Psoriasis is a chronic autoimmune condition that affects the skin, causing rapid skin cell production resulting in scaling on the skin’s surface. Characterized by patches of abnormal skin, these areas are typically red, itchy, and scaly. Psoriasis varies in severity, from small, localized patches to complete body coverage. This condition is not contagious, meaning it cannot be passed from person to person.
The exact cause of psoriasis is not fully understoodY, but it is believed to be related to an immune system problem with T cells and other white blood cells, called neutrophils, in the body. Normally, T cells help protect the body against infection and disease, but in the case of psoriasis, theyY mistakenly attack healthy skin cells, speeding up the skin cell production process.
Family history plays a crucial role. Having one parent with psoriasis increases your risk, and this risk doubles if both parents are affected. Certain infections such as strep throat can trigger psoriasis. High stress levels can impact the immune system and may trigger or worsen psoriasis. Tobacco use can increase the risk of developing psoriasis and may increase the severity of the disease. Excess weight increases the risk, and psoriasis may appear in skin folds.
Plaque Psoriasis is the most common form, characterized by raised, inflamed, red lesions covered by a silvery white scale.
Guttate Psoriasis often starts in childhood or young adulthood, showing up as small, water-drop-shaped sores on the trunk, arms, legs, and scalp. Inverse Psoriasis causes bright red, shiny lesions in areas such as the armpits, groin, under the breasts, and around the genitals. Pustular Psoriasis is characterized by white pustules surrounded by red skin. Erythrodermic Psoriasis is the least common type, which can cover your entire body with a red, peeling rash that can itch or burn intensely.
Symptoms of psoriasis vary depending on the type but may include Red patches of skin covered with thick, silvery scales, Small scaling spots, Dry, cracked skin that may bleed, Itching, burning, or soreness, Thickened, pitted, or ridged nails, Swollen and stiff joints etc.
Diagnosing psoriasis involves examining the affected skin. Sometimes, a biopsy is necessary to rule out other skin disorders. There are no special blood tests or diagnostic tools for psoriasis.
Living with psoriasis can be challenging, but with the right treatment and lifestyle adjustments, most people can manage their symptoms and lead active, healthy lives. It’s also important to seek support from friends, family, or support groups, as dealing with a chronic condition can be mentally and emotionally taxing.
Psoriasis is more than a skin condition; it is a chronic disease that, for many, requires lifelong management. Understanding the disease, its triggers, and treatment options can empower those affected to live better with psoriasis. Regular consultations with healthcare providers are crucial to effectively manage this condition and improve the quality of life.
Psoriatic arthritis (PsA) is a chronic, autoimmune inflammatory arthritis that affects some people with psoriasis, a condition characterized by red patches of skin topped with silvery scales. PsA can develop in individuals who have a history of psoriasis, although in some cases, the arthritis symptoms might appear before the skin lesions do. The condition can affect any part of the body, including fingertips and spine, and ranges from relatively mild to severe.
PATHOPHYSIOLOGY OF PSORIASIS
The pathophysiology of psoriasis is complex, involving an interplay between the immune system, genetics, and environmental factors that lead to the proliferation of skin cells and inflammation. At its core, psoriasis is considered an immune-mediated disease that results in hyperproliferation and aberrant differentiation of keratinocytes, which are the predominant cells in the outer layer of the skin.
Psoriasis has a strong genetic component, with multiple genes implicated in its pathogenesis. These genes are often involved in the immune system, particularly those affecting the regulation of T cells and the major histocompatibility complex (MHC). The disease process begins when certain environmental triggers (like infections, stress, or injury) activate the immune system. In psoriasis, T cells (a type of white blood cell) become overactive and migrate to the skin. These activated T cells release cytokines, particularly tumor necrosis factor-alpha (TNF-alpha), interleukin-17 (IL-17), interleukin-22 (IL-22), and interleukin-23 (IL-23), which cause inflammation and promote the rapid growth of skin cells. The cytokines create an inflammatory cascade that increases the production of keratinocytes and changes their differentiation process. The result is the thickened, scaly patches characteristic of psoriasis.
