Jaban M Moore alias The Toxic Person Toxin

Jaban M Moore is not licensed or approved by Missouri State Board of Chiropractic Examiners to advertise Toxic relationships can SIGNIFICANTLY impact YOUR physical health, fueling illness and contributing to autoimmune conditions as within their scope of practice.

Toxic relationships can SIGNIFICANTLY impact YOUR physical health, fueling illness and contributing to autoimmune conditions

Supports

High-quality evidence supports a link between chronic or severe psychological stress and adverse physical health, including increased risk and worse course of some autoimmune and inflammatory conditions. Chronic psychological stress is known to alter immunoregulatory networks, increasing risk for allergic and autoimmune diseases and worsening inflammatory disease activity.^[12] Psychological stress and psychosocial stressors can impair immune regulation and increase susceptibility to autoimmune disease through neuroendocrine and immune pathways.^[15] Large cohort studies show that clinically diagnosed stress-related disorders are associated with a significantly increased subsequent risk of autoimmune diseases (hazard ratio around 1.36 compared with unexposed individuals and siblings).^[13][14] Adverse childhood experiences and childhood traumatic stress (which often involve toxic or abusive relationships) are associated with a modest but significant increase in the prevalence and incidence of autoimmune diseases in adulthood, including Th1, Th2, and rheumatic autoimmune conditions.^{[2][5][10][11]} Psychological stress is also an important modifiable risk factor for cardiovascular disease, and relationship conflicts and psychosocial stress are implicated in functional hypothalamic amenorrhea and preclinical cardiovascular risk.^[18][20] In autoimmune gastrointestinal disease such as inflammatory bowel disease, accumulating evidence indicates that chronic psychological stress can trigger disease deterioration and relapse, supporting an impact of stress on disease activity.^[21] Overall, these data support that severe and persistent stress exposure, which can include toxic or abusive relationships, can significantly affect physical health and may contribute to onset or exacerbation of autoimmune and other stress-sensitive conditions.

Contradicts

The evidence does not show that any and all “toxic relationships” directly and independently cause autoimmune disease in a strong, deterministic way, and high-quality trials establishing causality for specific relationship patterns are lacking. Most data are observational, showing associations between chronic stress or adversity and autoimmune disorders rather than proving that toxic relationships alone fuel illness. The effect sizes for adverse childhood experiences on autoimmune disease risk are generally modest (e.g., hazard ratios around 1.1–1.2 per ACE), not large enough to support a blanket claim that toxic relationships themselves are a major or sole driver of autoimmunity.^[5][2][10] Existing reviews highlight that psychological stress is one of multiple environmental contributors interacting with genetic predisposition and other exposures, rather than a single dominant cause.^[12][15][22] There is also evidence that general psychological stress is not consistently associated with all physical disease endpoints; for example, some studies find no significant relationship between psychological stress and certain cardiovascular risk factors after adjustment, suggesting that stress effects can be context-dependent and mediated by other variables.^[18][23] High-quality randomized controlled trials directly testing whether changing or leaving a toxic relationship alters autoimmune disease incidence are not available, so causal claims about specific relationship types remain inferential rather than experimentally confirmed.

Mainstream view

The mainstream medical and scientific view is that chronic and severe psychological stress, including stress arising from adverse or abusive relationships, can significantly impact physical health and is one of several recognized risk and exacerbating factors for autoimmune and inflammatory diseases, cardiovascular disease, and other stress-sensitive conditions.^{[12][13][14][15][21][22]} Stress-related disorders and adverse childhood experiences are accepted as environmental risk factors that modestly increase autoimmune disease risk, likely through persistent dysregulation of neuroendocrine-immune pathways, but this operates in conjunction with genetic predisposition, infections, lifestyle, and other environmental exposures.^{[2][5][10][11][22]} Clinicians and guidelines generally regard addressing chronic psychological stress (through psychotherapy, social support, and stress management) as an important part of comprehensive care for autoimmune and cardiovascular conditions, while emphasizing that toxic relationships are one potential source of stress rather than a uniquely proven direct cause of autoimmunity. The prevailing position is therefore that toxic or highly stressful relationships can meaningfully contribute to physical illness and may play a role in autoimmune disease onset or flares in vulnerable individuals, but they are neither necessary nor sufficient causes, and causal strength varies between individuals and diseases. Deterministic PubMed cross-check found no matching indexed studies for these terms (absence of indexed evidence is not evidence against the claim).

In their own wordsWatch sourceArchived copy

“Toxic relationships can SIGNIFICANTLY impact YOUR physical health, fueling illness and contributing to autoimmune conditions through various mechanisms...”

Rule: Mo. Rev. Stat. §331.010 (20 CSR 2070)

Jaban M Moore is not licensed or approved by Missouri State Board of Chiropractic Examiners to diagnose, treat, or cure Stress in toxic relationships disrupts hormonal balance, affecting the endocrine system. Hormonal disruptions can impact immune function and exacerbate autoimmune responses.

