Environmental Management

http://www.drmyhill.co.uk/wiki/Autoimmune_diseases_-_the_environmental_approach_to_treating

autoimmune diseases - the environmental approach to treating

Contents

 [hide] 

1 How auto-immunity may be switched on2 Immune adjuvants.3 Treatment of Auto-immunity3.1 Reduce the infectious load through diet and probiotics3.2 Get rid of adjuvants by doing detox regimes3.3 Vitamin D3.4 Diet3.5 Essential fatty acids3.6 Anti-oxidants3.7 Low dose naltrexone3.8 Thyroid and adrenal function4 Related Tests5 Related Articles

Autoimmunity occurs when the immune system has made a mistake. The immune system has a difficult job to do, because it has to distinguish between molecules which are dangerous to the body and molecules which are safe. Sometimes it gets its wires crossed and starts making antibodies against molecules which are "safe". For some people this results in allergies, which is a useless inflammation against "safe" foreign molecules. For others this results in autoimmunity which is a useless inflammation against the body's own molecules. These are acquired problems - we know that because they become much more common with age.

It is likely we are seeing more autoimmunity because of Western lifestyles, diets and pollution. Chemicals, especially heavy metals, get stuck onto cells and change their "appearance" to the immune system. In this respect they act as haptens [1] to switch on inappropriate reactions.

How auto-immunity may be switched on

Viruses and chemicals: autoimmunity may be switched on by viruses or exposure to chemicals, in particular the pesticides and heavy metals. The result is a useless inflammation which causes symptoms wherever the inflammation arises. This inflammation will be made much worse by poor antioxidant status. See Antioxidants. Having poor antioxidant status is a disease amplifying process.

Molecular mimicry - the idea here is that the body makes antibodies against food or bacteria in the gut which then, through sheer chance, cross reacts with the body's own molecules. So for example ankylosing spondylitis is thought to be caused by molecular mimicry against klebsiella bacteria in the gut and those antibodies then cross react with spinal ligaments - one has to be a particular tissue type for this to happen namely HLA B27 positive. There is some evidence to suggest that rheumatoid arthritis may be partly due to molecular mimicry with bacteria proteus mirabilis and tissue types HLA DR1 and 4. Clinically one sometimes sees arthritis following viral infections (pallindromic rheumatism) and this too may be molecular mimicry.

Have a look at [[2]] where it is suggested that gluten sensitivty results in autoimmune thyroid disease.

The following combinations have been shown:

Epstein Barr Virus with genotype HLA DR-15 puts one at risk of multiple sclerosisEBV and HLA DR3 puts one at risk of autoimmune thyroiditisEBV and HLA DR4 puts one at risk of autoimmune cardiomyopathyEBV and HLA DR7 - puts one at risk of primary biliary cirrhosisEBV and HLA DR7 plus smokiong puts one at risk of rheumatoid arthritis and multiple sclerosisEBV has been associated with 33 autoimmune diseases, including systemic lupus erythematosis and Sjogren's syndromeCMV (cytomegalovirus) has also been associated with autoimmune reactions

Helicobacter pylori infection is associated with idiopathic thrombocytopeonic purpura (ITP), systemic sclerosis, Crohn's disease and Guillam Barre syndrome and other vasculitic conditionsEradication of H pylori has resulted in resolution of ITP and also anti-phospholipid syndromeBUT H. pylori infection is protective for childhood asthmaWegener's granulomatosis may be switched on by staphlococci in the nose

Antibodies against yeast (saccharomyces cerevisiae) ie ASCA are predictive of developing Crohn's diseaseASCA is associated with arteriosclerosis- this too may be an autoimmune diseaseParasitic worms are protective agaisnt many forms of autoimmunity. They have a proven track record in Inflammatory Bowel Disease. For further infomration see [[3]]Malaria is protective against SLEvaccination may well increase risk of autoimmunityswine flu vaccination has been followed by epidemics of Guillam Barre syndrome and narcolepsy.

Immune adjuvants.

Many chemicals are immune adjuvants and "turn on" the immune system. One example is hay fever rates in Japan which are much higher in the cities than the countryside although pollen counts are much higher in the countryside! It is diesel particulates that make the difference - they act as adjuvants to switch on an immune response against grass pollen.

Vaccinations all contain immune adjuvants (without which they do not work!) such as mercury (thiomersal,) aluminium, squalene (a toxic lipid) or whatever. These have the potential to switch on the immune system to trigger allergies and/or autoimmunity. My personal view is that the evidence for benefit of the annual flu vaccination is probably out-weighted by potential damage so I no longer recommend this for my patients. Instead I direct them toViral infections - good nutrition is highly protective against viral infection.

Pesticides are very good at switching on allergy and probably autoimmunity as well. They too are immune adjuvants.

Heavy metals such as nickel and mercury also seem to activate the immune system.

Silicone. Silicones and other synthetic materials are widely used in surgery and cosmetic surgery. Many are strong adjuvants - ie they switch on the immune system. Silicones will migrate out of implants and distribute widely throughout the body to switch on allergies and/or auto-immunity. Devices may be contained in silicone such as pacemakers. Also think of breast implants, repair mesh for hernias, micro-chips, contraceptive devices, injected silicones for body contouring etc. See Silicone Breast Implants and Injections. Some people react to surgical suture material!