Keratinocyte Hyperproliferation: Under normal conditions, skin cells (keratinocytes) mature and are replaced every 28 to 30 days. In psoriasis, this process is significantly accelerated, and skin cells can cycle every 3 to 5 days. This rapid turnover doesn’t allow for the normal shedding of skin cells, leading to the accumulation of cells on the skin’s surface, forming plaques. Angiogenesis: New blood vessel formation (angiogenesis) is also a feature of psoriatic lesions, further supporting the growth of plaques and inflammation.
While genetic predisposition plays a crucial role, environmental factors such as stress, skin trauma (the Koebner phenomenon), infections (especially streptococcal), and certain medications can trigger or exacerbate the disease.
Different types of psoriasis (e.g., plaque, guttate, inverse, pustular, and erythrodermic) share the fundamental pathophysiological process of immune dysregulation and skin proliferation but differ in their specific manifestations, triggers, and sometimes, the predominance of certain cytokines.
The pathophysiology of psoriasis involves a complex interaction between genetic susceptibility, immune system dysregulation, and environmental triggers leading to an overproduction of skin cells and inflammation. Understanding this interplay has led to the development of targeted therapies that aim to modulate the immune system, reduce inflammation, and normalize skin cell growth, providing more effective management options for those with psoriasis.
ROLE OF GENETIC FACTORS IN PSORIASIS
The role of genetics in psoriasis is significant, with numerous studies indicating that psoriasis has a strong hereditary component. While psoriasis is a complex disease influenced by multiple genes and environmental factors, genetics plays a crucial role in determining an individual’s susceptibility to developing the condition.
Individuals with a family history of psoriasis are at a higher risk of developing the disease. The risk increases if one or both parents have psoriasis. Studies have shown that the risk of psoriasis is about 10% if one parent has it and rises to as much as 50% if both parents are affected. Certain genetic markers are associated with an increased risk of developing psoriasis. The most significant genetic determinant identified is within the major histocompatibility complex (MHC), specifically HLA-Cw6, which is found to be present in a large number of individuals with psoriasis.
Many genes implicated in psoriasis are involved in the immune system, particularly those affecting the functioning of T cells and the regulation of inflammation. For example, genes within the IL23R-IL23A pathway are associated with psoriasis. This pathway is crucial for the differentiation and maintenance of Th17 cells, a subtype of T cells that produce interleukin-17 (IL-17) and are involved in the pathogenesis of psoriasis.
Genes that affect the skin barrier function, such as those involved in keratinocyte proliferation and differentiation, can also influence the susceptibility to psoriasis. Disruptions in the skin barrier make it easier for environmental triggers to initiate the psoriatic inflammation process.
While genetics lays the foundation for psoriasis, environmental factors often trigger the onset or exacerbate the condition in genetically predisposed individuals. These triggers include stress, skin injury (the Koebner phenomenon), infections (notably streptococcal infections), and certain medications. The interaction between genes and the environment is complex, and not all individuals with a genetic predisposition will develop psoriasis; likewise, psoriasis can occur in individuals without a known family history of the disease.
Advances in genetic research, including genome-wide association studies (GWAS), have identified numerous genes associated with psoriasis, offering insights into its pathogenesis and potential therapeutic targets. Ongoing research into the genetics of psoriasis aims to better understand the disease’s heritability, identify new genetic markers, and develop personalized treatment approaches based on an individual’s genetic makeup.
The strong genetic component of psoriasis highlights the importance of understanding genetic factors in its pathogenesis, diagnosis, and treatment. While having a genetic predisposition to psoriasis can increase the risk, environmental factors and lifestyle choices also play critical roles in the disease’s development and management. As research progresses, the hope is that genetic insights will lead to more effective, tailored treatments for individuals with psoriasis, improving their quality of life.
