Table of contents
Updated - January 3, 2026
Autoimmune diseases and immunomodulation are directly related. How essential oils have an immunomodulatory effect will be explained below in a way that is understandable for both medical laypersons and medical professionals (by means of studies).
First of all, three terms whose meaning should be clarified in order to avoid possible ambiguities:
- Autoimmunity
- Immunosuppression
- Immunomodulation
Autoimmunity
Autoimmunity is the term used to describe a pathological (pathological) Immune response of the human organism against the body's own antigens (e.g. bacteria, viruses) as a result of which healthy structures (e.g. cells, tissue) are attacked, which in turn lead to the formation of autoantibodies against the body's own proteins and inflammation, destruction of cells or tissue, as well as organ dysfunction (Dysfunction).
Autoimmunity is synonymous with autoimmune disease.
Immunosuppression
Immunosuppression is the suppression of one or both of the body's immune systems, the humoral (non-cellular components of body fluids (e.g. blood, lymph) and the acquired body fluid), cellular (represented by the „killer cells“, or. T-cells / -Lymphocytes) immune system.
It can be triggered by illness, stress, exposure to radiation or medical treatment.
Immunomodulation
Immunomodulation is the regulatory intervention in the immune system, both dampening and stimulating. The aim is to restore normal regulatory behavior (e.g. dampening (suppressive) in the presence of autoimmunity or promoting (stimulative) for immunodeficiency.
Normally, our immune system protects us from pathogens such as viruses and bacteria. In the case of autoimmune diseases, however, the immune system makes a mistake: it suddenly attacks the body's own healthy cells as if they were enemies.
The immune system produces too many „attack signals“ (inflammatory messengers such as TNF-α, IL-6, IL-1β). These keep the inflammation going, even if there is no real enemy.
Examples of autoimmune diseases:
- Multiple sclerosis (MS) - attack on Nerve sheaths
- Rheumatoid arthritis - attack on Joints
- Crohn's Disease & Ulcerative Colitis - Attack on the Colon
- Hashimoto's - attack on the Thyroid gland
- Lupus ... - Attack on various Organs (...)
- Type 1 diabetes - attack on Pancreas
Studies
All the studies listed are written in English. A summary in German follows each study link and thus provides a rough overview of the key findings of the respective study.
If the study is available in full text, this link was given preference. Studies that are not available in full text can usually be viewed in the respective publication for a fee, more rarely only with registration via an institution.
NoticeSome links require multiple „I am human“ verifications.
Essential oils
Chemotypes (Ct.)
Chemotypes are used to differentiate essential oils of a plant species whose main active ingredient content varies due to different growing conditions (e.g. soil conditions, altitude, climate, UV radiation, time of harvest) and thus also the effect of the resulting oil.
One example is thyme: Thyme (Ct. thymol) has a stronger stimulating, antiseptic, expectorant effect, while thyme (Ct. linalool) has a softer, calming and relaxing effect.
Depending on the intended effect, the knowledge and choice of chemotype is of fundamental importance.
Carrier oil
Essential oils (EO) are highly volatile substances. Some essential oils have an irritating effect on the skin when undiluted. Carrier oils are ideal for effectively counteracting both properties, minimizing volatility, diluting the oils and increasing bioavailability when used topically (on the skin) or internally.
All oils with skin-caring properties are suitable as carrier oils for topical application, e.g. Argan, jojoba, almond, coconut oil, for internal use all cold-pressed (native) edible oils.
Mechanisms of action
For a more detailed description, please refer to the article „Essential oils - why they work?“ referred to.
1. From the nose to the brain
When smelling (olfactory / aromatic) of an essential oil, its fragrance molecules reach the brain directly. There (in the limbic system) they can:
- Reduce stress (less cortisol)
- Improve the mood
- Calm the nervous system
- Indirectly influence the immune system positively
2. Through the skin into the blood
On the skin (topical) can be applied to the tiny molecules:
- get into the blood
- migrate to inflamed areas
- have a direct anti-inflammatory effect there
3. At the cellular level
As soon as the active ingredients enter the body's cells, they develop their systemic effect:
- Block inflammatory messengers
- calm misdirected immune cells
- Activate protective mechanisms
Essential oils - turn off the inflammation switch
Let's imagine that there is an „inflammation master switch“ (called NF-κB) in our cells. Many essential oils can turn this switch „OFF“.
... calm overzealous immune cells
Certain immune cells (T cells, macrophages) are overactive in autoimmune diseases. In concrete terms, this means that they constantly send out alarm signals, produce too many inflammatory messengers and attack healthy tissue like overzealous guard dogs that also bark at family members.
The consequences are, for example, permanent inflammation, swelling, pain and tissue damage.
Essential oils can „shut down“ these cells in the same way that you slow down an engine that is too loud. This makes the cells react less aggressively.
... change the balance
The immune system has „aggressive“ and „peaceful“ cells. The aggressive (Th1, Th17) are like attack troops fighting off intruders, but can also react far too aggressively.
The peaceful (Th2, Treg) are like diplomats, they appease and regulate.
In autoimmune diseases, there are too many aggressive cells. This leads to excessive immune reactions, chronic inflammation and tissue damage.
Some oils help to create more peaceful cells, which then keep the aggressive ones in check and reduce inflammation.
... block inflammatory substances
During inflammation, the body produces substances such as Leukotrienes and Prostaglandins, chemical messengers that trigger pain, swelling, redness and fever.
In autoimmune diseases, these substances are permanently produced in large quantities, which leads to chronic symptoms such as swollen, aching joints, persistent fatigue, tissue that feels warm and reddened.
Certain oils block the enzymes that produce these inflammatory substances, similar to pharmaceuticals such as. Aspirin or Ibuprofen, only in a natural way and without undesirable side effects.
... protect against oxidative stress
Inflammation produces aggressive molecules (free radicals), unstable particles that attack and damage healthy cells like small „projectiles“. This damage accumulates, causing cell membranes to become porous and DNA to be damaged, and tissue ages more quickly.
The result is even more inflammation, exhaustion and accelerated tissue breakdown.
Many essential oils contain antioxidants that neutralize these free radicals, like a protective shield that intercepts the „projectiles“ before they can do any damage.
