Atopic dermatitis, commonly referred to as eczema, is a chronic skin condition characterized by itchy, inflamed skin. It is the most common type of eczema, affecting millions of people worldwide, across all ages but most commonly seen in children. This condition not only affects the skin but can have profound impacts on quality of life, causing sleep disturbances and affecting mental health due to its visible and often uncomfortable symptoms.
Atopic dermatitis is part of what is known as the atopic triad, which also includes asthma and allergic rhinitis (hay fever). This association underscores the immunological aspect of the disease, where an overactive immune system response leads to skin inflammation. The exact cause of atopic dermatitis is unknown, but it is believed to be a combination of genetic, environmental, and immune system factors.
The symptoms of atopic dermatitis can vary significantly from person to person but commonly include dry, scaly skin, red and inflamed areas, severe itching, which can be worse at night, dark coloured patches of skin, swelling, oozing, or crusting. These symptoms can lead to a cycle of itching and scratching, causing further irritation, skin infections, and possibly scars.
Diagnosis is typically based on a physical examination of the skin and a review of the patient’s medical history. Doctors may also perform patch testing or other tests to rule out other conditions that could mimic atopic dermatitis, such as psoriasis or contact dermatitis.
While there is no cure for atopic dermatitis, treatments are available that can manage symptoms and flare-ups. Treatment plans are often tailored to the individual’s symptoms. Options include moisturizers used daily to help maintain the skin’s natural barrier, topical corticosteroids to reduce inflammation and relieve itching, topical calcineurin inhibitors for reducing inflammation, phototherapy using ultraviolet light to reduce itchiness and inflammation, systemic medications for severe cases, and drugs that suppress the immune system or biologics may be used. Lifestyle changes can also play a crucial role in managing atopic dermatitis. These may involve identifying and avoiding triggers such as certain soaps, fabrics, and allergens. Stress management techniques and maintaining a skin care routine are also beneficial.
Living with atopic dermatitis can be challenging, but with the right strategies and support, individuals can manage their symptoms and lead healthy lives. It’s important for patients and families to educate themselves about the condition and to work closely with healthcare providers to develop an effective treatment plan. Education on the condition, alongside support groups, can provide invaluable assistance to those affected, helping them to manage not only the physical but also the emotional and social impacts of the condition.
Atopic dermatitis is a complex skin condition that requires a multifaceted approach to management. Through a combination of medical treatment, lifestyle adjustments, and supportive care, individuals with atopic dermatitis can achieve relief from their symptoms and improve their quality of life.
PATHOPHYSIOLOGY OF ATOPIC DERMATITIS
The pathophysiology of atopic dermatitis (AD) is intricate, involving an interplay between genetic, environmental, immunological, and skin barrier factors. Understanding this complex interaction is crucial for developing targeted treatments and managing the condition effectively.
Atopic dermatitis has a strong genetic component, with a higher incidence in individuals with a family history of AD or other atopic diseases. Mutations in the gene encoding for filaggrin, a protein critical for skin barrier function, are found in a significant number of patients with AD. This mutation leads to a compromised skin barrier, making the skin more susceptible to irritants, allergens, and infections. Filaggrin is a crucial protein involved in maintaining the skin’s barrier function, playing a significant role in skin health and the pathophysiology of various dermatological conditions, including atopic dermatitis (AD). The name “filaggrin” derives from “filament aggregating protein,” reflecting its role in aggregating keratin filaments in skin cells, which is essential for the formation of the stratum corneum, the outermost layer of the skin. Filaggrin is synthesized as a large precursor molecule called profilaggrin, which is stored in the keratohyalin granules of the skin’s epidermal cells (keratinocytes). As these cells mature and move towards the skin surface, profilaggrin is broken down into smaller filaggrin units. Filaggrin plays a critical role by aggregating keratin filaments into tight bundles, contributing to the formation of a dense, protective layer that makes up the stratum corneum. This process is essential for the skin’s barrier function, preventing water loss and protecting against the entry of pathogens, allergens, and irritants. Mutations in the FLG gene, which encodes filaggrin, have been identified as a major risk factor for developing atopic dermatitis and are associated