ENZYME KINETICS INVOLVED IN PSORIASIS
The pathogenesis of psoriasis involves several key enzyme pathways that contribute to inflammation, keratinocyte proliferation, and the aberrant immune response characteristic of the condition. Targeting these pathways offers therapeutic potential. Below are the critical enzymes and related pathways involved in psoriasis, along with their activators and inhibitors.
Phosphodiesterase 4 (PDE4) is involved in the degradation of cyclic adenosine monophosphate (cAMP). High levels of PDE4 activity reduce cAMP levels, promoting the release of pro-inflammatory cytokines (TNF-α, IL-23, and IL-17) from immune cells. Inflammatory cytokines can enhance PDE4 expression, creating a feedback loop that exacerbates inflammation. PDE4 inhibitors (e.g., apremilast) increase cAMP levels, reducing the production of pro-inflammatory cytokines and modulating the immune response.
Janus Kinase (JAK) is the Signal Transducer and Activator of Transcription (STAT) Pathway. The JAK-STAT pathway is crucial for the signaling of cytokines and growth factors that contribute to the inflammatory and proliferative processes in psoriasis. Cytokines such as IL-23 and IL-22 activate the JAK-STAT pathway, promoting the differentiation and proliferation of T cells and keratinocytes. JAK inhibitors (e.g., tofacitinib) block cytokine signaling, reducing inflammation and keratinocyte proliferation.
Tumor Necrosis Factor-alpha (TNF-α) is a key pro-inflammatory cytokine that plays a significant role in the inflammatory process of psoriasis. Activated T cells and other immune cells produce TNF-α, which then activates keratinocytes and further immune cells, perpetuating the cycle of inflammation. Biologics that inhibit TNF-α (e.g., adalimumab, etanercept, infliximab) have been effective in treating psoriasis by reducing inflammation.
Interleukin Pathways (IL-17, IL-23, IL-12/23) are central to the activation and maintenance of the Th17 cell response, which is pivotal in psoriasis pathology. IL-23 from dendritic cells promotes the differentiation and expansion of Th17 cells, which produce IL-17 among other cytokines. Several biologics target these pathways. IL-23 inhibitors (e.g., guselkumab, tildrakizumab) and IL-17 inhibitors (e.g., secukinumab, ixekizumab) directly target these cytokines, reducing the inflammatory and proliferative responses in psoriasis.
Nuclear Factor-kappa B (NF-κB) is a transcription factor that regulates the expression of genes involved in immune and inflammatory responses, including the production of pro-inflammatory cytokines and adhesion molecules. Various stimuli, including TNF-α and IL-17, can activate the NF-κB pathway. Certain natural compounds and pharmaceuticals can inhibit the NF-κB pathway, thus offering potential therapeutic effects in psoriasis by reducing inflammation.
These enzyme pathways and their modulators play significant roles in the pathophysiology of psoriasis, offering targets for therapeutic intervention. By understanding the specific activators and inhibitors of these pathways, researchers and clinicians can develop more effective treatments to manage and alleviate the symptoms of psoriasis.
ROLE OF HORMONES IN PSORIASIS
The involvement of hormones in psoriasis underscores the complex interplay between the endocrine system and immune responses. Hormonal changes can influence the course and severity of psoriasis in some individuals. Here are key hormones implicated in the pathophysiology and modulation of psoriasis:
Cortisol is a glucocorticoid hormone produced by the adrenal cortex, known for its anti-inflammatory and immunosuppressive effects. It plays a crucial role in the body’s response to stress. Lower levels of cortisol or a blunted response to stress may exacerbate psoriasis due to the lack of sufficient anti-inflammatory action.
Estrogen and Progesterone, predominantly found in higher levels in females, have been shown to have immunomodulatory effects. Some women report improvement in psoriasis symptoms during pregnancy, a period characterized by high levels of estrogen and progesterone, suggesting these hormones might exert protective effects against psoriasis. However, postpartum flare-ups are common as hormone levels drop.