Essential oils - in detail
The following applies to all essential oils: they must be pure and natural WITHOUT any additives, ideally proven by a gas chromatographic analysis by a laboratory independent of the manufacturer. NO use of fragrance oils, synthetically produced, modified or mixed oils.
A analysis (using frankincense oil as an example) contain data (values in %) as follows:
alpha-Pinene
alpha-Thujene
Limonene
para-Cymene
Sabinene
Myrcenae
Octyl acetate
beta-Pinene
beta-Caryophyllene
Terpinen-4-ol
alpha-Phellandrene
delta-3-Carene
Camphene
...
37.44
10.80
9.46
5.75
4.09
3.53
3.22
1.83
1.81
1.47
1.24
1.24
1.20
...
The Effect of the individual main components:
alpha-Pinene
alpha-Thujene
Limonene
para-Cymene
Sabinene
Octyl acetate
beta-Caryophyllene
Terpinen-4-ol
Strongly anti-inflammatory
antimicrobial, immunomodulating
antioxidant, anti-inflammatory
analgesic, anti-inflammatory
antioxidant
soothing
CB2 receptor agonist (like Copaiba)
immunomodulating (as in tea tree oil)
Frankincense (Frankincense)
Two different products are obtained from the resin of the frankincense tree: the essential oil (contains Monoterpenes) and the boswellia resin (contains Boswellic acids).
Both substances have different effects, but complement each other perfectly (see below).
Frankincense (frankincense oil)
Frankincense oil has a dose-dependent effect on autoimmunity: while a low Dosage for normalization contributes to the activity of the immune system high Tins stimulating, which must be avoided in the case of autoimmunity! It is therefore essential to know the exact ingredients.
Based on the above analysis data, frankincense oil can be used in adults and children.
- Rheumatoid arthritis - Application to the affected joints
- Multiple sclerosis (MS) - Apply to the neck, spine and soles of the feet
- Crohn's disease / colitis - Massage the abdominal area in a clockwise direction
- Lupus ... - On joints and painful areas (avoid sun exposure)
topical in
- low dosage (for testing) - at 0.5 - 1 percent dilution (3 - 6 drops to 30 ml carrier oil),
for application, even over large areas - medium dosage (chron.) - at 1 - 2 percent dilution (6 - 12 drops to 30 ml carrier oil),
Apply 2-3 times a day to the affected areas - higher dosage (acute) - at 2-3% dilution (12 - 18 drops per 30 ml carrier oil),
max for 1-2 weeks (then back to medium dosage) applied 3-4 times daily
be applied.
Inhalative for systemic effects and stress reduction via ultrasonic nebulizer / diffuser 3 ... 5 trp. in water for 30 ... 60 min. 2 ... 3 times a day.
For products that Boswellic acid the content of AKBA (Acetyl-11-keto-β-boswellic acid) is decisive for quality and efficacy, which underlines the importance of independent batch analysis of such products (see also the study of the University of Ulm from 10.2019 „Comparative Investigation of Frankincense Nutraceuticals ...„).
Boswellic acids act through
- Blocking the Leukotriene production by inhibiting the enzyme 5-Lipoxygenase (5-LOX)
Leukotrienes are aggressive messenger substances that are released during inflammation.
They cause:
- Severe swelling (joints)
- Constriction of the bronchial tubes (shortness of breath with asthma)
- Increase in mucus production
- Accumulation of further inflammatory cells
- Chronic tissue damage - Inhibition of the Prostaglandin synthesis
Prostaglandins are inflammatory messengers that increase pain. - Suppression of the NF-κB signaling pathway
NF-κB is the „inflammation master switch“ in cells. When it is active, hundreds of pro-inflammatory genes are switched on. Boswellic acids turn off this master switch, stopping the entire inflammatory cascade. - Inhibition of the Complement system as part of the immune defense
In autoimmune diseases, it mistakenly attacks the body's own cells. Boswellic acids inhibit the key enzyme C3 convertase, which curbs autoimmune attacks. - Passage of the Blood-brain barrier
A particularly important property of boswellic acids in
- Multiple sclerosis (inflammation in the CNS)
- Brain tumors with swellings
- Cerebral edema after a stroke
because they work against
- Gehrin inflammation (neuroinflammation)
- Nerve cell damage (oxidative stress)
- Nerve degeneration (neurodegeneration)
These effects have been proven by studies:
- Multiple sclerosis (MS) - 800 .. 1,200 mg/d
Frontiers in Neurology (2022) - Crohn's disease - 900 .. 1,200 mg/d
Journal of Gastroenterology (2001) - Ulcerative colitis - 1.000 .. 3,600 mg/d
Planta Medica (2001) - Psoriasis - 1.000 .. 2,400 mg/d
Clinical, Cosmetic and Investigational Dermatology (2010) - Type 1 diabetes
Phytomedicine (2011)
The effect of boswellic acids is doubled due to their fat solubility when taken together with high-fat food!
Resulting dosage recommendation for an adult (70 kg) of AKBA in mg/d:
- Multiple sclerosis - 40 ... 60
- Crohn's disease - 40 ... 60
- Ulcerative colitis - 40 ... 60
- Rheumatoid arthritis - 50 ... 80
- Osteoarthritis, mild - 20 ... 30
- Osteoarthritis, severe - 50 ... 80
- Asthma - 30 ... 40
- Psoriasis - 40 ... 60
Frankincense (boswellic acid)
The main internal (systemic) anti-inflammatory active ingredients of boswellic acid are
- AKBA (3-O-acetyl-11-keto-β-boswellic acid - 5-LOX inhibition)
- KBA (11-keto-β-boswellic acid)
- β-BA (beta-Boswellic acid)
- Binds to TLR4 receptors (Toll-like Receptor 4) and blocks this
TLR4 is an alarm receptor that recognizes damaged molecules and activates inflammatory genes, creating a vicious circle in autoimmunity
- Inhibits the TLR4/IL-1R signaling pathway (anti-arthritic effect)
- Reduces MAPK p38/NF-κB activation
MAPK p38 is a signaling chain that activates inflammatory genes and cartilage-destroying enzymes (MMPs), COX-2, Cytokines produced; NF-κB activates 250 genes, some of which in turn NF-κB genes activate. (chronic inflammation)
- Inhibits the NLRP3 inflammasome (chronic inflammation)
- Lowers IL-6, TNF-α, COX-2 in joint chondrocytes
- Protects cartilage from degradation (osteoarthritis)
- Inhibits prostaglandin E synthase 1 (PGES-1), while protective prostacyclin remains untouched
PGES-1 produces the main inflammatory messenger substance that causes pain, fever and swelling PGE2
- Inhibits cathepsin G (Serine protease)
Cathepsin G destroys cartilage and connective tissue (RA), blood vessel walls (vasculitis), intestinal mucosa (IBD) and forms NETs (harmful in autoimmunity)
- achieves a higher bioavailability when taken orally due to better 100 times higher blood concentration as AKBA
AKBA and KBA can be a pro-inflammatory enzyme (5-Lipoxygenase) in the body so that it can has an anti-inflammatory effect. A unique property among natural substances!
