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Home » 2025 | November | Endocrinology and Metabolic Health » Clinically Proven Natural Support for Autoimmune Rheumatic Conditions

Clinically Proven Natural Support for Autoimmune Rheumatic Conditions

    Authors: Devin Miles, ND & Elizabeth Sutherland, ND

    Emerging research highlights how botanicals such as berberine, cordyceps, rehmannia, and rosmarinic acid can modulate immune pathways and reduce inflammation in autoimmune diseases like lupus and rheumatoid arthritis.

    Abstract

    Emerging clinical and pre-clinical evidence supports the use of botanicals like berberine, cordyceps, rehmannia, and rosmarinic acid in modulating immune pathways and reducing inflammation in autoimmune rheumatic disorders. These phytonutrients demonstrate immunoregulatory, antioxidant, and microbiome-balancing properties that complement conventional therapies to improve patient outcomes.

    Overview

    The prevalence of organ-specific and systemic autoimmune conditions is increasing worldwide.1 This rise is not attributable to improvements in diagnosis, but more likely to increasing exposure to a growing array of unavoidable environmental risk factors.

    Because autoimmune rheumatic disorders manifest in a diverse array of signs and symptoms, they can be extremely challenging to manage. Goals of treatment are manifold and include modulating immune activity, reducing or preventing organ damage and comorbidities, and alleviating pain and fatigue.2

    With regard to immune activity in autoimmune disorders, aberrant autoreactivity of CD4+ T helper cells leads, among other outcomes, to Th1 cells producing interferon gamma (IFNγ) and Th17 cells producing IL-17. IFNγ is considered central to the pathogenesis and clinical course of systemic lupus erythematosus (SLE),3 and IL-17 to the pathogenesis and clinical course of rheumatoid arthritis (RA).4 Drugs that modulate or suppress immune function, the core of conventional treatment for autoimmune disorders, have limited benefit and serious side effects. With the rising global prevalence of autoimmune diseases, it is all the more important to identify potentially effective and non-toxic options to support a holistic therapeutic approach.

    Certain phytoconstituents appear to exert downstream immunoregulatory and anti-inflammatory effects via their ability to modulate intracellular signaling. Among other mechanisms, these phytoconstituents are able to regulate the expression of cell-cycle proteins and other protein kinases involved in transcription of autoantibodies and inflammatory cytokines, both of which are implicated in the onset and worsening of autoimmune pathophysiology.5,6,7,8

    Phytoconstituents with Immunomodulatory Properties 

    Berberine

    Berberine is an isoquinoline alkaloid9 found in multiple plant species, including Hydrastis canadensis (goldenseal), Coptis chinensis (Chinese goldthread), Phellodendron anureses (Amur cork tree), Tinospora cordifolia, Eschscholzia californica (Californian poppy),10 Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), and Berberis aristata (tree turmeric).11

    Pre-clinical and cell culture studies suggest that berberine impedes cell signaling pathways that promote the differentiation and function of pro-inflammatory Th1 and Th17 cells. Berberine may also inhibit the biosynthesis of interferons that trigger the apoptosis cascade in SLE.9 Berberine has been shown to redress the imbalance of the Treg to Th17 cell ratio, which is a hallmark of autoreactivity, both directly, by inducing differentiation of Treg cells, and indirectly, by selectively influencing gut microbiome composition to promote Treg development.12

    In addition, berberine has been found to mitigate autoreactivity by decreasing the expression of M1 macrophages, which produce pro-inflammatory cytokines, and promoting the M2 phenotype, which produces anti-inflammatory factors and supports tissue repair.13 In an animal model of RA, berberine considerably improved clinical signs, such as joint destruction, and downregulated several pro-inflammatory factors, including IL-1β, IL-6, and IL-17.14,15

    Berberine has also been shown to inhibit NF-κB gene expression, thus impeding the production of inflammatory mediators, such as IL-1β, IL-6, IL-8, and TNF-α.  Berberine’s ability to modulate gut microbiota also promotes suppression of TNF-α.16 

    Addressing gut health is a vital part of any therapeutic approach to mitigating autoimmune conditions. Intestinal inflammation and infection have been treated with berberine for years. Toll-like receptors (TLRs) are part of innate immunity.  Cell surface TLR dimers that recognize microbial membrane lipids include TLR4/MD-2, TLR1/TLR2, and TLR6/TLR2.  Intracellular TLR dimers that recognize microbial nucleic acids include TLR3, TLR7, TLR8, and TLR9.  Cell-surface TLRs detect lipopolysaccharides (LPS) or lipopeptides in microbial membranes.  TLR4 is an LPS receptor.  LPS/TLR4 signaling is either MyD88-dependent or MyD88-independent, both of which can promote pathways of inflammation regulated by NF-kB and MAPK, which are important for inflammatory cytokine production. Berberine has demonstrated inhibition of LPS-induced TLR4 and MyD88 expression, as well as greater affinity to the TLR4/MD2 receptor than LPS.16 

