Lupus is a chronic inflammatory autoimmune disease with a wide range of clinical manifestations that include multiple organ system effects.
Patients with lupus experience a loss of self-tolerance as a result of abnormal immunological function and the production of autoantibodies (immune proteins that mistakenly attack a person’s own tissues), which lead to the formation of immune complexes that create damage to healthy tissue.
Patients experience periodic flares of varying severity or periods in which no observable signs or symptoms are present (remission).
Although the precise underlying cause of lupus is unknown, genetic, hormonal, and environmental factors, as well as immune abnormalities, have been identified.
Associations between the onset of lupus and age, sex, geography, and race have also been established.
Management of this disease should be individualized and should include both pharmacological and non-pharmacological approaches for symptom relief and resolution, as well as improved quality of life.
Diagnosis of lupus can be challenging and while several classification criteria have been verified, their utility in the clinical setting is still a matter of debate.
Types of Lupus
There are four main classifications of lupus: neonatal, discoid, drug-induced, and systemic lupus erythematosus (SLE).
1) Neonatal Lupus Erythematosus (NLE)
It is a rare form of lupus observed in newborns and results from maternal autoantibodies passing through the placenta, although only 1% of newborns testing positive for autoantibodies end up developing it.
It usually involves the heart, liver, and skin. In most children with neonatal lupus and other organ involvement (e.g. skin, liver, and blood), signs and symptoms often resolve spontaneously within 4 to 6 months .
2) Discoid Lupus Erythematosus (DLE)
It manifests as chronic scarring and atrophic photosensitive dermatosis (skin disease where lesions are formed upon sun exposure), and may progress to systemic lupus erythematosus (SLE), or may occur in patients with pre-existing SLE.
Its cause is thought to be genetic, with the highest prevalence in women, African-Americans, and people between 20 and 40 years of age.
The diagnosis is frequently made through biopsy of a rash on the scalp, face, neck, or arms.
Chemical and physical sunblocks, topical corticosteroids, or antimalarial medications are commonly used to prevent DLE flares and manage symptoms .
3) Drug-induced Lupus (DIL)
It materializes in genetically susceptible individuals after exposure to a medication, causing an autoimmune response .
Various organ systems may be affected.
Hydralazine (Apresoline) was the first agent to be associated with the development of lupus-like symptoms in 1954 .
Since then, more than 100 drugs have been identified as the cause of drug-induced lupus, with the list expanding with the development of newer biologic compounds each year.
Drug-induced lupus (DLE) tends to be less severe than systemic lupus erythematosus (SLE), with symptoms typically resolving after the discontinuation of the offending agent.
4) Systemic Lupus Erythematosus (SLE)
Commonly referred to as “lupus”, systemic lupus erythematosus (SLE) is the most common type of lupus, and differs from the other types, because it affects multiple organ systems.
It has varying clinical presentations ranging from mild mucocutaneous (affecting the skin and mucous membranes) manifestations to multi-organ and severe central nervous system involvement.
The incidence of systemic lupus erythematosus (SLE) or lupus varies among ethnic groups and by geographic location, sex, and age.
It is estimated that systemic lupus erythematosus (SLE) affects 250,000 Americans .
Black people in Africa have a much lower incidence of lupus than African-Americans in the U.S, implying a correlation between lupus and a western-type diet and lifestyle (as in most autoimmune diseases) .
The disease is more severe in African-Americans followed by Asian and Hispanic populations, and then by Caucasians.
Sex and Age
Lupus predominantly affects women of childbearing age, with a female to male ratio of 9 to 1.
The risk, however, decreases after menopause in women despite still being twice as compared to men.
This increased female incidence may be attributed to hormones, namely estrogen, as studies have shown that women who had an early menarche (first occurrence of menstruation), or who used oral contraceptives, or hormonal therapies, had an increased risk for lupus [8, 9].
Concerning men, studies have indicated that although rarer, lupus in males tends to be more harsh and aggressive.
Age plays also an important role in lupus, and although the disease is more common in women of childbearing age, it has been well reported in the pediatric and elderly population.