AKBA does not directly block the active center by means of oxidation/reduction, as is usually the case with other inhibitory substances, but binds 3 nm away from the center, exactly between the membrane-binding and catalysis parts, and restructures the enzyme form.
This will LOX-5 induces less inflammation-promoting Leukotrienes at position 5 the Arachidonic acid but - in position 12/15 - less inflammation-promoting and also inflammation-dissolving Lipoxins and Resolvine to produce (15-LOX activation).
This study describes the Enzyme binding from AKBA, these study the 15-LOX activation.
Copaiba
β-Caryophyllene binds to CB2-receptors of immune cells, similar to cannabis, but without the intoxicating component of cannabis.
Copaiba calms aggressive immune cells, which leads to a reduction in the inflammatory reactions caused, both in affected tissues and in the brain and spinal cord, which in turn means a reduction in pressure due to reduced swelling and a functional improvement in nerve cells, such as a reduction in numbness and paralysis.
In multiple sclerosis, the myelin layer that protects the nerve fibres, but which has become porous due to the immune reaction, is remyelized, which improves nerve conductivity.
In the brain, the microglia immune cells are switched from „attack“ to „heal“, allowing the removal of cell remnants and preventing further damage to the nerve cells.
This results in the scope of application
- Multiple sclerosis (MS)
- Neurological autoimmune diseases
- Neuropathic pain
- Inflammation of the central nervous system
which have been proven in the following studies:
- Alberti TB et al. (2017) - „(-)-β-Caryophyllene, a CB2 Receptor-Selective Phytocannabinoid, Suppresses Motor Paralysis and Neuroinflammation in a Murine Model of Multiple Sclerosis“
Basic MS study - BCP inhibited microglial cells, CD4+/CD8+ T lymphocytes and proinflammatory cytokines - Reduced axonal demyelination - Modulated Th1/Treg balance through CB2 activation - Askari VR et al. (2023) - „Low Doses of β-Caryophyllene Reduced Clinical and Paraclinical Parameters of an Autoimmune Animal Model of Multiple Sclerosis„
Low-dose study - Low doses (2.5-5 mg/kg) were optimal - Shifted immune system from M1/Th1/Th17 (inflammatory) to M2/Th2/Treg (curative) - Increased IL-10 (anti-inflammatory), reduced TNF-α, IL-6, IL-17 - Acted more on systemic than CNS immune system - Askari VR & Shafiee-Nick R (2017) - „β-Caryophyllene ameliorates the development of experimental autoimmune encephalomyelitis in C57BL/6 mice„
Mechanism study - Protected oligodendrocytes (myelin-producing cells) from LPS toxicity - Acted via CB2 → Nrf2/HO-1 (low doses) and PPAR-γ (high doses) - Reduced ROS, NO, TNF-α - Promoted M2 microglia phenotype (healing) - Vafa Baradaran Rahimi, Vahid Reza Askari (2022) - „A mechanistic review on immunomodulatory effects of selective type two cannabinoid receptor β-caryophyllene„
Comprehensive overview of all mechanisms - Antioxidant through Nrf2/HO-1 axis - Immunomodulatory through CB2 activation - Inhibits MAPK p38 and NF-κB
Oregano
Oregano can be seen as a „brake“ on overactive T cells, the command center of the immune system, as it reduces the production of inflammatory messengers by up to 70%. This results in significantly fewer IL-2 and IFN-γ key messengers, which accelerate inflammation and damage tissue.
It also stops overzealous T cells that attack healthy tissue because they receive false information suggesting that the healthy cells in the tissue need to be fought.
In multiple sclerosis (MS), it activates the MBP and OLIG2 genes responsible for cell regeneration, which are specifically responsible for repairing the myelin layer that has become patchy as a result of the disease.
In the brain, it prevents inflammatory cells from entering and spreading by breaking this inflammatory cascade and thereby reducing neurological symptoms.
This results in the following areas of application
- Multiple sclerosis (MS)
- Rheumatoid arthritis
- T-cell-induced autoimmune diseases
which are substantiated by these studies:
- Khorsandi L et al. (2019) - „Carvacrol ameliorates experimental autoimmune encephalomyelitis through modulating pro- and anti-inflammatory cytokines„
Basic EAE study - Reduced clinical scores significantly (p<0.001) - Reduced IFN-γ, IL-6, IL-17 (pro-inflammatory) - Increased TGF-β, IL-4, IL-10 (anti-inflammatory) - Reduced leukocyte infiltration into the CNS - Ahmadi M et al. (2023) -
„Effect of Carvacrol on histological analysis and expression of genes involved in an animal model of multiple sclerosis„
Gene expression study - Reduced NF-κB, IL-1 and IL-17 gene expression significantly - Increased MBP (myelin basic protein) and OLIG2 (oligodendrocyte marker) - Promoted remyelination - Histology showed less demyelination and infiltrates - Fahad Khan Thareen (2024)
Review: „Carvacrol Essential Oil as a Neuroprotective Agent„
Comprehensive overview: 59 studies analyzed (2009-2024) - Neuroprotective in MS, Alzheimer's, Parkinson's, ischemia, epilepsy - Has antioxidant, anti-inflammatory, immunomodulatory effects - Regulates intracellular Ca2+ homeostasis
Lavender
Mode of action dose-dependent!
