The word Paleo means ancient or older. The Paleo diet, as its name states, is a diet based around focusing on foods that have been eaten by humans for thousands of years during their evolution. Foods that existed before the introduction of agriculture. These foods are fresh and free of any added preservatives, mainly consisting of vegetables and meats. Paleo advocates claim that this way of eating can improve all aspects of your health, including your weight, reduction of disease activity and prevention of some chronic diseases like heart disease and type 2 diabetes. The Paleo diet provides that we should be eating what heals and supports our immune system. This diet includes diet the following diet recommendations as shown in the above graphic:
Hormonal mechanisms could explain the increased incidence of SLE in females. The onset of SLE could be attributed to the elevated hydroxylation of estrogen and the abnormally decreased levels of androgens in females. In addition, differences in GnRH signalling have also shown to contribute to the onset of SLE. While females are more likely to relapse than males, the intensity of these relapses is the same for both sexes.[12]
DHEA (dehydroepiandrosterone) has been helpful in reducing fatigue, improving thinking difficulties, and improving quality of life in people with SLE. Recent research indicates that DHEA diet supplementation has been shown to improve or stabilize signs and symptoms of SLE. DHEA is commonly available in health-food stores, pharmacies, and many groceries.
Neurological disorders contribute to a significant percentage of morbidity and mortality in people with lupus.[37] As a result, the neural side of lupus is being studied in hopes of reducing morbidity and mortality rates.[30] One aspect of this disease is severe damage to the epithelial cells of the blood–brain barrier. In certain regions, depression affects up to 60% of women with SLE.[38]
Kaposi observed that lupus assumed two forms: the skin lesions (now known as discoid lupus) and a more aggravated form that affected not only the skin but also caused fever, arthritis, and other systemic disorders in people.[112] The latter also presented a rash confined to the face, appearing on the cheeks and across the bridge of the nose; he called this the "butterfly rash". Kaposi also observed those patients who developed the "butterfly rash" (or malar rash) often were afflicted with another disease such as tuberculosis, anemia, or chlorisis which often caused death.[110] Kaposi was one of the first people to recognize what is now termed systemic lupus erythematosus in his documentation of the remitting and relapsing nature of the disease and the relationship of skin and systemic manifestations during disease activity.[113]
The modern period, beginning in 1920, saw major developments in research into the cause and treatment of discoid and systemic lupus. Research conducted in the 1920s and 1930s led to the first detailed pathologic descriptions of lupus and demonstrated how the disease affected the kidney, heart, and lung tissue.[115] A major breakthrough was made in 1948 with the discovery of the LE cell (the lupus erythematosus cell—a misnomer, as it occurs with other diseases as well). Discovered by a team of researchers at the Mayo Clinic, they discovered that the white blood cells contained the nucleus of another cell that was pushing against the white's cell proper nucleus.[116] Noting that the invading nucleus was coated with antibody that allowed it to be ingested by a phagocytic or scavenger cell, they named the antibody that causes one cell to ingest another the LE factor and the two nuclei cell result in the LE cell.[117] The LE cell, it was determined, was a part of an anti-nuclear antibody (ANA) reaction; the body produces antibodies against its own tissue. This discovery led to one of the first definitive tests for lupus since LE cells are found in approximately 60% of all people diagnosed with lupus.[118] The LE cell test is rarely performed as a definitive lupus test today as LE cells do not always occur in people with SLE and can occur in individuals with other autoimmune diseases. Their presence can be helpful in establishing a diagnosis but no longer indicates a definitive SLE diagnosis.
The medical doctors who treat lupus are rheumatologists who specialize in arthritis and other inflammatory disorders. However, depending on the individual, case treatment may involve a wide range of health professionals including clinical immunologists (doctors specializing in immune system disorders), nurses, psychologists, social workers, nephrologists (kidney disease specialists), hematologists (specialists in blood disorders), dermatologists, and neurologists.
Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium). This prevents the heart ventricles from expanding fully. The excess pressure from the fluid prevents the heart from working properly. As a result, the body does not get enough blood.