Stress in toxic relationships disrupts hormonal balance, affecting the endocrine system. Hormonal disruptions can impact immune function and exacerbate autoimmune responses

Supports

There is strong evidence that psychological stress activates neuroendocrine pathways (especially the hypothalamic–pituitary–adrenal axis and sympathetic nervous system) and thereby influences hormonal balance and endocrine function, which in turn modulates immunity.^[8][15][18] Encyclopedic and review sources on endocrine–immune interactions describe that multiple hormones (glucocorticoids, prolactin, sex steroids, thyroid hormones) have direct, well‑characterized effects on immune cell function and inflammatory responses. Classic endocrine and immunology references also note that hormonal milieu changes (e.g., in pregnancy) alter immune responses, illustrating how endocrine shifts modulate immunity. Psychoneuroimmunology reviews and autoimmune‑focused articles conclude that chronic stress can contribute to immune dysregulation, cytokine imbalance, and loss of tolerance via stress‑induced hormonal changes, supporting a mechanistic link between stress, endocrine disruption, and autoimmunity.^{[3][4][10][15][16][18]} Several narrative reviews on autoimmune diseases report that a high proportion of patients retrospectively describe major stressors before disease onset and that stress can exacerbate autoimmune disease activity, consistent with stress‑related endocrine and immune perturbations.^{[4][7][11][13][16][18]} Overall, high‑quality reviews and authoritative texts support the general chain: chronic or severe psychosocial stress → altered stress‑hormone/endocrine signaling → immune modulation → potential contribution to onset or exacerbation of autoimmune phenomena, even though “toxic relationship” is not a formal clinical term.

Contradicts

The influencer’s claim is more specific and categorical than current evidence supports. Most high‑quality sources describe stress as a contributing or modulating factor in endocrine and immune dysregulation, not as a universally causal driver of autoimmune disease. Large guidelines for autoimmune disorders generally do not list psychological stress or “toxic relationships” as primary etiologic causes; rather, they emphasize genetic predisposition, specific environmental exposures, and infections, with stress regarded as a possible trigger or exacerbating factor. Reviews of stress and autoimmunity routinely note that mechanisms, dose–response relationships, and causality remain incompletely defined, and much of the evidence is observational, retrospective, or based on experimental models rather than large prospective RCTs.^{[3][4][6][7][13][15][18]} The claim implies that any toxic relationship will disrupt hormonal balance and exacerbate autoimmune responses, but the literature supports heterogeneity: stress responses, endocrine changes, and immune consequences vary widely among individuals and conditions, and not all stressed individuals develop autoimmune disease or clinically significant endocrine disruption. Moreover, the index paper on zinc supplementation in PCOS shows that endocrine and immune changes in that condition are influenced by metabolic and micronutrient factors, not just stress, underscoring that endocrine–immune abnormalities have multifactorial causes beyond relationship stress. Evidence specifically tying “toxic relationship” stress, as opposed to generic chronic psychosocial stress, to measurable endocrine disruption and autoimmune exacerbations is sparse; most data aggregate diverse stressors without distinguishing relationship dynamics. Therefore, while parts of the pathway are plausible and supported in principle, the influencer’s phrasing overstates certainty and generalizability.

Mainstream view

The mainstream medical and scientific view is that there is a bidirectional, clinically important interaction between the nervous system, endocrine system, and immune system. Stress activates neuroendocrine axes (notably the HPA axis and sympathetic nervous system), causing changes in hormone secretion that can modulate immune function and inflammatory responses.^{[8][14][15][18]} Authoritative endocrine and immunology references recognize that hormones such as cortisol, prolactin, sex steroids, thyroid hormones, and pregnancy‑related hormones have well‑documented immunomodulatory effects. Psychoneuroimmunology and autoimmune disease reviews generally regard chronic psychological stress as a risk or exacerbating factor for some autoimmune and inflammatory conditions, operating partly through stress‑hormone and cytokine pathways, but they stop short of calling stress a sole or dominant cause.^{[3][4][7][10][13][15][16][18]} Mainstream position is that: (1) chronic or severe psychosocial stress can alter endocrine stress‑response systems and thereby influence immune regulation; (2) such alterations may contribute to the onset or worsening of autoimmune disease in susceptible individuals; (3) mechanisms involve complex, context‑dependent changes in glucocorticoids, catecholamines, prolactin, and other hormones rather than a simple uniform “hormonal imbalance”; and (4) evidence is strongest Deterministic PubMed cross-check found no matching indexed studies for these terms (absence of indexed evidence is not evidence against the claim).

In their own wordsWatch sourceArchived copy

“Stress in toxic relationships disrupts hormonal balance, affecting the endocrine system. Hormonal disruptions can impact immune function and exacerbate autoimmune responses.”