Lupus is more severe in children, while in the elderly, it tends to have a more insidious onset and more pulmonary involvement and serositis (inflammation of the tissues that line the inside of various organs, such the heart and lungs), but less Raynaud’s disease symptoms (medical condition where there is spasm on the arteries, causing reduced blood flow), malar rash (butterfly-like rash on the cheeks), nephritis (kidney inflammation), and neuropsychiatric complications .
Lupus is a multifactorial disease with unknown exact etiology, however, several genetic, immunological, endocrine, and environmental factors play a role in its pathogenesis.
Studies investigating a potential connection between genetics and lupus have revealed a genetic predisposition within families.
First-degree relatives of patients with lupus have a significantly higher chance of getting the disease compared with the rest of the population.
A study focusing on children of mothers with lupus documented that 27% of 195 children tested positive for antinuclear antibodies (ANAs) .
Multiple studies addressing the incidence of lupus in identical and fraternal twins have confirmed a strong relationship, especially with identical twins.
In another study of non-identical twins, concordance rates of 3% to 10% were reported .
Research on the mechanisms by which genetic factors affect the incidence of lupus has led to the discovery of several gene variants linked to lupus expression.
It seems that a combination of specific genetic variants leads to the clinical manifestation of lupus.
For example, the complement component C1q that eliminates necrotic cellular waste (apoptotic material) in healthy individuals, is often deficient in patients with lupus, leading to disease expression.
A second example of genetic variance is a possible deficiency in complement component 4, a protein identified in the elimination of self-reactive B cells.
When the overall genetic profile of a patient with systemic lupus erythematosus (SLE) is taken into account, the additive effects of these genetic variances significantly increase the risk of disease progression .
The effect of hormones on the speed of occurrence and the severity of lupus has been of particular interest to researchers.
The mechanism by which hormones affect the prevalence of lupus remains unclear.
One hypothesis proposes the potential role of estrogen, progesterone, testosterone, dehydroepiandrosterone (DHEA), and prolactin in immune system responsiveness.
Estradiol in mice has an inhibitory effect on apoptosis (programmed cell death), allowing the survival of B cells that produce high-affinity anti-DNA antibodies .
DHEA, an androgen that is a precursor to testosterone and estrogen, has immunosuppressive properties.
In patients with systemic lupus erythematosus (SLE), DHEA levels may be suboptimal .
Normally, prolactin levels should stay low in both men and women, except during pregnancy and lactation .
The role of the immune system in lupus has to do with the patient’s loss of “self-tolerance.”
The process of phagocytosis (cellular removal mechanism against pathogens and cell debris) is compromised in lupus patients, leading to the inappropriate removal of apoptotic cells and immune complexes.
A hallmark characteristic of lupus is the formation of autoantibodies that go on to form immune complexes (in combination with antigens), leading to inflammation and tissue damage.
Environmental factors affecting the incidence of lupus include certain viruses and ultra-violet (UV) light.
UV light stimulates keratinocytes (the primary type of cells found in the epidermis- the outer layer of the skin) leading to B-cell stimulation and antibody production; it may also stimulate T-cell activity, resulting in additional production of autoantibodies [24, 25, 26].
Epstein–Barr virus (EBV) has also been linked with the onset of lupus in children.
Lupus patients have higher titers of antibodies against EBV .
Smoking, silica exposure, and some hair products (e.g., dyes) may also be possible triggers of lupus.
Symptoms can be complex and widespread, considering the number of organ systems affected by the disease.
Patients experience flare-ups to varying degrees, as well as spontaneous periods of disease remission.
Although certain signs and symptoms are common in lupus, every patient presents with unique symptomatology.
The most common signs and symptoms observed in lupus include fever, fatigue, and weight loss.
Lupus patients who report skin symptoms most commonly exhibit a red rash on their nose and cheeks manifesting after sun exposure.
This butterfly-shaped rash, know as “malar rash”, is characteristically identified in a significant number of lupus patients at some point during the disease course.
Patients reporting photosensitivity reactions also experience skin rashes on other parts of the body that were exposed to the sun.
Other skin-related lupus symptoms include alopecia (hair loss, either in small patches or widespread), Reynaud’s phenomenon (medical condition in which spasms of the arteries cause episodes of reduced blood flow), and sores in the mouth or nose.