Inflammation of the heart muscle, usually in the U.S. as a consequence of infections (viruses, esp. coxsackie virus, and occasionally as a consequence of bacterial, protozoan or fungal infections); immunological-rheumatological conditions (e.g., systemic lupus erythematosus, ulcerative colitis, hypersensitivity reactions, or transplant rejection); exposure to chemicals or toxins (e.g., cocaine, doxorubicin, methamphetamine); nutritional or metabolic abnormalities (e.g., thiamine deficiency or hypophosphatemia); or radiation. Myocarditis also is occasionally found in pregnancy and with advanced age. The myocardium is infiltrated by leukocytyes, lymphocytes, and macrophages, leading to inflammation, necrosis of muscle cells, and fibrosis. Inflammatory damage to heart muscle fibers may resolve spontaneously or may cause progressive deterioration of the heart with pericarditis, arrhythmias, chronic dilated cardiomyopathy, and heart failure.
Jump up ^ Smyth, Andrew; Guilherme H.M. Oliveira; Brian D. Lahr; Kent R. Bailey; Suzanne M. Norby; Vesna D. Garovic (November 2010). "A Systematic Review and Meta-Analysis of Pregnancy Outcomes in Patients with Systemic Lupus Erythematosus and Lupus Nephritis". Clinical Journal of the American Society of Nephrology. 5 (11): 2060–2068. doi:10.2215/CJN.00240110. PMC 3001786. PMID 20688887. Archived from the original on 2016-01-26.
Infections and diseases of the cardiovascular, renal, pulmonary, and central nervous systems are the most frequent causes of death in patients with systemic lupus erythematosus.8,23,32–37 Since the 1950s, the five-year survival rate for patients with systemic lupus erythematosus has increased from 50 percent to a range of 91 to 97 percent.8,23,32–34,38,39 It is not known how much of this increase in survival is due to improved management versus diagnosis of earlier and milder disease. Higher mortality rates are associated with seizures, lupus nephritis, and azotemia.36,37,40
An antibody, produced by B cells in response to an altered autoantigen on one type of the body’s own cells, that attacks and destroys these cells. Autoantibodies are the basis for autoimmune diseases such as rheumatoid arthritis and diabetes mellitus. Several theories exist about why autoantibodies are formed. The most common theory proposes that AAbs develop as the result of a combination of hereditary and environmental risk factors that cause an autoantigen to be falsely recognized as alien by B cells; as a result, antibodies are produced for its destruction.
In SLE patients with serious brain (lupus cerebritis) or kidney disease (lupus nephritis), plasmapheresis is sometimes used to remove antibodies and other immune substances from the blood to suppress immunity. Plasmapheresis is a process of removing blood and passing the blood through a filtering machine, then returning the blood to the body with its antibodies removed. Rarely, people with SLE can develop seriously low platelet levels, thereby increasing the risk of excessive and spontaneous bleeding. Since the spleen is believed to be the major site of platelet destruction, surgical removal of the spleen is sometimes performed to improve platelet levels. Other treatments have included plasmapheresis and the use of male hormones.
Certain people may need to follow a slightly different diet. For example, pregnant women need to avoid eating certain foods; people with lupus nephritis (lupus affecting the kidneys) need to follow advice from their hospital dietician; and dietary advice for people over 60 and for children of various ages may also be different. The British Nutrition Foundation provides further advice and information about healthy eating and alternative diets. You can also find a lot more information in the links for further reading at the end of this article.

An increase in the size of an organ, structure, or the body due to growth rather than tumor formation. This term is generally restricted to an increase in size or bulk that results not from an increase in the number of cells but from an increase in a cellular component, e.g., proteins. It applies to any increase in size as a result of functional activity.
In more severe cases, medications that modulate the immune system (primarily corticosteroids and immunosuppressants) are used to control the disease and prevent recurrence of symptoms (known as flares). Depending on the dosage, people who require steroids may develop Cushing's syndrome, symptoms of which may include obesity, puffy round face, diabetes mellitus, increased appetite, difficulty sleeping and osteoporosis. These may subside if and when the large initial dosage is reduced, but long-term use of even low doses can cause elevated blood pressure and cataracts.