Prescription drugs which are of course chemicals! Practolol, a beta blocker, was taken off the market because it could trigger retroperitoneal fibrosis - now thought to be an autoimmune disorder. Hydralazine, another drug for blood presssure, may induce systemic lupus erythematosis.

Hormones Dydrogestone, a synthetic progesterone, can trigger autoimmune hepatitis. Indeed female sex hormones have profound effects on the immune systme and explain why autoimmuity is much more common in women than men.

Treatment of Auto-immunity

Conventional medicine uses steroids and immuno-suppressives to suppress this useless inflammation. But suppressing the immune system is a risky business, making patients more susceptible in the long term to infections and possibly cancer.

The environmental approach can be used to treat autoimmunity in the following ways:

Reduce the infectious load through diet and probiotics

By treating the upper fermenting gut. See [[4]]

Get rid of adjuvants by doing detox regimes

Do a good chemical clean up and detox regime. To read about detoxing follow links, or look for articles under 'Toxic Problems: Pollution and Poisoning'.Multiple Chemical Sensitivity - Detoxification - how to reduce your chemical load using physical methods and micronutrientsDetoxing and Treatment of Multiple Chemical Sensitivity (MCS): - see Chemical Poisoning and Multiple Chemical Sensitivity (MCS) - how to reduce the body loadDetoxing - Far Infrared Sauna (FIRS)Silicones cannot be got rid of in this way - they are large tough molecules which cannot be broken down by enzyme systems nor can they be excreted.

Vitamin D

Vitamin D has profound immune modulating properties. Vitamin D is made in the skin through the action of sunlight on cholesterol. Sunshine has marked pro-inflammatory properties so when it lands on the skin vitamin D is made from cholesterol - which counteracts this tendency to pro-inflammation. Thus vitamin D has profound anti-inflammatory effects locally in the skin - it then diffuses into the rest of the body where it modulates inflammation there. Vitamin D is probably the most powerful nutritional tool we have in the fight against auto-immunity.

Although vitamin D is present in some foods, it is there in such tiny amounts that changing one's diet hardly makes any difference in vitamin D levels. It is all about getting enough sunshine and failing that one simply has to take supplements. I like everybody to take at least 2000i.u. daily and for people with autoimmunity give them up to 50 000i.u. weekly. This is roughly equivalent to an hour of good sunshine daily landing directly on the skin of someone in shorts and T-shirt. The incidence of autoimmunity increases in people who live away from the equator with the best example of this being multiple sclerosis.

Diet

The strongest antigens appear to be gluten, milk protein and probably yeast. Sugar and refined carbohydrate are similarly pro-inflammatory. Everybody with autoimmunity should aim to do aStone Age Diet.

Essential fatty acids

Broadly speaking, the omega 3 and 6 fats feed into hormone and prostaglandin pathways, which tend to suppress inflammation so:

take evening primrose oil (4 capsules daily).take cod liver oil (4 capsules daily). Must be filtered oil: cod liver oil needs filtering to remove pesticides, check with your supplier. Eat oily fish.

Anti-oxidants

Good anti-oxidant status protects against many of the malign effects of inflammation. SeeAntioxidants

Low dose naltrexone

The idea here is to boost one's own production of opiates (endophines). This is achieved by giving a tiny dose of a morphine blocker naltrexone (4mgs, compared to a therapeutic dose of 50mgs) in the evening which partly inhibits endogenous morphine production but that is followed by a rebound increase in endogenous production. See LOW DOSE NALTREXONE

Thyroid and adrenal function

Both thyroid and adrenal hormones have immune modulating effects. Well worth getting both checked! See Thyroidand Adrenal Gland - the gear box of the car (DHEA and cortisol) – underactive

Opthalmology & HLA B27

http://www.reviewofophthalmology.com/content/c/29627/

About our DNA .....

PREVALENCE
The prevalence of HLA-B27 varies between populations— from 50% in Haida Indians to 0/ nil in Australian Aborigines. In the UK general population it is about 8%. HLA-B27 is rare in the American black population whereas Eskimo populations carry it much more frequently than Western Europeans, with prevalence rates of 25% or more. This antigen is associated with ankylosing spondylitis in virtually all racial groups studied. 

PATHOGENESIS
HLA-B27 positive Caucasians have a 20-fold risk of developing any spondylarthropathy, particularly ankylosing spondylitis and undifferentiated spondarthritis.

Family and twin studies of ankylosing spondylitis have shown a polygenic pattern of genetic susceptibility with heritability in excess of 90%. The contribution of HLA-B27 to genetic susceptibility has been estimated to be 20–50% of the total.

Other HLA alleles, most notably HLA-B60 and HLA-DR1, may predispose to ankylosing spondylitis either independently of B27 or in conjunction with it.

MECHANISMS
The main natural function of HLA-B27 is to form a complex with β2microglobulin which can bind short antigenic peptides such as those derived from intracellular microorganisms. Following presentation at the cell surface, the complexes are specifically recognised by cytotoxic lymphocytes which then kill the infected cell.

Viral?/Organisms have been shown to trigger reactive arthritis, including Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia, Mycobacteria and possibly Brucella, all of which habitually survive intracellularly. HLA-B27 appears to enhance the invasion of Salmonella into intestinal epithelial cells.

