A simple guide to Homocysteine

What is homocysteine?

Homocysteine is an amino acid that is produced by the body, usually as a byproduct of consuming meat. Amino acids are naturally made products, which are the building blocks of all the proteins in the body.

Why is it important to monitor homocysteine levels?

Elevated levels of homocysteine (>10 micromoles/liter) in the blood may be associated with atherosclerosis (hardening and narrowing of the arteries) as well as an increased risk of heart attacks, strokes, blood clot formation, and possibly Alzheimer's disease.

In 1969, Dr. Kilmer S. McCully reported that children born with a genetic disorder called homocystinuria, which causes the homocysteine levels to be very high, sometimes died at a very young age with advanced atherosclerosis in their arteries. However, it was not until the 1990's that the importance of homocysteine in heart disease and stroke was appreciated.

What are the possible symptoms or features of elevated homocysteine levels?

Theoretically, an elevated level of homocysteine in the blood (hyperhomocysteinemia) is believed to cause narrowing and hardening of the arteries (atherosclerosis). This narrowing and hardening of the vessels is thought to occur through a variety of ways involving elevated homocysteine. The blood vessel narrowing in turn leads to diminished blood flow through the affected arteries.

Elevated levels of homocysteine in the blood may also increase the tendency to excessive blood clotting. Blood clots inside the arteries can further diminish the flow of blood. The resultant lack of blood supply to the heart muscles may cause heart attacks, and the lack of blood supply to the brain causes strokes.

Elevated homocysteine levels also have been shown to be associated with formation of blood clots in veins (deep vein thrombosis and pulmonary embolism). The mechanism is complex, but it is similar to the way that they contribute to atherosclerosis. In some studies, even moderate levels of homocysteine level showed higher rates of repeated incidence of blood clot formation.

What is considered a high level for homocysteine?

Homocysteine levels are measured in the blood by taking a blood sample. Normal levels are in the range between 5 to 15 micromoles (measurement unit of small amount of a molecule) per liter. Elevated levels are classified as follows:

• 15-30 micromoles per liter as moderate
• 30-100 micromoles per liter as intermediate
• Greater than 100 micromoles per liter as severe

What causes elevated homocysteine levels?

Homocysteine is chemically transformed into methionine and cysteine (similar amino acids) with the help of folic acid, vitamin B12, and vitamin B6. This transformation utilizes a set of mediator molecules (called enzymes) and happens via a delicate sequence of specific steps.

Therefore, insufficient amounts of these vitamins in the body can hamper the natural breakdown of homocysteine. In addition, if there are any deficiencies in the mediator molecules, the breakdown is also hampered. This can cause homocysteine to accumulate in the blood because its breakdown is slow and inadequate.

Can elevated homocysteine levels be genetic?

Homocysteine levels in the blood may be elevated for many reasons as briefly described in the above section. More specifically, these can be divided into severe genetic causes and other milder causes.

In the genetic condition called homocystinuria, there is a deficiency or lack of an important mediator molecule (enzymes) in the complicated homocysteine breakdown pathway. This leads to severely elevated levels of homocysteine. In this rare and serious condition, there is a constellation of symptoms that include developmental delay, osteoporosis (thin bones), visual abnormalities, formation of blood clots, and advanced atherosclerosis (narrowing and hardening of blood vessels). This condition is mainly recognized in childhood.

Milder genetic variations are more common causes of elevated homocysteine levels (hyperhomocysteinemia). In these conditions, the mediator molecules malfunction and are less efficient because of minor abnormality in their structure. They also lead to elevation of homocysteine levels, although much milder than in homocystinuria, by slowing down the breakdown of homocysteine.

Can nutritional problems cause elevated homocysteine levels?

The other more common (5%-7% of the population) and less severe type of elevated homocysteine level may be caused by nutritional deficiencies in folate, vitamin B6 and vitamin B12, chronic (long-term)kidney disease, and cigarette smoking.

