Mar 13, 2012

Primary Prevention: The Challenge of the Future

In an attempt to reverse the observed epidemiological trend, primary prevention strategies for decades aimed at avoiding risk factors and inhibiting their mechanism of action. More recently, attempts were initiated to promote protecting factors and stimulate their mechanisms of action.

Alimentary Ways to Protect
For numerous reasons, breast-feeding is the preferred method of infant nutrition; however, there is still controversy as to whether breast-feeding protects against the
development of allergic diseases.

On the basis of the available data, an “Expert Group” of the “European Academy of Allergology and Clinical Immunology” recommends exclusively breast-feeding for 4 to 6 month irrespective of family history of atopy.

For a long time, primary prevention strategies for asthma were almost exclusively focused on allergen avoidance measures early in life, which were supposed to prevent primary sensitization to both food and inhalant allergens.

For several years, the use of hydrolyzed formula was recommended as an alternative for infants, for whom breast milk was not available and who were genetically predisposed to atopic diseases. Indeed, the German Infant Nutritional Intervention (GINI) Study demonstrated that extensively as well as certain partially hydrolyzed formulas compared to unhydrolyzed infant formulas resulted in a lower incidence of atopic eczema during the first 3 years of life. This study still represents the only large and well-designed trial when comparing different formulas in relation to primary prevention of atopic dermatitis and sensitization to food proteins.

More recently, new alimentary strategies to prevent allergic manifestations are being studied. These include supplementation with probiotics (e.g., lactobacilli) or prebiotics (oligosaccharides influencing the intestinal microflora). So far, the information from the initial studies on supplementation with probiotics is inconclusive.
It will be interesting to see the outcomes of well-designed intervention studies focused on the efficacy of this approach.

Endotoxin

Microbial exposures are abundant in these environments and microbial studies investigating stables report a large variety of gram-negative and gram-positive germs as well as a diversity of molds and fungi.
In addition, nonviable parts of microbes, such as endotoxin from the outer wall
of gram-negative bacteria, are found in abundance in stables and also in elevated
concentrations in indoor environments of adjacent farmhouses.
Endotoxins are a family of molecules called lipopolysaccharides (LPS) and are intrinsic parts of the outer membranes of gram-negative bacteria. LPS and other bacterial wall components are found in high concentrations in stables, where pigs, cattle, and poultry are kept engaged with antigen-presenting cells via CD14 ligation to induce strong interleukin (IL)-12 responses. IL-12, in turn, is regarded as an obligatory signal for the maturation of naive T cells into Th1-type cells. Endotoxin concentrations were recently found to be highest in stables of farming families and
also in dust samples from kitchen floors and mattresses in rural areas in southern Germany and Switzerland.

These findings support the hypothesis that environmental exposure to endotoxins and other bacterial wall components is an important protective determinant related to the development of atopic diseases. Indeed, endotoxin levels in samples of dust from children’s mattresses were found to be inversely related to the rate of occurrence of hay fever, atopic asthma, and atopic sensitization.
On the other hand, high exposure to endotoxins may only be a surrogate marker for other bacterial products such as nonmethylated cytidine-guanosine, dinucleotides specific for prokaryotic DNA (CpG motifs). Cell wall components from atypical mycobacteria or gram-positive bacteria, such as lipoteichoic acid, are known to affect immune responses in ways similar to endotoxin.

Mar 6, 2012

Farming Environment

In farming environments where animals such as cattle, pigs, and poultry are kept, microbial products are particularly abundant. Accumulating evidence indicates that children growing up on traditional dairy farms have a significantly lower prevalence of atopic sensitization, hay fever, and asthma when compared with children from the same rural areas but not raised on farms. Interestingly, no protective effect of a farming environment was seen for the prevalence of atopic dermatitis.

Contact with livestock and poultry was found to explain much of the relation between farming and atopy. Exposure to the farm environment during the first year of life or even before birth, and the dose and duration of exposure from the first to the fifth years of life were crucial for this protective effect. Children exposed to animal stables or unpasteurized milk in the first year of life, in contrast to later exposure, had a significantly reduced prevalence of asthma, whereas
continued exposure was relevant for the protection from atopy and hay fever.