    Cordyceps sinensis

    Cordyceps sinensis is a fungus with a long history of therapeutic use in Chinese medicine as an adaptogenic agent in a multitude of complex health conditions.17 In an animal model of SLE, oral administration of C. sinensis at 2.4 mg/g/day mitigated disease severity, increased survival, lowered proteinuria, and decreased antibodies to anti-double-stranded DNA, potentially through its ability to modulate the ratio of CD4 to CD8 T lymphocytes.18 A bioactive constituent of Cordyceps, cordycepin, was found to modulate inflammation by inhibiting IL-1β-induced chemokine production in synovial fibroblasts, suggesting it might help attenuate connective tissue damage in RA and related autoimmune disorders.19

    In one study, 10 healthy men and 10 healthy women received either a beverage of fermented Cordyceps militaris (FCM) containing 2.85mg of cordycepin or a placebo, for eight weeks.  Compared with placebo, participants who received the FCM beverage experienced an increase in NK (natural-killer) cell activity, and a reduction in IL-1β and IL-6 levels, two interleukins associated with an inflammatory immune response. The study demonstrated the immunomodulatory capabilities of cordyceps without toxicity to the liver, kidneys, or blood components.20

    In another study, 61 patients with lupus nephritis (LN) were randomly assigned to either a treatment or a control group. The treatment group received oral doses of cordyceps (2-4g/d before a meal) and artemisinin (0.6mg/d after a meal) in three doses for three years, while the control group was given tripterygiitotorum and/or Baoshenkang tablets. Complement C3 level stabilized in the treatment group at above normal range.  The treatment group also experienced fewer side effects than the control group.21

    In an in vitro study, human osteoarthritis chondrocytes were pretreated with cordycepin and then stimulated with IL-1β for 24 hours.  Prostaglandin E2 and nitric oxide induced by IL-1β were both significantly inhibited by pretreatment with cordycepin. IL-1β genetic expression and production of MMP-13, IL-6, iNOS, and COX-2 were all reduced. Activation of NF-κB by IL-1β was also mitigated. These results demonstrate the potential anti-inflammatory activity of cordyceps in joint health.22

    Rehmannia glutinosa 

    Rehmannia glutinosa is another adaptogenic botanical with a long history of use in Chinese medicine. Studies that highlight the potential neuroprotective effects of Rehmannia suggest it has powerful antioxidant and anti-inflammatory properties.23 In addition, recent evidence shows that the polysaccharide constituents of Rehmannia glutinosa may favorably influence Th1/Th2 balance, suggesting it has potential as an immune modulator.24

    Methanol-extracted Rehmanniae radix has been shown to decrease IL-2, IL-6, IL-10, IFN-γ, and TNF-α in animal models of SLE.  Rehmannia’s ability to downregulate TNF-α and T-cell-dependent cytokines demonstrates its benefit in the treatment of immune disorders.25

    An ethylacetate extract of Rehmannia glutinosa was shown to attenuate nitric oxide by decreasing inducible NOS (iNOS) expression, NF-kB activation, reactive oxygen species (ROS), and IL-6, thus showing promise for mitigating inflammatory components of various rheumatic diseases, such as rheumatoid arthritis.26

    In a study of 16,645 newly diagnosed SLE patients, Rehmannia was integrated into herbal prescriptions for SLE. Participants who received conventional treatment plus the herbal medicine prescription had a lower adjusted hazard ratio for lupus nephritis than those who had only received conventional treatment.27

    Rehmanniae Radix (RR) contains Catalpol (CAT), which has been found to regulate immunity. In an animal model of RA, CAT had an immunomodulating effect on the differentiation of Tregs-to-Th17 cells by up-regulation of the Micro-RNA let-7g-5p, which decreased expression of the transcription factor STAT3.28

    In a Sjogren’s mouse model, CAT improved salivary flow rates and water consumption. It also attenuated lymphocytic infiltration and ectopic germinal center formation, as well as decreasing IFN-γ and BAFF levels in the serum and submandibular glands.29

    Rosmarinic acid

    Rosmarinic acid is a polyphenolic compound found in plants such as Rosmarinus officinalis. Multiple in vitro and in vivo studies have corroborated its extensive anti-oxidative, anti-apoptotic, and anti-inflammatory effects.30,31,32 Rosmarinic acid was found to limit intracellular production of IFN by inhibiting the expression of IFN-stimulated genes. This is significant because a deranged response to self-nucleic acids results in the sustained production of type 1 IFN, which is a hallmark of autoimmune reactivity.33

    Rosmarinic acid has been shown to inhibit the signal transduction of lymphocyte-specific protein tyrosine kinase (Lck), which regulates many cellular processes, including T-cell development and homeostasis. Interestingly, the net effect of this inhibition triggered apoptosis only in active, proliferating T cells, preventing the expression of pro-inflammatory cytokines such as IL-2 and IFNγ.34 It is possible, therefore, that rosmarinic acid could play a role in re-establishing immune homeostasis under autoreactive conditions. In an in vivo study of RA, rosmarinic acid was found to induce apoptosis in activated T cell subsets far more than in naïve T cells and did so in a dose-dependent manner via the mitochondrial pathway of apoptosis. T cells in particular contribute to the onset and clinical progression of RA, and so the potentially preferential apoptosis of pathogenic T cells is an important consideration.35