PREDICTIVE
{Insert genome suscept.
-first degree}
Generally, the value of testing for HLA-B27 depends upon the particular clinical situation. Beginning with a clinical estimate of the likelihood of ankylosing spondylitis or a related spondarthropathy.

Seronegative Spondarthritides

Ankylosing spondylitis
Reactive arthritis (Reiter’s syndrome)
Psoriatic arthropathy
Enteropathic arthropathy
Acute anterior uveitis
Juvenile spondarthritis
Undifferentiated spondarthritis
Isolated peripheral enthesitis

ASSOCIATIONS
HLA-B27 and ankylosing spondylitis remains the strongest known relationship between a major histocompatibility complex (MHC) antigen and a disease!

Enthesitis, defined as inflammation of the origin and insertion of ligaments, tendons, aponeuroses, annulus fibrosis and joint capsules, is a hallmark.

The concept of entheseal organ prone to pathological changes in spondyloarthritis is well recognized.

The relevant role of peripheral enthesitis is supported (heel pain or other well-defined enthesopathic pain), axial and peripheral spondyloarthritis.

Episodes of Achilles tendinitis, plantar fasciitis, posterior tibial tendinitis, & dactylitis. Also seen are lateral epicondyle, insertion of the patella tendon into the inferior pole of the patella, femoral quadriceps, and posterior tibial tendons. {continue}Hip disfunct:

Upper lobe fibrosis is the lung condition best known to correlate with HLA-B27.  The antigen may be positively, neutrally or negatively associated with asbestosis. Claims have also been made for an association with other pulmonary diseases, especially pleurisy, pleural abscess, bronchitis and pneumonia and pneumothorax, independently of the presence of ankylosing spondylitis.

Aortic regurgitation occurs in 2–10% of patients with ankylosing spondylitis, and cardiac conduction abnormalities including atrioventricular and intraventricular blocks have been found in one-third of patients with spondylitis.

HLA-B27 related cardiac lesions may be found in the absence of other rheumatological manifestations.
Indeed, an HLA-B27 associated cardiac syndrome comprising severe cardiac conduction system abnormalities and lone aortic regurgitation has been defined, whose link with B27 is almost as strong as that between B27 and ankylosing spondylitis.

Significant association has been reported between HLA-B27 and acute leukaemia, particularly acute myeloid leukaemia.HLA-B27 carriers may have an increased risk of acute leukaemia whilst those with concomitant ankylosing spondylitis may be predisposed to lymphoid malignancies.

While infection with HIV predisposes to spondyloarthropathy,HLA-B27 is the HLA class I molecule most closely associated with non-progression of HIV infection to AIDS.

HLA-B27 can be helpful in a patient complaining of low back pain of an inflammatory character in the absence of radiological signs of sacroiliitis or in patients with an asymmetrical oligoarthritis but without other features of spondarthritis. This has been acknowledged with the inclusion of HLA-B27 positivity as a criterion in the Amor classification criteria for spondyloarthropathy.

Likewise, testing for HLA-B27 can help to differentiate between alternative aetiologies in iritis and aortic regurgitation.

PROGNOSTIC VALUE

Whereas HLA-B27 does not seem to influence the severity of ankylosing spondylitis, in psoriatic spondylarthropathy it may determine not only susceptibility to the condition but also its clinical expression.

It correlates most strongly with isolated axial disease and it may confer some protection against peripheral joint erosions.

Patients with Reiter’s disease and Yersinia andSalmonella triggered reactive arthritis who are HLA-B27 positive have more severe acute disease, more extra-articular features and more frequent chronic back pain and sacro-iliitis.

In C. trachomatis reactive arthritis, more severe or chronic disease could be due to lower concentrations of interferon-γ in the synovial fluid of patients who are HLA-B27 positive than those who are HLA-B27 negative, with consequent impaired clearance of infective agents.

With regard to cardiac disease, the relative risk that a HLA-B27 positive man will need a permanent pacemaker has been calculated to be 6.7 compared with a man who has other B alleles. This association is not, however, present in female patients.

A poor outcome of back surgery has been found in patients possessing HLA-B27.

Atlanto-axial subluxation can occur.

HLA-B27 positive patients with rheumatoid arthritis have about twice the risk of developing subluxation of the cervical spine and an almost threefold risk of subaxial subluxation.

Thus, HLA-B27 may transpire to be a useful prognostic indicator for the later development of instability of the cervical spine and its complications in rheumatoid arthritis.

The discovery of the link between HLA-B27 and a large family of inflammatory rheumatic diseases was one of the seminal advances in rheumatology in the last century. Associations have subsequently been identified with other musculoskeletal and non-rheumatic diseases.

The Test
http://labtestsonline.org/understanding/analytes/hla-b27/tab/test/

The HLA-B27 test is primarily ordered to help strengthen or confirm a suspected diagnosis of ankylosing spondylitis (AS),reactive arthritis, juvenile rheumatoid arthritis (JRA), or sometimes anterioruveitis. The HLA-B27 test is not a definitive test that can be used to diagnose or rule out a disorder. It is one piece of evidence used along with the evaluation of signs,symptoms, and other laboratory tests to support or rule out the diagnosis of certain autoimmune disorders, such as ankylosing spondylitis and reactive arthritis.