Systemic lupus erythematosus is a multisystem inflammatory disease that is often difficult to diagnose. Before the diagnosis can be established, four of 11 clinical and laboratory criteria must be met. Antinuclear antibody titer is the primary laboratory test used to diagnose systemic lupus erythematosus. Because of the low prevalence of the disease in primary care populations, the antinuclear antibody titer has a low predictive value in patients without typical clinical symptoms. Therefore, as specified by the American College of Rheumatology, this titer should be obtained only in patients with unexplained involvement of two or more organ systems. Pa tients with an antinuclear antibody titer of 1:40 and characteristic multiorgan system involvement can be diagnosed with systemic lupus erythematosus without additional testing; however, patients with an antibody titer of 1:40 who fail to meet full clinical criteria should undergo additional testing, including tests for antibody to doublestranded DNA antigen and antibody to Sm nuclear antigen. While an antinuclear antibody titer of less than 1:40 usually rules out systemic lupus erythematosus, patients with persistent, characteristic multisystem involvement may be evaluated for possible antinuclear antibody–negative disease.
Useful medication for the disease was first found in 1894, when quinine was first reported as an effective therapy. Four years later, the use of salicylates in conjunction with quinine was noted to be of still greater benefit. This was the best available treatment until the middle of the twentieth century, when Hench discovered the efficacy of corticosteroids in the treatment of SLE.[121]
Hydroxychloroquine (Plaquenil) is an antimalarial medication found to be particularly effective for SLE people with fatigue, skin involvement, and joint disease. Consistently taking Plaquenil can prevent flare-ups of lupus. Side effects are uncommon but include diarrhea, upset stomach, and eye-pigment changes. Eye-pigment changes are rare but require monitoring by an ophthalmologist (eye specialist) during treatment with Plaquenil. Researchers have found that Plaquenil significantly decreased the frequency of abnormal blood clots in people with systemic lupus. Moreover, the effect seemed independent of immune suppression, implying that Plaquenil can directly act to prevent the blood clots. This fascinating study highlights an important reason for people and doctors to consider Plaquenil for long-term use, especially for those SLE people who are at some risk for blood clots in veins and arteries, such as those with phospholipid antibodies (cardiolipin antibodies, lupus anticoagulant, and false-positive venereal disease research laboratory test). This means not only that Plaquenil reduces the chance for re-flares of SLE, but it can also be beneficial in thinning the blood to prevent abnormal excessive blood clotting. Plaquenil is commonly used in combination with other treatments for lupus.
Corticosteroids, such as prednisone, hydrocortisone, methylprednisolone, and dexamethasone, are related to cortisol, which is a natural anti-inflammatory hormone. They work by rapidly suppressing inflammation. Corticosteroids can be given by mouth, in creams applied to the skin, by injection, or by intravenous (IV) infusion (dripping the drug into the vein through a small tube). Because they are potent drugs, the doctor will seek the lowest dose required to achieve the desired benefit.
Neonatal lupus Technically neonatal lupus is not a form of lupus. The condition is the result of autoantibodies passing from a pregnant woman with lupus (or related condition) through the placenta and to the baby developing in the womb, causing mostly temporary symptoms, explains Virginia Pascual, MD, the director of the Gale and Ira Drukier Institute for Children’s Health at Weill Cornell Medicine in New York City. Some infants are born with symptoms, such as skin rash, liver problems, or white blood cell counts. But those symptoms disappear within a few months and leave no lasting effects.
Lupus disease, especially when active, could lead to accelerated atherosclerosis (clogging of the arteries) which can develop in young women and could also lead to heart attacks, heart failure, and strokes. Thus, it is vital that patients with lupus, in addition to controlling their disease, exercise and lower other risk factors for heart disease, such as smoking, high blood pressure, and high cholesterol.
The aim of this review is to provide an up-to-date overview of treatment approaches for systemic lupus erythematosus (SLE), highlighting the multiplicity and heterogeneity of clinical symptoms that underlie therapeutic decisions. Discussion will focus on the spectrum of currently available therapies, their mechanisms and associated side-effects. Finally, recent developments with biologic treatments including rituximab, epratuzumab, tumor necrosis factor (TNF) inhibitors, and belimumab, will be discussed.