with a more severe disease course. These genetic mutations lead to a reduction or absence of functional filaggrin protein, compromising the skin barrier. As a result, the skin becomes more permeable to allergens and irritants, leading to increased inflammation and the characteristic symptoms of AD, such as dryness, itching, and recurrent rashes. In addition to AD, filaggrin mutations are associated with a higher risk of developing other allergic conditions, such as asthma and allergic rhinitis, in a phenomenon known as the “atopic march.” These mutations have also been linked to ichthyosis vulgaris, a skin condition characterized by dry, scaly skin, which further underscores the importance of filaggrin in maintaining normal skin hydration and barrier function. Understanding the role of filaggrin in skin barrier function and its implications in atopic dermatitis has led to the development of targeted therapeutic strategies. Treatments aimed at repairing the skin barrier, such as the use of moisturizers containing ceramides (lipids that are also important for barrier function) and other barrier-enhancing ingredients, can help mitigate the effects of filaggrin deficiency. Additionally, ongoing research is exploring the potential for gene therapy and other molecular approaches to directly address the underlying genetic defects in filaggrin and improve skin barrier function in individuals with AD. Filaggrin plays a vital role in skin health by maintaining the barrier integrity of the skin. Mutations in the filaggrin gene significantly contribute to the development and severity of atopic dermatitis, highlighting the importance of the skin barrier in the pathogenesis of this condition. Advances in understanding the molecular mechanisms underlying filaggrin function and dysfunction are guiding the development of more effective treatments for atopic dermatitis and related skin conditions.
The skin serves as the body’s primary barrier against environmental threats. In AD, this barrier is compromised due to alterations in the composition and organization of lipids in the stratum corneum (the outermost layer of the skin), reduced production of antimicrobial peptides, and structural defects from filaggrin mutations. This dysfunction allows allergens and microbes to penetrate the skin and initiate immune responses, leading to inflammation and the characteristic symptoms of AD.
Atopic dermatitis is marked by an imbalance in the immune system, particularly an overactive T-helper cell (Th2) response. This imbalance leads to increased levels of certain cytokines (signaling proteins) such as interleukin (IL)-4, IL-13, and IL-31, which play key roles in inflammation and itchiness. The Th2 response also promotes the production of immunoglobulin E (IgE), which further contributes to allergic responses.
In chronic stages of AD, there is a shift towards a mixed immune response involving Th1 and Th17 pathways, indicating the complexity of the immune dysregulation in AD.
Environmental factors, including allergens, irritants, microbial flora, and climate conditions, can exacerbate AD. For instance, house dust mites, pollen, and pet dander may trigger immune responses in sensitive individuals. Additionally, certain soaps and detergents can strip the skin of its natural oils, worsening the skin barrier dysfunction.
The microbiome of the skin also plays a role in AD. Patients with AD often have an imbalance in skin flora, with an over colonization of Staphylococcus aureus, which can exacerbate skin inflammation and barrier damage. Here comes the relevance of using potentized form of homeopathic nosode Staphylococcin 30 in the treatment of atopic dermatitis
Stress and emotional factors can worsen AD symptoms, possibly through stress-induced changes in immune function and skin barrier properties. Hormonal changes, particularly during puberty, pregnancy, and certain phases of the menstrual cycle, can also influence AD symptoms, indicating a hormonal influence on the disease’s pathophysiology.
The pathophysiology of atopic dermatitis is complex and multifactorial, involving genetic predispositions, skin barrier defects, immune dysregulation, and environmental factors. This complexity underscores the importance of a holistic approach to treatment, targeting not just the symptoms but also the underlying mechanisms driving the disease. Advances in understanding the molecular and cellular pathways involved in AD have led to the development of targeted therapies, offering hope for more effective management strategies.
ROLE OF ENZYMES IN ATOPIC DERMATITIS
Atopic dermatitis (AD) is characterized by inflammation and barrier disruption of the skin, involving a complex network of immune cells, cytokines, and signalling pathways. Enzymes play a crucial role in the pathophysiology of AD, contributing to both the development and exacerbation of the condition. Below, we explore some of the key enzymes involved in AD, along with their activators and inhibitors, which are pivotal in understanding the disease mechanisms and the development of targeted therapies.
