If you’re navigating life with lupus, you’ve probably come across the carnivore diet as a possible solution. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multiple organ involvement, including the skin, joints, kidneys, lungs, central nervous system and the haematopoietic system, with a large number of complications. Despite years of study, the etiology of SLE remains unclear; thus, safe and specifically targeted therapies are lacking. In the last 20 years, researchers have explored the potential of nutritional factors on SLE and have suggested complementary treatment options through diet. Nutritional therapy including restrictions on carbohydrate and protein and the use of nutritional supplements (i.e., vitamins, minerals and polyphenols) is a promising way to control inflammatory responses in SLE. At MGI Clinics, we help patients uncover the root causes of autoimmune symptoms, especially when it comes to gut microbiome imbalance and chronic inflammation. Lupus is an autoimmune condition rooted in immune dysregulation and gut inflammation. This gut microbiome imbalance often shows up as fatigue, pain, and unpredictable flares.
What is the Carnivore Diet?
The carnivore diet is an all-animal-product diet that includes meat, fish, eggs, and sometimes dairy, while excluding all plant-based foods like fruits, vegetables, grains, and legumes. It’s often described as an extreme elimination diet, aiming to reduce potential dietary triggers of inflammation.
How the Carnivore Diet May Impact Lupus Symptoms
Rheumatic diseases are often driven by chronic inflammation and autoimmune responses, leading to joint pain, stiffness, and fatigue. The carnivore diet for lupus cuts out all carbohydrates-meaning no starches, sugars, or even plant-based fibers. Proponents claim that removing carbs starves pathogenic gut microbes, which can temporarily reduce inflammation and ease lupus flare symptoms.
Potential Benefits
Reduces Inflammation: By eliminating plant-based foods that may contain anti-nutrients (e.g., lectins, oxalates), the diet may lower inflammation for some individuals. Some individuals have reported significant symptom relief from autoimmune conditions after adopting the carnivore diet, though these are anecdotal and not supported by large-scale clinical trials. That’s why some people use the carnivore diet as a lupus flare-up diet, especially when symptoms are severe.
Why the Carnivore Diet Sometimes Helps with Lupus Flare-Ups
Bad gut bacteria and fungi thrive on dietary carbohydrates, producing inflammatory toxins. By cutting out all carbs, the carnivore diet can rapidly reduce these microbial populations, leading to a short-term drop in inflammatory markers and symptom relief during a flare.
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Potential Drawbacks of the Carnivore Diet for Lupus
While the carnivore diet may help manage short-term lupus flare-ups, it’s not a lasting solution.
Phytonutrient Deficiency
By eliminating all plant-based foods, the carnivore diet creates a serious phytonutrient deficiency. Eliminating all plant foods causes phytonutrient deficiency-loss of polyphenols, flavonoids, and resistant fibers essential for gut lining repair and immune regulation. Without these compounds, your body loses access to key antioxidants and anti-inflammatory tools that form the foundation of any effective autoimmune inflammation diet. Phytonutrients from plants serve as antioxidants and anti-inflammatory agents that nourish beneficial microbes and strengthen gut barrier function.
Imbalanced Gut Microbiome
One of the biggest misconceptions is that avoiding carbs equals healing the gut. While carb restriction reduces harmful bacteria temporarily, it does not rebuild a healthy microbiome. It also fails to rebuild a balanced microbiome, since beneficial bacteria rely on plant fibers for growth. In patients following the carnivore diet for lupus, we’ve never found a balanced microbiome.
Food Sensitivity
Another key concern with a meat-heavy diet is food sensitivity in lupus. Complex animal proteins aren’t always fully broken down, especially in those with compromised digestion.
Nutritional Factors and Systemic Lupus Erythematosus (SLE)
The contribution of lifestyle-associated factors is still a matter of controversy in SLE; however, dietary habits and dietary-related microbiome composition are receiving more attention from researchers. Indeed, some SLE-related clinical features are associated with nutrition; perhaps not as an aetiological factor but as a clinical repercussion. Thus, SLE represents a mosaic of metabolic changes and mineral and vitamin deficiencies superimposed by the systemic presentation of arthritis, nephritis, vascular events and organ damage to the heart, CNS, kidneys, and skin, which contribute to increases in the morbidity and mortality of these patients.
