

You will receive a letter saying you have been subbed and giving directions for posting the
list. Send in your family info and let us see if we can help you. I know that you will be able
to help someone as well! I will look forward to hearing from you and seeing you on the list.

There is also a Melungeon chat list for more cultural, social gathering and getting to know
one and other, that you might enjoy. Pam Cresswell can give you directions forsubbing this
list. Visit her URL at:

http://cresswells.com/alhn/melung/index.html

Here are several other sites with Melungeon queries and information:

http://geocities.datacellar.net/Heartland/Pointe/3778/

http://www.clinch.edu/appalachia/melungeon/mel_nmr.htm

http://www2.privatei.com/~bartjean/mainpage.htm

Common Melungeon Surname List

North Carolina, Virginia, Tennessee, Kentucky, West Virginia

ADAMS ADKINS ALLEN ALLMOND ASHWORTH * BARKER BARNES BASS
BECKLER BELCHER

BEDGOOD BELL BENNETT BERRY BEVERLY BIGGS BOLEN BOLLING
BOLTON BOONE BOWLIN

BOWLING BOWMAN BRADBY BRANHAM BRAVBOY BRIGER/BRIDGER
BROGAN BROOKS BROWN

BUNCH BULLION BURTON BUTLER BUTTERS BUXTON BYRD * CAMPBELL
CARRICO CARTER CASTEEL

CAUDILL CHAPMAN CHAVIS CLARK CLOUD COAL COFFEY COLE
COLEMAN COLES COLLEY

COLLIER COLLINS COLLINSWORTH COLYER COOPER CORMAN COUNTS
COX COXE CRIEL

CROSTON CROW CUMBA CUMBO CUMBOW CURRY CUSTALOW * DALTON
DARE DAVIS

DENHAM DENNIS DIAL DOOLEY DORTON DOYLE DRIGGERS DULA DYE
DYESS * ELY EPPS EVANS

* FIELDS FREEMAN FRENCH * GALLAGHER GANN GARLAND GIBSON
GIPSON GOINS GOINGS

GORVENS GOWAN GOWEN GRAHAM GREEN(E) GWINN * HALL HAMMON(D)
HARMON HARRIS

HARVIE HARVEY HAWKES HENDRICKS HENDRIX HILL HILLMAN HOGGE
HOLMES HOPKINS HOWE

HYATT * JACKSON JAMES JOHNSON JONES * KEITH(E) KENNEDY KISER *
LANGSTON LASIE

LAWSON LOCKLEAR LOPES LOWRY LUCAS * MADDOX MAGGARD MAJOR
MALE MALONE(Y)

MARSH MARTIN MAYLE MINARD MINER MINOR MIZER MOORE MORLEY
MOSELY

MOZINGO MULLINS * NASH NELSON NEWMAN NICCANS NICHOLS NOEL
NORRIS * ORR OSBORN

OSBORNE OXENDINE * PAGE PAINE PATTERSON PERKINS PERRY PHELPS
PHIPPS PRINDER POLLY

POWELL POWERS PRITCHARD PRUITT * RAMEY RASNICK REAVES REVELS
REEVES RICE

RICHARDSON RIDDLE RIVERS ROBERSON ROBERTSON ROBINSON RUSSELL
* SAMMONS

SAMPSON SAWYER SCOTT SEXTON SHAVIS SHEPHARD SHEPHERD SHORT
SHORTT SIZEMORE

SMILING SMITH STALLARD STANLEY STEEL STEVENS STEWART
STROTHER SWEATT SWETT

SWINDALL * TALLY TACKETT TAYLOR THOMPSON TIPTON TOLLIVER
TUPPANCE TURNER *

VANOVER VICARS VICCARS VICKERS * WARE WATTS WEAVER WHITE
WHITED WILKINS

WILLIAMS WILLIAMSON WILLIS WILSON WISBY WISE WOOD WRIGHT
WYATT WYNN

THE MELUNGEONS:
THE PIONEERS of the INTERIOR SOUTHEASTERN UNITED STATES
1526-1997
by Eloy J. Gallegos