Musculoskeletal involvement includes arthralgias (joint paint), myalgias (muscle pain), and/or arthritis.
Patients with pulmonary symptoms report painful breathing, coughing, and shortness of breath.
Pleural effusion (excess fluid build-up between the thin membranes lining the lungs, called pleura) and pulmonary hypertension have also been documented .
Additionally, lupus affects the cardiovascular, nervous, gastrointestinal, renal, and hematological systems.
Cardiovascular effects often include pericarditis (inflammation of the double-walled sac containing the heart, called pericardium), myocarditis (inflammation of the heart muscle, called myocardium), endocarditis (infection of the inner lining of the heart, called endocardium), and coronary artery disease [38, 39].
It has been theorized that certain drugs used to treat lupus (e.g., immunosuppressants and corticosteroids) increase the susceptibility for coronary artery disease in lupus patients, along with the traditional risk factors seen in the general population .
It has been estimated that 20 to 70 percent of people with lupus experience some sort of GI complications at some point in their lives.
This makes digestive issues extremely common among lupus patients, though usually not serious .
Lupus can attack any part of the GI system, including the esophagus, stomach, pancreas, liver, gall bladder, bile ducts, small and large intestine.
It can be challenging for a doctor to identify whether lupus is the direct cause of a particular GI complication or a side effect of a medication or a malfunction of another organ caused by lupus inflammation.
The primary gastrointestinal symptoms present in lupus include GERD (gastroesophageal reflux disease), dysphagia (trouble swallowing), nausea, vomiting, diarrhea, constipation, peritonitis (inflammation of the peritoneum- the membrane that lines the inner abdominal wall and covers the organs within the abdomen), pancreatitis (inflammation of the pancreas), liver disease (e.g., enlarged liver, hepatic vasculitis, autoimmune hepatitis), and peptic ulcers.
Also, drugs used to combat the disease, such as non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids, can oftentimes be the cause of GI disturbances.
Hematological changes reported in lupus include anemia (low red blood cell count), leukopenia (low white-well count), or thrombocytopenia (low platelet count) .
Also, the presence of antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant, and anti-β2 glycoprotein) in lupus patients can lead to thrombosis (blood clot formation in blood vessels) and fetal loss .
Nervous System Involvement
Lupus can affect all parts of the nervous system: the central nervous system (CNS), the peripheral nervous system (PNS), and the autonomic nervous system (ANS).
When the nervous system is affected, lupus patients can experience several complications.
The symptoms may come on suddenly or come and go, but they will vary depending upon the location and extent of the tissue injury.
Central Nervous System
When lupus affects the central nervous system (CNS), the main symptoms include headaches, confusion, fatigue, depression, seizures, strokes, vision problems, mood swings, and concentration difficulties.
Peripheral Nervous System
When lupus affects the peripheral nervous system (PNS), the primary symptoms involve vision problems, facial pain, ringing in the ears, dizziness, drooping of an eyelid, and carpel tunnel syndrome.
Autonomic Nervous System
When lupus affects the autonomic nervous system (ANS), symptoms, such as tingling, burning and numbness, mental confusion, headaches, and nervous system-related gastrointestinal disturbances (nausea, vomiting, constipation, or diarrhea) can manifest.
Kidney (Renal) Symptoms
Renal involvement in lupus typically results in diminished kidney function (reduced GFR), which may result in elevated serum creatinine levels and proteinuria.
Patients with renal involvement have a poorer prognosis, with likely progression to end-stage renal disease, which can be life-threatening.
Approximately 50% of lupus patients develop nephritis (inflammation of the nephrons, the functional units of the kidneys), also called lupus nephritis, which happens when lupus autoantibodies affect the functional structures of the kidneys that filter out waste (nephrons).
Lupus nephritis greatly increases morbidity and mortality rates among lupus patients, if the disease remains untreated for prolonged periods, resulting in significant, irreversible end-organ damage.
Arriving at the correct diagnosis of lupus is a challenge, considering the multitude of clinical presentations observed.
The disease can affect the kidneys, lungs, skin, nervous system, and musculoskeletal system, as well as other organs of the body.
The signs and symptoms of lupus may also vary over time and overlap with those of other disorders.