A skeletal disorder characterized by compromised bone strength predisposing to an increased risk of fracture. Bone strength reflects the integration of two main features: bone density and bone quality. Bone density is expressed as grams of mineral per area or volume and in any given individual is determined by peak bone mass and amount of bone loss. Bone quality refers to architecture, turnover, damage accumulation (e.g., microfractures) and mineralization. A fracture occurs when a failure-inducing force (e.g., trauma) is applied to osteoporotic bone. Thus, osteoporosis is a significant risk factor for fracture, and a distinction between risk factors that affect bone metabolism and risk factors for fracture must be made.
Vitamin tablets and supplements are not an alternative to eating healthily. It is always wise to talk with your GP or consultant about what supplements you wish to take as they can have a serious effect on some medications you may be on, such as warfarin. They may also suggest that you supplement your diet if they find that there is a deficiency. If you eat a good balance, particularly of fruit and vegetables, this should give you sufficient vitamins. It is relatively easy to overdose on the fat-soluble vitamins and this can be dangerous to your health (particularly vitamin A) as well as wasting your money.
Lupus, also known as Systemic Lupus Erythematosus or SLE, is a complex disease that can be difficult to diagnose. It affects many areas of body including the joints, skin and kidneys. More than 200,000 people in the U.S. are diagnosed with lupus each year.  Like other autoimmune diseases, in lupus, cells essentially make the bad decision to attack the body’s own cells.
The monoclonal antibody belimumab (Benlysta), a B-lymphocyte stimulator–specific inhibitor, has been found to reduce disease activity and possibly decrease the number of severe flares and steroid use in patients with SLE when used in combination with standard therapy. [114] In March, 2011, the US Food and Drug Administration (FDA) approved the use of belimumab in combination with standard therapies (including steroids, nonbiologic DMARDS [eg, hydroxychloroquine, azathioprine, methotrexate]) to treat active autoantibody-positive SLE. [115]  In July 2017, a subcutaneous (SC) formulation was approved that allows patients to self-administer a once-weekly dose. [162]
ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE.[10] The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases.[10] Other ANA that may occur in people with SLE are anti-U1 RNP (which also appears in systemic sclerosis and mixed connective tissue disease), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögren's syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.[71]
While there is no cure for lupus, there are treatments that can help prevent flares, treat symptoms and reduce organ damage. Early diagnosis and treatment is the key to successful management of lupus. Treatment depends on the type and severity of the symptoms. Like all medications, these treatments have potential side effects. It is very important that you communicate with your health care professional about the potential benefits and potential side effects of any treatment.
Kaposi observed that lupus assumed two forms: the skin lesions (now known as discoid lupus) and a more aggravated form that affected not only the skin but also caused fever, arthritis, and other systemic disorders in people.[112] The latter also presented a rash confined to the face, appearing on the cheeks and across the bridge of the nose; he called this the "butterfly rash". Kaposi also observed those patients who developed the "butterfly rash" (or malar rash) often were afflicted with another disease such as tuberculosis, anemia, or chlorisis which often caused death.[110] Kaposi was one of the first people to recognize what is now termed systemic lupus erythematosus in his documentation of the remitting and relapsing nature of the disease and the relationship of skin and systemic manifestations during disease activity.[113]
The term undifferentiated connective tissue diseases is used to define conditions characterized by the presence of signs and symptoms suggestive of a systemic autoimmune disease that do not satisfy the classificative criteria for defined connective tissue diseases (CTD) such as systemic lupus erythematosus (SLE), Sjögren’s syndrome (SS), rheumatoid arthritis (RA) and others. A small percentage of patients presenting with an undifferentiated profile will develop during the first year follow up of a full blown CTD, however an average of 75% will maintain an undifferentiated clinical course. These patients may be defined as having a stable undifferentiated connective tissue diseases (UCTD). The most characteristic symptoms of UCTD are represented by arthritis and arthralgias, Raynaud’s phenomenon, leukopenia, while neurological and kidney involvement are virtually absent. Eighty percent of these patients have a single autoantibody specificity, more frequently anti-Ro and anti-RNP antibodies. Stable UCTD are considered as distinct clinical entities and therefore it has been proposed to define those conditions as UCTD. Classificative criteria have also been proposed and a work to better define them is still under way.