Lavender counteracts the consequences of permanent stress, thus the inflammation-promoting Cortisolrelease, which not only irritates the immune system but also provokes flare-ups. It lowers cortisol levels and thus has an anti-inflammatory effect.
It promotes sleep and supports the regeneration of the immune system during the deep sleep phases: inflammation is reduced and tissue damage is repaired.
The nervous system is calmed, activates the Parasympathetic nervous system, which triggers the rest and digestion mode to promote healing processes.
Lavender also blocks inflammatory messengers on a cellular basis and therefore has an anti-inflammatory effect,
Lavender is therefore suitable as an accompanying therapy for
- all autoimmune diseases
- relapses triggered by stress
- chronic diseases
as the following studies also confirm:
- Horvath G et al. (2021) - „Anti-inflammatory effect of lavender (Lavandula angustifolia Mill.) essential oil prepared during different plant phenophases on THP-1 macrophages„
Linalool and lavender oil reduced IL-6, IL-8, IL-1β, TNF-α Significant - Similar to NFκB inhibitors - Best effect: oil from the beginning of the flowering period - Silva GL et al. (2015) - „Antioxidant, analgesic and anti-inflammatory effects of lavender essential oil„
In vivo anti-inflammatory - Carrageenan-induced pleurisy: lavender oil reduced inflammation - Croton oil-induced edema: effect similar to Dexamethasone - Formalin test: pain relief similar to Tramadol - Cardia GFE et al. (2018) - „Effect of Lavender (Lavandula angustifolia) Essential Oil on Acute Inflammatory Response„
Dose dependence in the mode of action: Low dosesAnti-inflammatory (reduced NO, MPO, edema) - High doses: Irritant (pro-inflammatory) - Mechanism: Prostanoids, cytokines, NO, histamine - Gostner JM et al. (2014) - „Lavender oil suppresses indoleamine 2,3-dioxygenase activity in human PBMC„
Inhibits IDO (Indoleamine 2,3-dioxygenase) - important for autoimmunity - Reduced Tryptophan breakdown and Neopterin (immune activation marker) - Relevant for chronic immune activation, autoimmune syndromes
Eucalyptus
The main active ingredient in eucalyptus 1,8-Cineole activates macrophages, the scavenger cells of the immune system. Their task is to clear up cell debris, dead cells and inflammatory substances. The property of eucalyptus is the activation of macrophages in the aforementioned direction, whereas in autoimmune diseases macrophages attack healthy cells and tissue in overzealousness, which is counterproductive.
Swelling is reduced, which reduces pressure, thus ensuring better mobility in the joints and reducing pain, but also by inhibiting pain messengers.
At the same time, the improvement in well-being has a mood-enhancing effect, which reduces depression - especially in the case of chronic pain.
Eucalyptus thus proves to be
- Rheumatoid arthritis
- Autoimmune diseases of the respiratory tract
- Joint pain
effective according to the following studies:
- Yin C et al (2020) - „Eucalyptol alleviates inflammation and pain responses in a mouse model of gout arthritis„
Gouty arthritis mouse model - Eucalyptol reduced pain and swelling in a dose-dependent manner - Efficacy comparable to indomethacin (NSAID) - Inhibited NLRP3 inflammasome activation - Reduced oxidative stress (increased SOD, CAT, GPx; lowered ROS) - Suppressed TRPV1 overexpression (pain receptor) - Mechanism: Antioxidant effect → inhibits NLRP3 → reduces IL-1β - Juergens UR et al. (2004) - „Inhibitory activity of 1,8-cineol (eucalyptol) on cytokine production in cultured human lymphocytes and monocytes„
Fundamental immune cell study - Human lymphocytes: 1.5 μg/ml (10-⁵M) significantly inhibited: TNF-α by 92%, IL-1β by 84%, IL-4 by 70%, IL-5 by 65% - Human monocytes: Same concentration inhibited TNF-α by 99%, IL-1β by 84%, IL-6 by 76%, IL-8 by 65% - Mechanism: Suppression of NF-κB - Therapeutic concentrations without cytotoxicity - Greiner JFW et al. (2013) - „1,8-Cineole inhibits nuclear translocation of NF-κB p65 and NF-κB-dependent transcriptional activity„
Molecular NF-κB mechanism - 1,8-cineole blocks NF-κB p65 translocation into the cell nucleus - Inhibits NF-κB-dependent transcriptional activity - Increases IκBα level in a dose-dependent manner - Acts on MAPK pathway - Khan A et al (2014) - „1,8-Cineole (Eucalyptol) Mitigates Inflammation in Amyloid Beta Toxicated PC12 Cells„
Neuroinflammation (relevance for MS) - Reduced TNF-α, IL-1β, IL-6 in neuronal cells - Inhibited NF-κB activation - Antioxidant effect (increased SOD, CAT, GSH) - Relevant for neurodegenerative autoimmune diseases - Venkataraman B et al. (2023) - „Molecular docking identifies 1,8-cineole (eucalyptol) as a novel PPARγ agonist that alleviates colon inflammation„
PPARγ agonist in colitis - 1,8-cineole binds to PPARγ (like thiazolidinediones in diabetes) - Reduced colitis symptoms in DSS-induced model - Reduced MPO activity, IL-6, TNF-α, iNOS - Increased IL-10 (anti-inflammatory) - Mechanism: PPARγ activation → inhibits NF-κB - Jun YS et al. (2013) - „Effect of Eucalyptus Oil Inhalation on Pain and Inflammatory Responses after Total Knee Replacement„
Clinical study in knee replacement - Eucalyptus inhalation after TKR significantly reduced pain - Lowered CRP (C-reactive protein) - Inflammation markers - Reduced blood pressure (parasympathetic activation) - 1,8-cineole inhibits cytokine secretion by T lymphocytes - Suppresses edema formation - Brown SK et al (2017) - Review: „1,8-cineole: An Underappreciated Anti-inflammatory Therapeutic„
Multiple clinical studies demonstrate potent anti-inflammatory activity - Use in arthritis, type 2 diabetes, cardiovascular disease - As primary therapy or adjuvant to synthetic drugs - Safe profile, low side effects - Salvatori G et al. (2023) - „Anti-Inflammatory and Antimicrobial Effects of Eucalyptus spp. Essential Oils„
Antimicrobial and anti-inflammatory - 1,8-cineole inhibits arachidonic acid pathway → inhibits inflammatory mediators - Common mechanism with glucocorticoids - α-pinene (also in eucalyptus): Anti-inflammatory in osteoarthritis, antioxidant - Eucalyptol inhibits TNF, IL-1, leukotrienes, thromboxane
Carnation
CaveClove oil can increase the effect of blood thinners!