Ankylosing spondylitis and reactive arthritis are both chronic, progressive conditions that occur more frequently in men than women. The first symptoms typically occur when a person is in their early 30's. Often, the initial symptoms of these autoimmune disorders are subtle and may take several years before characteristic degenerative changes to bones and joints are visible on X-rays.

Ankylosing spondylitis is characterized by pain, inflammation, and a gradual stiffening of the spine, neck and chest.Reactive arthritis is a group of symptoms that includes inflammation of the joints,urethra, and eyes as well as skin lesions.Juvenile rheumatoid arthritis is a form ofarthritis that occurs in children.Anterior uveitis is associated with recurring inflammation of the structures of one or both eyes.

The HLA-B27 test may be ordered as part of a group of tests used to diagnose and evaluate conditions causing arthritis-like chronic joint pain, stiffness, and inflammation. This group of tests may include an RF (rheumatoid factor) with either an ESR (erythrocyte sedimentation rate) or a CRP (C-reactive protein). HLA-B27 is sometimes ordered to help evaluate someone with recurrent uveitis that is not caused by a recognizable disease process.

When is it ordered?

An HLA-B27 test may be ordered when a person has acute or chronic pain andinflammation in the spine, neck, chest, eyes, and/or joints, and the doctor suspects the cause is an autoimmune disorder that is associated with the presence of HLA-B27. An HLA-B27 may also be ordered when someone has recurrent uveitis.

The HLA-B27 test is not diagnostic, but the results add information, increasing or decreasing the likelihood that the person being evaluated has the suspected autoimmune disorder.

Doctors frequently use the HLA-B27 test result when they suspect ankylosing spondylitis but the disease is in an early stage and the vertebrae in the spine have not yet undergone the characteristic changes that would be seen on X-ray.

What does the test result mean?

If a person is positive for HLA-B27 and has symptoms such as chronic pain,inflammation, and/ or degenerative changes to his bones (as seen on X-ray), then it supports a diagnosis of ankylosing spondylitis, reactive arthritis, or anotherautoimmune disorder that is associated with the presence of HLA-B27. This is especially true if the person is young, male, and if he experienced his first symptoms before the age of 40.

If HLA-B27 is negative, then the marker was not detected. This does not mean, however, that the person tested does not have the suspected condition since people who do not have the HLA-B27 antigen can also develop these autoimmune diseases. Likewise, someone who has the HLA-B27 antigen will not necessarily develop one of these conditions. Researchers are trying to determine what factors contribute to the higher likelihood of people with HLA-B27 developing these particular diseases and what actually triggers them.

Whether or not certain HLA antigens will be present is genetically determined. Their production is controlled by genes that are passed from parents to their children. If two members of the same family are HLA-B27 positive and one of them develops a disease associated with HLA-B27, then the other person is at an increased risk of developing a similar disease.

Is there anything else I should know?

Though the diseases associated with HLA-B27 occur more frequently in men, women can also be affected. However, the signs and symptoms related to the diseases can often be milder in women.

With new genetic testing methods, it is now possible to separate HLA-B27 into subtypes. So far, more than 70 different subtypes have been identified, such as HLA B27*05 and HLA B27*02. How the presence of these specific subtypes affects the likelihood of developing an autoimmune disease is not yet known

About our DNA ?!