Phosphodiesterase 4 (PDE4) is involved in the regulation of cyclic adenosine monophosphate (cAMP) levels in cells. High PDE4 activity reduces cAMP, promoting the release of inflammatory cytokines. In AD, PDE4 overexpression contributes to inflammation. Inflammatory cytokines can enhance PDE4 expression. PDE4 inhibitors, such as crisaborole, are used topically to treat AD by reducing inflammation. Molecular imprints of inflammatory cytokines will be helpful in managing the over expression of PDE4.
Kallikrein-Related Peptidase 7 (KLK7) is a serine protease that degrades corneodesmosomes, the protein structures that hold skin cells together. Overactivity of KLK7 can lead to impaired skin barrier function, a hallmark of AD. Inflammatory cytokines and dysregulated skin pH can increase KLK7 activity. Specific serine protease inhibitors and maintaining an optimal skin pH can help to control KLK7 activity. Here also, molecular imprints of inflammatory cytokines will be helpful in managing the over expression of enzyme KLk7.
Janus Kinases (JAK) are involved in the signalling pathways of various cytokines implicated in AD. JAK activation leads to the transcription of pro-inflammatory genes. Cytokines such as interleukins (IL-4, IL-13) bind to their receptors and activate the JAK-STAT pathway, promoting inflammation. JAK inhibitors, such as tofacitinib and baricitinib, block cytokine signaling and are being explored as treatments for AD. Molecular imprints of inflammatory cytokines will be helpful in managing the over expression of enzyme JAK.
Matrix Metalloproteinases (MMPs) are enzymes that degrade extracellular matrix proteins. They are involved in tissue remodeling and inflammation. Elevated levels of MMPs can contribute to skin barrier dysfunction and inflammation in AD. Inflammatory cytokines and UV radiation can increase MMP expression. Tetracyclines and synthetic MMP inhibitors can reduce MMP activity, potentially benefiting AD patients by preserving skin structure. Molecular imprints of inflammatory cytokines will be helpful in managing the over expression of enzyme Matrix Metalloproteinases (MMPs).
Omega-Hydrolase is an enzyme involved in the metabolism of fatty acids and lipids in the skin. Dysregulation can affect the skin barrier and inflammatory processes. Dysregulated lipid metabolism pathways can increase the activity of omega-hydrolases. Research is ongoing to understand the regulation of omega-hydrolases and their potential as therapeutic targets in AD.
Transglutaminase enzyme is involved in the formation of the cornified cell envelope, a critical component of the skin barrier. Its altered activity is associated with the disrupted skin barrier in AD. Calcium ions and retinoic acid can stimulate transglutaminase activity. Certain isoforms of transglutaminase may be overactive in AD, and inhibitors are being studied as potential treatments.
Inflammatory cytokines are small signalling proteins released by cells that have a specific effect on the interactions and communications between cells. They play a pivotal role in the immune system, particularly in the body’s response to infection and injury, by mediating and regulating inflammation, immunity, and hematopoiesis (the formation of blood cellular components). However, when produced in excess or not adequately regulated, these cytokines can contribute to inflammatory and autoimmune diseases.
Interleukin-1 (IL-1) is a key mediator of the inflammatory response and is involved in a variety of cellular activities, including cell proliferation, differentiation, and apoptosis (cell death). It is also one of the cytokines involved in the fever response. Overproduction is associated with various conditions, including rheumatoid arthritis, psoriasis, and inflammatory bowel diseases. Interleukin-6 (IL-6) plays a role in inflammation and the maturation of B cells (a type of white blood cell). It is also involved in the body’s response to infections and tissue injuries. Elevated levels are found in chronic inflammatory and autoimmune diseases such as rheumatoid arthritis, lupus, and osteoporosis. Tumour Necrosis Factor-alpha (TNF-α) is involved in systemic inflammation and stimulates the acute phase reaction, which is part of the body’s immune response. It has a range of actions including the induction of fever, apoptotic cell death, cachexia (wasting syndrome), and inflammation. High levels of TNF-α have been implicated in a variety of diseases, including rheumatoid arthritis, Crohn’s disease, and ankylosing spondylitis. Interferon-gamma (IFN-γ) is produced primarily by natural killer cells and T lymphocytes. It has antiviral, immunoregulatory, and anti-tumor properties, playing a crucial role in innate and adaptive immunity. Its dysregulation is associated with autoimmune diseases like multiple sclerosis and type 1 diabetes. Interleukin-17 (IL-17) is produced by Th17 cells and plays a role in inducing and mediating proinflammatory responses. IL-17 stimulates the production of many other cytokines, chemokines, and prostaglandins that, in turn, increase inflammation. It is implicated in conditions such as psoriasis, rheumatoid arthritis, and asthma.