As mentioned above, these vitamins are essential in the breakdown of homocysteine. In some studies, lower levels of these vitamins, especially folate, have been demonstrated in people with elevated homocysteine levels. On the other hand, other studies have suggested that adequate intake of folate, Vitamin B6, and Vitamin B12 have resulted in lowering of the homocysteine level.

How common is hyperhomocysteinemia?

Mild hyperhomocysteinemia levels are seen in about 5%-12% of the general population. In specific populations such as, alcoholics (due to poor vitamin intake) or patients with chronic kidney disease, this may be more common. The severe genetic form, homocystinuria, is rare.

How can homocysteine levels be lowered?
The consumption of folic acid supplements or cereals that are fortified with folic acid, and to a lesser extent vitamins B6 and B12, can lower blood homocysteine levels. These supplements may even be beneficial in people with mild genetic hyperhomocysteinemia to lower their homocysteine levels. However, it is noteworthy that so far there is no compelling data to support the treatment of hyperhomocysteinemia for prevention of heart disease or treatment of known heart disease or blood clots. There are many studies underway to determine whether there may be any benefit to treat high levels of homocysteine in patients with known heart disease or blood clots. Further recommendations may be available when these studies are completed.

How many vitamins should I take to lower my homocysteine level?

Daily recommended doses of folate, B vitamins, and multivitamins are generally sufficient in regard to lowering homocysteine levels. These daily doses are recommended by the Food and Drug Administration (FDA) and the doses in a specific product are printed on the label of the vitamin bottle by the manufacturer. Usually, folate supplementation is recommended at 1 milligram daily; vitamin B6 is recommended at 10 milligram per day; and vitamin B12 at one-half milligram per day.

Does lowering homocysteine levels prevent heart attacks and strokes?

Currently, there is no direct proof that taking folic acid and B vitamins to lower homocysteine levels prevents heart attacks and strokes. However, in a large population study involving women, those who had the highest consumption of folic acid (usually in the form of multivitamins) had fewer heart attacks than those who consumed the least amount of folic acid. In this study, the association between dietary intake of folate and vitamin B6 and risk of heart disease was more noticeable than between dietary intake of vitamin B12 and heart disease, which was minimal.

Many other observational studies have been performed to assess the effect of folate and the other B vitamins on heart disease. Most of these studies have concluded that oral intake of folate has been associated to lower risk of heart disease, possibly because due to lowering of homocysteine levels. The relation between oral intake of vitamin B12 and B6 and heart disease was not as obvious in many of these studies.

In one study, it was concluded that even in people with elevated homocysteine levels due to genetic reasons, oral intake of folate and possibly the other B vitamins was related to lower incidence of heart disease.

Most of these data, however, are obtained from observational studies rather than purely controlled scientific data. Therefore, it is important to mention that despite these studies suggesting an association between the intake of these vitamins and the lower incidence of heart disease, in general, there is no compelling clinical evidence to treat hyperhomocysteinemia other than homocystinuria (the severe genetic form) in regards to heart disease, stroke, or blood clots.

What should I do to prevent heart attacks and strokes?

Losing excess weight, exercising regularly, controlling diabetes and high blood pressure, lowering the bad LDL cholesterol, and stopping cigarette smoking are crucial steps in preventing heart attacks and strokes. The association between homocysteine levels and atherosclerosis is generally weaker compared to the known risk factors of diabetes, high blood pressure (hypertension), high cholesterol level, and cigarette smoking.

It is recommended that healthy adults eat more fresh fruits and vegetable, eat less saturated fat and cholesterol, and take one multivitamin daily. One multivitamin will supply 400 mcg (microgram or one-one thousandth of a gram)/day of folic acid in addition to vitamins B6, B12, and other important vitamins.

Who should undergo testing for homocysteine blood levels?

Some doctors screen for elevated homocysteine levels in patients with early onset of blood clot formation, heart attacks, strokes, or other symptoms related to atherosclerosis, especially if these patients do not have typical risk factors, such as smoking cigarettes, diabetes, high blood pressure, or high LDL cholesterol levels.

