Allergy and True Allergy
Perhaps if scientists refrain from using terms like “allergy” and “true allergy”, “immunological” and “non-immunological” to describe exactly the same symptoms of allergy, the problems associated with oilseed rape/rapeseed and its effects on human health may have been resolved many years ago.
In some instances scientists appear to pooh-pooh people who have been found to suffer allergy type symptoms but have tested negative during allergy testing. The scientists tend to be almost dismissive of persons who do not respond to immunological testing but say they suffer from allergic type symptoms.
The fact that scientists often use these terms to differentiate the mechanisms of allergy symptoms clearly indicates that a serious gulf exists in scientific knowledge/teaching about immunological mechanisms and the effects of environmental factors (e.g. exposure to airborne chemicals) on the immune system.
Being a lay-person, I do not wish to convey my thoughts on allergy and the effects of environmental factors. However, I wish to point out that a number of well written books have been published on environmental allergy/illness and are readily available from good book stores.
However, I would stress that it is about time that scientists came to a consensus of opinion on the above terms and how they should used and interpreted by scientists, doctors, allergists and the general public. It would appear that the scientific literature on immunology needs to be updated to reflect general acceptance that knowledge has moved on since immunologists deliberately restricted the meaning of allergy back in 1923.
As advocated by many allergists, the term allergy should be all-encompassing and be used to describe both immunological and non-immunological reactions. The definition adopted by immunologists in 1923 is far too restrictive and cannot explain the huge increase in allergy type symptoms over the last 50 years. Furthermore, it is recognised that doctors using the immunological definition of allergy to describe or test for food allergy/sensitivity and food intolerance run into great difficulty with the explanations as these mechanisms do not fit the narrow antibody-mediated reactions defined by the immunologists.
I would argue that Scientists cannot use terms like “allergy” and “true allergy” otherwise we must also have terms like “science” and “true science”.
The definition of allergy
The term allergy was coined by Clemens von Pirquet in 1906. His original wording (translated) was:-
“For this general concept of a changed reactivity, I propose the term allergy. Allos implies deviation from the original state... a foreign substance which by one or more applications stimulate the organism to a change in reaction is an allergen. This term traces its origin to the word antigen, which implies a substance capable of giving rise to the production of antibodies. The term allergen is more far-reaching. The allergen comprises beside the antigen proper, the many protein substances which lead to no production of antibodies, but to supersensitivity.”
The term allergy was later debated and subsequently redefined (in 1923) so that its meaning was restricted to mean only antibody-mediated reactions and exclude all others. This definition is the one that has been accepted in many of the learned journals and advocated by immunologists. However, it must be stated that this definition has been strongly contested by pragmatic allergists ever since.
Pirquets defintion is supported by logic and by the subsequent demonstration that T-lymphocytes can carry immunological specificity, and by the other types of immunological damage which have since been described. During the course of reactions of all the Gell and Coombs types, inflammation may be induced, and mediators released with a variety of mainly physiological effects. Some of these mediators are many times more potent than histamine, with the potential for causing a wide range of symptoms and pathological consequences.
Allergy In The UK
Allergists in the UK are represented by two societies, namely; the British Society for Allergy and Environmental Medicine (BSAEM), and the British Society for Allergy and Clinical Immunology (BSACI).
The BSAEM endorse Pirquets all-imbracing definition of allergy and believe that reactions cannot be ignored irrespective of whether the immunological mechanisms have been fully elucidated. The BSAEM fully acknowledge that there are two overlapping sides of allergy; antibody-mediated and cell-mediated reactions.
In contrast, the BSACI consider that allergists should restrict their practice to conditions associated with antibody-mediated reactions only. This definition has effectively restricted and redefined Pirquets original definition of allergy by excluding cell-mediated reactions.
This type of allergy, often called classic allergy, sensitisation or IgE antibody-mediated allergy, is generally defined on the basis that individuals with an abnormally high level of IgE antibodies in their blood and who also respond unfavourably upon repeated exposure to common substances (eg, pollen) which do not effect most people.
Physicians (more particularly those involved in occupational medicine) have recently extended this definition to also cover exposure to biological agents and chemicals which are not normally encountered outwith the occupational setting. It is now recognised that repeated exposure to these substances can also initiate a wide range of allergic disorders in normally healthy individuals as well as susceptible individuals.
The term sensitisation is rather ambigous. Allergists and immunologists define it as a measurable antibody-mediated response to a substance [sensitiser], usually evaluated using clinical techniques like skin prick tests or RAST tests. Where as physicians in occupational medicine define it [sensitisation] in a similar way, however the allergy patient must also show measurable symptoms in addition to an immunological response.
Immunologists and allergists from both societies (the British Society for Allergy and Environmental Medicine, and the British Society for Allergy and Clinical Immunology) are very much aware that all immune system reactions are orchestrated by T-lymphocytes (T-cells), which, in basic terms, act as messengers, helpers and suppressors, thereby controlling the immunological defence against environmental factors which threaten our well being. Although T-cells do not directly control the release of antibodies, they have a fundamental role in managing the approprate level of defence against environmental factors and should therefore be extremely important when conducting allergy investigations.