Eugenol, the main active ingredient in clove oil, blocks the enzyme COX-2, which produces inflammatory substances (prostaglandins), as well as NF-κB, both of which are responsible for the usual symptoms of inflammation, such as redness, pain, swelling, etc.
It interrupts the signaling pathways of the causative substances at several points and is therefore effective for
- severe joint inflammation
- acute pain
- systemic inflammations
as the following studies confirm:
- Kang HJ et al. (2024) - „Eugenol alleviates the symptoms of experimental autoimmune encephalomyelitis in mice by suppressing inflammatory responses„
Multiple sclerosis EAE model - MOG-induced EAE in C57BL/6 mice - Daily oral administration of eugenol significantly reduced clinical symptoms - Inhibited immune cell infiltration and proinflammatory mediators - Histology: Reduced inflammation and demyelination in the spinal cord - Mechanism: Anti-inflammatory, antioxidant, neuroprotective - Ferrari JG et al. (2025) - „Antioxidant and Anti-inflammatory Activity of Eugenol, Bis-eugenol, and Clove Essential Oil„
TLR4/NF-κB pathway - In vitro study on LPS-stimulated macrophages - Eugenol and clove oil significantly reduced TLR4 levels - NF-κB activation inhibited - Bis-eugenol (dimeric form): Only substance that simultaneously suppressed TLR4/NF-κB, upregulated NRF2 (antioxidant) and increased IL-10 (anti-inflammatory) - DPPH radical scavenging activity: ~80% at 25 μg/mL - TNF-α level decreased at all concentrations - Barboza JN et al (2018) - Review: „Anti-inflammatory Potential and Antioxidant Profile of Eugenol„
Inhibits NF-κB signaling pathway (p50/p65 phosphorylation) - Reduces COX-2, TNF-α, IL-6, IL-1β, NO - Improves antioxidant enzymes: SOD, CAT, GPx, GST - In lung injury: Reduced neutrophil infiltration, TNF-α, NF-κB - Dosage: 10.7 mg/kg/day in rats showed optimal effect - Daniel AN et al. (2009) - „Clove and eugenol in noncytotoxic concentrations exert immunomodulatory/anti-inflammatory action„
Immunomodulation - Macrophages incubated with clove/eugenol (24h) - Clove oil (100 μg/well) inhibited IL-1β, IL-6, IL-10 - Eugenol (50-100 μg/well) inhibited IL-6 and IL-10 - Acted preventively and therapeutically against LPS stimulation - Mechanism: suppression of NF-κB by eugenol - Khalil AA et al. (2021) - Review: „Biological Properties of Eugenol“
Inhibits 5-LOX and COX-2 (dual action!) - Prevents neutrophil/macrophage chemotaxis - Inhibits prostaglandin and leukotriene synthesis - Eugenol dimers show chemopreventive properties - Could replace NSAIDs in osteoarthritis and inflammatory diseases - Safe dose: 2.5 mg/kg body weight
Tea tree
Terpinen-4-ol, the main active ingredient in tea tree oil, calms monocytes and macrophages, both immune cells that are overactive in many autoimmune diseases: They migrate en masse into the tissue, releasing large quantities of inflammatory messengers and summoning further immune cells. Tea tree oil interrupts this self-reinforcing inflammatory cycle.
In addition to reducing inflammatory messengers such as TNF-α, IL-1β and other aggressive signaling molecules, its strong antimicrobial effect (bacteria, viruses, fungi) reduces autoimmune relapses and modulates not only monocytes but also leukocytes, the white blood cells, which has a broad spectrum of efficacy in, among others
- Skin autoimmune diseases
- systemic inflammations
- as a broad immune module
as these studies show:
- Hart PH et al (2000) - „Terpinen-4-ol, the main component of the essential oil of Melaleuca alternifolia (tea tree oil), suppresses inflammatory mediator production by activated human monocytes„
Basic human monocyte study - Human peripheral blood monocytes (not animal model) - Water soluble components at 0.125% reduced: TNF-α by ~50%, IL-1β by ~50%, IL-10 by ~50%, PGE2 by ~30% - Only terpinen-4-ol (not α-terpineol or 1,8-cineole) was active - Suppression of all five mediators: TNF-α, IL-1β, IL-8, IL-10, PGE2 - Nogueira MNM et al. (2014) - „Terpinen-4-ol and alpha-terpineol (tea tree oil components) inhibit the production of IL-1β, IL-6 and IL-10 on human macrophages“
Mechanism study - U937 macrophages (human cell line) - TTO and terpinen-4-ol significantly reduced IL-1β, IL-6, IL-10 - Mechanism: Interference with NF-κB, p38 or ERK MAPK pathways - Effect NOT through NF-κB/p38 activation changes, but downstream - Effective on TLR4 and TLR2/TLR4 activation - Carson CF et al. (2006) - „Melaleuca alternifolia (Tea Tree) Oil: a Review of Antimicrobial and Other Medicinal Properties„
Comprehensive review - Systematic overview of all immunomodulatory effects - TTO inhibits TNF-α, IL-1β, IL-10 (50%) and PGE2 (30%) in human monocytes - Terpinen-4-ol modulates edema formation after histamine injection - Reduces erythema in nickel-induced contact hypersensitivity - Topical application modulates contact hypersensitivity response in mice - Ninomiya K et al. (2012) - „Suppression of inflammatory reactions by terpinen-4-ol in a murine model of oral candidiasis„
Oral candidiasis model - Terpinen-4-ol (40mg/mL, 50µL orally) 3h after Candida infection - Suppressed myeloperoxidase activity significantly - Reduced Macrophage Inflammatory Protein-2 (MIP-2) - In vitro: 800µg/mL inhibited cytokine production of cultured macrophages
Thyme
CaveNote chemotype!