Other autoimmune diseases and conditions that can mimic lupus include rheumatoid arthritis, Adult Still’s disease, Behcet disease, and Sarcoidosis.
Some viral and bacterial infections, particularly hepatitis B and C, Epstein-Barr virus (EBV), Parvovirus B19, Cytomegalovirus (CMV), and HIV can also induce lupus-like symptoms.
In general, if systemic lupus erythematosus (SLE) is suspected, patients’ subjective complaints, as well as laboratory abnormalities and demographic characteristics, may help to pinpoint the diagnosis.
Typically, the first signs of lupus include fatigue, fever, joint pain, and weight fluctuations.
Concerning bloodwork, antinuclear antibodies (ANA) are the hallmark of the disease and shall be the first biomarker to be examined.
Immunofluorescence assay is considered the gold standard test for ANA, and although other methods of detection, such as ELISAs and multiplex assays, are widely available, they lack sensitivity.
A positive ANA is seen in more than 97% of cases of lupus, although it can also be present in several other disorders, as well as a significant proportion of the healthy population, and has a specificity of only 20%.
Other autoimmune diseases associated with a positive ANA including autoimmune hepatitis, multiple sclerosis, Hashimoto’s thyroiditis, and idiopathic thrombocytopenic purpura.
Several infections and malignancies have also been reported to be associated with a positive ANA.
Hence, a positive ANA test does not confirm the diagnosis of lupus, but a negative ANA makes it very unlikely.
Another less common, but highly specific to lupus marker is Anri-Smith antibodies.
Anri-Smith antibodies are seen in less than 30% of lupus patients, but have a 99% specificity for lupus.
However, they are mainly observed in African-American lupus patients.
Addiotnaly, markers of inflammation, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may be elevated.
Other tests that should be performed include complete blood counts, liver function tests, and renal function tests including serum creatinine, urinalysis, and urine protein quantification (24-hour urine protein, or spot urine protein/creatinine ratio), in order to assess organ involvement.
In lupus, synovial fluid aspiration, a procedure that removes fluid from the space around a joint using a needle and syringe, often reveals tissue inflammation (inflammatory fluid).
Joint radiographs can be used to demonstrate periarticular osteopenia (indication of past inflammation around a certain joint), deformities, or subluxation (when a joint doesn’t work the way it’s supposed to, often due to misalignment), and to exclude the possibility of erosions.
Chest imaging with CT-scan, cardiac workup including echocardiography (trans-esophageal, if Libman-sacks endocarditis is suspected), CNS work up with magnetic resonance imaging (MRI), and / or lumbar puncture (needle insertion between two lumbar bones / vertebrae to remove a sample of cerebrospinal fluid), can all be pursued if specific organ involvement is suspected.
Renal biopsy shall always be performed if there is suspicion of lupus nephritis.
Skin biopsies can be considered as well, especially if atypical findings are suspected.
Treatment / Management
The goal of treatment in lupus is to prevent organ damage and achieve remission.
The choice of treatment is dictated by the organ system/systems involved and the severity of involvement, and ranges from minimal treatment (NSAIDs, antimalarials) to intensive treatment (cytotoxic drugs, corticosteroids) [44, 45, 46].
Patient education, physical and lifestyle interventions, and emotional support play a central role in the management of systemic lupus erythematosus (SLE).
Patients shall be well educated on the disease pathology, potential organ involvement including brochures, and the importance of medication and monitoring compliance.
Stress reduction techniques, good sleep hygiene, daily exercise, and use of emotional support shall be encouraged.
Smoking and recreational drug use can worsen symptoms, leading to systemic inflammation and possible complications, such as infections.
Patients shall be educated about the importance of smoking and recreational drug use cessation.
Dietary recommendations shall involve an anti-inflammatory diet rich in nutrient-dense foods, avoiding some legumes and echinacea, and including as many vitamin D rich foods as possible, like oily fish, liver, egg yolks (on top of vitamin D supplementation).
Photoprotection is also vital, and all patients with lupus shall avoid direct sun exposure by timing their activities appropriately, by wearing light-weight, loose-fitting dark clothes covering a big portion of the body, and using natural, mineral-based, broad-spectrum (UV-A and UV-B) sunscreens with a sun protection factor (SPF) of 30 or more.