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Macronutrients and SLE
Macronutrients represent the group of environmental substances widely used by organisms for vital processes such as growth, body development, and bodily functions. Carbohydrates are among the macronutrients that provide energy and, when consumed in excess, contribute to increased energy storage and subsequent weight gain. Although there is no clear evidence that altering the proportion of total carbohydrate in the diet is an important determinant of energy intake, nutritional imbalance, and excess carbohydrate dietary intake have been suggested as risk factors that exacerbate clinical manifestations of several autoimmune diseases such as rheumatoid arthritis and SLE.
Obesity and Inflammation in SLE
Obesity is a well-known risk factor for low-grade inflammation characterized by activation of several pathways involved in the expression of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. Activation of these proinflammatory pathways significantly contributes to the perpetuation of the inflammatory response, which are at least partly responsible for the severe co-morbidities seen in SLE patients. Indeed, several studies have shown that up to 35% of SLE patients are overweight and 39% are obese, and these patients are characterized by a higher concentration of inflammatory markers including C-reactive protein (CRP). Recent studies have suggested that obesity is associated independently with SLE disease activity. Corticosteroids remain the first choice of treatment for SLE, but their administration is linked to excess weight gain and the development of corticosteroid-induced diabetes.
Calorie Restriction and Immune Response
Mouse models provide excellent insight into the pathogenesis of SLE and the observation of dietary-induced changes. Notably, the restriction of calorie intake leads to substantial changes in the immune response. For example, in a study with a lupus-prone mouse model (NZB/NZW F1), calorie intake restriction effectively delayed the onset of proteinuria and significantly decreased serum levels of anti-dsDNA antibodies. Calorie restriction also had a significant impact on the B-cell population, resulting in a reduction of their frequency and activity. Parallel to this, a decline in CD8+ T cells and a higher proportion of naïve CD4+ and CD8+ T cells have been observed. This finding is of special importance as it shows the direct impact of calorie restriction on B-cell and T-cell compartments, key immunocompetent cell compartments involved directly in SLE pathogenesis. In another SLE-prone mouse model, when a 40% calorie-restricted diet was provided, B:T cell and CD4+:CD8+ T-cell ratios were significantly lowered compared with the control group. The impact of calorie intake on autoimmune system functioning is not restricted to immune executive cells. At the end of the last century, Troyer et al. showed that a calorie-restricted diet was successful in modulating the key inflammatory ligand platelet-derived growth factor (PDGF) subunit A and the thrombin receptor, resulting in the suppression of murine lupus nephritis. Less is known about the humoral response in this regard. The influence of calorie restriction on the expression of main cytokines and synthesis of immunoglobulin (Ig)G has been tested in NZB/NZW F1 mice.
Obesity and SLE Disease Activity
During the last several decades, the prevalence of excess body weight has increased rapidly worldwide and is now recognized as a main public health crisis. Obesity has a strong impact on organism functioning and is linked to the development of all diseases of civilization, including metabolic syndrome, atherosclerosis and T2DM. Strong evidence also links obesity to many autoimmune disorders including SLE. Obesity in SLE patients is associated with a poorer outcome, higher disease activity and higher cumulative organ damage. Therefore, the importance of prevention and treatment of obesity is widely acknowledged. The influence of body weight reduction on SLE activity has been addressed by Davies et al. They enrolled 23 overweight female subjects (BMI: >25 kg/m2) with SLE who were on corticosteroid therapy. A 6-week controlled trial where a low glycaemic index diet (n = 11) or a calorie-restricted diet (n = 12) was implemented resulted in significant weight loss, reduction in waist and hip measurements and fatigue in both treatment groups. Of note, caloric restriction did not cause any flares of disease. However, these results must be interpreted with caution because they from only one study that addresses this issue, and the population studied was small. Nevertheless, it is surprising that such an important problem has not yet attracted greater attention, and more studies in this field are required. Presently, evidence supports the idea that a hypocaloric diet reduces the disease activity of SLE. By contrast, however, not all obese patients share inflammatory profiles, and not all individuals in a healthy weight range are metabolically healthy. This underscores the need for proper nutrition or weight loss as only two factors of many for lupus patients. Lifestyle modifications such as meditation and exercise can also ameliorate lupus symptoms.