Testosterone is a male sex hormone that also possesses immunomodulatory properties. There is some evidence to suggest that higher levels of testosterone may be protective against the development or severity of psoriasis in men, though the exact mechanism and the extent of this effect are not fully understood.
Thyroid hormones, including thyroxine (T4) and triiodothyronine (T3), play a critical role in metabolism and also affect immune function. Disorders of the thyroid gland, such as hypothyroidism or hyperthyroidism, can affect the severity of psoriasis. The link suggests a potential influence of thyroid hormones on the disease process, although the exact relationship remains complex and not fully elucidated.
Prolactin is a hormone produced by the anterior pituitary gland, primarily known for its role in lactation. It also has immunomodulatory functions. Elevated levels of prolactin have been associated with increased severity of psoriasis. Prolactin may promote inflammation by stimulating the production of pro-inflammatory cytokines.
Although not a hormone in the traditional sense, vitamin D functions like a hormone in the body. It is crucial for bone health, calcium absorption, and immune function. Vitamin D modulates the immune system and reduces inflammation. Topical and systemic vitamin D analogs are effective treatments for psoriasis, underscoring the hormone’s protective role against the disease.
Hormonal influences on psoriasis are multifaceted, involving both exacerbation and amelioration of the disease depending on the hormonal milieu. This understanding suggests potential therapeutic avenues, such as hormone therapy, might be beneficial in managing psoriasis for some patients. However, the use of hormonal treatments must be carefully considered, taking into account the individual’s overall health and the potential side effects of such therapies.
ROLE OF INFECTIOUS DISEASES IN PSORIASIS
Certain infectious diseases have been associated with the onset or exacerbation of psoriasis, highlighting the complex interplay between infections and the immune system in the pathogenesis of this skin condition. These infectious triggers can induce or worsen psoriasis through various mechanisms, including molecular mimicry, superantigen stimulation, and direct immune system activation. Here are some of the key infectious diseases linked to psoriasis:
Streptococcal throat Infections is perhaps the most well-documented infectious trigger for psoriasis, particularly guttate psoriasis. The onset of guttate psoriasis often follows a streptococcal pharyngitis or tonsillitis by a few weeks. The proposed mechanism involves molecular mimicry, where the immune response against streptococcal antigens cross-reacts with similar antigens in the skin, triggering psoriasis in genetically predisposed individuals.
Human Immunodeficiency Virus (HIV) infection can both trigger the onset of psoriasis in someone previously unaffected and exacerbate the condition in those with existing psoriasis. Psoriasis may appear at any stage of HIV infection but is often more severe and difficult to treat in advanced stages of HIV/AIDS. The immunosuppressive nature of HIV, along with immune activation and increased levels of certain cytokines (such as TNF-α and IFN-γ), are thought to contribute to the worsening or development of psoriasis in HIV-infected individuals.
There is an observed association between chronic hepatitis C infection and the exacerbation of psoriasis. Treatment of HCV with interferon can also trigger or worsen psoriasis. The mechanisms are not fully understood but may involve direct immune activation and the pro-inflammatory state induced by chronic HCV infection, along with specific treatment effects.
Staphylococcus aureus colonization, particularly in the nasal cavity, has been linked to the severity and flares of psoriasis. The bacteria can produce superantigens that activate a significant proportion of T cells, leading to systemic inflammation that can exacerbate psoriasis.
Candida albicans, a type of yeast, has been associated with psoriasis, especially in cases of inverse psoriasis where yeast overgrowth is common in the skin folds. The immune response to Candida in the skin may exacerbate inflammation in psoriasis, though the exact mechanisms are still being investigated.
Management of psoriasis in the context of infectious diseases involves treating the underlying infection alongside standard psoriasis therapies. For example, antibiotics may be used for streptococcal infections, and antiretroviral therapy is crucial for managing psoriasis in HIV-infected individuals. Awareness and prompt management of these infections can help mitigate their impact on psoriasis.