In this presentation, Ms. Everett covers the relationship of diet and nutritional considerations and lupus, osteoporosis, medication side effects, and vitamins and supplements. This is the first of a two-part presentation. In Part II, Ms. Everett will focus more specifically on nutrition and the importance of heart health and kidney health for people with lupus. Before beginning the presentation, Ms. Everett highlighted that nutrition has become an important area of research in regard to lupus.


Symptoms, causes, and treatment of chronic kidney disease Chronic kidney disease or failure is a progressive loss of kidney function that sometimes occurs over many years. Often the symptoms are not noticeable until the disease is well advanced, so it is essential that people who are at risk of developing kidney problems, such as those with diabetes, have regular check-ups. Read now
I recommend having your MTHFR genes tested, as this genetic mutation can impact how you detoxify mercury and other heavy metals. There are multiple options for heavy metal testing, however I’ve found the DMPS “challenge” test to be the gold standard. To assess whether someone is being exposed to mycotoxins, I use the test from Real Time Lab. If either heavy metals or mycotoxins are an issue for you, work on minimizing your exposure to these toxins, and be sure to support your detox pathways while you work to flush them out.

If your CBC comes back with high numbers of RBCs or a high hematocrit, it could indicate a number of other issues including lung disease, blood cancers, dehydration, kidney disease, congenital heart disease, and other heart problems. High WBCs, called leukocytosis, may indicate an infectious disease, inflammatory disease, leukemia, stress, and more. 


A primary lymphoid organ located in the mediastinal cavity anterior to and above the heart, where it lies over the superior vena cava, aortic arch, and trachea. The thymus comprises two fused lobes, the right larger than the left. The lobes are partially divided into lobules, each of which has an outer cortex packed with immature and developing T lymphocytes (thymocytes) and an inner medulla containing a looser arrangement of mature T lymphocytes.
Next, Ms. Everett reviewed some of the key foods that are important for your diet. She emphasized that balance is essential – that is, to not eat too much of one thing and not enough of another. Different foods have different nutritional components. Included in the important foods that Ms. Everett highlighted were a variety of fruits and vegetables; foods low in calories and saturated fats; and foods high in antioxidants, fiber, calcium, vitamin D, and Omega 3 fatty acids.
And it’s important to point out that people who are initially diagnosed with systemic lupus (or SLE) can also get lupus rashes. One of the common rashes that occurs in people with systemic lupus is malar rash. It’s alternatively called a butterfly rash, and it spreads across the bridge of the nose and cheeks and is telltale sign of the disease because its appearance is so distinctive, Caricchio says. A malar rash can be flat or raised. While it usually isn’t painful, it can itch and burn. (3) And the rash can show up on other parts of the body, including the arms, legs, and torso.
ANA screening yields positive results in many connective tissue disorders and other autoimmune diseases, and may occur in normal individuals. Subtypes of antinuclear antibodies include anti-Smith and anti-double stranded DNA (dsDNA) antibodies (which are linked to SLE) and anti-histone antibodies (which are linked to drug-induced lupus). Anti-dsDNA antibodies are highly specific for SLE; they are present in 70% of cases, whereas they appear in only 0.5% of people without SLE.[10] The anti-dsDNA antibody titers also tend to reflect disease activity, although not in all cases.[10] Other ANA that may occur in people with SLE are anti-U1 RNP (which also appears in systemic sclerosis and mixed connective tissue disease), SS-A (or anti-Ro) and SS-B (or anti-La; both of which are more common in Sjögren's syndrome). SS-A and SS-B confer a specific risk for heart conduction block in neonatal lupus.[71]

If your doctor suspects you have lupus based on your symptoms, a series of blood tests will be done in order to confirm the diagnosis. The most important blood screening test is ANA. If ANA is negative, you don’t have lupus. However, if ANA is positive, you might have lupus and will need more specific tests. These blood tests include antibodies to anti-dsDNA and anti-Sm, which are specific to the diagnosis of lupus.

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Please Note: The material on this site is provided for informational purposes only and is not medical advice. Always consult your physician before beginning any diet or exercise program.

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