As explained in the introduction with regard to chemotypes, the curvature is different. While thyme Linalool is indicated for autoimmune diseases with its calming and modulating effect, thyme has a Thymol with its intensive immunostimulating properties is counterproductive and can provoke relapses, inflammation and pain.
The study situation on thyme:
- Gholijani N et al. (2015) - „Modulation of Cytokine Production and Transcription Factors Activities in Human Jurkat T Cells by Thymol and Carvacrol„
T-cell modulation (most important study for autoimmunity) - Human T cells (Jurkat T cell line) - thymol and carvacrol at 25 µg/ml significantly reduced IL-2: from 119.4±8 to 66.9±6.4 pg/ml (thymol) and 32.3±3.6 pg/ml (carvacrol), IFN-γ: from 423.7±19.7 to 311.9±11.6 pg/ml - Mechanism: Reduced NFAT-2 to 44.2% (thymol) and 91.4% (carvacrol) - c-Fos to 31.2% (thymol) and 27.6% (carvacrol) - NFAT-2 and AP-1 are critical for T cell activation in autoimmunity - Amirghofran Z et al. (2015) - „Modulatory effects of thymol and carvacrol on inflammatory transcription factors in lipopolysaccharide-treated macrophages„
Macrophage study - J774.1 Mouse macrophages, LPS-stimulated - Carvacrol significantly reduced IL-1β and TNF-α (protein + mRNA) - Thymol significantly reduced IL-1β - Western Blot: Both reduced c-Fos, NFAT-1, NFAT-2 - Carvacrol lowered phospho-SAPK/JNK and phospho-STAT3 - Modulated JNK, STAT-3, AP-1, NFATs - Horvath G et al. (2022) - „Antioxidant and Anti-Inflammatory Effects of Thyme (Thymus vulgaris L.) Essential Oils„
Phenophase study - TEO from the beginning of flowering inhibited IL-6, IL-8, IL-1β, TNF-α potently - TEO from the end of flowering less effectively - Not just thymol, but synergism of all components Responsible - Increased CAT and SOD activity (antioxidant) - Fachini-Queiroz FC et al (2012) - „Effects of Thymol and Carvacrol, Constituents of Thymus vulgaris L. Essential Oil, on the Inflammatory Response„
In vivo study - TEO and carvacrol inhibited inflammatory edema and leukocyte migration - Important: Thymol showed irritative effect (chemoattractant) - Carvacrol was responsible for anti-inflammatory effects - Carvacrol (10mg/ear topical) reduced edema - Gago C. et al. (2025) - „Anti-Inflammatory Activity of Thymol and Thymol-Rich Essential Oils„
Review - Thymol (50 µg/mL) inhibited TLR4/MyD88/NF-κB/IL-1β signaling - Prevented cell aggregation, reduced necroptosis and pyroptosis - Standardized extract (0.3% thymol) in HBEpC/HTEpC: Reduced NF-κB p65 and p52, lowered IL-1β, IL-8, Muc5ac - Thymol: FDA „generally recognized as safe“ - Waheed F et al. (2024) - „Phytochemical Profiling and Therapeutic Potential of Thyme (Thymus spp.): A Medicinal Herb„
Comprehensive Review - Thymol reduces MAPK and NF-κB signaling pathways - Immunomodulating effects in autoimmune diseases - Can restore immune balance in dysregulated immune responses - Promising natural remedy for immunological disorders
Rosemary
Improves blood circulation and thus brings more oxygen and nutrients to inflamed areas, as inflamed tissue has an increased metabolism and needs more „fuel“ to heal. At the same time, waste products and inflammatory mediators need to be removed, which build up when circulation is poor, hindering healing and causing pain.
It therefore promotes healing processes thanks to improved blood circulation, faster removal of inflammatory substances and an intensified supply of repair material (amino acids, vitamins, minerals).
Muscle and joint pain is alleviated. The improved circulation relaxes hardened muscles, reduces stiffness and promotes mobility.
Rosemary activates the mind, which is particularly important in cases of chronic fatigue, because „Fatigue“ (extreme exhaustion) is a major symptom of autoimmune diseases. The invigorating effect on the brain and nervous system also has an anti-inflammatory effect by blocking the inflammatory pathways (NF-κB, COX-2).
Accordingly, rosemary is helpful for
- Rheumatoid arthritis
- Muscle stiffness
- Chronic tiredness (fatigue)
as the following studies show:
- Benincá JP et al. (2011) - „Analysis of the anti-inflammatory properties of Rosmarinus officinalis L. in mice„
Colitis model (relevant for IBD) - Rosemary essential oil in the diet reduced TNBS colitis - Preventive administration: reduced damage scores, wet weight, MPO activity - α-pinene and borneol (further components) enhanced the effect - α-pinene inhibits NF-κB translocation in LPS-stimulated THP-1 cells - 1,8-cineole inhibits prostaglandin/cytokine formation - Belkhodja H et al. (2021) - „Anti-osteoarthritis potential of peppermint and rosemary essential oils in a nanoemulsion form„
Osteoarthritis MIA model - Rosemary nanoemulsion significantly reduced osteoarthritis score - Reduced cartilage degradation and joint inflammation - Histology: Less mononuclear cell infiltration, thicker cartilage - Rosemary reduced migrating cells and inflammatory exudate - Effective in formalin test, writhing test, paw edema test - Borges RS et al (2019) - „Rosmarinus officinalis essential oil: Phytochemistry, anti-inflammatory activity, and mechanisms„
Review - Main components: 1,8-cineole, α-pinene, camphor - Mechanisms: NF-κB inhibition, arachidonic acid cascade suppression - Antioxidant activity prevents ROS damage - Smooth muscle relaxation (important in respiratory diseases) - Low toxicity - Khalil DY & Hassan OM (2024) - „Anti-inflammatory and Antioxidant Activity of Rosemary Essential Oil„
Iraqi study - GC-MS: eucalyptol (34,25%), α-pinene (20,98%), camphor (13,75%) - protein denaturation assay: significant anti-inflammatory effect - Inhibition rate of free radicals: 87.45% - At 50mg/mL comparable to diclofenac sodium - High antioxidant activity, comparable to Trolox - Zuzarte M et al. (2011) - „Chemical composition and antifungal activity of the essential oils of Lavandula viridis, Lavandula stoechas subsp. lusitanica, and Rosmarinus officinalis„
Anti-inflammatory and antioxidant study - Rosemary oil showed strong antioxidant activity - Inhibited lipid peroxidation - Protected against oxidative damage in cells - Rašković A et al. (2014) - „Antioxidant and anti-inflammatory activity of rosemary (Rosmarinus officinalis L.) essential oil„
In vivo inflammation models - Carrageenan-induced paw edema: Dose-dependent inhibition - Formalin test: Significant analgesic effect - Both test phases (neurogenic and inflammatory) affected - DPPH radical scavenging activity: IC50 = 8.7 mg/mL - Comparable to synthetic antioxidants
Citrus oils (orange, lemon, bergamot)
The main effect of citrus oils is on a psychological level and are therefore also immunomodulatory: anyone suffering from depression due to chronic pain, for example, also experiences a weakening of their immune system. A vicious circle that citrus oils are able to break.