The relationship between infectious diseases and psoriasis underscores the importance of a comprehensive approach to managing psoriasis that includes screening for and treating underlying infections. Understanding these connections can help healthcare providers tailor treatment strategies to individual patients, potentially improving outcomes for those with psoriasis influenced by infectious diseases. Homeopathic nosodes prepared from these infectious agents in 30 c potency obviously plays a leading role in the MIT therapeutics of psoriasis
ROLE OF IMMUNE SYSTEM IN PSORIASIS
The role of immunology in psoriasis is central to understanding the pathogenesis and the development of targeted treatments for this chronic inflammatory skin condition. Psoriasis is characterized by hyperproliferation of keratinocytes in the skin and is considered an immune-mediated disease. The involvement of various immune cells and cytokines plays a pivotal role in its development and exacerbation.
Psoriasis is driven primarily by an abnormal activation of T cells, a type of lymphocyte that plays a central role in the adaptive immune response. In psoriasis, these T cells become activated mistakenly and migrate to the skin, where they release inflammatory cytokines. Specifically, Th1 (T helper 1) and Th17 cells are subsets of T cells implicated in psoriasis. Th17 cells, in particular, are considered crucial in the pathogenesis due to their production of interleukin-17 (IL-17), a cytokine that induces keratinocyte proliferation and the expression of other inflammatory mediators. IL-17, along with tumor necrosis factor-alpha (TNF-α), interleukin-22 (IL-22), and interleukin-23 (IL-23), are key cytokines involved in the inflammatory process of psoriasis. These cytokines stimulate keratinocytes to proliferate and produce other inflammatory molecules, perpetuating the cycle of inflammation. Understanding the role of these cytokines has led to the development of targeted biologic therapies that significantly improve psoriasis symptoms for many patients. These include monoclonal antibodies directed against TNF-α, IL-17, and IL-23.
Beyond the adaptive immune system, components of the innate immune system, particularly dendritic cells, are also involved in psoriasis. Dendritic cells in the skin can present antigens to T cells, activating them and promoting the production of cytokines that contribute to inflammation and disease progression. Neutrophils and macrophages, other innate immune cells, are found in increased numbers in psoriatic lesions and contribute to the inflammatory milieu.
Psoriasis has a strong genetic component, with multiple genes related to the immune system implicated in its pathogenesis. Some of these genes are involved in the pathways that regulate innate immunity and inflammatory responses, contributing to the autoinflammatory nature of psoriasis.
The skin acts as a physical barrier, and its disruption can lead to psoriasis flare-ups. The interplay between skin barrier dysfunction and immune response, including the role of antimicrobial peptides and other skin-derived signals, influences psoriasis severity. Emerging research suggests that the skin microbiome—the community of microorganisms residing on the skin—can also influence immune responses and may play a role in psoriasis, although this area requires further investigation.
Immunology plays a crucial role in psoriasis, with the disease representing a complex interplay between adaptive and innate immune responses leading to chronic inflammation and skin cell proliferation. The understanding of these immunological mechanisms has been instrumental in developing targeted treatments that have significantly improved the quality of life for many people with psoriasis. Continued research in immunology and genetics promises to uncover new therapeutic targets and strategies for managing psoriasis more effectively.
ROLE OF HEAVY METALS AND MICROELEMENTS IN PSORIASIS
The relationship between heavy metals, microelements, and the exacerbation or initiation of psoriasis is an area of ongoing research. Both heavy metals and certain microelements, depending on their levels in the body, can influence the severity and occurrence of psoriasis.
Mercury exposure, especially in its organic forms found in certain fish, can exacerbate psoriasis symptoms. Mercury can induce oxidative stress and inflammation, potentially worsening psoriasis. High levels of lead have been associated with various health problems, including potential exacerbation of autoimmune diseases like psoriasis. Lead can disrupt immune function and enhance inflammatory responses. Exposure to arsenic, whether through water, air, or food, has been linked to the worsening of psoriasis. Arsenic can induce oxidative stress and inflammation. Cadmium can accumulate in the body through smoking or dietary sources, contributing to oxidative stress and possibly exacerbating psoriasis.