Currently, there are no official recommendations as to who should undergo testing for homocysteine blood levels. Before more scientific data become available from the currently ongoing studies, many experts do not recommend a screening test for blood homocysteine levels, even in patients with unexplained blood clot formation. In addition, the consensus recommendation is against treating elevated homocysteine levels with vitamins to prevent heart disease.

There is also no consensus as to the optimal dose of folic acid and other B vitamins for the treatment of elevated blood homocysteine levels. (For example, treatment of patients with high homocysteine levels may require higher doses of folic acid and other B vitamins than the amounts contained in a multivitamin.) Therefore, a decision regarding testing should be individualized after consulting with your doctor.

Are you allergic to Blomia tropicalis?

Latin name: Blomia tropicalis
Source material: Whole body culture
Family: Glycyphagidae
Sub family: Acari
Common names: Storage mite, Flour mite, Grain mite

Geographical distribution

Blomia tropicalis, a Storage mite, was earlier found predominantly in agricultural environments but is now being recognised as an important contributor to the allergen content in house dust in indoor urban dwellings.
B. tropicalis is a notable mite species in many parts of the world, and the most common and most important mite species in tropical countries. B. tropicalis and Dermatophagoides pteronyssinus occur in a significant percentage of homes in tropical and subtropical regions of the United States and Europe, and in Central and South America and Asia, along with the House dust mites Euroglyphus maynei and Dermatophagoides farinae. Blomia tropicalis is the 4th most common mite in the United States.

Unexpected exposure

Mites were found in 21% of 571 samples of cereal-based food products purchased at food retail outlets in the UK, and in 38% of 421 samples, derived from the 571 samples, which were examined after 6 weeks of storage in volunteers’ homes. The most common species were A. siro, T. putrescentiae, L. destructor and G. domesticus.

Allergens
In a study of 60 Taiwanese patients, B. tropicalis extract was shown to contain at least 30 protein components. The most frequently detected allergens were proteins with molecular weights of 14.3, 106.5, 94.0, 72.0, 91.9, 63.7, 100.3, 43.6, 27.3, 62.0, 34.7, 18.3, 41.1 and 21.9 kDa. The frequencies of IgE binding of 60 patient sera to those proteins were, respectively, 87.0, 65.2, 56.5, 43.4, 39.1, 39.1, 34.8, 30.4, 30.4, 17.4, 17.4, 17.4, 13.0 and 8.7%.

In a study investigating the IgE reactivity of allergens present in extracts of B. tropicalis and comparing the IgE responses to these allergens in asthmatics and patients with atopic dermatitis and allergic rhinitis, as well as in 199 non-atopic volunteer controls, 18 out of 29 protein bands present in Blomia extracts were recognised by the allergic and control sera. Of these allergens, 4 showed a high IgE binding frequency; these had molecular weights of 104, 80, 68 and 14 kDa. The 14 kDa allergen demonstrated the highest IgE binding frequency. The authors concluded that extracts from pure bodies of B. tropicalis contain 1 immunodominant and 3 important allergens.

At least 23 IgE-binding components have been demonstrated for B. tropicalis. 

The following allergens have been characterised:
Blo t 1, a Group 1 mite allergen, a cysteine protease, a major allergen, and a homologue of Der p 1.
Blo t 2, a 14.5 kDa protein, a Group 2 mite allergen

Blo t 3, a Group 3 mite allergen, a trypsin like protease

Blo t 4, a Group 4 mite allergen, an alphaamylase

Blo t 5, a 14 kDA Group 5 mite allergen, a homologue of Der p 5.