Early Exposure to Infections or Microbial Products?

One hypothesis that has attracted considerable interest is that a decline in certain childhood infections or a lack of exposure to infectious agents during the first years of life associated with smaller families in the middle class environments of industrialized countries may be causal for the recent epidemic in atopic disease and asthma. Although this hypothesis is obviously very complex, various sources of information appear to support it. Studies from several countries provide indirect evidence for the hypothesis that early exposure to viral infections, although triggering lower airway symptoms during early life, may exert long-lasting protective effects. Children born into families with several siblings, especially older siblings, have been found to have reduced risk of allergic sensitization and asthma at school age. Studies in children who attended day-care centers during infancy support this concept. Infections are known to produce long-lasting nonspecific systemic effects on the nature of the immune response to antigens and
allergens. For example, recovery from natural measles infection reduces the incidence of atopy and allergic responses to house dust mites to half the rate found in vaccinated children.
Obviously, the fact that certain infections induce a systemic and nonspecific switch to Th1 cells may be responsible for inhibiting the development of atopy during childhood.

Observations from Japan suggesting that strong positive tuberculin responses in children predict a lower incidence of asthma, lower serum IgE levels, and cytokine profiles biased toward a Th1-type were supported by animal experiments demonstrating that IgE responses to ovalbumin in mice could be down-regulated by a previous infection with bacillus Calmette-Guerin (BCG).
Unfortunately, cohort studies from Europe were unable to describe any protective
effect of BCG vaccination.
Although these observations on the relationship of immune responses to infectious agents, atopic sensitization, and disease expression are stimulating and challenging, conclusions regarding the relevance of the atopic march should be drawn with care.

In different parts of the world, completely different infectious agents have been addressed in different study settings. It appears to be fashionable to join Rook and Stanford who, in a recent review article pleaded “Give us this day our daily germs”—but which germ, at what time, under which circumstances, and at what price?

Mar 2, 2012

Lifestyle

Obviously, a long list of lifestyle-related factors possibly associated with the apparent allergy and asthma epidemic of the late twentieth and early twenty-first centuries may have relevance to the atopic march in children.

Taking into account that the risk of atopic sensitization and disease manifestation early in life is particularly high in industrialized Western countries, and that within these countries concomitant variations in the socioeconomic status and the prevalence of atopy are evident, the question arises as to what factor related to Western lifestyle may be responsible for increasing the susceptibility to atopic sensitization?

In a recent Swedish study, the prevalence of atopy in children from anthroposophic families was lower than in children from other types of families.

This led the authors to the conclusion that lifestyle factors associated with anthroposophy
(no vaccination, low exposure to antibodies, etc.) may lessen the risk of
atopy in childhood.

Several studies focusing on differences between the former socialist countries and Western European countries reported lower prevalence rates for atopy in the former East.
The differences were particularly striking in the areas with few genetic differences such as East and West Germany where it was found that the critical period during which lifestyle mainly influences the development of atopy is probably the first years of life. These observations point in the same direction as studies reporting lower prevalence rates for children born into families that have few siblings. Recent observations from Germany suggest that within the population of
an industrialized country with a Western lifestyle, high socioeconomic status must be considered as a risk factor for early sensitization and the manifestations of atopic dermatitis and allergic airway disease. Turkish migrants living in Germany exhibited higher prevalences of atopy and asthma after cultural assimilation. Differences in the intestinal microflora as a major source of microbial stimulation of the immune system in early childhood has been proposed as a possible explanation for this observation. The intestinal microflora have been shown to enhance Th1-type responses. The results of a comparative study of Estonian and Swedish children demonstrated differences in intestinal microflora. In Estonia, the typical microflora included more lactobacilli and fewer clostridia organisms that are associated with a lower presence of atopic disease. Intervention studies are needed to demonstrate the relevance of these findings and examine the effects of adding probiotics to infant formulas. In one study from Finland, which unfortunately
was not blinded, infants with milk allergy and atopic dermatitis exhibited milder symptoms and fewer markers of intestinal inflammation if they were fed lactobacilli-fortified milk formula.
Few reports have described an association between the use of antibiotics during the first 2 years of life and increased risks of asthma. It seems too early to draw final conclusions from these publications.