PREVALENCE The prevalence of HLA-B27 varies between populations— from 50% in Haida Indians to 0/ nil in Australian Aborigines. In the UK general population it is about 8%. HLA-B27 is rare in the American black population whereas Eskimo populations carry it much more frequently than Western Europeans, with prevalence rates of 25% or more. This antigen is associated with ankylosing spondylitis in virtually all racial groups studied.  PATHOGENESIS HLA-B27 positive Caucasians have a 20-fold risk of developing any spondylarthropathy, particularly ankylosing spondylitis and undifferentiated spondarthritis. Family and twin studies of ankylosing spondylitis have shown a polygenic pattern of genetic susceptibility with heritability in excess of 90%. The contribution of HLA-B27 to genetic susceptibility has been estimated to be 20–50% of the total. Other HLA alleles, most notably HLA-B60 and HLA-DR1, may predispose to ankylosing spondylitis either independently of B27 or in conjunction with it. MECHANISMS The main natural function of HLA-B27 is to form a complex with β2microglobulin which can bind short antigenic peptides such as those derived from intracellular microorganisms. Following presentation at the cell surface, the complexes are specifically recognised by cytotoxic lymphocytes which then kill the infected cell. Viral?/Organisms have been shown to trigger reactive arthritis, including Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia, Mycobacteria and possibly Brucella, all of which habitually survive intracellularly. HLA-B27 appears to enhance the invasion of Salmonella into intestinal epithelial cells. PREDICTIVE {Insert genome suscept. -first degree} Generally, the value of testing for HLA-B27 depends upon the particular clinical situation. Beginning with a clinical estimate of the likelihood of ankylosing spondylitis or a related spondarthropathy. Seronegative Spondarthritides Ankylosing spondylitis Reactive arthritis (Reiter’s syndrome) Psoriatic arthropathy Enteropathic arthropathy Acute anterior uveitis Juvenile spondarthritis Undifferentiated spondarthritis Isolated peripheral enthesitis ASSOCIATIONS HLA-B27 and ankylosing spondylitis remains the strongest known relationship between a major histocompatibility complex (MHC) antigen and a disease! Enthesitis, defined as inflammation of the origin and insertion of ligaments, tendons, aponeuroses, annulus fibrosis and joint capsules, is a hallmark. The concept of entheseal organ prone to pathological changes in spondyloarthritis is well recognized. The relevant role of peripheral enthesitis is supported (heel pain or other well-defined enthesopathic pain), axial and peripheral spondyloarthritis. Episodes of Achilles tendinitis, plantar fasciitis, posterior tibial tendinitis, & dactylitis. Also seen are lateral epicondyle, insertion of the patella tendon into the inferior pole of the patella, femoral quadriceps, and posterior tibial tendons. {continue}Hip disfunct: Upper lobe fibrosis is the lung condition best known to correlate with HLA-B27. The antigen may be positively, neutrally or negatively associated with asbestosis. Claims have also been made for an association with other pulmonary diseases, especially pleurisy, pleural abscess, bronchitis and pneumonia and pneumothorax, independently of the presence of ankylosing spondylitis. Aortic regurgitation occurs in 2–10% of patients with ankylosing spondylitis, and cardiac conduction abnormalities including atrioventricular and intraventricular blocks have been found in one-third of patients with spondylitis. HLA-B27 related cardiac lesions may be found in the absence of other rheumatological manifestations. Indeed, an HLA-B27 associated cardiac syndrome comprising severe cardiac conduction system abnormalities and lone aortic regurgitation has been defined, whose link with B27 is almost as strong as that between B27 and ankylosing spondylitis. Significant association has been reported between HLA-B27 and acute leukaemia, particularly acute myeloid leukaemia.HLA-B27 carriers may have an increased risk of acute leukaemia whilst those with concomitant ankylosing spondylitis may be predisposed to lymphoid malignancies. While infection with HIV predisposes to spondyloarthropathy,HLA-B27 is the HLA class I molecule most closely associated with non-progression of HIV infection to AIDS. HLA-B27 can be helpful in a patient complaining of low back pain of an inflammatory character in the absence of radiological signs of sacroiliitis or in patients with an asymmetrical oligoarthritis but without other features of spondarthritis. This has been acknowledged with the inclusion of HLA-B27 positivity as a criterion in the Amor classification criteria for spondyloarthropathy. Likewise, testing for HLA-B27 can help to differentiate between alternative aetiologies in iritis and aortic regurgitation. PROGNOSTIC VALUE Whereas HLA-B27 does not seem to influence the severity of ankylosing spondylitis, in psoriatic spondylarthropathy it may determine not only susceptibility to the condition but also its clinical expression. It correlates most strongly with isolated axial disease and it may confer some protection against peripheral joint erosions. Patients with Reiter’s disease and Yersinia andSalmonella triggered reactive arthritis who are HLA-B27 positive have more severe acute disease, more extra-articular features and more frequent chronic back pain and sacro-iliitis. In C. trachomatis reactive arthritis, more severe or chronic disease could be due to lower concentrations of interferon-γ in the synovial fluid of patients who are HLA-B27 positive than those who are HLA-B27 negative, with consequent impaired clearance of infective agents. With regard to cardiac disease, the relative risk that a HLA-B27 positive man will need a permanent pacemaker has been calculated to be 6.7 compared with a man who has other B alleles. This association is not, however, present in female patients. A poor outcome of back surgery has been found in patients possessing HLA-B27. Atlanto-axial subluxation can occur. HLA-B27 positive patients with rheumatoid arthritis have about twice the risk of developing subluxation of the cervical spine and an almost threefold risk of subaxial subluxation. Thus, HLA-B27 may transpire to be a useful prognostic indicator for the later development of instability of the cervical spine and its complications in rheumatoid arthritis. The discovery of the link between HLA-B27 and a large family of inflammatory rheumatic diseases was one of the seminal advances in rheumatology in the last century. Associations have subsequently been identified with other musculoskeletal and non-rheumatic diseases.

Great GrandParents Rena Bell Burgess & James "Murphy" Morris

Rena Bell Burgess
Married
James Murphy Morris

(Georgetown, SC ~ also where the paternal side of my tree hails from)

 

/aka; Murphy Howard on the attached link(s).

(Last Name taken forward was Morris although tree indicates otherwise

>ie: Hazel Howard

 vs. Hazel Morris,  middle daughter, my grandmother)

 

Mammy & Apo; as we referred to my Great Grandparents, would have been first cousins (once removed)... Not unusual for the times!

Check your history ~google the Roosevelt's~

there's a great PBS special about Teddy, FDR & Eleanor and even a Mercer that features prominently in the Ken Burns series but, i digress...

 

Murphy/Apo:
(The last name Howard confused as 2 marriages subsequent to his father's death with same surname*  Alice Britt & Sue Morris  -both married men with last name Howard- 

Sue may have brought her younger brother (Apo) into her family but, was actually his sister.

David Morris (died 1905/Apo age 5)
Alice Britt (remarried;  Howard).

 

David's parents/Apo's Paternal Grandparent's were:
Hansford Richard Morris
& Melvina Burgess (had a brother named John W. Burgess)

 

John W. Burgess (Mammy's GrandFather) married to Jane Morris were the parents of
Sarah "Mamie" Morris
who is Rena Bell's/Mammy's Mother.