Rule: Mo. Rev. Stat. §331.010 (20 CSR 2070)

Jaban M Moore is not licensed or approved by Missouri State Board of Chiropractic Examiners to advertise Stressful environments, including toxic relationships, might interact with genetic predispositions, potentially triggering or worsening autoimmune conditions in susceptible individuals as within their scope of practice.

Stressful environments, including toxic relationships, might interact with genetic predispositions, potentially triggering or worsening autoimmune conditions in susceptible individuals

Supports

There is substantial observational evidence that psychological stress and stressful life events are associated with an increased risk of developing autoimmune diseases and with disease exacerbations in susceptible individuals. ^{[17][18][19][20]} A systematic review and meta-analysis of retrospective case–control studies found that patients with autoimmune diseases had a significantly higher number of major stressful events in the premorbid period than healthy controls, with a moderate effect size, supporting stress as an environmental risk factor for autoimmunity. ^[22] A dedicated review of stress as an environmental risk factor for autoimmune diseases summarizes multiple studies showing that chronic stress and negative life events are linked to the onset or flare of several autoimmune disorders, although most data are observational. Large cohort studies of stress-related psychiatric disorders (e. g. , PTSD and other stress-related diagnoses) show elevated subsequent risk of a range of autoimmune diseases compared with matched unexposed individuals and siblings, suggesting that severe or chronic stress can precede autoimmune onset in real-world populations. ^[8][7] A recent systematic review and meta-analysis reported that PTSD is associated with a significantly increased risk of several autoimmune diseases, including SLE, MS, RA, and IBD, again supporting a link between severe stress and autoimmune development or expression in susceptible people. Systematic reviews and meta-analyses of stress and immune function show that chronic psychological stress is associated with dysregulation and suppression of cellular and humoral immune responses, and with links to both hypo- and hyper-immune conditions, including autoimmune diseases, providing a biologically plausible mechanism by which stress might interact with genetic susceptibility to influence disease onset or course. A meta-analysis of risk factors for primary Sjögren’s syndrome identified both negative stressful life events and specific IRF5 gene polymorphisms as independent risk factors, implying that environmental stressors and genetic predisposition can co-occur as contributors to disease risk. ^[21] Reviews on genetic predispositions to stressful conditions note that inherited differences in stress reactivity and neuroendocrine response can modify how individuals respond biologically to environmental stressors, which conceptually supports gene–environment interaction in stress-related health outcomes, including immune-mediated conditions.

Contradicts

Despite consistent associations, the evidence is largely observational and does not definitively prove that stressful environments or toxic relationships causally trigger autoimmune diseases; reverse causation and residual confounding (e. g. , socioeconomic status, comorbid mental health conditions, health behaviors) remain concerns. The main meta-analysis of stressful life events and autoimmune disease emphasizes that prospective data are needed to establish causality, explicitly stating that only longitudinal studies can clarify whether stress is a true cause rather than a correlate. ^{[17][18][19][20][21][22]} Many studies rely on retrospective self-report of stressful events, which is vulnerable to recall bias—patients already diagnosed with autoimmune disease may remember or interpret past stress differently than controls, potentially inflating associations. ^[8][7] Some autoimmune diseases (e. g. , RA, SLE, inflammatory bowel disease) show clear evidence that stress can exacerbate symptoms or flares, but evidence that interpersonal stressors like “toxic relationships” specifically trigger disease onset in genetically predisposed individuals is indirect; most studies aggregate different life stressors and do not isolate relationship toxicity as a distinct exposure. While there is evidence that genetic factors predispose both to stress-related disorders and to autoimmune diseases, direct demonstration of specific gene–stress interaction models (e. g. , defined HLA or IRF5 variants whose penetrance is substantially modified by psychosocial stress) is limited and still emerging, so the gene–environment interaction aspect remains more inferred than conclusively demonstrated. No major autoimmune disease guideline currently frames psychosocial stress or toxic relationships as proven primary triggers of autoimmunity; rather, stress is recognized as a modifiable factor that can impact symptoms, quality of life, and possibly flare risk, reflecting the uncertainty around its causal role in disease initiation.

Mainstream view

The mainstream medical position is that autoimmune diseases arise from complex interactions between genetic predisposition and environmental factors (such as infections, smoking, hormones, and other exposures), with psychosocial stress recognized as one of several potential environmental contributors but not as a sole or universally causal trigger. High-quality evidence from systematic reviews and large cohort studies indicates that chronic or severe stress and stressful life events are associated with increased risk of developing autoimmune diseases and with worse disease activity in Deterministic PubMed cross-check found no matching indexed studies for these terms (absence of indexed evidence is not evidence against the claim). ^{[17][18][8][7][19][20][21][22]}

In their own wordsWatch sourceArchived copy

“While not solely related to toxic relationships, stressful environments, including toxic relationships, might interact with genetic predispositions, potentially triggering or worsening autoimmune conditions in susceptible individuals.”

Rule: Mo. Rev. Stat. §331.010 (20 CSR 2070)