By using the Serotonin- and Dopamine-release in the brain, they noticeably lift the mood, which reduces anxiety and depression when fear of relapses, worry about the future and frustration about restrictions no longer dominate.
They support the immune system indirectly by reducing stress, because a good mood means fewer stress hormones and this in turn means better immune regulation.
The antimicrobial effect of Limes also acts directly against bacteria and viruses, which can prevent infections that may trigger flare-ups.
Lemon oils are therefore effective for
- Depression resulting from chronic illnesses
- Stress management
- and as a pleasant addition to mixtures
according to the results of the following studies:
- Amorim JL et al (2016) - „Anti-Inflammatory Properties and Chemical Characterization of the Essential Oils of Four Citrus Species„
Four citrus species in comparison - C. limon, C. aurantifolia, C. limonia showed anti-inflammatory effects - Reduced cell migration, cytokine production, protein extravasation (carrageenan) - Pure limonene showed the same effects as the complete oils - limonene (31.1-65.7%), β-pinene (5.1-13.1%), γ-terpinene (10.8-12.2%) - Limonene inhibits cell migration and cytokine production - Kummer R et al. (2013) - „Evaluation of Anti-Inflammatory Activity of Citrus latifolia Tanaka Essential Oil and Limonene„
Citrus latifolia/limonene - Limonene (62% of the oil) reduced neutrophil migration to fMLP and LTB4 - 500mg/kg limonene significantly reduced TNF-α levels - Mechanism: inhibition of proinflammatory mediators in exudate - inhibition of leukocyte chemotaxis - In vitro: 1, 3, 10µg/mL limonene effective - Yoon WJ et al (2010) - „Anti-inflammatory Effects of Limonene from Yuzu (Citrus junos Tanaka) Essential Oil on Eosinophils„
Eosinophil study - Limonene (7.34mM) inhibited ROS production in eotaxin-stimulated HL-60 cells - 14.68mM decreased MCP-1 production via NF-κB activation - Comparable to proteasome inhibitor MG132 - Inhibited cell chemotaxis p38 MAPK-dependently (like SB203580) - Potential for asthma treatment via cytokine/ROS inhibition - Hirota R et al. (2010) - „Anti-inflammatory effect of essential oil through blocking JNK, ERK and NF-κB pathways„
Fingered Citron (C. medica) - Limonene (52,44%) + γ-Terpinene (28,41%) = 98,97% of oil - Inhibited NO and PGE2 by suppression of iNOS and COX-2 - Suppressed TNF-α, IL-1β, IL-6 - Mechanism: NF-κB activation prevented, IκB-α phosphorylation inhibited - Additionally: JNK and ERK pathway inhibition - Lee GH et al. (2023) - „Anti-Inflammatory Effects of Essential Oils from the Peels of Citrus Cultivars„
21 Citrus cultivars screening - C. japonica and C. maxima showed superior anti-inflammatory activity - Inhibited inflammatory mediator + proinflammatory cytokine expression - Active components: α-pinene, myrcene, limonene, β-ocimene, linalool, α-terpineol - α-Terpineol showed the strongest anti-inflammatory effect - Limonene was the main component in all 21 oils - El Omari N et al. (2024) - „Chemical Composition and Assessment of Anti-inflammatory, Antioxidant Activities of Citrus sinensis Essential Oil„
Citrus sinensis/Limonene Review - Limonene (70,15%) as main component - Dose-dependent NO and PGE2 reduction in RAW 264.7 macrophages - Elastase inhibition (IC50 = 65.72µg/mL), tyrosinase (IC50 = 102µg/mL) - Better than quercetin standard - Dermatoprotective - relevant for psoriasis, skin autoimmunity
Oil combinations for various autoimmune diseases
Multiple sclerosis (MS)
3 drops Copaiba (nerve protection, remyelination)
2 drops Incense (anti-inflammatory)
2 drops Oregano (T-cell balance)
1 drop Lavender (Stress)
In 30ml Carrier oil (e.g. jojoba oil)
Application:
Massage into the neck and spine twice a day
Additional inhalation (1-2 drops on a handkerchief)
Rheumatoid arthritis
3 drops Incense (cartilage protection, leukotriene inhibition)
2 drops Eucalyptus (macrophage modulation)
2 drops Rosemary (blood circulation)
1 drop Carnation (COX-2 inhibition)
In 30ml Carrier oil
Application:
Apply directly to affected joints
Massage in gently
2-3x daily
Crohn's disease / colitis
3 drops Incense (specific for intestine)
2 drops Lavender (gut-brain axis, stress)
2 drops Thyme Linalool (gentle antimicrobial effect)
1 drop Bergamot (mood)
In 30ml Carrier oil
Application:
Massage onto the abdomen in a clockwise direction
For cramps as a warm compress
Lupus (Systemic Lupus Erythematosus)
3 drops Copaiba (CB2 system)
2 drops Lavender (oxidative stress)
2 drops Oregano (T-cell balance)
1 drop Tea tree oil (monocyte modulation)
In 30ml Carrier oil
Application:
Especially joints and painful areas
Full body massage (avoid sun-exposed areas)
Interactions with biologics
What are biologics?
Biologics are biotechnologically produced drugs that specifically intervene in the immune system. They are used to treat moderate to severe autoimmune diseases.
Main classes of biologics
TNF-α inhibitors
Block tumor necrosis factor-alpha, a cytokine that promotes inflammation, e.g.