Immunizations against infectious diseases do not appear to influence the risk of early sensitization or development of atopy. Physicians should therefore support successful immunization programs such as those targeting measles.

Feb 23, 2012

Pollutants and Tobacco Smoke

Other environmental factors have attracted the interest of epidemiologists and experimental researchers. Although they do not serve as allergens, these factors are capable of up-regulating existing IgE responses or leading to disease manifestation or aggravation of symptoms. Guinea pig and mouse experiments suggested an increase of allergic sensitization to ovalbumin after experimental exposure to trafficor industry-related pollutants. A strong association between allergic rhinitis caused by cedar pollen allergy and exposure to heavy traffic was reported in Japan.

Important sociodemographic confounders turned out to be problems in interpreting study results. Other investigators were unable to describe any relationship between traffic exposure and the prevalence of hay fever or asthma. The role of tobacco smoke, a complex mixture of various particles and organic compounds, was extensively studied.

Recent review studies consistently demonstrate that the risk of lower airway diseases such as bronchitis, recurrent wheezing in infants, and pneumonia is increased. Whether passive tobacco smoke exposure is causally related to the development of asthma is still disputed.
Until recently, data about the risk of sensitization have been lacking. The prospective birth cohort MAS in Germany suggests that an increased risk of sensitization is found only in children whose mothers smoked up to the end of their pregnancies and continued to smoke after childbirth. In this subgroup of the cohort, a significantly increased sensitization rate of IgE antibodies to food proteins, particularly to hen’s egg and cow’s milk, was observed during infancy.
The effect of environmental tobacco smoke exposure is particularly strong in families with susceptibility for atopy

Allergen Exposure

Exposure to environmental allergens is the most extensively studied potential risk factor for sensitization and manifestation of atopy and asthma. From a number of cross-sectional studies performed in children and adults, it has become obvious that there is a close association between allergen exposure, particularly in the domestic environment, and sensitization to that specific allergen. Longitudinal studies such as the MAS (Multicenter Allergy Study) study in Germany have clearly demonstrated that during the first years of life there is a dose–response relationship between indoor allergen exposure to dust mite and cat allergens and the risk of
sensitization to cat and mites, respectively.

As far as the manifestation of atopic dermatitis and asthma are concerned, the situation is much less clear. Early studies performed by Sporik suggested that exposure of sensitized children to dust mite allergens determines not only the risk of asthma but also the time of the onset of the disease. More recent investigations by the same group, however, suggest that other factors besides allergen exposure are important in determining which children develop asthma.
In a comprehensive meta-analysis, evaluated several environmental factors said to be responsible for the incidence and severity of atopic diseases, particularly asthma. After comparing the strengths of the various effects, she concluded that on the basis of the literature, indoor allergen exposure is the environmental component with by far the strongest impact on the manifestation of asthma. In recent years, however, the paradigm that exposure induces asthma with airway inflammation via sensitization has been challenged. In several countries, the prevalence of asthma in children has been increasing independent of allergen exposure.

Data sets obtained from the MAS birth cohort suggest that while domestic allergen exposure is a strong determinant for early sensitization in childhood, it cannot be The Allergy Epidemic: A Look into the Future considered as a primary cause of airway hyper-responsiveness or asthmatic symptoms, since during the first 3 years of life the manifestation of wheeze is not related to elevated serum IgE levels or specific sensitization. Studies following up birth cohorts to adolescence have recently indicated that 90% of children with wheeze but without atopy lose their symptoms at school age and retain normal lung function in puberty. By contrast, sensitization to perennial allergens (house dust mites, cats, and dogs) developing in the first 3 years of life was associated with a loss of lung function at school age. Concomitant exposure to high levels of perennial allergens early in life aggravates this process. Such exposure also enhances the development of airway hyper-responsiveness in sensitized children with wheeze.
From these data, it can be concluded that impairment of lung function during school age is determined by continuing allergic airway inflammation beginning in the first 3 years of life.

