scholarly journals Review of Toxins Associated with Autoimmune Diseases

Author(s):  
Domina Petric

Aim of this article is to review the literature about the toxins that might be involved in the pathogenesis of autoimmune diseases. Almost 70% of all autoimmune diseases are caused by environmental factors, including toxic chemicals. Genetic factors contribute to approximately 30% of all autoimmune diseases.

2021 ◽  
Vol 28 (4) ◽  
pp. 513-543
Author(s):  
Aristo Vojdani ◽  
Elroy Vojdani

Autoimmune diseases affect 5–9% of the world’s population. It is now known that genetics play a relatively small part in the pathophysiology of autoimmune disorders in general, and that environmental factors have a greater role. In this review, we examine the role of the exposome, an individual’s lifetime exposure to external and internal factors, in the pathophysiology of autoimmune diseases. The most common of these environmental factors are toxic chemicals, food/diet, and infections. Toxic chemicals are in our food, drink, common products, the air, and even the land we walk on. Toxic chemicals can directly damage self-tissue and cause the release of autoantigens, or can bind to human tissue antigens and form neoantigens, which can provoke autoimmune response leading to autoimmunity. Other types of autoimmune responses can also be induced by toxic chemicals through various effects at the cellular and biochemical levels. The food we eat every day commonly has colorants, preservatives, or packaging-related chemical contamination. The food itself may be antigenic for susceptible individuals. The most common mechanism for food-related autoimmunity is molecular mimicry, in which the food’s molecular structure bears a similarity with the structure of one or more self-tissues. The solution is to detect the trigger, remove it from the environment or diet, then repair the damage to the individual’s body and health.


Leukemia ◽  
2021 ◽  
Author(s):  
Geffen Kleinstern ◽  
J. Brice Weinberg ◽  
Sameer A. Parikh ◽  
Esteban Braggio ◽  
Sara J. Achenbach ◽  
...  

AbstractMonoclonal B-cell lymphocytosis (MBL) is a precursor to CLL. Other than age, sex, and CLL family-history, little is known about factors associated with MBL risk. A polygenic-risk-score (PRS) of 41 CLL-susceptibility variants has been found to be associated with CLL risk among individuals of European-ancestry(EA). Here, we evaluate these variants, the PRS, and environmental factors for MBL risk. We also evaluate these variants and the CLL-PRS among African-American (AA) and EA-CLL cases and controls. Our study included 560 EA MBLs, 869 CLLs (696 EA/173 AA), and 2866 controls (2631 EA/235 AA). We used logistic regression, adjusting for age and sex, to estimate odds ratios (OR) and 95% confidence intervals within each race. We found significant associations with MBL risk among 21 of 41 variants and with the CLL-PRS (OR = 1.86, P = 1.9 × 10−29, c-statistic = 0.72). Little evidence of any association between MBL risk and environmental factors was observed. We observed significant associations of the CLL-PRS with EA-CLL risk (OR = 2.53, P = 4.0 × 10−63, c-statistic = 0.77) and AA-CLL risk (OR = 1.76, P = 5.1 × 10−5, c-statistic = 0.62). Inherited genetic factors and not environmental are associated with MBL risk. In particular, the CLL-PRS is a strong predictor for both risk of MBL and EA-CLL, but less so for AA-CLL supporting the need for further work in this population.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yisong Huang ◽  
Shaoyong Su ◽  
Harold Snieder ◽  
Frank Treiber ◽  
Gaston Kapuku ◽  
...  

AbstractIncreased arterial stiffness measured by pulse wave velocity (PWV) is an important parameter in the assessment of cardiovascular risk. Our previous longitudinal study has demonstrated that carotid-distal PWV showed reasonable stability throughout youth and young adulthood. This stability might be driven by genetic factors that are expressed consistently over time. We aimed to illustrate the relative contributions of genetic and environmental factors to the stability of carotid-distal PWV from youth to young adulthood. We also examined potential ethnic differences. For this purpose, carotid-distal PWV was measured twice in 497 European American (EA) and African American (AA) twins, with an average interval time of 3 years. Twin modelling on PWV showed that heritability decreased over time (62–35%), with the nonshared environmental influences becoming larger. There was no correlation between the nonshared environmental factors on PWV measured at visit 1 and visit 2, with the phenotypic tracking correlation (r = 0.32) completely explained by shared genetic factors over time. Novel genetic influences were identified accounting for a significant part of the variance (19%) at the second measurement occasion. There was no evidence for ethnic differences. In summary, novel genetic effects appear during development into young adulthood and account for a considerable part of the variation in PWV. Environmental influences become larger with age for PWV.


Cephalalgia ◽  
2002 ◽  
Vol 22 (8) ◽  
pp. 624-632 ◽  
Author(s):  
E Loder

Susceptibility to migraine is determined by genetic factors and is therefore subject to the forces of natural selection. Migraine is a common and ancient disorder whose prevalence may be increasing, suggesting that a migraine-prone nervous system may be associated with reproductive or survival advantages. Five evolutionary explanations are reviewed that might account for the persistence of migraine: (i) migraine as a defence mechanism; (ii) migraine as a result of conflict with other organisms; (iii) migraine as result of novel environmental factors; (iv) migraine as a trade-off between genetic harms and benefits; and (v) migraine as a design constraint. An evolutionary perspective on migraine allows the generation of important hypotheses about the disorder and suggests rewarding possibilities for further research.