Zinc plays a crucial role in maintaining skin health, immune function, and inflammation regulation. Both zinc deficiency and excess have been implicated in psoriasis. Adequate zinc levels can support skin health and modulate the immune response, potentially benefiting psoriasis patients. Selenium is an antioxidant that helps combat oxidative stress. Low selenium levels have been observed in psoriasis patients, suggesting that adequate selenium might help manage psoriasis symptoms. Copper is involved in various enzymatic reactions that are essential for skin health. However, an imbalance in copper levels, particularly in conjunction with zinc levels, may influence psoriasis severity.
Heavy metals can induce oxidative stress by generating free radicals, leading to cell damage and inflammation, which can exacerbate psoriasis. Metals can modulate the immune system, potentially leading to the activation of pathways that exacerbate psoriasis, such as increased production of pro-inflammatory cytokines. Some metals might contribute to skin barrier dysfunction, increasing the susceptibility to environmental triggers and infections that can worsen psoriasis.
For individuals with psoriasis, testing for heavy metal exposure and levels of essential microelements can be informative. Avoiding known sources of heavy metals and addressing any imbalances with dietary adjustments or supplements, under medical supervision, may help manage psoriasis symptoms. A balanced diet rich in antioxidants and essential nutrients can support skin health and reduce inflammation. However, supplementation should be approached with caution and under medical guidance to avoid exacerbating psoriasis through imbalances.
While heavy metals are generally harmful and can exacerbate psoriasis, the role of microelements is more nuanced, with both deficiencies and excesses potentially impacting the disease. Understanding the complex interactions between these elements and psoriasis can aid in the development of comprehensive management strategies. Always consult with healthcare professionals before making significant changes to diet or starting new supplements, especially for conditions like psoriasis.
Arsenic, a naturally occurring element in the environment, has had a complex relationship with psoriasis. Historically, small doses of arsenic were used as a treatment for psoriasis due to its immunosuppressive and anti-proliferative effects on the skin. However, this practice has been discontinued due to the long-term toxicity and carcinogenic potential of arsenic. Today, exposure to arsenic is recognized more for its potential to aggravate psoriasis and for being a risk factor for the development of the disease in some cases. People can be exposed to arsenic through contaminated water, air, and food. Chronic arsenic exposure has been linked to various health problems, including skin lesions, cancer, cardiovascular diseases, and diabetes. There is evidence to suggest that arsenic exposure can exacerbate psoriasis symptoms. Arsenic can induce oxidative stress and inflammation, contributing to the pathogenesis and exacerbation of psoriasis. Additionally, arsenic has immunomodulatory effects that may negatively affect the immune dysregulation already present in psoriasis. Arsenic induces oxidative stress by generating reactive oxygen species (ROS), which can damage cells and tissues, contributing to the inflammatory process in psoriasis. Arsenic can activate signaling pathways that lead to the production of pro-inflammatory cytokines, exacerbating the inflammatory response in psoriatic lesions. Arsenic may alter the immune response by affecting the function of T cells and other immune cells involved in the pathogenesis of psoriasis. As such, molecular imprints of arsenic as Ars Alb 30 can play a big role in the MIT therapeutics of psoriasis.
ROLE OF PHYTOCHEMICALS IN PSORIASIS
Phytochemicals, or plant-derived compounds, have a wide range of effects on human health, including impacts on chronic conditions like psoriasis. While many phytochemicals have beneficial effects, such as anti-inflammatory and antioxidant properties, there are some that may aggravate psoriasis in susceptible individuals. It is important to note that the interaction between phytochemicals and psoriasis is complex and can vary greatly among individuals, depending on genetic factors, the nature of their psoriasis, and other health conditions.
