Voltando á ligaçao Alergias>> Depressão:Psicose:Inflamaçao CerebralTive aqui um casal amigo, trouxeram-me bolinhos, bons por acaso. O gajo estava porreiro, ela toda rebentada, da cabeça, depressao, 43 anos. Falou do problema, ele estava calado.
Perguntei-lhe as coisas basicas, voces estao bem, isto e aquilo, trabalho, empresa, etc. tudo fino. Noto os olhos dela imensamente inchados e sintoma de muco no nariz, assoava-se etc. Perguntei se estava consitipada, disse que nao, que eram alergias, que sempre teve mas hoje em dia andava pior. Mudaram de casa ha uns meses, para um sitio mais natural, mais campo, mais natureza. Eu disse lhe logo, a tua depressao é alergica. Ela disse, ai querido, era bom. E eu disse, mas é mesmo. Como tinha o tablet á mao, mostrei-lhe umas coisas, que nao sao totalmente a resposta ao problema, mas podem ser uma pista. O que sugeri foi, se fosse possivel, sair de casa um mes para outro sitio e ver como sentia. Ainda me fez uma festinha na cabeça e disse, es tao querido tu, achas mesmo que é isso? E eu disse, nao sei se é mesmo mas é muito possivel. A parte chata é que a nivel de medicina, vao te dar bomba e mais bomba. A tua soluçao é nao abrires as janelas ou mudares de casa novamente, mas isto, depois de fazeres a experiencia.
Eu ja tinha falado aqui ha umas semanas da relaçao entre alergia e depressao.
Falar disto a um alergologista de categoria media em portugal é complicado, ele vai abanar a cabeça e dizer, voce voce anda no google.
MAs é verdade, a histamina, tem uma profunda acçao a nivel dos neurotransmissores. Sejam alergenos que produzam histamina ou ate mesmo comidas que sao ricas em histamina.
A soluçao nunca passa por retirar o agente insultuoso á pessoa,mas sim, dar-lhe um imunosupressor para continuar a comer queijo, ou poder ter cao ou gato ou viver no pó(len).
Leiam, porque se nao tiver aplicaçao pratica para voces, pode ter a alguem que conheçam, e mudam-lhe a vida, para melhor.
Vejam bem este artigo
Allergen Specific IgE, Number and Timing of Past Suicide Attempts, and Instability in Patients with Recurrent Mood Disorders.
uicide and decompensation of mental illness peak in spring and, to a lesser extent, in fall. Several recent studies reported that suicide and decompensation peaks coincided with spring and fall aeroallergen peaks. Allergic symptoms occur as the result of a complex biochemical cascade initiated by IgE antibodies (sensitization) and allergens (triggers). Animal models have shown molecular/neurochemical changes in the brain, as well as relevant behavioral chang
https://www.ncbi.nlm.nih.gov/pubmed/19043595Allergy: a risk factor for suicide?
https://www.ncbi.nlm.nih.gov/pubmed/18782509
completo
Changes in Severity of Allergy and Anxiety Symptoms Are Positively Correlated in Patients with Recurrent Mood Disorders Who Are Exposed to Seasonal Peaks of Aeroallergens
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678838/Supported by grant R21 MH075891-01A1 from the
National Institute of Mental Health (Principal Investigator: Teodor T. Postolache), by
research funds from the Johns Hopkins University Dermatology Allergy and Clinical Immunology (DACI) Reference Laboratory and by the University of Maryland General Clinical Research Center Grant M
Do mesmo autor
Airborne inflammatory factors: "from the nose to the brain".
The intranasal pathway is a direct route of communication between the environment and the brain. This pathway is currently used for the delivery of several experimental therapeutic peptides and vaccines because it bypasses the blood brain barrier. It is also a route of entrance to the brain for several viruses and toxic substances. Airborne infectious, allergic and pollution agents are among the most common inflammatory factors which may affect brain function via the brain-nose interface. The inflammatory processes triggered in the upper respiratory tract by these agents are positioned to influence the immune response of the brain and therefore, influence its function and alter behavior. Several clinical and epidemiological studies find an association between inflammatory factors affecting the intranasal pathway and neurological disorders such as multiple sclerosis, Alzheimer and Parkinson diseases as well as mental disorders including anxiety and mood disorders. However the mechanisms of interaction between the immune response in the nasal epithelium and the brain are poorly understood. This article discusses current evidence about these mechanisms and associations with neurological and mental diseases.