Protein Restriction and Amino Acids
The restriction of dietary protein has been addressed in several studies in patients with SLE and animal models. These data should be interpreted in a wider context as diet composition rather than protein restriction alone may show beneficial effects on SLE course. As an example, a traditional Mediterranean diet provides protection from certain chronic diseases including autoimmune disorders. This diet consists of vegetables, fruits, nuts, grains, olive oils and fish with limited meat consumption. Reduction of protein intake may be a reasonable approach in cases of lupus nephropathy as high protein intake contributes to reduced renal filtration, directly leading to the progression of kidney damage. Indeed, Milovanov et al. observed that early restriction of dietary protein (0.6 g/kg/day) slowed the decline in glomerular filtration rate in patients with SLE-induced chronic kidney disease. It has also been postulated that not only proteins but also selected amino acids may influence the course of SLE. In a case-controlled study, levels of serum L-canavanine (a non-proteinogenic amino acid) was significantly high (p < 0.01) in a group of Mexican patients with SLE (n = 100) compared with those of healthy controls (n = 100). Among the many mechanisms by which amino acids modulate the immune response, regulation of mechanistic target of rapamycin (mTOR) attracts special attention. The signaling of mTOR is recognized as the most important intracellular pathway that coordinates local nutrients and systemic energy status at the organismal and cellular levels. Moreover, it is deeply involved in the immune response; thus, any dysfunction in this pathway may result in an aberrant immune response and predisposition to the development of autoimmunity. The role of the mTOR pathway is usually discussed in the context of T-cell function. It has been shown recently that T-cell dysfunction observed in SLE is at least partially due to the activation of mTOR caused by reduced glutathione (GSH) depletion via mitochondrial hyperpolarisation. It was established that supplementation with N-acetylcysteine (NAC), a precursor of GSH, significantly improved the activity of SLE disease by profoundly blocking mTOR activity (p < 0.0009) in T cells and reversing GSH depletion. Regarding the other amino acids, in case-controlled studies, lower levels of tryptophan and higher levels of kynurenine (a metabolite of tryptophan) with activation of the kynurenine pathway were detected in patients with SLE. Indeed, an interventional study showed that NAC treatment significantly reduced the levels of kynurenine (p = 2.8 × 10−7) in patients with SLE. Contrary to this, a diet low in phenylalanine and tyrosine showed a protective role against nephropathy and reduced autoantibody production in a mouse model (NZB/W) of SLE. Considering the role of proteins and amino acids, it should be emphasized that a diet of moderate protein intake is recommended, and a high-protein diet should be avoided especially by patients with lupus-related kidney diseases (e.g., overt lupus nephropathy).
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Fatty Acids and SLE
Fatty acids (FAs), especially polyunsaturated FAs (PUFAs), are an effective and essential dietary factor for patients with SLE. Among PUFAs, omega-3 (ω-3) fatty acids [i.e., docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)] can reduce the level of inflammatory mediators as well as CRP. In a lupus-prone mouse model, when animals were fed with DHA, IFN-related genes were suppressed besides reduced autoantibody levels and glomerulonephritis. In another lupus-prone mouse model (female NZBWF1), the autoimmune response (i.e., increased levels of proinflammatory cytokines) was triggered by airway silica exposure, resulting in glomerulonephritis, lung damage and autoantibody formation. In the mid-1980s, Kelley et al. in his pioneer study demonstrated the direct impact of a fish oil diet (rich in EPA) on prostanoid metabolism and function that ultimately led to reduction of the inflammatory response in MRL/lpr mice. Many years later, the mechanism of this phenomenon was explained. The direct anti-inflammatory effect of EPA was due to the inhibition of cyclooxygenase (COX)-1, a key enzyme in the prostanoid synthesis pathway. Parallel to the inhibition of COX, fish oil ω-3 PUFA suppressed autoantibody production and reduced the gene expression of inflammatory response-related products, especially in the spleen and kidney of a murine SLE model. These mechanisms ultimately lead to the inhibition of glomerulonephritis and inflammation and prolong the lifespan of lupus-prone mice. Fish oil maintained the enzymatic ratios of reduced GSH to oxidized GSH (GSH:GSSG) and the antioxidant profile in lupus-prone aged B/W mice.
Dietary Approaches Recommended Instead of the Carnivore Diet for Lupus
A personalized “Mind-Gut-Immunity” protocol balances clean proteins, healthy fats, and gut-safe carbohydrates, while emphasizing high-phytonutrient foods and targeted prebiotic/probiotic support. The carnivore diet may provide relief during a flare, but long-term remission requires a comprehensive strategy focused on gut health, food sensitivity awareness, and nutrient diversity. For personalized guidance and support, schedule a discovery call with Dr. Chanu Dasari at MGI Clinics. Discover the transformative power of the Mind-Gut-Immunity Method! Over the past decade, Dr. Dasari has helped countless clients reduce inflammation and find relief from autoimmune issues, often in just 3-6 weeks. Now, you can start your journey to better health with our free training.