Psoralen is found in high concentrations in certain plants like figs, celery, and parsley. While psoralen is used therapeutically in PUVA (psoralen plus UVA) treatment for psoriasis, accidental exposure to high amounts of psoralen (e.g., from handling or consuming these plants) followed by sun exposure can exacerbate psoriasis symptoms in some individuals due to its photosensitizing effects.
Solanine is a glycoalkaloid found in nightshade vegetables, such as tomatoes, potatoes, and eggplants. Anecdotal reports suggest that solanine can exacerbate psoriasis for some people, possibly due to its impact on inflammation and the immune system. However, scientific evidence supporting this claim is limited.
Capsaicin is the active component in chili peppers that gives them their heat. While capsaicin is used topically for pain relief and has shown benefits in reducing itching and inflammation in psoriasis plaques, oral ingestion can irritate the gut lining in some individuals, potentially exacerbating psoriasis symptoms indirectly through effects on gut health and inflammation.
Some herbal remedies and tinctures contain significant amounts of alcohol. Alcohol consumption is known to potentially aggravate psoriasis, and thus, alcohol-based herbal extracts might also contribute to worsening symptoms, particularly if used in large quantities.
The impact of these phytochemicals on psoriasis can vary widely among individuals. What exacerbates symptoms in one person may have no effect or even benefit another. Patients with psoriasis are often advised to monitor their diet and lifestyle to identify any personal triggers for their symptoms. Keeping a food diary can be a helpful tool in understanding how certain foods and phytochemicals affect one’s condition. It’s important for individuals with psoriasis to consult with healthcare professionals, including dermatologists and nutritionists, before making significant dietary changes or using herbal remedies. This ensures that treatments are safe and effective and that they do not interfere with other medications or therapies.
In conclusion, while many phytochemicals offer health benefits, individuals with psoriasis should be mindful of how certain plant-derived compounds may affect their condition and consult healthcare providers to tailor a management plan that considers their unique triggers and sensitivities.
ROLE OF NUTRITION IN PSORIASIS
The relationship between diet and psoriasis remains an area of active research, with many individuals reporting variations in their symptoms in response to certain food items. It is important to note that dietary triggers can be highly individual, but there are several common food groups and items that have been reported to potentially aggravate psoriasis in some people.
Alcohol consumption can exacerbate psoriasis symptoms for many reasons, including its effect on inflammation, the immune system, and liver function. Alcohol may also interfere with the effectiveness of psoriasis treatments.
High consumption of saturated fats found in red meat and certain dairy products can contribute to inflammation, potentially worsening psoriasis symptoms. Some people also report sensitivity to casein, a protein found in cow’s milk.Individuals with psoriasis may have a higher prevalence of gluten sensitivity or celiac disease. For those affected, consuming gluten can trigger or worsen psoriasis flare-ups.
Vegetables such as tomatoes, potatoes, eggplants, and peppers belong to the nightshade family and contain solanine, which some people with psoriasis report as aggravating their symptoms. The evidence is anecdotal, and the effect is highly individual.
Foods high in processed sugars and unhealthy fats can increase inflammation throughout the body, potentially leading to worsening psoriasis symptoms. These include fast foods, snacks, sweets, and beverages high in sugar. Specific types of fats, such as trans fats found in some fried foods and baked goods, can promote inflammation and may exacerbate psoriasis.
One approach to identifying food triggers is through an elimination diet, where you systematically exclude certain foods for a period and then gradually reintroduce them to observe any changes in symptoms. This should be done under the guidance of a healthcare professional to ensure nutritional needs are met. Adopting a diet that focuses on anti-inflammatory foods, such as fruits, vegetables, whole grains, lean protein, and healthy fats (e.g., omega-3 fatty acids found in fish and flaxseeds), may help some people manage their psoriasis symptoms better. Adequate hydration is also important for skin health. Drinking plenty of water can help keep the skin moisturized and possibly reduce the severity of psoriasis patches. Because dietary needs and triggers can vary greatly among individuals with psoriasis, consulting with a healthcare provider or a dietitian who can tailor dietary recommendations to your specific condition and nutritional requirements is essential. Identifying and avoiding personal dietary triggers can be a valuable part of managing psoriasis, alongside medical treatments. Given the individual nature of the condition, what exacerbates symptoms in one person may not affect another, making personal observation and professional guidance crucial in managing the disease through diet.
