(Text-only) Autism and TH1/TH2 Balance

Vaccinations induce antibodies by a T cell Helper 2 response (TH2). Antibodies are thought to protect the individual from parasites, toxins and other 'outside' environmental exposures. This is known as the humoral response.

TH2 is an anti-inflammatory, suppressive component of the immune system and is the dominant part of the immune system that is at work during a mother's pregnancy. Although it makes antibodies, it doesn't react with an inflammatory response that could potentially damage the developing fetus. The neonates passive immunity is therefore TH2 based.
There is also a T helper 1 (TH1) response, known as the cellular response which helps to bring about immunity within our cells to viruses, yeast, cancer by inducing an inflammatory response from the cells. TH1 response stimulates skin reactions to diseases (inflammation, rashes etc) and hypersensitivity reactions. We have both TH1 and TH2 to balance out our immune response so that we can produce antibodies to infection without incuring too much inflammation and tissue damage.

The British Medical Journal wrote:

'Th1-type cytokines tend to produce the proinflammatory responses responsible for killing intracellular parasites and for perpetuating autoimmune responses. Interferon gamma is the main Th1 cytokine. Excessive proinflammatory responses can lead to uncontrolled tissue damage, so there needs to be a mechanism to counteract this. The Th2-type cytokines include interleukins 4, 5, and 13, which are associated with the promotion of IgE and eosinophilic responses in atopy, and also interleukin-10, which has more of an anti-inflammatory response. In excess, Th2 responses will counteract the Th1 mediated microbicidal action. The optimal scenario would therefore seem to be that humans should produce a well balanced Th1 and Th2 response, suited to the immune challenge.'

Put basically, we need a balanced amount of T cell 1 and 2 in order to have a healthily functioning immune system.

What vaccination does is over-stimulate the TH2 immune system, which simultaneously suppresses TH1. This causes vaccinated individuals to become hypersensitive to toxins, allergens and bacteria while not responding to viruses, yeast and cancer. This is a large reason why we now have 1 in 3 people who get cancer and an epidemic of children with asthma, eczema, hayfever and food allergies.

BMJ also wrote:

'Many researchers regard allergy as a Th2 weighted imbalance, and recently immunologists have been investigating ways to redirect allergic Th2 responses in favour of Th1 responses to try to reduce the incidence of atopy.'

Their investigations involve developing more vaccines rather than just letting the immune system function as mother nature designed it to.

This over-activation of TH2 gives us a hypersensitive immune system that over-reacts to bacteria, toxins and environmental pollutants, increasing the likelihood of eczema, asthma, hayfever, RH arthritis, MS, type 1 diabetes, food allergies and other inflammatory diseases. The down-regulation of TH1 means that the immune system will under-respond to challenges in the cells, for instance, cancer and yeast. In addition to crazy cancer levels, many people have chronic yeast problems such as vulvodynia, intersital cystitis, recurrent candida infections, UTI's, gum infections and more.

Depression and anxiety have also been on the increase in recent decades and it isn't just because of greater awareness. Recent discoveries have found that inflammation can trigger anxious and depressed behaviours.
In 2008, researchers used BCG vaccine to induce anxious behaviour in rats. Brain, behaviour and immunity wrote:

'Although cytokine-induced sickness behavior is now well-established, the mechanisms by which chronic inflammation and depression are linked still remain elusive. Therefore this study aimed to develop a suitable model to identify the neurobiological basis of depressive-like behavior induced by chronic inflammation, independently of sickness behavior. We chose to measure the behavioral consequences of chronic inoculation of mice with Bacillus Calmette-Guerin (BCG), which has been shown to chronically activate both lung and brain indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolizing enzyme that mediates the occurrence of depressive-like behavior following acute innate immune system activation. BCG inoculation induced an acute episode of sickness (approximately 5 days) that was followed by development of delayed depressive-like behaviors lasting over several weeks. Transient body weight loss, reduction of motor activity and the febrile response to BCG were dissociated temporarily from a sustained increase in the duration of immobility in both forced swim and tail suspension tests, reduced voluntary wheel running and decreased preference for sucrose (a test of anhedonia). Moreover, we show that a distinct pattern of cytokine production and IDO activation parallels the transition from sickness to depression. Protracted depressive-like behavior, but not sickness behavior, was associated with sustained increase in plasma interferon-gamma and TNF-alpha concentrations and peripheral IDO activation. Together, these promising new data establish BCG inoculation of mice as a reliable rodent model of chronic inflammation-induced depressive-like behaviors that recapitulate many clinical observations and provide important clues about the neurobiological basis through which cytokines may have an impact on affective behaviors.'

So if you have a family history of auto-immune disease, allergies or cancer and you have depression or anxiety that isn't due to a stressful situation, you are probably chronically inflammed.
Vaccination doesn't strengthen the immune system, it skews it towards a TH2 response and this imbalance causes disease.

When vaccines were invented, no one knew anything about the TH1 and TH2 responses.

Sources: Alternative Medicine Review, Volume 8, number 3, 2003.

BMJ. 2000 Aug 12; 321(7258): 424

A study in 2006 found that autistic children had higher levels of TH1 and TH2 than neurotypical children, with a dominance of TH2. The study suggested that children with autism cannot down-regulate their TH1/TH2 system so it's always ramped up even when it is not needed. The elevation of these pro-inflammatory cytokines may be the reason why autistic children often have other illnesses such as inflammatory bowel disease and gluten allergy.

Elevated cytokine levels in children with autism spectrum disorder.

Abstract

This study compared production of IL-2, IFN-gamma, IL-4, IL-13, IL-5 and IL-10 in peripheral blood mononuclear cells from 20 children with autism spectrum disorder to those from matched controls. Levels of all Th2 cytokines were significantly higher in cases after incubation in media alone, but the IFN-gamma/IL-13 ratio was not significantly different between cases and controls. Cases had significantly higher IL-13/IL-10 and IFN-gamma/IL-10 than controls.

CONCLUSION:

Children with ASD had increased activation of both Th2 and Th1 arms of the adaptive immune response, with a Th2 predominance, and without the compensatory increase in the regulatory cytokine IL-10.

Source: J Neuroimmunol. 2006 Mar;172(1-2):198-205. Epub 2005 Dec 19.

Elevated immune response in the brain of autistic patients.

Abstract

This study determined immune activities in the brain of ASD patients and matched normal subjects by examining cytokines in the brain tissue. Our results showed that proinflammatory cytokines (TNF-alpha, IL-6 and GM-CSF), Th1 cytokine (IFN-gamma) and chemokine (IL-8) were significantly increased in the brains of ASD patients compared with the controls. However the Th2 cytokines (IL-4, IL-5 and IL-10) showed no significant difference. The Th1/Th2 ratio was also significantly increased in ASD patients.

CONCLUSION:

ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.

Source: J Neuroimmunol. 2009 Feb 15;207(1-2):111-6. doi: 10.1016/j.jneuroim.2008.12.002. Epub 2009 Jan 20.