In chronic inflammatory diseases such as atopic dermatitis, the prolonged production of inflammatory cytokines can cause tissue damage and contribute to the disease pathology. This understanding has led to the development of cytokine inhibitors as therapeutic agents. MIT Homeopathy proposes to use molecular imprinted forms these inflammatory cytokines in 30c potency as therapeutic agents for atopic dermatitis.
The enzymes involved in AD play significant roles in the disease’s pathophysiology, influencing inflammation, skin barrier integrity, and immune responses. Understanding the activators and inhibitors of these enzymes is crucial for developing targeted therapies that can more effectively manage AD symptoms and improve patient outcomes. The therapeutic landscape for AD continues to evolve as research uncovers new targets and strategies to modulate enzyme activity within the skin.
ROLE OF ANTIBODIES IN ATOPIC DERMATITIS
Antibodies themselves are not causative agents of atopic dermatitis (AD), but certain immune responses involving antibodies can play a significant role in the pathogenesis and exacerbation of this condition. AD is characterized by a complex interplay between genetic, environmental, and immunological factors, with dysregulated immune responses being central to its development and persistence. Among these immune responses, the role of Immunoglobulin E (IgE) antibodies is particularly noteworthy.
Immunoglobulin E (IgE) is a class of antibodies that plays a crucial role in the body’s response to allergens. In many individuals with AD, especially those with the moderate to severe form of the disease, elevated levels of IgE are observed. These elevated IgE levels are associated with hypersensitivity reactions to environmental allergens, foods, and other triggers. In susceptible individuals, exposure to specific allergens can lead to the production of allergen-specific IgE antibodies. These antibodies bind to the surface of mast cells and basophils in the skin and other tissues. Upon re-exposure to the allergen, it can cross-link with the bound IgE on these cells, leading to cell activation and the release of inflammatory mediators such as histamine, cytokines, and leukotrienes. This inflammatory cascade can result in the symptoms of AD, including redness, swelling, and intense itchiness. The chronic activation of the immune system and the ongoing inflammatory response in the skin can disrupt the skin barrier function, making it more susceptible to infections and further allergen penetration. This creates a vicious cycle of inflammation, barrier disruption, and sensitization to new allergens, exacerbating the condition.
While IgE-mediated responses are prominent in the pathophysiology of AD, other antibody-related mechanisms can also contribute indirectly to the disease. For example, autoantibodies targeting skin components have been identified in some patients with AD, suggesting that autoimmunity might play a role in the disease’s development or exacerbation in certain cases.
Understanding the role of IgE and other immunological factors in AD has led to the development of targeted therapies. For instance, monoclonal antibodies that block IgE (e.g., omalizumab) or interfere with the pathways activated by IgE and other cytokines involved in AD (e.g., dupilumab, which targets the interleukin-4 receptor alpha) have shown promise in managing severe cases of AD. These treatments can significantly reduce the severity of symptoms and improve the quality of life for individuals with AD.
While antibodies themselves are not the cause of atopic dermatitis, the immune response involving IgE antibodies to environmental and dietary allergens plays a pivotal role in the development, persistence, and exacerbation of this condition. Targeting these immune responses offers a therapeutic avenue for managing AD, especially in its more severe forms. Immunoglobulin E is an ideal target in MIT approach also.
ROLE OF HORMONES IN ATOPIC DERMATITIS
Hormones play a significant role in atopic dermatitis (AD), influencing both the course of the disease and its symptom severity. The interplay between hormones and AD underscores the complexity of this skin condition, which is affected by a myriad of factors including genetic predisposition, environmental triggers, and now, hormonal fluctuations. Here are some key hormones implicated in the pathophysiology of atopic dermatitis and their roles:
Cortisol, often referred to as the “stress hormone,” is produced by the adrenal glands in response to stress. It has potent anti-inflammatory effects and plays a role in regulating the immune response. In the context of AD, chronic stress can lead to dysregulation of cortisol production and secretion, potentially exacerbating inflammation and worsening AD symptoms. Reduced cortisol levels or sensitivity could impair the body’s ability to suppress inflammatory responses, contributing to the severity of AD flare-ups.
