GSE
ALLERGIC RHINITIS
Causes of allergic rhinitis
Causes of allergic rhinitis
Predisposing factors
These include a family history of similar symptoms and a personal history
of eczematous dermatitis, urticaria, and/or asthma.
Likely causes
The most blamed culprit is the allergen to which
the I.S. is over-reacting. However, since some
people are not affected by AR we should look to other explanations:
Lifestyle
A study of nearly 4,300 German
adults found that those whose partners had hay fever were at greater risk of developing
such allergies themselves, and the longer
couples lived together, the higher the hay fever risk climbed. The authors of the
study published in the journal Allergy say the findings point to the importance
of environment and lifestyle in the risk of developing allergies, since cohabitating
couples have many of these factors in common.
Diet
An immune system that has a controlled, as opposed to overzealous response
to allergens, requires
- A balance of
anti-inflammatory essential fats. In
particular, there is a general excess of inflammatory
omega-6 fatty acids typically found in grocery
store oils and processed foods, and used in restaurants.
- An adequate supply
of antioxidants to combat
reactive oxygen species
(ROS) produced during
the inflammatory process. Chronic inflammation can damage healthy
tissue (called oxidative stress). Combative antioxidants
would include:
• Vitamins A, B, C, E and flavonoids (E.g. quercetin). Found in fruits
and vegetables and supplements;
•
VITAMIN D. Produced in
skin exposed to sunlight. VITAMIN D
levels are lower in children who have allergies.
• MELATONIN.
H ormone produced in the body during a good night's sleep
• Others.
E.g. supplemental CoQ10.
• "In-house"
antioxidants SOD, CAT, and GPx. Produced
by body, but require antioxidant support
nutrients including copper,
iron,
manganese,
selenium
and zinc.
Processes associated with AR
In most cases, AR is an allergic reaction to a
specific allergen in the nasal mucosa. The allergen binds to
the immunoglobulin E (IgE) antibody (specific to the allergen e.g. cat dander)
on the surface of the immune system mast cell, which initiates:
- Initial-Response
Phase - Recruitment of numerous
chemoattractants and inflammatory mediators, which signal infiltration of eosinophils,
basophils, neutrophils, and monocytes.
- Delayed-response
phase (~2-8 hours after exposure)-inflammatory
mediators in tissue lead to damage of mucosal epithelial cells. This phase is associated
with increased sensitivity to allergens after repeated exposure and hyper-responsiveness
to irritants.
Mast cells - are
found in high concentrations in blood vessels of the sub-epithelial connective tissue
of the respiratory tract and conjunctiva. Mast cell degranulation (release of active
substances) accounts for ~ half AR symptoms.
HISTAMINE (main inflammatory
mediator in AR) - is released by mast cells in the immediate-response phase and
basophils in the delayed-response phase. When histamine binds to H1-receptors, it
increases vasodilation, capillary permeability and smooth muscle contraction,
resulting in rapid fluid leakage into nasal tissues and swollen, secretory nasal
linings
Evans R III. Epidemiology and natural history of asthma,
allergic rhinitis, and atopic dermatitis. In: Middleton E Jr, Reed CE, Ellis EF,
et al, eds. Allergy Principles and Practice 4th ed. St. Louis,
MO: Mosby; 1993:1109-1136.