On p. 80 of the above text, Eloy Gallegos provides a Table giving the Mean Measure of
Divergence (MMD) of Melungeons from Other Populations taken from a 1990 study by
James L. Guthrie. Dr. Gallogos stated (p.79) that, “Overall, I believe the
gene frequency approach taken to resolve Melungeon origins is the best available given the
limited funding and time available for the project, however, it is equally important to
support gene frequency studies with historical, cultural, linguistic, and archaeological
information which might be obtained from the Melungeon group.
Finally, a study of human values, traits of
this group...etc, world-view, religious aspirations, motivational traits, eccentric and
habitual behavior, and idiosyncrasies could be used in support of establishing Melungeon
origins when compared to other world population groups.”

A perfect match meaning that a person is to be considered absolutely pure blooded, would
equal 0.000. I believe that the most distant match indicating no connection whatsoever
would be 0.999.

POPULATION MMD

Libya (Tripoli*) 0.017
Cyprus (Toodos-Greek) 0.017
Malta* 0.018
Canary Islands (Spanish) 0.019
Italy (Veneto) 0.022 Close Matches
Portugal 0.024
Italy (Trentino) 0.026
Spain (Galacia) 0.027
U. S. Whites (Minnesota)+ 0.028
Ireland# 0.029
Italy 0.030
Sweden 0.030
Libya (minus Fezzan) 0.030
Germany 0.031
Britain 0.031
Greece 0.032
Netherlands 0.032
Wales 0.033
Corsica 0.034
France 0.035
Spain 0.036
U. S. Whites 0.036
England 0.040
Sicily 0.040
Iceland 0.041
Northern Ireland 0.042
Finland 0.046
Sardinia 0.051
Turkey 0.053
Cyprus 0.058
U.S. Blacks 0.189 Distant Matches
Gullas (Blacks South Carolina) 0.222
Seminole, Oklahoma 0.241
Cherokee 0.256
Seminole, Florida 0.308

* The Arab/Berber (Moorish) component of the Spanish/Portugese of today.
+Probably Swedes. Could reflect the Moorish in Swedes.
# Married into Melungeon families in the S. E. U. S. Does not include
Northern Ireland.

In spite of the close corrolation between the Turks and the Melungeons, Dr. Gallegos,
who is of Spanish/Portugese extraction, does not agree with Dr. N. Brent Kennedy on
Melungeon origins. His book is aimed toward the Spanish/Portugese expeditions prior to
the establishment of the English on the American continent in 1607. In the * above, he
says that the Moorish component came through the Spanish/Portugese whose genes
combined with the Moors, rather than from that group of people themselves.

MEDITERREAN DISEASES WHICH MAY AFFECT MELUNGEON DESCENDANTS

BECHET’SYNDROME is a relapsing, multi-system inflammatory disease in which there
are oral/genital ulcers. There may be inflammation of the eyes, joints, blood vessels,
central nervous system and gastrointestinal tract involvement. Attacks last about a week
to a month and recur spontaneously. Onset is usually between 20-30 years of age with
symptoms ocurring up to several years after the onset. Twice as many men as women are
affected. There is a genetic predisposition, with autoimmune mechansism and viral
infection which may all play a part. Related disorders are Reiters Syndrome, Stevens
Johnson Syndrome, and Ulcerative Colitis.

JOSEPH’S DISEASE is a disorder of the central nervous system with slow degeneration
of particular areas of the brain. Lurching gait, difficulity in speaking, muscle rigidity,
impairment of eye movement, are involved. Mental alertness and intellect are preserved.
Joseph’s disease is inherited through autosomal dominant mode of transmission,
which means that it takes only one parent with the marker for you to have a 50% chance of
inheriting the disease.
Type I, begins about age 20 years,
Type II, about 30 years and
Type III, Machado’s after 40 years
This disease is very similar to Parkinson’s Disease. Medicine is baclofen.