Estrogen has been observed to influence skin barrier function, immune response, and inflammation. Its effects on AD are complex and can vary depending on the levels and context. Some studies suggest that high levels of estrogen can exacerbate AD symptoms, while others indicate it might have protective effects, especially in improving skin barrier function. Estrogen can modulate the immune system and influence the production of skin lipids, which are essential for maintaining the skin barrier. However, fluctuations in estrogen levels, such as those occurring during the menstrual cycle, pregnancy, or menopause, can impact AD severity.
Thyroid hormones, including thyroxine (T4) and triiodothyronine (T3), are crucial for regulating metabolism and can also affect skin health. Abnormal levels of thyroid hormones have been associated with various skin conditions, including AD. Both hyperthyroidism and hypothyroidism can influence skin barrier function and immune responses, potentially affecting AD. The mechanisms may involve alterations in skin hydration, lipid metabolism, and immune regulation.
Androgens, such as testosterone, can influence skin health and have been linked to changes in AD symptoms. The role of androgens in AD is complex and not fully understood, with research suggesting both exacerbating and mitigating effects on the disease. Androgens can influence skin thickness, sebum production, and immune function. These effects can indirectly affect the skin’s barrier function and inflammatory responses, thereby impacting AD severity.
Growth Hormone and Insulin-like Growth Factor-1 (IGF-1) play roles in skin development and regeneration. They can influence AD through effects on skin barrier function and immune responses. GH and IGF-1 can promote skin cell proliferation and differentiation, essential for maintaining a healthy skin barrier. However, they can also influence inflammation and immune responses, potentially affecting AD pathology.
Prolactin, primarily known for its role in lactation, also has immunomodulatory effects. Elevated prolactin levels have been associated with autoimmune diseases and may influence AD severity. Prolactin can enhance inflammatory responses and influence skin barrier integrity, potentially exacerbating AD symptoms.
Hormones significantly influence the pathophysiology of atopic dermatitis, affecting both the immune response and skin barrier function. These effects can vary based on the hormonal balance within an individual, which may be influenced by factors such as stress, gender, age, and overall health. Understanding the hormonal influences on AD can provide insights into individual variations in disease severity and response to treatment, offering potential avenues for personalized therapeutic strategies.
ADVERSE EFFECTS OF ALLOPATHIC DRUGS IN ATOPIC DERMATITIS
Atopic dermatitis (AD) is primarily an inflammatory skin condition with a multifactorial etiology, including genetic predisposition, environmental factors, and immune system dysfunction. However, certain medications have been associated with exacerbating or potentially contributing to the development of AD symptoms in susceptible individuals. It’s important to note that while these drugs can influence AD, they do not cause the condition in the traditional sense but can trigger flares in people with a predisposition to the disease.
Topical Corticosteroids, even though a mainstay in the treatment of AD to reduce inflammation and symptoms, overuse or inappropriate use can lead to worsening of the condition or a rebound effect upon withdrawal. This phenomenon is known as “topical steroid withdrawal” (TSW) or “red skin syndrome” and can result in severe exacerbation of AD symptoms.
Beta-blockers, used to treat high blood pressure and other cardiovascular conditions, have been reported to induce or exacerbate AD in some cases. The mechanism may involve the suppression of anti-inflammatory pathways or alteration of immune responses.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) can exacerbate skin conditions, including AD, in susceptible individuals. The exact mechanism is not entirely understood but may involve alterations in prostaglandin metabolism and immune function.
Angiotensin-Converting Enzyme (ACE) Inhibitors, another class of blood pressure medication, have been associated with the exacerbation of AD. The mechanism may involve modulation of the renin-angiotensin system, which can affect inflammatory processes.
Certain antimicrobials and antibiotics, especially when used excessively or inappropriately, can disrupt the skin and gut microbiota. This disruption can potentially influence AD severity due to the crucial role of microbiota in modulating immune responses and maintaining skin barrier integrity.
Some psychotropic drugs, including lithium and antipsychotics, have been reported to exacerbate skin conditions like AD. These drugs can influence immune function and inflammatory pathways, potentially worsening AD symptoms.