https://www.ncbi.nlm.nih.gov/pubmed/15599378outro
Schizophrenia (SCZ) and type 2 diabetes (T2D) are clinically associated, and common knowledge attributes this association to side effects of antipsychotic treatment. However, even drug-naive patients with SCZ are at increased risk for T2D. Dopamine dysfunction has a central role in SCZ. It is well-known that dopamine constitutively inhibits prolactin (PRL) secretion via the dopamine receptor 2 (DR2D). If dopamine is increased or if dopamine receptors hyperfunction, PRL may be reduced. During the first SCZ episode, low PRL levels are associated with worse symptoms. PRL is essential in human and social bonding, as well as it is implicated in glucose homeostasis. Dopamine dysfunction, beyond contributing to SCZ symptoms, may lead to altered appetite and T2D. To our knowledge, there are no studies of the genetics of the SCZ-T2D comorbidity focusing jointly on the dopamine and PRL pathway in the attempt to capture molecular heterogeneity correlated to possible disease manifestation heterogeneity. In this dopamine-PRL pathway-focused-hypothesis-driven review on the association of SCZ with T2D, we report a specific revision of what it is known about PRL and dopamine in relation to what we theorize is one of the missing links between the two disorders. We suggest that new studies are necessary to establish the genetic role of PRL and dopamine pathway in SCZ-T2D comorbidity.
outro
Abstract
Selective serotonin reuptake inhibitors (SSRIs) reduce platelet serotonin and are associated with increased gastrointestinal bleeding, an effect that is enhanced when taken with NSAIDs or aspirin. The best method to evaluate hemorrhagic events in patients taking SSRIs has not been determined. Platelet aggregation, which is not widely available, shows SSRI inhibition of platelet function; we tested whether a platelet function analyzer could detect SSRI inhibition of platelet function. Two groups of outpatients with mood disorders were recruited; each patient was taking a stable dose of either an SSRI or bupropion for at least 6 weeks. They were tested using the platelet function analyzer-100 (PFA-100; Dade International Inc, Miami, Fla) concomitantly with platelet aggregation. Fifty-eight patients were analyzed. We detected significant differences between the groups using aggregation methods with arachidonic acid (aggregation, P = 0.00001; release, P = 0.009) and collagen (aggregation, P = 0.016; release, P = 0.006). The PFA-100 did not detect differences between the groups or results outside the reference range. The PFA-100 does not detect the inhibitory effects of SSRIs on platelet function, but it can be used to direct evaluation of bleeding in a patient taking an SSRI. Abnormal PFA-100 results suggest additional evaluation for von Willebrand disease, other platelet inhibitory medications, or underlying intrinsic platelet
outro
Abstract
Suicide is the third-leading cause of death for adolescents between 15 and 24 years of age in the United States and its rate has been increasing. Factors that contribute to rate of, risks for, or protection against depression and suicide may be different for people from cultures with different values and health beliefs. Although typically seen as affecting Caucasians more than other groups in the U.S., the rates of suicide among African Americans, Latinos, and others have been increasing. 87 studies were reviewed looking at rates for suicide/suicidal ideation, risk factors for suicide, protective factors/coping mechanisms, service delivery/barriers to care, and specific treatment or management of suicidal thoughts for adolescents from different ethnic groups in the U.S. The following ethnic groups in the U.S. were compared: African American, Latino, Asian American, Native American/Alaskan Native, and Hawaiian American. Although studies report conflicting rates, most studies still show an overall higher risk for suicidal behavior among Caucasian youth than any other group. Rates for suicidal behavior are growing for African American teens (perhaps more in boys), Latino teens (especially Latina girls), Asian American youth, Native American youth, Alaskan Native youth, and Hawaiian American youth. Details about these differences are discussed along with recommendations for clinicians working with youth at risk for suicide from minority cultures in the U.S.
outro
The Role of Vitamin D in Atherosclerosis Inflammation Revisited: More a Bystander than a Player?Mangge H1, Weghuber D, Prassl R, Haara A, Schnedl W, Postolache TT, Fuchs D.
Abstract
Levels of 25-hydroxy vitamin D [25(OH)D] are reported to be decreased in cardiovascular disease (CVD) and in other chronic immunopathologies. Vitamin D (vitD) has been shown to be significantly linked to mortality, and is thought to be a predictor of survival. Therefore, supplementation with vitD has been suggested as an option to improve clinical outcomes. In contrast to the causal assumption, we hypothesize that the decreased vitD levels, seen in patients with CVD and chronic immunopathologies is secondary to inflammation and not as pathophysiologically relevant as currently suggested. Under these conditions, low vitD might be mainly caused by oxidative stress that results from chronic, immune-mediated vascular and systemic inflammation seen in patients with CVD. The oxidative environment most likely causes biodegradation of vitD and interferes with key enzymes, disturbing the biosynthesis of 25(OH)D and 1,25(OH)D. Thus far, no clear evidence of a beneficial effect of vitD supplements exists, beyond treating vitD deficiency to improve skeletal health. Moreover, a prolonged and/or high dose vitD supplementation, unless needed to correct actual vitD deficiency [levels of 25(OH)D<20 ng/ml)] may even be immunologically harmful by downregulating Th1 immune responses and indirectly upregulating Th2 immune activation with potential detrimental metabolic and cardiovascular effects. Large randomized controlled studies of vitD with multiple outcomes (skeletal, metabolic, cardiovascular and mental) are urgently needed.
PMID: 24329737
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