 

 

| Therefore; Apo's Grandmother Melvina was the sister of Mammy's Grandfather John W.
|Clementina Anderson (mother of both Melvina & John W) is shared GG
| Because they share the same Great - Grandmother they are First Cousins (once removed) as the connection is separated from first degree relative by one generation; a grandparent.

 

Here's a link that will help you track it down for yourself; incase you are related to me on the maternal side .... http://familytreemaker.genealogy.com/users/g/l/a/Louise-S-Gladden/WEBSITE-0001/UHP-1089.html

 

???????????
If I have followed the genome graph correctly indicating I have rcvd DNA from GGrandMother's familial tree,
that come to find out is the same as my GGrandFather's roots, duplicated to their child/my grandmother & passed via my mother..
Does that mean I received multiple copies /defects / mutations
¿???????????? 

Mamie (my great-great grandmother) died in the early 70s I actually have early recollection (&some pics) visiting her in Jax. & growing up my Great GrandParents were very close until deaths (5yrs apart - near the time of my highschool graduation & early 20s, They knew Jacque' as a baby!) & Meemaw still praising God everyday @ 88.. so longevity is not the issue, its the suffering until then...

 

I have not back tracked the other Morris Burgess branch connections further, although there are several... and as mentioned, not unusual for the times; seeing how both sides of my family tree come from the same geographic area I wouldn't be surprised if there was some co-mingling there as well.

 

But, I struggle now with what information is relative and useful & how to pass this on to my heirs (since they already have the stuff... I think I just need to word the disclaimer at this point??)

 

They say if you can find your wound you can begin to heal, I have hit the jackpot recently and am just trying to work it all out.

 

If you read further posts ... just know that most of these articles relate to signs & symptoms that I have utilized in my personal treatment & pursuit of care.  There are only a few narrative type, from the beginning/scroll to the bottom, if you're interested in that kind of thing.

Indeed, there have been no rigorous attempts to define the basic science of UCTD. It is presumed that many of the same immunologic mechanisms that play a role in lupus and rheumatoid arthritis may be involved. Theories in those diseases include a genetic predisposition, which is subsequently triggered by some environmental factor, such as an infection, that is improperly handled by the immune system. This in turn causes the immune system to be "turned up high," or activated, when it shouldn't be and to target the tissues of one's body instead of foreign invaders

http://www.hss.edu/conditions_undifferentiated-connective-tissue-disease-overview.asp

Important to speak to first degree relatives... !

It is important to inform first degree relatives regarding genetic predilection to associated conditions & syndromes in light of a positive HLA B27 result..

http://ghr.nlm.nih.gov/glossary=firstdegreerelative

This information (follow the link re: manifestations & diagnosis of polymyalgia) should have been entitled... Stella!!!

http://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-polymyalgia-rheumatica?source=outline_link&view=text&anchor=H5#H5

Arthritis, Diagnosing, Treatment (s) AU {spondyloarthropathy}

General Practice
Recognition (types)/Treatment/Referral...

http://murtagh.fhost.com.au/html/general_practice/9780070134591_001_ch35.htm

Cutaneous Fistulas Overview

I am looking into this after a series of occurrences (which may or may not be related; shingles type rash on back (2yr), carbunkle (1yr), basal cleft sinus (6wks)) most recent a sinus drain of crystalline amber fluid from a small cutaneous opening directly between my eyes.

http://emedicine.medscape.com/article/1077808-overview#showall

Vertigo explained (HLA B27 association Meniere)

http://experts.umn.edu/pubDetail.asp?n=Peter+A+Santi&u_id=2444&oe_id=1&o_id=23&id=77951517783

http://www.mayoclinic.org/diseases-conditions/menieres-disease/basics/definition/con-20028251

Seronegative Arthritis /HLA B27

(3rd Party Info.) illness is suggestive of spondyloarthropathy.

What Is Seronegative Spondyloarthropathy?
In the broadest sense, the term spondyloarthropathy includes joint involvement of vertebral column from any type of joint disease, including rheumatoid arthritis and osteoarthritis.  But the term seronegative  spondyloarthropathy is often used for a specific group of disorders with certain common features.  You can group yourself under this seronegative spondylarthropathies. 

Typically, patients of this group have an increased incidence of HLA-B27, as well as negative rheumatoid factor and anti-nuclear antibodies (ANA).

Seronegative spondyloarthropathy can further be of various types, such asankylosing spondylitis,  psoriatic arthritis with associated skin problems, spondylitis with associated inflammatory bowel or Crohn’s disease and reactive arthritis.

How to Diagnose Seronegative Spondyloarthropathy?
The presence of following characteristic features helps concluding a diagnosis:

Asymmetric peripheral arthritis(which serves as an important distinguishing factor with rheumatoid arthritis) is present. Any joint big or small can be affected.
Lower back pain is the most common clinical presentation. This back pain is unique because it decreases with activity.There is a relation to HLA-B27.
Inflammatory arthritis, generallysacroiliitis (hip girdle) and spondylitis (lumbar spine) is often there.Enthesitis (inflammation of the sites where tendons or ligaments insert into the bone) is there. For example,joints of the ribs. Patient feels pain on chest expansion.
The disease condition often runs in the family.
Rheumatoid factor is not present. Blood test for RF and ANA is negative.
Extra-articular features, such as involvement of eyes, skin and genitourinary tract may be found.
ESR and other acute-phase reactants (eg, C-reactive protein) are inconsistently elevated in patients in patients with active disease.