- Infliximab (Remicade)
- Adalimumab (Humira)
- Etanercept (Enbrel)
Use for rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis
Interleukin inhibitors
Block specific interleukins (IL-1, IL-6, IL-12/23, IL-17, IL-23).
- Tocilizumab (IL-6)
- Ustekinumab (IL-12/23)
- Secukinumab (IL-17)
Use for rheumatoid arthritis, psoriasis, psoriatic arthritis
B-cell depletors
Reduce B lymphocytes that produce antibodies.
- Rituximab (MabThera)
Use in rheumatoid arthritis, certain vasculitides
T-cell costimulation inhibitors
Block the activation of T cells.
- Abatacept (Orencia)
Use for rheumatoid arthritis
Integrin antagonists
Prevent the migration of immune cells into inflammatory foci.
- Vedolizumab (Entyvio)
- Natalizumab (Tysabri)
Use in chronic inflammatory bowel disease, multiple sclerosis
Potential additive anti-inflammatory effects
| Essential oil | Main active ingredients | Biologics class | Possible synergy mechanism | Potential advantages |
|---|---|---|---|---|
| Frankincense (Boswellia) | Boswellic acids | TNF-α inhibitors | Inhibition of leukotrienes + TNF-α blockade | Increased inhibition of inflammation |
| Turmeric (essential oil) | Turmeron, ar-Turmeron | IL-6 inhibitors | NF-κB inhibition + IL-6 blockade | Reduced systemic inflammation |
| Ginger | Gingerols, Shogaols | TNF-α inhibitors | COX-2 inhibition + TNF-α reduction | Pain relief, reduction of inflammation |
| Lavender | Linalool, linalyl acetate | All classes | Stress reduction, cortisol modulation | Improved disease control through stress management |
| Peppermint | Menthol, menthone | TNF-α inhibitors | Local pain relief + systemic anti-inflammation | Symptom relief |
Immunomodulatory effects
| Essential oil | Immune effect | Possible synergy with biologics | Hints |
|---|---|---|---|
| Tea tree oil | Antimicrobial, immunostimulant | Potentially counterproductive in immunosuppression | Caution with severe immunosuppression |
| Thyme | Antimicrobial, immunostimulant | Potentially protective against infections | Could reduce the risk of infection |
| Oregano | Highly antimicrobial | Potentially protective in immunosuppression | Only highly diluted and with caution |
| Camomile | Anti-inflammatory, calming | Additive anti-inflammatory effect | Well tolerated, no immune stimulation |
Theoretical risks
Increased immunosuppression
Biologicals specifically suppress parts of the immune system. Some essential oils could enhance this effect:
Risk scenario:
- Mechanism: Additive immunosuppressive effect
- Oils concerned: Frankincense, myrrh (high doses), turmeric
- Consequence: Increased risk of infection, delayed wound healing
- Clinical relevance: Probably low with topical application, higher with oral administration
Increased risk of infection
Biologics increase the risk of bacterial, viral and fungal infections, especially tuberculosis and opportunistic infections.
Critical considerations:
- Immunostimulating oils: Could theoretically weaken the effect of biologics (e.g. tea tree oil, oregano, thyme)
- Antimicrobial oils: Could have a protective effect, but cannot replace medical infection prophylaxis
- Paradox: Excessive immune stimulation could exacerbate autoimmune reactions
Allergic reactions and skin reactions
Patients on biologics often have more sensitive skin and an altered immune system.
Risks:
- Contact dermatitis due to essential oils
- Photosensitization (citrus oils)
- Exacerbation of skin manifestations of psoriasis or eczema
- Reactions at injection sites
Liver metabolism and drug interactions
Some essential oils affect cytochrome P450 enzymes.
Potential interactions:
- Oils with CYP enzyme induction/inhibition: Peppermint, grapefruit, bergamot
- Risk: Altered clearance of other drugs (but not of the biologics themselves, as these are proteolytically degraded)
- Clinical relevance: More relevant with concomitant use of DMARDS (e.g. methotrexate)
Specific considerations for immunosuppressants
TNF-α inhibitors + essential oils
Moderate risks:
- Frankincense: Could have additive anti-inflammatory effects, but could also increase immunosuppression
- Ginger: Relatively safe, predominantly symptomatic effect
- Turmeric: caution with high doses, note the risk of bleeding
Recommendation: Topical application probably safe, discuss oral supplementation with doctor
Interleukin inhibitors + essential oils
Take special care:
- IL-17 inhibitors increase the risk of candidiasis: antifungal oils such as tea tree oil could theoretically help, but caution when applied to the skin
- IL-6 inhibitors: Increased risk of infection, no strong immunosuppressive oils
B-cell depletors (rituximab)
Extreme caution:
- Strongly immunosuppressive
- Long-term immunosuppression (6-12 months)
- Avoid all potentially immunomodulating essential oils in therapeutic doses
- Only mild, symptomatic oils in low doses (lavender for relaxation)
Practical recommendations
Safe use with biologics therapy:
- Always discuss with the treating rheumatologist/gastroenterologist
- Preferred topical application (lower systemic absorption)
- Use low concentrations (1-2% in carrier oil)
- Antimicrobial oils: Only if specifically required and in consultation
- Avoid immunostimulant oils during active biologics therapy
- Perform patch test due to increased skin sensitivity
Relative safety - Recommended oils:
- Lavender: Relaxation, sleep promotion
- Camomile: Anti-inflammatory, calming
- Peppermint: Symptomatic pain relief (topical, diluted)
- Ginger: Nausea, moderate anti-inflammatory effect
... to be avoided or only after consultation with a doctor:
- Frankincense/Myrrh: In high doses
- Oregano/thyme: Strongly immunomodulating
- Tea tree oil: Immunostimulating
- All oral income therapeutic doses
Conclusion
The interaction between essential oils and biologics has been the subject of little scientific research. The theoretical risks mainly concern increased immunosuppression and risk of infection. Topical application of mild essential oils in low concentrations is probably safe, but any application should be discussed with the treating physician. For autoimmune diseases undergoing biologic therapy, safety is paramount.
Important: This is not medical advice. Any use of complementary therapies for autoimmune diseases must be individually agreed with the specialist.