Foods to Avoid in Lupus
Some foods tend to exacerbate lupus and should be avoided.
These foods include:
Gluten is a protein complex comprised of 2 components: gliadin (the water-soluble component) and glutenin (the water-insoluble component).
Gluten is found in wheat, barley, rye, triticale, and most flour-containing products.
Gluten can create several problems for most people, and especially autoimmune patients, because it’s a protein resistant to digestion, ending up passing undigested through the GI tract.
Undigested proteins are dietary antigens- food-derived substances that can instigate an autoimmune response, as the body mistakes them for pathogenic material.
Gluten intolerance is extremely common and oftentimes comes with no overt symptomatology, remaining undiagnosed for a very big percentage of people.
Gluten has also been shown to increase – even in healthy subjects – gut permeability, by causing disassembly of the tight junctions of the intestinal epithelium, promoting the development of leaky gut syndrome, intestinal and systemic inflammation, or triggering a lupus flare-up.
Gluten is a gluey and gooey substance that is very difficult to be broken down by alimentary enzymes.
Due to its physical and chemical qualities, it is used extensively in dough making and bread baking, since : 1) It absorbs twice its weight in water 2) It is sticky 3) It is extensible, meaning that it stretches when pulled 4) It is elastic, meaning that when it is stretched it returns to near its original size.
It’s no mystery that most people – both healthy or sick – can not fully digest gluten, and feel bloated after eating pizza, pasta, or bread.
How to Protect Yourself From Gluten
If you have gluten or even casein by mistake, the side-effects will vary, depending on your physiology and genetics, how much gluten/casein you consumed, your gut integrity status (how permeable it is), how long you have been gluten-free, and other factors.
From individual to individual, reactions to gluten can vary from severe, unpleasant reactions – like headaches, stomach ache, bloating, constipation, diarrhea, brain fog, severe depression – which can develop quickly, to those where the person does not even realize he/she has ingested gluten.
The individuality factor is so strong that even siblings who both suffer from Celiac disease can exhibit completely different symptomatology when they get “glutened”.
However, in all cases and no matter the overt symptoms, gluten ingestion will lead to autoimmune activity and damage – the intestinal villi will get attacked by the immune system – which will aggressively respond to the semi-digested/undigested gluten molecules floating in the digestive tract.
The nasty side effects (and not the damage) of involuntary gluten consumption may be minimized by a product called Gluten Guardian, which has been shown to minimize cross-contamination symptoms in Celiac patients and gluten-intolerant individuals.
It is a formula blend of 6 plant-based proteolytic enzymes that includes Peptidase DPP-IV (an enzyme clinically proven to help break down gluten) — as well as three enzymes that break down starches and sugars into monosaccharides.
It may be used as a precautionary measure (and not a cure) for anyone dealing with gluten/casein sensitivity or intolerance, Celiac disease, autoimmune issues, bloating, indigestion, excessive gas, or constipation.
2) Processed Sugar
A high processed sugar consumption is linked with an increased risk of many conditions, like autoimmune disease, type-2 diabetes, depression, liver disease, dementia, and even certain types of cancer.
In lupus patients, too much sugar can increase the severity of their symptoms, as it overstimulates an already over-stimulated and exhausted immune system.
3) Trans Fats
Trans fats are industrially manufactured fats created through the process of hydrogenation, which is used to stabilize polyunsaturated fatty acids (PUFAs), prevent them from becoming rancid, and keep them solid at room temperature.
Trans fats are primarily found in:
- Stick margarine
- Vegetable oils, such as soybean oil, sunflower oil, safflower oil, canola oil, peanut oil, cottonseed oil
- Commercial ice creams and candy bars, such as Ben & Jerry’s and Mars
- Baked goods, such as cakes, waffles, cookies, and pies
- Microwave popcorn
- Frozen pizza
- Refrigerated dough, such as biscuits and rolls
- Fried foods, including french fries, doughnuts, and fried chicken
- Non-dairy coffee creamers
- Toast bread
- Nut butter
Additionally, 99% of plant-based oils used for homemade, high-heat cooking and frying are rich in PUFAs, which turn into trans fats under high-temperatures.