FAMILIAL MEDITERREAN FEVER is a hereditary genetically restricted disease
commonly found among Jews originating from North African countries, Armenians, Turks
and Arabs. Closely following the pattern of autosomal recessive inheritance
(both parents must carry a recessive gene), FMF is
recognized by two independent manifestations: 1.) acute, short-lived painful, bouts of
stomach pain, (may be followed by diahrrea); pleuritis, an inflammation of the lining of
the body cavities, and/or some of its internal organs, which in its acute stage may
produce, stabbing pain in the side or affected cavity, possible fever of 101-103 degrees,
similar to gallbladder/kidney stone attacks/inflammation, and short, dry cough and body
pain similar to arthritis and fibromyalgia and 2.) nephropathic amyloidosis, which can lead
to terminal renal failure even at a young age. In half of the people this disease appears
before age ten. The gene for FMF is located on the short arm of chromosome 16, yet the
exact nature of the disease remains unclear. Foggy-headedness (inability to think clearly)
may also be a part of the symptoms because of inflammation of the brain lining which
causes the brain to swell. Fatigue (severe) can also be a problem. Infertility and pregnancy
loss in women with FMF is much more common than it is in the general population.

The identification of FMF is based on clinical findings, family history, physical examination
and laboratory results obtained from patients experiencing attacks. No specific diagnostic
test is available. There are four gene mutations that cause FMF. The genes have been
identified and I have heard that this should lead to the development of a blood test to
identify the disease in people. Amyloidosis affects most untreated FMF patients.
In its early stage it can be recognized by protein in the urine.

The medicine colchicine which comes from a plant that grows in the Mediterrean and is
also used to treat gout, is effective in controlling this disease. Colchicine treatment was
first introduced in 1973 and in a dose of 1-2 mg/day on a continuous basis, has been
found to prevent attacks in most patients and amyloidosis in all patients. Colchicine
treatment has been shown to be safe and entirely suitable for FMF patients.

Through genealogical research and coming across this medical information, I realized that
I suffer with FMF. I asked my doctor to diagnose it, by giving me a short course of
colchicine to see if it would work. He didn’t think I had FMF but agreed to my wishes and
within two hours of taking the first dose, I knew it was going to help.
I believe that I have had this disease since about 8 years of age.
It took 50 years to diagnose it. At first, I took 0.06mg once a day,
and have increased that after 6 weeks to twice a day. My previously diagnosed
FIBROMYALGIA is gone! I still have RA-like symptoms, but even those seem to be improving,
however. If you take a few days worth of colchicine and your symptoms are not
gone, then in my opinion you don’t have FMF.

SARCOIDOSIS is a disorder which affects many body systems. It is characterized by
small round lesions of granulation tissue. The ones I have seen are about the size of a
quarter and flat. Symptoms may vary with the severity of the disease. Fever,
weight loss, joint pain, with liver involvement and enlarged lymph nodes are common. Cough
and difficulty in breathing may occur. Skin disease marked by tender red nodules
with fever and joint pain is a frequent manifestation. Onset is usually between 20 and 40
years.

THALLASEMIA, a blood disorder.

If you have had a mysterious disease that physicians have had trouble diagnosing, and you
have any of the above symptoms, it is imperative that you bring this to your physician’s
attention.

The opinions in this post are strictly my own, but have been based upon my reading and
research of various materials noted herein.

Just a few weeks ago I was diagnosed, with Familial Mediterrean Fever, a disease which I
believe that I have had since I was about 8 years old. My doctors and some of my family
thought that I was a hypochondriac because of the many and varied symptoms that I
presented. I was told ‘it is all in your head.’
I was diagnosed previously and erroneously, it turns out,
with fibromyalgia, rheumatoid arthritis, chronic recurrent chemical depression,
sleep apnea, sleep disorder with myoclonus, and Restless Leg Syndrome, colitis, spastic
colon, gallbladder inflammation, appendicitis, possible kidney stones with their concurrent
problems of vomiting and diahrrea, and so many other things that I can’t even remember
them. I had chronic respiratory problems, sinus infections, allergies and asthma. I had
even looked into Chronic Fatigue Syndrome as a possible cause of my problems. All of
these things didn’t happen at once, but the diagnoses kept being added and they grew
worse as I grew older. Sound like I was a wreck? I was, but I am beginning to improve. It
is like a miracle.