PEDIATRICS ◽  
1982 ◽  
Vol 70 (4) ◽  
pp. 648-650
Author(s):  
K. M. Laurence

It is generally agreed that neural tube defects (NTD) have a multifactorial etiology when genetic factors render the developing fetus susceptible to intrauterine environmental factors acting during the fourth week of gestation to interfere with the orderly closure of the neural tube.1 As there is little likelihood that anything can be done about the genetic background, primary prevention would therefore be dependent on eliminating these factors from the environment or avoiding them. My intention here is to enlarge on some aspects of primary prevention of NTD as outlined by Smithells in an earlier issue (Pediatrics 69:498, 1982).2 One environmental factor, poor maternal nutrition and, more particularly, folic acid deficiency seems now to have been identified, but there are almost certainly a number of others.


1979 ◽  
Vol 134 (4) ◽  
pp. 343-351 ◽  
Author(s):  
Svenn Torgersen

SummaryBy means of a twin study an attempt was made to throw light upon the aetiology and nosology of phobic fears. Factor analyses revealed five factors, namely separation fears, animal fears, mutilation fears, social fears and nature fears. The study demonstrated that, apart from separation fears, genetic factors play a part in the strength as well as content of phobic fears. Environmental factors, affecting the development of dependence, reserve and neurotic traits generally, seemed also to be of some importance. It was further demonstrated that phobic fears were related to emotional and social adjustment and this was true to an even greater extent for separation fears.


2019 ◽  
Vol 8 (1) ◽  
pp. 115 ◽  
Author(s):  
Yu-Huei Huang ◽  
Chang-Fu Kuo ◽  
Lu-Hsiang Huang ◽  
Mei-Yun Hsieh

Psoriasis is considered to result from the interaction of genetic factors and environmental exposure. The evidence for familial aggregation in psoriasis has been reported but population-based studies related to the magnitude of genetic contribution to psoriasis are rare. This study aimed to evaluate the relative risks of psoriasis in individuals with affected relatives and to calculate the proportion of genetic, shared, and non-shared environmental factors contributing to psoriasis. The study cohort included 69,828 patients diagnosed with psoriasis enrolled in National health Insurance in 2010. The adjusted relative risks (RR) for individuals with an affected first-degree relative and affected second-degree relative were 5.50 (95% CI (Confidence Interval), 5.19–5.82) and 2.54 (95% CI, 2.08–3.12) respectively. For those who have affected first-degree relatives, their RR was 1.45 (95% CI, 1.17–1.79) for Sjogren’s syndrome and 1.94 (95% CI, 1.15–3.27) for systemic sclerosis. This nationwide study ascertains that family history of psoriasis is a risk factor for psoriasis. Individuals with relatives affected by psoriasis have higher risks of developing some autoimmune diseases.


2020 ◽  
Author(s):  
Joshua M. Tybur ◽  
Laura Wesseldijk ◽  
Patrick Jern

Dozens of studies indicate that individuals more prone to experiencing disgust have stronger symptoms of anxiety disorders – especially contamination sensitivity. However, no work has informed the degree to which this relationship arises from genetic versus environmental factors. The present study fills this gap by measuring disgust proneness and contamination sensitivity in a sample of 7,199 twins and siblings of twins, including 1,411 complete twin pairs. Disgust proneness was related to contamination sensitivity, r = .32. Multivariate twin modeling revealed that genetic factors accounted for 34% and 40% of the variance in disgust proneness and contamination sensitivity, respectively, and that the correlation between the two traits reflected overlapping genetic (54%) and unshared environmental (46%) – but not shared environmental – influences. While consistent with work indicating that disgust proneness relates to contamination sensitivity, results suggest that parental-modeling hypotheses for explaining this relationship be re-evaluated.


Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1937
Author(s):  
Malgorzata Gabriela Wasniewska ◽  
Artur Bossowski

Autoimmune diseases (ADs) are characterized by a multifactorial etiology, in which genetic and environmental factors are responsible for the loss of immunological tolerance [...]


PEDIATRICS ◽  
1975 ◽  
Vol 56 (3) ◽  
pp. 459-462
Author(s):  
Robert J. Touloukian ◽  
Raymond Duncan

Hirschsprung's disease is presumably caused by intrauterine environmental or genetic factors which prevent the migration and formation of the intramural ganglion cell (IMG) in the distal colon. While the IMG is known to be particularly sensitive to anoxemia and other postnatal environmental factors, its selective loss following such stress has not been substantiated in an unoperated patient. The following report of a stressed premature newborn with the clinical and radiographic features of Hirschsprung's disease clearly documents the histologic disappearance of the IMG from the distal colon. CASE REPORT D.J. (#88-65-29), a 1,525-gm male infant, was born to a healthy 22-year-old abortus 0, gravida 1, para 0 mother following an uncomplicated 30-week gestation, ending in a spontaneous uncomplicated delivery.


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