It is crucial for patients with atopic dermatitis to discuss any potential medication-related concerns with their healthcare provider. In many cases, the benefits of using these medications for their intended purposes outweigh the potential risks of exacerbating AD. However, in individuals with severe AD or those particularly sensitive to medication-induced flares, alternative treatments may need to be considered, and careful monitoring is advised to manage both the underlying condition and AD symptoms effectively.
ROLE OF ELEMENTAL CHEMICALS IN ATOPIC DERMATITIS
Atopic dermatitis (AD) is a complex condition influenced by a combination of genetic, environmental, and immunological factors. Although elemental chemicals themselves do not directly cause AD, certain elements can exacerbate symptoms in susceptible individuals or contribute to conditions that promote the development or worsening of AD. Here are some elemental chemicals and how they may relate to AD:
Nickel is a well-known skin irritant and allergen. Exposure to nickel, often through jewelry, buttons, and other metal objects, can trigger allergic contact dermatitis, which can exacerbate AD symptoms in sensitized individuals.
Similar to nickel, chromium can cause allergic contact dermatitis. Occupational exposure to chromium compounds, as well as exposure through leather products treated with chromium, can worsen skin conditions like AD.
Cobalt, another common allergen, is often found in metal-plated objects, cosmetics, and some medical implants. Sensitivity to cobalt can manifest as allergic contact dermatitis, potentially aggravating AD.
Mercury, especially in its organic form (e.g., methylmercury), can be a potent neurotoxin and immunotoxin. Exposure to high levels of mercury is associated with immune system dysregulation, which could potentially influence the severity or incidence of immune-related conditions like AD.
Lead exposure has been linked to various health issues, including potential impacts on the immune system. While the direct relationship between lead exposure and AD is less clear, minimizing exposure to lead is recommended due to its other well-documented health risks.
While not elemental chemicals themselves, the minerals calcium (Ca) and magnesium (Mg) in high concentrations contribute to hard water, which has been associated with an increased risk of developing AD. Hard water can affect the skin’s barrier function by leaving a residue that irritates the skin and potentially exacerbates AD symptoms.
Elements such as sulfur (S) and nitrogen (N) in air pollutants, including sulfur dioxide (SO2) and nitrogen oxides (NOx), can contribute to the formation of fine particulate matter and ground-level ozone. These pollutants can irritate the respiratory tract and skin, potentially worsening conditions like AD.
ROLE OF PHYTOCHEMICALS IN ATOPIC DERMATITIS
Phytochemicals, naturally occurring compounds found in plants, are widely recognized for their health benefits, including anti-inflammatory, antioxidant, and immunomodulatory properties. However, their effects on atopic dermatitis (AD) can vary greatly, with some phytochemicals potentially exacerbating the condition in susceptible individuals. While the therapeutic potential of many phytochemicals in managing AD is promising, awareness of their potential adverse effects is essential for those with the condition. Here are some phytochemicals that can have adverse effects on AD:
Fragrance compounds, which are common in plant extracts used in cosmetics and personal care products, can act as irritants or allergens for those with AD. Natural products are not inherently safe, and substances like limonene, linalool, and geraniol, despite being naturally derived, can cause contact dermatitis and exacerbate AD symptoms.
Essential oils, highly concentrated phytochemicals, can sometimes worsen AD. For instance, tea tree oil, while having antimicrobial properties, can irritate the skin and trigger AD flares in some individuals. Similarly, peppermint and eucalyptus oils, despite their soothing reputations, can be irritants.
Certain herbal extracts can irritate the skin or trigger allergic reactions, exacerbating AD. For example, some people might react negatively to witch hazel, calendula, or chamomile, despite these herbs often being recommended for their soothing properties. The reaction can vary significantly from person to person.
Alkaloids found in some plants can have strong biological effects, and their impact on the skin can sometimes be detrimental to individuals with AD. For example, capsaicin (from chili peppers) can cause burning sensations and irritate the skin, potentially worsening AD symptoms.
Phenols, like eugenol found in clove oil, can act as irritants or allergens, exacerbating skin conditions like AD. While they have antimicrobial and anti-inflammatory properties, their potential to cause skin irritation must be considered.
Natural latex from the rubber tree contains phytochemicals that can cause allergic reactions. People with AD may have a heightened sensitivity to latex, leading to contact dermatitis and exacerbation of their symptoms.