A better, healthier alternative is the more stable and less-prone-to-oxidation saturated fats, like organic butter, lard, and beef tallow (fats our ancestors used to cook with before the industrial revolution).
Trans fats are extremely inflammatory; many people attribute the unprecedented rates of chronic disease we face today to their consumption, as well as the recent addition of carbohydrates into our diet.
Trans fats have also been shown to contribute to the onset of cardiovascular disease (CVD), GI problems, hypo-endocrine conditions (i.e., hypothyroidism), diabetes, and certain types of cancer [47, 48, 49, 50, 51, 52].
Alcohol depletes the body of fluids and B vitamins (which are crucial for energy levels and healthy nerves) , is toxic to the liver , creates blood sugar imbalances , suppresses the immune system , interferes with the production of pancreatic enzymes (impairing digestion) , reduces testosterone and progesterone (the hormone of youth), and increases estrogen (a risk factor for breast cancer and ovarian cancer in women) .
All these factors can greatly increase symptomatology and induce a lupus flare.
Caffeine is the most extensively used psychoactive substance on the planet.
Like other wake-promoting drugs and stimulants, caffeine exerts its effects by antagonizing adenosine A2A receptors (A2AR) in the brain and by stimulating β-adrenergic receptors in the heart.
This can create symptoms of anxiety, jitters, tremors, cold sweats, and even panic attacks in already anxious and psychologically distressed lupus patients.
Caffeine also seems to negatively interfere with several autoimmune conditions, such as Hashimoto’s thyroiditis (coffee decreases the absorption of levothyroxine), type-1 diabetes Mellitus (coffee decreases insulin sensitivity), Celiac disease (coffee consumption is associated with cross-reactivity with gliadin antibodies in celiac patients .)
6) Certain Legumes
Alfalfa sprouts, broad beans, snow beans, jack beans, soybeans, peanuts, and several other legumes contain the non-proteinogenic amino acid L-canavanine, which has been shown to trigger lupus flare-ups in some lupus patients [61, 62, 63].
Canavanine-sensitive lupus patients who consume these legumes usually react with muscle pain and fatigue, and exhibit negative blood alterations during check-ups.
Lupus, also called Systemic Lupus Erythematosus (SLE), is a chronic autoimmune condition in which the immune system mistakenly attacks the body’s own healthy tissues and organs.
During lupus, high levels of persistent inflammation are present in the body, and multiple organs can be affected: the heart, joints, muscles, kidneys, brain, lungs, endocrine glands, gastrointestinal system, etc.
Because the symptoms of lupus are very similar to many other health conditions- such as rheumatoid arthritis, thyroid disorders, chronic infections – lupus can be very hard to diagnose.
Lupus tends to cause periods of unpredictable “flare-ups” (exacerbation of symptoms), followed by periods of remission (minimal or no symptomatology).
Common signs and symptoms of lupus include fatigue, headaches, sun sensitivity, joint pain, insomnia, GI issues, and skin rashes.
The medications available include non-steroidal anti-inflammatory drugs (NSAIDs), antimalarial medications, steroids, immunosuppressive agents, and monoclonal antibodies, which are used to control flares, maintain remission, and manage symptoms, but may also create serious side-effects, and even long-term health problems.
Despite that many lupus patients aren’t satisfied with the benefits of their prescriptions, most feel they have no alternatives, and are desperate to find a solution to their problem.
However, natural remedies for lupus, including stress manipulation, supplements, exercise, and a healthy diet high in anti-inflammatory foods can all contribute to symptom management and improved immunity, without the side-effects of the commonly prescribed synthetic agents.
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About George Kelly
George Kelly M.Sc is a Sports Nutritionist, Functional Nutritional Therapy Practitioner (FNTP), and Metabolic Type expert. He is the CEO and lead author of Metabolic Body.
This content is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of such advice or treatment from a personal physician. All readers/viewers of this content are advised to consult their doctors or qualified health professionals regarding specific health questions. Neither Metabolic Body nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this educational content. All viewers of this content, especially those taking prescription or over-the-counter medications, should consult their physicians before beginning any nutrition, supplement or lifestyle program.