I came across the diagnosis of Familial Mediterranean Fever through my genealogical
research and that story is told in another paper. Suffice it to say, that I diagnosed myself,
told my doctor about it, and asked for the medicine colchicine as a trial. My doctor did not
think that I had FMF, even though I had the ancestry, but he was willing to give me a trial
prescription. Two hours after I took the first dose, I knew it was going to work.

At the point when I took the medicine, I could not rise from a seated position without
pushing or pulling myself up with my hands. My hands, arms, and shoulders in particular
were in constant pain, both in the muscles and the joints. I could not hold a cup of coffee
or a glass of water without using two hands, no thumbs to hold them. I moaned and
groaned as I came down the steps in the morning, turned sideways and taking one step at
a time while holding on to the rail with my finger tips from underneath the railing. My
brain was foggy; I could not think clearly, nor concentrate for longer than a few minutes. I
had trouble doing simple arithmetic in order to balance a checkbook. MY life was
miserable. I was very unhappy and I hurt so much at times that I was sure I could not
stand it. Stress seemed to make it more intolerable.

The medicine colchicine, which I started taking in 0.06mg daily doses,once daily and now
take twice a day, and which the Merck Manual says can be taken in that amount 3 times a
day, is made from a plant called the Autumn Crocus which grows in the Mediterranean. It
is not harmful taken in small doses for a short time even if you do NOT have the disease.
It needs to be carefully monitored by your doctor and is available only through
prescription.

I cannot claim to diagnose or prescribe as I am not a doctor. I am a genealogist with a
scientific bent. I can tell you my story and tell you what I think, however.

This information is copied from the paper that the National Organization of Rare Diseases
(NORD) sent to me. I have added a few comments in parentheses with the words
“I,my,mine” included. If the parenthesis does not include these words then the
parentheses are NORDs.

FAMILIAL MEDITERRANEAN FEVER

Other names that FMF may be called are:

Armenian Syndrome
Benign Paroxysmal Peritonitis
Familial Paroxysmal Polyserositis
FMF
MEF
Periodic Amyloid Syndrome
Periodic Peritonitis Syndrome
Polyserositis, Recurrent
Reimann Periodic Disease
Reimann’s Syndrome
Siegel-Cattan-Mamou Syndrome

Familial Mediterranean Fever (FMF) is a rare (I am not so sure about the rare.)
inflammatory disease characterized by recurrent attacks of fever and acute inflammation of
the membranes that line the abdominal cavity (peritonitis) and/or the lungs (pleuritis); pain
and swelling of the joints (arthritis); and/or in some cases, skin rashes. In addition, some
affected individuals may experience a serious complication known as amyloidosis, which is
characterized by abnormal accumulation of a fatty-like substance (amyloid in various parts
of the body. If amyloid accumulates in the kidneys (renal amyloidosis), kidney function
may be impaired and life-threatening complications may occur. In most cases,
Familial Mediterranean Fever is thought to be inherited as an autosomal recessive
genetic trait.

SYMPTOMS

The symptoms of Familial Mediterranean Fever, which may be recurring, typically include
fever, severe abdominal pain, and/or chest pain. This pain occurs due to inflammation of
the delicate membranes that line the abdomen and lungs (polyserositis). The abdominal
pain, which usually occurs in the lower right quadrant, may be acute and severe; it is
frequently confused with acute appendicitis. The attacks generally last up to 24 hours but
may continue for 4 days. (My attacks were also confused with gallbladder attacks
(inflammation and gallstones), colitis, spastic colon, bladder spasms and possible kidney
stones, as well as appendicitis. I had numerous upper respiratory problems, including
asthma and allergies, and infections.)

Approximately 75 percent of people with Familial Mediterranean Fever have episodes of
joint pain (arthritis). The pain, which may be accompanied by swelling, may be severe and
limit the range of motion in the affected joints. Attacks of arthritis usually
subside within 7 days and joint function is restored. However, in some affected individuals,
these episodes can also continue for several weeks or months. (Mine have been periodic for
many years.) Some individuals with Familial Mediterranean Fever have painful swollen red
(erythematous) skin lesions (pyoderma) on the lower legs.