Certain foods high in phytochemicals can sometimes trigger AD flares in people with food sensitivities or allergies. For example, citrus fruits, tomatoes, and nuts contain various phytochemicals that can exacerbate AD in some individuals through allergic reactions or food intolerances.
It is important to note that the response to phytochemicals is highly individual, and what exacerbates AD in one person may not affect or could even benefit another. The complexity of AD, coupled with the diverse effects of phytochemicals, underscores the importance of a personalized approach to managing the condition. Individuals with AD should patch test any new products containing phytochemicals and consult healthcare providers before incorporating new phytochemicals into their treatment regimen, especially if they have a history of sensitivities or allergies.
MIT HOMEOPATHY APPROACH TO ATOPIC DERMATITIS
MIT or Molecular Imprints Therapeutics refers to a scientific hypothesis that proposes a rational model for biological mechanism of homeopathic therapeutics.
According to MIT hypothesis, potentization involves a process of ‘molecular imprinting’, where in the conformational details of individual drug molecules are ‘imprinted or engraved as hydrogen- bonded three dimensional nano-cavities into a supra-molecular matrix of water and ethyl alcohol, through a process of molecular level ‘host-guest’ interactions. These ‘molecular imprints’ are the active principles of post-avogadro dilutions used as homeopathic drugs. Due to ‘conformational affinity’, molecular imprints can act as ‘artificial key holes or ligand binds’ for the specific drug molecules used for imprinting, and for all pathogenic molecules having functional groups ‘similar’ to those drug molecules. When used as therapeutic agents, molecular imprints selectively bind to the pathogenic molecules having conformational affinity and deactivate them, thereby relieving the biological molecules from the inhibitions or blocks caused by pathogenic molecules.
According to MIT hypothesis, this is the biological mechanism of high dilution therapeutics involved in homeopathic cure. According to MIT hypothesis, ‘Similia Similibus Curentur’ means, diseases expressed through a particular group of symptoms could be cured by ‘molecular imprints’ forms of drug substances, which in ‘molecular’ or crude forms could produce ‘similar’ groups of symptoms in healthy individuals. ‘Similarity’ of drug symptoms and diseaes indicates ‘similarity’ of pathological molecular inhibitions caused by drug molecules and pathogenic molecules, which in turn indicates conformational ‘similarity’ of functional groups of drug molecules and pathogenic molecules. Since molecular imprints of ‘similar’ molecules can bind to ‘similar ligand molecules by conformational affinity, they can act as the therapeutics agents when applied as indicated by ‘similarity of symptoms. Nobody in the whole history could so far propose a hypothesis about homeopathy as scientific, rational and perfect as MIT explaining the molecular process involed in potentization, and the biological mechanism involved in ‘similiasimilibus- curentur, in a way fitting well to modern scientific knowledge system.
If symptoms expressed in a particular disease condition as well as symptoms produced in a healthy individual by a particular drug substance were similar, it means the disease-causing molecules and the drug molecules could bind to same biological targets and produce similar molecular errors, which in turn means both of them have similar functional groups or molecular conformations. This phenomenon of competitive relationship between similar chemical molecules in binding to similar biological targets scientifically explains the fundamental homeopathic principle Similia Similibus Curentur.
Practically, MIT or Molecular Imprints Therapeutics is all about identifying the specific target-ligand ‘key-lock’ mechanism involved in the molecular pathology of the particular disease, procuring the samples of concerned ligand molecules or molecules that can mimic as the ligands by conformational similarity, preparing their molecular imprints through a process of homeopathic potentization upto 30c potency, and using that preparation as therapeutic agent.
Since individual molecular imprints contained in drugs potentized above avogadro limit cannot interact each other or interfere in the normal interactions between biological molecules and their natural ligands, and since they can act only as artificial binding sites for specific pathogentic molecules having conformational affinity, there cannot by any adverse effects or reduction in medicinal effects even if we mix two or more potentized drugs together, or prescribe them simultaneously- they will work.
Based on above discussions, potentized forms of Cortisol 30, Diethylstilbesterol 30, Staphylococcin 30, Immunoglobulin E 30, Lithium carb 30, Prolactin 30, Testosterone 30, Thyroidinum 30, Sulphur 30, Niccolum 30, Cobaltum 30 etc should be incorporated in the MIT prescriptions for Atopic Dermatitis.
REDEFINING HOMEOPATHY 