A number of intervention studies to examine the effects of indoor allergen elimination on the incidence of asthma are currently being performed in cohorts followed prospectively from birth. The results will have a strong impact on public health policies because they will determine whether considering indoor allergen elimination as an important element of primary prevention of various atopic manifestations is meaningful. Even if the result is that other factors play major parts in determining whether an atopic child will develop asthma, so that allergen elimination as a measure of primary prevention is inefficient, reduction of allergen exposure will still remain as a very important element in secondary prevention.

Feb 21, 2012

The Atopic March

The term “atopic march” refers to the natural history of atopic manifestations, characterized
by the typical sequences of immunoglobulin E (IgE) antibody responses and clinical symptoms that appear during a certain age period, persist over years and decades, and often show a tendency for spontaneous remission with time.

Prospective cohort studies have shown that sensitization to food allergens occurs usually during the first months of life with the antibody response to cow’s milk and hen’s egg occurring most frequently. Sensitization against inhalant allergens usually develops after the first 2 years of life. Most of these children will develop IgE responses to a wide array of environmental allergens such as house dust mites, animal dander, and pollen.

Specific patterns of atopic sensitization are associated with certain atopic illnesses. Atopic eczema is primarily related to IgE responses to dietary allergen, while individuals with allergic rhinitis tend to become sensitized to seasonal outdoor allergens. Specific IgE responses in asthmatic children are usually directed against perennial and indoor allergen such as house dust mites. Several studies have shown that early sensitization during infancy is a predictor for the persistence of childhood asthma until adolescence.

In the German Multicenter Allergy Study, food sensitization before age 1 to 2 years with or without concurrent inhalant sensitization was a strong predictor for the development of asthma and airway hyper-responsiveness until school age.
Our understanding of the determinants of the natural history of allergic diseases is limited. Although a strong genetic basis for atopy and asthma has been described and several genes have been identified, which are associated with different phenotypes, a variety of modifiable environmental and lifestyle factors have been discovered in the past, which might offer future options for primary prevention.

Feb 13, 2012

How Do Steroids Treat Allergies?

Many people in the U.S. suffers from hay fever. Steroid medications don't just make life easier; they are lifesaving and are normally prescribed to be used as needed.
Sterois are also prescribed after a life-threatening health scare, such as an anaphylactic reaction.

There are several types of steroid medications, including but not limited to Prednisone, Nasacort, Nasonex, Flonase, AeroBid, Pulmicort and Beclovent.

Food and environmental allergies are both immune system responses, one to food and the other to pollens, dust and mold spores. Steroid medications suppress the immune system response, therefore minimizing inflammation, pain and discomfort.


Side effects of steroids can include weight gain, fluid retention, mood swings, increased risk of infection, suppressed adrenal gland hormone production and increased blood pressure. It is highly recommended that people on corticosteroids stay away from those with contagious infections.

Buy anabloic steroids online safe and secure.

Feb 2, 2012

The Allergy Epidemic: A Look into the Future

U. Wahn


Over the past decades, the increasing rates of allergic conditions among affluent societies have posed a heavy burden on healthcare systems. Cross-sectional studies such as the International Study of Asthma and Allergies in Childhood (ISAAC) have confirmed that atopic diseases such as atopic dermatitis, asthma, and seasonal allergic rhinoconjunctivitis represent major health problems in many countries, particularly in childhood.

During the past 2 decades, two general hypotheses have been proposed in the literature in connection with the observed increases of atopy and asthma in childhood:
- New risk factors that were not known several decades ago might have become relevant in connection with nutrition, environmental exposure, and lifestyle. Protective factors related to a more traditional lifestyles common in the past might have been lost, which could have led to increased susceptibility to atopic diseases.