Individuals with FMF may also experience depression and other psychological
difficultiies.(I have suffered bouts of recurrent chronic chemical depression
for years,worsening as I becane older.)

Some individuals with the disorder may experience a serious complication known as
amyloidosis. In this condition, a fatty-like substance (amyloid) accumulates in various
parts of the body. If amyloid accumulates in the kidneys (renal amyloidosis), kidney
function may be impaired and life-threatening complicatins may occur. Some affected
individuals may experience intestinal obstruction (My grandfather died of an intestinal
obstruction.) and inflammation of the membranes that line the brain (meningitis) as
complications of amyloidosis associated with Familial Mediterranean Fever. (I believe this
caused confusion, inability to concentrate, and mood swings, among other things in my
case.I wonder about ADHD and even Alzheimer’s Disease.) Affected individuals from
certain ethnic populations (such as those of Turkish or Sephardic Jewish descent) may
have a relatively high incidence of amyloidosis when compared with those from other
ethnic groups.

CAUSES

In most cases, FMF is thought to be inherited as an autosomal recessive genetic trait.
Human traits, including the classic genetic diseases, are the product of the
interaction of two genes, one received from the father and one from the mother.

In recessive disorders, the condition does not appear unless a person inherits
the defective gene for the same trait from each parent. If an individual receives one
normal gene and one gene for disease, the person will be a carrier for the disease, but
usually will not show symptoms.
The risk of transmitting the disease to the children of the couple, both of
whom are carriers for a recessive disorder, is 25 percent. Fifty percent of their children
risk being carriers of the disease, but usually will not show symptoms of the disorder.
Twenty-five percent of their children may receive both normal genes, one from each
parent, and will be genetically normal (for that particular trait). The risk
is the same for each pregnancy.

Two teams of researchers have identified the gene responsible for Familial Mediterranean
Fever. The disease gene, which is located on the short arm (p) of chromosone 16
(16p13)*, encodes for a protein (named “pyrin” or “marenostrin”) that is thought to play
an important role in controlling inflammation. Researchers have identified four mutations
of the gene during genetic analysis of affected individuals in several ethnic
groups.

*Chromosomes are found in the nucleus of all body cells. They carry the genetic
characteristics of each individual. Pairs of human chromosomes are numbered from 1
through 22, with an unequal 23rd pair of X and Y chromosomes for males, and two X
chromosones for females. Each chromosone has a short arm designated ‘p’ and a long
arm identified by the letter “q.” Chromosones are futher subdivided into
bands that are numbered.

One of the research teams suggested that different mutations of the FMF gene may be
associated with different levels of disease severity. (I believe this may account for
fibromyalgia and chronic fatigue syndrome on the scale of the diseases severity.) For
example, the researchers stressed that a particular FMF gene mutation (known as
“Met694Val”) is common in certain populations with more severe disease including earlier
disease onset, increased frequency of inflammation of the joints (arthritis) and the
membranes that line the lungs (pleuritis), and a high occurrence of amyloidosis, while a
different FMF gene mutation (called “Val726Ala”) is often present in other populations in
which the disease tends to be more mild and amyloidosis occurs less frequently.
Accordingly, the research team suggested that inheriting two copies or one copy of the
‘milder’ FMF mutation (i.e., Val726Ala homozygotes or compound heterozygotes) may
be “protective” against amyloidosis. Yet it is important to note that some cases later
reported in the medical literature demonstrated the development of amyloidosis in affected
individuals who inherited one copy of the ‘milder’ mutation (i.e., Val726Ala heterozygotes).
Therefore, additional studies are needed to further examine the role
specific FMF gene mutations may play in potentially determining disease severity and
potential risk of amyloidosis. Such informatin may be essential since ongoing preventive
(prophylactic) therapy with the medication colchicine may prevent amyloidosis from
developing in those at risk for this serious complication.