Diagnosis is confirmed by a rheumatologist after examination and blood work, showing negative RF and ANA. Increased ESR and other acute-phase reactants.

Presence of HLA B-27 may or may not be confirmed. Long standing ankylosing spondylitis may also lead to the fusion of vertebrae known as bamboo spine.

Treatment

Medications to reduce pain and suppress joint inflammation and muscle spasm are the first to be given. They increase the range of motion, which facilitates exercise and prevents contractures. Most NSAIDs do work and tolerance and toxicity towards them dictate the drug choice.The daily dose of NSAIDs should be as low as possible, but maximum doses may be needed with active disease. Drug withdrawal should be attempted only slowly, after systemic and joint signs of active disease have been suppressed for several months.Another drug called sulfasalazine may help reduce peripheral joint inflammation. Dosage should be started at 500 mg/day and increased by 500 mg/day at 1-wk intervals to 1 to 1.5 g bid maintenance.Methotrexate is another drug which has to be given judiciously, but is quite effective in this illness.Systemic corticosteroids are sometimes used. Intra-articular depot corticosteroids may be given, particularly when one or two peripheral joints are more severely inflamed than others; like injecting corticosteroids into the sacroiliac joints (hip girdle).

Treatment differs from case to case. All you need is an expert rheumatologist.

Physiotherapy
For proper posture and joint motion, daily exercise and other supportive measures (eg, postural training, therapeutic exercise) are vital to strengthen muscle groups that oppose the direction of potential deformities (ie, the extensor rather than flexor muscles).

Reading while lying prone and pushing up on the elbows or pillows and thus extending the back may help keep the back flexible.Because chest wall motion can be restricted, which impairs lung function, cigarette smoking, which also impairs lung function, is strongly discouraged.Heat may be used for stiffness, including hot baths and warm showers.Ice packs can be put over swellings.Some patients feel comfort with gentle massage therapy.Electrical stimulators are tried for pain (TENS or TNS units).Losing weight to lessen stress on joints usually help.

Seronegative Arthritis /HLA B*27

(3rd Party Info.) illness is suggestive of spondyloarthropathy.

What Is Seronegative Spondyloarthropathy?

In the broadest sense, the term spondyloarthropathy includes joint involvement of vertebral column from any type of joint disease, including rheumatoid arthritis and osteoarthritis.  But the term seronegative  spondyloarthropathy is often used for a specific group of disorders with certain common features.  You can group yourself under this seronegative spondylarthropathies. Typically, patients of this group have an increased incidence of HLA-B27, as well as negative rheumatoid factor and anti-nuclear antibodies (ANA).

Seronegative spondyloarthropathy can further be of various types, such asankylosing spondylitis,  psoriatic arthritis with associated skin problems, spondylitis with associated inflammatory bowel or Crohn’s disease and reactive arthritis.

How to Diagnose Seronegative Spondyloarthropathy?

The presence of following characteristic features helps concluding a diagnosis:

Asymmetric peripheral arthritis(which serves as an important distinguishing factor with rheumatoid arthritis) is present. Any joint big or small can be affected.Lower back pain is the most common clinical presentation. This back pain is unique because it decreases with activity.There is a relation to HLA-B27.Inflammatory arthritis, generallysacroiliitis (hip girdle) and spondylitis (lumbar spine) is often there.Enthesitis (inflammation of the sites where tendons or ligaments insert into the bone) is there. For example,joints of the ribs. Patient feels pain on chest expansion.The disease condition often runs in the family.Rheumatoid factor is not present. Blood test for RF and ANA is negative.Extra-articular features, such as involvement of eyes, skin and genitourinary tract may be found.ESR and other acute-phase reactants (eg, C-reactive protein) are inconsistently elevated in patients in patients with active disease.

Diagnosis is confirmed by a rheumatologist after examination and blood work, showing negative RF and ANA. Increased ESR and other acute-phase reactants. Presence of HLA B-27 may or may not be confirmed. Long standing ankylosing spondylitis may also lead to the fusion of vertebrae known as bamboo spine.

Treatment

Medications to reduce pain and suppress joint inflammation and muscle spasm are the first to be given. They increase the range of motion, which facilitates exercise and prevents contractures. Most NSAIDs do work and tolerance and toxicity towards them dictate the drug choice.The daily dose of NSAIDs should be as low as possible, but maximum doses may be needed with active disease. Drug withdrawal should be attempted only slowly, after systemic and joint signs of active disease have been suppressed for several months.Another drug called sulfasalazine may help reduce peripheral joint inflammation. Dosage should be started at 500 mg/day and increased by 500 mg/day at 1-wk intervals to 1 to 1.5 g bid maintenance.Methotrexate is another drug which has to be given judiciously, but is quite effective in this illness.Systemic corticosteroids are sometimes used. Intra-articular depot corticosteroids may be given, particularly when one or two peripheral joints are more severely inflamed than others; like injecting corticosteroids into the sacroiliac joints (hip girdle).

Treatment differs from case to case. All you need is an expert rheumatologist.