ROLE OF DRUGS IN PSORIASIS
Certain medications and chemical substances can trigger or exacerbate psoriasis in some individuals. The reaction to these drugs can vary widely among patients, with some experiencing worsening of existing psoriasis or the onset of new psoriasis plaques.
Beta-blockers are commonly prescribed for hypertension (high blood pressure) and other cardiovascular conditions. These drugs can worsen psoriasis symptoms in some individuals, potentially by increasing the level of T cells and cytokines that contribute to psoriasis inflammation.
Lithium is a medication used primarily to treat bipolar disorder. It can exacerbate psoriasis in existing patients or induce psoriasis in predisposed individuals, possibly through altering immune function or affecting skin cell growth.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as ibuprofen and naproxen, are widely used to relieve pain, reduce inflammation, and lower fever. Although they are anti-inflammatory, NSAIDs can paradoxically worsen psoriasis symptoms for some people, particularly those with a subtype of psoriasis known as psoriatic arthritis.
Antimalarial medications, including chloroquine and hydroxychloroquine, are used to prevent and treat malaria. They’re also prescribed for autoimmune diseases like lupus and rheumatoid arthritis. These drugs can induce psoriasis flares or initiate the onset of psoriasis in some cases. The mechanism might involve changes in skin pH that affect enzyme activity related to psoriasis.
Angiotensin-Converting Enzyme (ACE) inhibitors are used to treat hypertension and congestive heart failure. They can worsen psoriasis in some patients, although the exact mechanism is not fully understood. It may involve modulation of the immune system or direct effects on skin cells.
Interferons are used to treat various conditions, including hepatitis C and certain types of cancer. These medications can trigger or exacerbate psoriasis due to their immunomodulatory effects, which may stimulate the pathways involved in psoriasis pathology.
Terbinafine is an antifungal medication used to treat fungal infections of the nails and skin. It has been reported to exacerbate psoriasis in some cases, although such instances are relatively rare.
Patients with psoriasis should inform their healthcare providers about their condition when discussing treatment options for any other health issues. A thorough review of current medications can help identify potential triggers. If a medication is suspected to exacerbate psoriasis, healthcare providers may recommend alternative treatments that have a lower risk of affecting the condition. Patients may need to be closely monitored when starting a new medication known to potentially aggravate psoriasis. Early detection and management of a flare-up can help reduce its severity.
While certain medications can trigger or exacerbate psoriasis, it’s essential to weigh the benefits of these drugs against their potential to affect psoriasis negatively. Changes to medication should always be made under the guidance of a healthcare provider, who can help manage both psoriasis and other underlying conditions in a balanced and informed way.
MIT APPROACH TO PSORIASIS THERAPEUTICS
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 involved in potentization, and the biological mechanism involved in ‘similia similibus- 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 the above discussions above regarding the molecular pathology, MIT suggest the following drugs in 30 C homeopathy dilutions for using in the therapeutics of disease: Arsenic Album 30, Zincum Met 30, Ibuprofen 30, Hydroxychloroquine 30, Interferon Alpha 30, Lithium 30, Gluten 30, Lac Caninum 30, Casein 30, Capsicum 30, Solanine 30, Psoralea 30, Mercurius 30, Prolactin 30, Thyroidinum 30, Sulphur 30., Candida Ablicans 30, Staphylococcus 30, Hepatitis C 30, HIV 30, Streptococcin 30
REDEFINING HOMEOPATHY 