The four mutations of the FMF gene that have been identified to date are present in
approximately 85 percent of individuals who have or are carriers for FMF. According to
the medical literature, there may be other FMF gene mutations that have not yet been
identified. In addition, some researchers suggest that, in rare cases, there may be other
factors that may be able to trigger the expression of the disease in those who have
inherited only one mutated FMF gene, (multifactorial inheritance). It has also been
suggested that certain FMF gene mutations may be inherited as an autosomal dominant
trait, meaning that only a single copy of the disease gene is needed to result in expression
of the disorder. According to researchers, such theories may be supported by reports in
the medical literature in which individuals with just one copy of a known FMF gene
mutation have developed the characteristic features associated with the disorder.
Additional research is needed to further understand the specific causes of FMF in
individuals who currently appear to carry just one FMF disease gene for the
disorder.(I have heard that since the genes have been identified, it should not be too
long before a blood test could be developed to identify the disease.)

AFFECTED POPULATION

Familial Mediterranean Fever is a rare disorder that affects more males than females. The
symptoms generally begin during childhood or teen years. Episodes of symptoms typically
continue throughout life. Most affected individuals have ancestors who lived in areas
around the Mediterranean Sea. Shephardic and Iraqui Jews, Turks, Levantine Arabs, and
Armenians are at a higher risk for this disease than other populations.

Approximately 50 percent of the people with Familial Mediterranean Fever have no
known family history of this disease.

RELATED DISORDERS

Symptoms of the following disorders can be similar to those of Familial Mediterranean
Fever. Comparisons may be useful for a differential diagnosis:

Appendicitis is a common disorder characterized by the acute inflammation of the
appendix. The symptoms usually include the sudden onset of pain in the stomach and
abdomen, nausea, and/or vomiting. After a few hours, the pain becomes more localized to
the lower right portion of the abdomen. (I have been diagnosed with appendicitis since
childhood, yet I never had my appendix removed until another surgery was performed and
the appendix was removed prophylactically.)

The following disorders may be associated with FMF as secondary characteristics. They
are not necessary for a differential diagnosis:

Amyloidosis is a term applied to a group of metabolic disorders in which amyloid (a
fibrous protein) accumulates in the tissues of the body. The excessive accumulation of
amyloid caused the affected organ to malfunction. The accumulation may be localized,
general or systemic.The nephrotic (kidney) syndrome associated with amyloidosis is
usually accompanied by increased levels of protein in the urine (proteinuria), which
worsens as the disease progresses and may finally result in kidney failure.
The kidneys become small, pale and hard.

STANDARD THERAPIES

Diagnosis
Because certain gene mutations known to cause FMF have been identified, precise genetic
testing may be possible in some cases. However, such testing may only be available
through research laboratories with a special interest in this disease. In addition, because
the four mutations of the FMF gene that have been identified to date are present in only
about 85 percent of the individuals who have or are carriers for FMF, precise diagnosis
may be difficult in some cases, such as in individuals with symptoms
characteristic of FMF who appear to carry just one FMF disease gene.
Further research is needed to better understand the genetic causes
and to improve the diagnosis of FMF.

Therapies
For reasons that are not yet clearly understoood, the medication colchicine may prevent or
reduce attacks in FMF. In addition, if an attack is ongoing, colchicine therapy may often
halt the symptoms. Studies have also shown that ongoing preventive (prophylactice)
therapy with colchicine may prevent amyloidosis from developing in those at risk for this
serious complication. Colchicine therapy may also help treat amyloidosis in affected
individuals who have developed this condition.

Costicosteroid drugs have not proven effective for the treatment of this disease. Narcotic
medications should not be used routinely to control pain because of the
possiblity of drug addction. For more information, contact:

Dr. Deborah Zemer
Dr. Avi Livneh
Helller Institute for Medical Research
Sheba Medical Center
Tel Hashomer
Israel

When the function of the kidneys has been severely impaired by amyloidosis associated
with FMF, renal dialysis and kidney transplantation may become necessary.