    In two studies using animal models of RA, rosmarinic acid was found to substantially lower levels of inflammatory markers, such as COX-2, in synovial tissue, with associated improvements in the arthritis index and clinical signs of treated animals.36,37

    Rosmarinic acid reduced injury to liver tissue in a carbon tetrachloride (CCL4)-induced liver injury mouse model.38

    Rosmarinic acid was able to reduce local paw edema. In liver ischemia-reperfusion (I/R) and thermal injury animal models, it was able to decrease multi-organ dysfunction markers by modulating NF-κB and metalloproteinase-9.  Thus, rosmarinic acid was shown to decrease inflammation locally and systemically.39

    A Word on the Microbiome

    Evidence for the fundamental contribution of gastrointestinal health and, in particular, the gut microbiome, to immune function and dysfunction is irrefutable and growing.40 As a consequence, any Restorative Medicine approach to autoimmune disorders must also focus on gut health. The ability of berberine to shift microbiome composition toward Treg development has already been mentioned.12 In addition, Lactobacillus has been shown to have many immunomodulatory effects, including reducing the population of pro-inflammatory ILC3 and Th17 cells, inhibiting IL-17 production, shifting the Treg/Th17 balance toward the Treg phenotype, and stimulating production of IL-10, which protects against hyper-immune reactivity.41,42 In pre-clinical studies of RA, Lactobacillus casei was found to decrease joint swelling, arthritis scores, and serum inflammatory cytokine levels.43,44

    MicroRNAs (miRNAs) are known to play an extensive regulatory role in immune cell function. Studies have shown an association between dysregulated expression of some miRNAs, such as miR-155 and miR-181a, and the pathogenesis and clinical severity of SLE.

    Interestingly, an in vivo study found that Lactobacillus rhamnosus and Lactobacillus delbrueckii attenuated the activity of miR-155 and miR-181a in SLE patients.45

    Dosage Recommendations for Autoimmune Support

    Based on published research and expert clinicians’ experience, the following doses are recommended for treating autoimmune conditions: 

    • Cordyceps fruiting body: 400mg
    • Rehmannia: 400mg
    • Rosmarinic acid: 200-400mg
    • Berberine: 300 mg
    • Probiotic Support: 50B+ 

    Key Clinical Takeaways

    • Certain phytoconstituents may be helpful as part of a therapeutic protocol for autoimmune rheumatic conditions, as they have been shown to have immunoregulatory effects in experimental and pre-clinical studies.
    • By modulating intracellular signaling pathways, they downregulate or upregulate downstream immune and inflammatory factors to re-establish immune balance.
    • The mechanisms of action are complex and can involve impeding or promoting gene expression at the level of transcription.
    • Important phytoconstituents and plants with immunomodulatory properties via intracellular signaling pathways include berberine, Cordyceps sinensis, Rehmannia glutinosa, and rosmarinic acid.
    • Berberine exerts some of its immunomodulatory effects by shifting microbiome composition in a favorable direction for immune balance. Certain Lactobacillus sp. have also been shown to be significant regulators of systemic immune function.
    • Rosmarinic acid may help reduce inflammation locally and systemically.

    Dr. Miles is a clinician who provides integrative and natural approaches to kidney function, cardiovascular health, digestion, autoimmunity, and prevention.  She graduated from Sonoran University of Health Sciences (previously Southwest College of Naturopathic Medicine) in Arizona. She enjoys educating via social media, webinars, and in-person presentations and has been interviewed in various podcasts and radio shows. Dr. Miles has also launched an online course sharing natural support for kidney and blood pressure health.  She is a medical writer and has written for traditional, integrative, naturopathic, and functional medicine sources. Dr. Miles is a Medical Advisor for Restorative Formulations.

    Dr. Elizabeth (Liz) Sutherland began her undergraduate degree at the University of Cambridge in Classics and finished it at Tufts University with a BS in Biopsychology. She earned her doctorate in naturopathic medicine (ND) from National University of Natural Medicine (NUNM), in Portland, OR, after which she completed post-doctoral research fellowships at the Kaiser Permanente Northwest (KPNW) Center for Health Research (where she subsequently became the first KPNW Research Associate to hold an ND degree) and the University of Arizona College of Medicine. She also earned a Certificate in Human Investigations for clinical trials at Oregon Health and Science University. Dr. Sutherland has served as co-investigator on a number of NIH-funded studies and is primary author or co-author on multiple peer-reviewed publications. She was Chair of the Institutional Review Board at NUNM, and also taught and redesigned the Mind-Body medicine curriculum. Currently, Dr. Sutherland serves as Vice President of Continuing Education Compliance for AARM, and editor in chief of the Journal of Restorative Medicine. In addition, she helps physicians and scientists from several wellness and medical disciplines write grant proposals, books, and manuscripts for submission to academic journals.

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