Recognition that cell-mediated reactions have an immunological basis underpins Environmental Medicine (Clinical Ecology). Practitioners in environmental medicine advocate that dysfunction of the T-lymphocytes can lead to in-numerable manifestations ranging from chronic fatigue and headaches to activation and disregulation of antibody-mediated reactions.
Orthodox immunologists give lip service to environmental medicine by recognising the importance of the cell-mediated side of allergy. Immunological testing of the T-cell helper/suppressor ratio and testing of other T-cell sub-populations are now endorsed as a far more accurate method of evaluating a patients allergic status than conventional skin prick or RAST tests.
Acquired immune system dysfunction can lead to atopy
It is highly plausible that acquired immune system dysfunction in individuals could become an inherited characteristic in their future offspring. Acquired immune system dysfunction happens at cellular level and is therefore capable of being passed across the placenta, unlike antibody-mediated reactions which are very much dependant upon exposure and sensitisation in the offspring.
Acquired immune system dysfunction due to changes in our environment is a natural characteristic. Darwinists would advocate that man needs time to adapt to our chemically adulterated world. As a result of the heavy chemical assaults over such a relatively short passage of time, our bodies are failing to develop a positive tolerance to these exposures and acquired immune system dysfunction is merely a sign that we are not successfully coping with the pervasive chemicals present in our environment.
The hypothesis that cell-mediated reactions can cause normally healthy individuals to develop antibody-mediated allergy (acquired immune system dysfunction) is a valid one. It can explain why more and more people today are becoming allergic, even although they do not have a family history of allergy. The orthodox definition of allergy used by the British Society for Allergy and Clinical Immunology (BSACI) is too narrow and cannot explain this modern phenomenon, often called the disease of the 20th Century. Instead the BSACI offer weak theories like non-specific hyper-sensitivity and reject the well documented effects of chemical exposure on the immune system (cell-mediated reactions). Incidentally the BSACI also have difficulty explaining food allergy and intolerance which also cause manifestations like headache, joint pains and flu, in fact the BSACI have great difficulty explaining all manifestations that do not fit antibody-mediated reactions.
All the manifestations described above have been reported in learned journals as causal symptoms associated with chemical exposure. This association has been demonstrated during rigorous double-blind tests and confirms that environmental exposure to chemical agents, can, and does, lead to immune system dysfunction.
Burge reported that the difference between asthma induced by allergic [antibody-mediated] and presumed irritant [cell-mediated] mechanisms is becoming very blurred. It may be that irritants can also induce hypersensitivity, or that the mechanism is able to run the same course. Some regard irritant induced [cell-mediated] asthma at work as a different (and by implication less worrying) disease than antibody-mediated asthma. There is accumulating evidence that this view warrants reappraisal.
Frew reported that a considerable body of evidence has now accumulated suggesting that asthma is an immunological disorder in which T-lymphocytes (T-cells) serve to orchestrate the inflammatory response. Increased numbers of activated T-cells are found in peripheral blood during acute episodes of asthma, and their numbers decrease as the acute exacerbation resolves. Our understanding of the precise role(s) of T-cells in asthma has been hampered by a lack of knowledge about the specificity of airway T-cells in health and disease. The T-cell repertoire has a direct influence on the type and strength of immunological responsiveness to a variety of antigens and it is conceivable that the combination of T-cell repertoire and the HLA haplotype may predispose individuals to atopy. During life the expressed T-cell repertoire may be modified by proliferation of T-cells responding to antgenic stimulation. In humans an association has recently been found between responsiveness to particular major allergens and genetic polymorphisms. This study suggests that a gene (or genes) within the T-cells modifies specific IgE antibody-mediated responses.
Steele claimed that his research supported the hypothesis of the 18th Century French biologist, Jean Baptiste Lamarck, that acquired immune system characteristics could be inherited by offspring. In 1994 Steel published work based on DNA sequences which provided further support for this hypothesis though many scientists remain scepticle.
Scientists in occupational medicine are now aware that exposure to low molecular weight chemicals [this includes volatile organic compounds] well below the occupational exposure threshold limits can cause disorders like asthma and rhinitis in non-susceptible individuals. However, scientists report that the reactions are not allergic because the mechanisms are not antibody-mediated. The scientists are only partially correct because the haptenic reaction is at cellular level and causes immune system dysfunction of the T-cells which causes a bypass of the bodies biochemical communication system and thereby (in some cases) non-activation of IgE antibodies [non-antibody-mediated]. The reactions are in fact immunological in basis and can best be described as allergic. Antibody-mediated mechanisms are over-riden when foreign chemicals combine with proteins within the host. It must be realised that IgE antibodies can cause the release of histamine whilst still attached to the mast cells and therefore an elevated and measurable level of IgE antibody in the blood will not be present. With this in mind it is easy to see why orthodox physicians using conventional (RAST) techniques fail to detect and understand this type of allergic reaction.
Author - Armitage; copyright 2007