Studies on FMF are being conducted. For more information on these studies,
please contact:

Association Francaise Contre Les Myopathies
1 Rue De L’Internationale
BP 59-91002
Evry CEDEX, Nancy
France
Phone: 011 33 88 1 69 47 28 28
Fax: o11 33 88 60 77 12 16

A COMPARISON OF FIBROMYALGIA, CFIDS, AND FAMILIAL MEDITERRANEAN FEVER

The following list compares symptoms given for fibromyalgia and chronic fatigue
syndrome with the symptoms that I have had with Familial Mediterranean Fever. The
fibromyalgia symptoms and the Chronic Fatigue Symptoms were taken from the internet
sites of both groups. I have taken the symptoms of FMF from the paper on the disease,
sent to me from the National Organization of Rare Diseases. I believe that the
symptoms of FMF are erroneously diagnosed in many patients because I believe the
heredity behind the disease is unknown by many people and is much more prevalent than
previously thought.I BELIEVE THAT FIBROMYALGIA AND CHRONIC FATIGUE
SYNDROME ARE JUST A CONTINUUM OF THE SAME DISEASE. I have starred
the symptoms normally listed for FMF, and perhaps explained why some of the symptoms
for FMF which are not listed may occur and why they may have been misdiagnosed
with Fibromyalgia and CFIDS patients. I also had the symptoms w/o the stars.All the
muscle pain, trigger spots and muscle soreness of my ‘diagnosed,’ fibromyalgia are
gone. I have marked those symptoms that are improving with a plus (+). IF I HAD
FIBROMYALGIA THEN I BELIEVE fibromyalgia is UNDIAGNOSED FMF. Is Chronic Fatigue also
undiagnosed FMF? I believe that it is. Are these two diseases milder forms of FMF
or just misdiagnosed? I believe that it is both.

FIBROMYALGIA CHRONIC FAMILIAL
FATIGUE MEDITERRANEAN
SYNDROME FEVER

1 fatigue + 1. Pronounced fatigue 1. fatigue, severe
2.widespread pain/GONE 2. joint aches and pains 2. widespread
pain/mscles/jnts
3 mos. duration 3. 6 mos duration, recurrent *3. periodic/recurrent
4 fever not necessary 4. lowgrade fever *4. periodic fever 101-103
degrees
5. headache + 5. headache 5. headache
6.sleep disturbance + 6. sleep disturbance 6. sleep disturbance
7.morning stiffness 7. ? 7. morning stiff.
8. depression + 8. depression *8. depression
9. anxiety + 9. anxiety 9. anxiety
10. ? 10. sore throat 10. ?
11. ? 11. chills/nightsweats *11.
(assoc.w/fever)
12. ? 12. swollen lympth nodes 12. periodic swln.lymph nodes
13.? 13. muscles weakness 13. muscle weakness
14. ? 14. skin rash *14. skin rash
15.? 15. confusion/disorientation 15. confusion/disorien
16. ? 16. memory loss 16. memory loss
17 ? 17. difficulty concentrating 17. diff. concentratng
18. ? 18. inability to exercise 18. inability to exercise
19. ? 19. reduced sex drive 19. reduced sex drv.
20. ? 20. dizziness/lt. headedness 20. dizziness/lt.head.
21. ? 21. irritability 21. irritibility
22. ? 22. personality changes 22. personality changes
23. ? 23. mood swings 23. mood swings
24. poss. heredity? 24. ? *24. hereditary
25. ? 25. ? *25. acute, short-lived
painful, bouts of
stomach pain, (may
be followed by
diahrrea)
26. ? 26 ? *26. pleuritis, inflam-
mation of the lining
of the body cavi-
ties, which in
acute stage may
produce stabbing
pain in the side.
27. ? 27. ? *27. short, dry cough
*28. nephropathic
28. ? 28? amyloidosis which
can lead to kidney failure.
29.? 29.? *29. Infertility and preg
loss more commn.

The stomach pain in my case has been mis-diagnosed as inflammation of the gallbladder,
colitis, appendicitis, etc and usually had vomiting and diahrrea as well.
Everyone has a cough from time to time, and flu-like symptoms.

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