The Melungeon Health Education and Support Network


I  am Nancy Sparks Morrison, Co-author of the Sparks Genealogy Web Site at:

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I am not a doctor. I can neither diagnose nor prescribe. I am a lay person, who because of my own personal health problems, has done extensive research on some Mediterranean illnesses which seem to run throughout my Melungeon connected families. The information that I am providing here is to be used for educational purposes only.  It should not be used for diagnostic or treatment purposes.  Here is an overview of the four major medical problems that some Melungeon descendants inherit.


Behçet's 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 reoccur 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 mechanism and viral infection which may all play a part.  Related disorders are Reiters Syndrome, Stevens Johnson Syndrome, and Ulcerative Colitis.

Click here for more on Behçet's Syndrome.
Click here to access the Behcet's Disease Web page at:

FAMILIAL MEDITERRANEAN 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 diarrhea);  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 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 Mediterranean 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.  Many FMF patients appear to be getting diagnoses of fibromyalgia and chronic fatigue syndrome.

Familial Mediterranean Fever

Familial Mediterranean Fever, long-mysterious, has now yielded up its secrets.   The cause is a lack of pyrin, a neutrophil protein which slows down neutrophils when enough have reached an area (Hosp. Pract. 33: 131, April 15, 1998.)  Lacking pyrin, neutrophils mob body cavities every once in a while. In addition to fever, patients may have pleuritis, arthritis, peritonitis, and/or a hot rash (looks like a strep infection) on the ankles.  Colchicine, famous for its ability to slow down neutrophils (as in acute gout), controls the attacks and prevents the dread complication of secondary amyloidosis. As you can imagine, FMF can mimic most diseases. "Don't miss it". genetic diagnosis: Ann. Int. Med. 129: 539, 1998.
Related links

 Nancy's Personal Experiences with FMF.

Map suggesting likely distribution of two main mutations responsible for FMF

HOW Familial Mediterranean Fever Works: Chart - Suggested pathogenesis of FMF

SARCOIDOSIS is a disorder which affects many body systems.  In recent years new data on Sarcoidosis, which was once considered a rare disease, shows that it is a common chronic illness that appears all over the world.  It is now thought to be the most common of the fibrotic lung disorders, and occurs often enough in the United States for Congress to have declared a national Sarcoidosis Awareness Day in 1990.

While it was once thought to indicate Mediterranean or African origins, further research has concluded that this is incorrect.  Anyone can get sarcoidosis.  It occurs in all races and in both sexes.  Onset is usually between 20 and 40 years and the risk is greater if you are a young black adult, especially a black woman, or of Scandinavian, German, Irish, or Puerto Rican origin.  No one knows why.  This illness is also being found among SOME Melungeon descendants.

New research estimates that today about 5 in 100,000 white people in the United States have sarcoidosis.  And among black people, it occurs more frequently.  The rate is thought to be 40 out of 100,000 people.  We can but guess at how many people are affected.  White women are just as likely as white men to get sarcoidosis, but the black female gets sarcoidosis twice as often as the black male.  Some scientists believe that these figures greatly underestimate the percentage of sarcoidosis patients in America.

Sarcoidosis 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.  Sarcoidosis can escape diagnosis or be mistaken for several other diseases.

While no direct research has been done at present on the involvement of Melungeon ancestry with sarcoidosis, we might expect that our involvement lies somewhere between the white and black estimates since our ancestry is mixed.  I also found information that shows that there appears to be 20 cases per 100,000 in cities on the EAST coast and somewhat fewer in rural locations, but no data on whether or not it is found in the mid-west or west.  Some pockets of sarcoidosis are being found in the Appalachian Mts of NC/VA/KY/TN/WV and more research will be needed to see exactly what this means.

Click here: NSRC-GLOBAL
Click here: Sarcoidosis Center
Click here: Sarcoidosis Home Page
Click here: So What is Sarcoidosis?

THALASSEMIA, Thalassemia is a rare blood disorder. There is not just one disease called Thalassemia, but several of them. All are chronic, inherited forms of anemia that affect an estimated 6 percent of the world's population. These illnesses are among the most common inherited illnesses and are particularly common in people of Mediterranean, African, Southeast Asian and Chinese ancestry.   Patients with Thalassemia don't produce enough red blood cells and cannot properly utilize iron. Some forms of the illness are mild, others are life-threatening.

Thalassemia major, also called Cooley’s Anemia after the doctor who identified the illness in the 1920s, is the most severe. Thalassemia major is a rare blood disorder characterized by a marked increase in F hemoglobin and a decrease in the production of certain oxygen carrying proteins in red blood cells. It is the most severe form of the chronic familial anemias that result from the premature destruction of red blood cells.  Cooley’s anemia patients often die of heart failure or other complications in their 20s or 30s.  Although they usually appear fine at birth, children with Cooley’s anemia eventually develop symptoms such as fatigue, slow growth patterns, shortness of breath, jaundice, spleen enlargement and bone deformities.

Another type of Thalassemia is designated Alpha Thalassemia. Some people do not produce enough alpha protein which causes them to have alpha-thalassemia.   It is commonly found in Africa, the Middle East, India, Southeast Asia, southern China, and occasionally the Mediterranean region. There are seven types of alpha thalassemias that range from mild to severe in their effect on the body.

Some people who do not produce enough beta protein have Beta-Thalassemia. It is found in people of Mediterranean descent; such as Italians and Greeks, and is also found in the Arabian Peninsula, Iran, Africa, Southeast Asia, and southern China. There are three types of beta-thalassemia that also range from mild to severe in their effects on the body.

In addition to the thalassemias mentioned above, there are other related disorders that occur when the abnormal gene for alpha or beta-thalassemia combines with another abnormal or mutant globulin gene.

In E. Beta Thalassemia, there is a hemoglobin E which is one of the most common abnormal hemoglobins. It is usually found in people of Southeast Asian ancestry, such as Cambodians, Vietnamese and Thai. When combined with the beta thalassemia trait, Hemoglobin E produces E. Beta Thalassemia, a moderately severe anemia which has similar symptoms to Beta Thalassemia Intermedia.

There is also a Sickle Beta Thalassemia. Sickle Beta is caused by a combination of beta thalassemia trait and the Hemoglobin S trait, the abnormal hemoglobin found in people with Sickle Cell Disease. It is commonly found in people of Mediterranean ancestry, such as Italians, Greeks, Turks, and in people from the Caribbean. The severity of Sickle Beta varies according to the amount of normal beta globin produced by the beta gene. When there is no beta globin produced by the beta gene, the condition is almost identical with Sickle Cell Disease. The more beta globin produced by the beta gene, the less severe the condition.

To learn more about Thalassemia, see Stanley M. Diamond's Web Site, at:

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