Role of Physiotherapy

For proper posture and joint motion, daily exercise and other supportive measures (eg, postural training, therapeutic exercise) are vital to strengthen muscle groups that oppose the direction of potential deformities (ie, the extensor rather than flexor muscles).

Reading while lying prone and pushing up on the elbows or pillows and thus extending the back may help keep the back flexible.Because chest wall motion can be restricted, which impairs lung function, cigarette smoking, which also impairs lung function, is strongly discouraged.Heat may be used for stiffness, including hot baths and warm showers.Ice packs can be put over swellings.Some patients feel comfort with gentle massage therapy.Electrical stimulators are tried for pain (TENS or TNS units).Losing weight to lessen stress on joints usually help.

B type HLA = Native American

http://ldsmag.com/ldsmag/ancients/050712dna2.html

HLA Studies

Another method of tracing the origin of some of one’s ancestors is to examine the human lymphocyte antigens (HLAs) that make up the immune system. HLAs are proteins or white blood cells produced by specific genes passed from parent to child. In recent years, medical experts have had to pay more attention to these HLAs because they, like blood types (A, B, AB, O) and other blood characteristics (Rhesus, Kell, and Duffy), play a role in the rejection of transplanted organs.

The actual number of human alleles responsible for HLAs is relatively small. According to a recent study by James L. Guthrie,

some isolated South American tribes possess only a few types that are common throughout the Americas. But other groups, especially those near sites of former Mesoamerican and Andean urban societies, exhibit HLA alleles that are rare in America but common in certain Afro-Asiatic, southern Asian, and European populations. These unexpected genes account, on the average, for 6-7% of the [Native] American HLA total, but range as high as 24% [in some groups]. The atypical genes are postulated to have been acquired by assimilation of foreign populations in various times after initial colonization of the hemisphere but prior to the sixteenth-century influx of Europeans and Africans, because they suggest gene-flow from places that were, according to some scholars, in ancient contact with the Americas, such as North Africa and Southeast Asia. [28]

Guthrie notes that “This diversity gives population geneticists a powerful tool for tracing ancient migrations, and, at present, HLA distributions are more informative in this regard  than are any other genetic system except DNA.” [29] At the time the article was published in 2001, there were, worldwide, “29 HLA families for which there are enough data to construct useful distribution maps,” with “many more types that are less well mapped at the present time.” [30] “Only twelve type-A and 17 type-B HLAs were sufficiently well sampled for useful worldwide comparison,” and there were some geographical regions that were not well represented by the sampling. [31]

Native American populations “near the urban societies of Mesoamerica and the Andes have the most” HLA alleles (up to 26), while “some marginal tribes of South America have the fewest. The degree of HLA diversity in a population may be a measure of its former size and cosmopolitan nature.” [32] Four of the type-A HLAs account for 94% of the American HLA-A total, while six of the type-B HLAs account for 93% of the HLA-B total, and these are to be considered as markers for Native Americans. Significantly, “some [isolated] South American tribes apparently have only these alleles, whereas those near former urban centers tend to have significant percentages of HLAs that now are most common in the Near East, India, Africa, Northwest Europe, or Southeast Asia (including Pacific Oceania),” and hence are due to admixture with outside groups. [33]

While “some anomalies may be explainable as recent admixtures ... the apparently foreign HLA alleles are usually less characteristic of Spain, Portugal, or West Africa than of places alleged [by some archaeologists and linguists] to have had earlier contact, such as Pacific Oceania, North Africa, or Southwest Asia [i.e., the Near East].” [34] On the basis of HLA distribution, Guthrie postulates ties to various parts of the Old World. Here, we shall deal only with possible ties to the ancient Near East. Of the 18 “non-Indian” alleles, the 9 that seem to have originated among Afro-Asiatic peoples (i.e., the Near East and North Africa) account for 47% of the total found in Native American populations, with 28% from the 5 southern Asian alleles and 25% from the 4 European. [35]

Guthrie notes that the highest world frequencies of Afro-Asiatic HLAs are represented by alleles B*21, A*32, and A*30, attested in Middle Eastern populations of Saudi Arabia, Jordan/Palestine, [36] the Berber and Tuareg of North Africa, and the Tigre of Ethiopia (where Semitic languages distantly related to Arabic and Hebrew are still spoken). [37] Significantly, all three of these alleles are attested in Central America in the range of 6.5-7.5%. Alleles A*32 and A*30 appear in even higher percentages in Samoa than in the Near East. [38]

Guthrie notes that “Central Amerind composite sample is unique in that all of its ‘non-Indian’ HLAs are of the Afro-Asiatic set” and concludes that “significant Afro-Asiatic contact with western Mexico and/or the Caribbean region almost certainly occurred, probably from Arabia or North Africa.” [39] According to Guthrie, of the foreign alleles, “A*33 seems to trace movement of a Near-Eastern population to Southeast Asia and South America,” [40]and contributes “70-80% to the second principal component, with its strongest effect in eastern North America and Panama.” [41]

He warns that, “Because human distributions have changed with time, arguments based on the present situation are not convincing unless combined with other kinds of evidence,” [42] by which he, being a diffusionist, means archaeological and linguistic findings that suggest to some scholars that there were Old World/New World contacts in precolumbian times.

HLA B27 positive

What It's LIke to Live with Ankylosing Spondylitis: http://youtu.be/RkyuphVynPA