Blo t 6, chymotrypsin, a protease

Blo t 7

Blo t 8, a glutathione-S-transferase

Blo t 9, a collagenolytic serine protease

Blo t 10, a tropomyosin
Blo t 11, a Group 11 mite allergen, a paramyosin
Blo t 12, a 14.2 kDa protein
Blo t 13, a Group 13 allergen, a fatty acid binding protein
Blo t 14
Blo t 15, a chitinase
Blo t 18, a 60 kDa protein, a chitinase
Blo t 19
Blo t 20, an arginine kinase
Blo t 21
The following recombinant allergens have been produced to date: 
rBlo t 3
rBlo t 5
rBlo t 12
rBlo t 13

Recombinant Blo t 1 has been shown to have a 90% frequency of reactivity with IgE in sera from asthmatic children and a 65% frequency in sera from asthmatic adults, indicating that it represents a major allergen. Cross-reactivity between the Group 1 mite allergens of B. tropicalis (Blo t 1) and D. pteronyssinus (Der p 1) was demonstrated to be low.

Of 80 B. tropicalis-sensitive Taiwanese patients, 7% were allergic to Blo t 2. However, among sera from Brazilian and Swedish patients, more than 80% revealed sensitisation to this allergen.
Of 80 B. tropicalis-sensitive Taiwanese patients, 4.7% were allergic to Blo t 3. However, in a study of mite-allergic subjects in Singapore, the frequency of IgE reactivity to the recombinant Blot t 3 was 50%; but the IgE titer was generally low. A study in this population, using native Blo t 3 in 44 mite-allergic sera, reported an IgE reactivity frequency of 57% .
Among 80 B. tropicalis-sensitive Taiwanese patients, 7.5% were shown to be allergic to Blo t 4.

Frequencies of sensitisation to Blo t 5 in Taiwanese and Malaysian patients’ sera were shown to be 91.8% and 73.5%, respectively. Other studies have reported Blo t 5 to be a major allergen, with sensitisation rates of up to 70% in populations prone to B. tropicalis allergy. Most patients appear to be concurrently sensitised to D. pteronyssinus, and around 18% of patients may be found to be sensitised to B. tropicalis as a result of cross-reactivity of D. pteronyssinus. In a Colombian study, 24% of mite-allergic patients were shown to have IgE binding to B. tropicalis extract. A study compared the importance of 2 types of sensitisation: to B. tropicalis and D. pteronyssinus among asthma patients from Florida, Puerto Rico, and Brazil; and to D. pteronyssinus among patients from the United States and the United Kingdom. IgE antibodies to recombinant Blo t 5 were found in 45% of sera from B. tropicalis-allergic asthmatics in the group from Florida, Puerto Rico, and Brazil, compared to 69% of similar patients in the United States and United Kingdom group. In vivo and in vitro comparisons of IgE responses to B. tropicalis, D. pteronyssinus, rBlo t 5, and rDer p 5 showed that B. tropicalis has unique allergens that cause allergen-specific IgE responses, suggesting that B. tropicalis is an independent cause of sensitisation.

Blo t 5 is a major allergen of B. tropicalis, with up to 92% of allergic patients sensitised to it. Native Blo t 5 has been purified and shown to consist of multiple isoforms. In a study in Barbados, Blo t 5 sensitivity was present in 46% of 261 subjects and was associated with younger age, higher total serum IgE level, and asthma – the prevalence of asthma in the Blo t 5-sensitive subjects was more than 3-fold greater (42 vs. 13%). Der p 1 sensitivity was less common (27%) but showed similar associations with age, IgE, and asthma. Of the 261 subjects sensitised to Blo t 5, 116 were also sensitised to Der p 1; they were younger, had higher total and Blo t 5-specific IgE levels, and had more than twice the asthma prevalence as those sensitised to Blo t 5 alone (59 vs. 29%). As in other studies, Der p 1 sensitivity without Blo t 5 sensitivity was uncommon; 90% of those sensitised to Der p 1 were also sensitised to Blo t 5.

A study of asthmatics’ homes in Hong Kong concluded that Der p 1 and Blo t 5 were the major allergens found in this region, and that Blo t 5 was a more potent allergen in Hong Kong, probably reflecting the high level of exposure to B. tropicalis.
Sensitisation to Blo t 6 has been reported in 11.1% of 80 B. tropicalis-sensitive Taiwanese patients.
A study using rBlo t 10 demonstrated that up to 96% amino acid identity was shared with tropomyosin of other mites, and skin specific IgE and ELISA IgE immunoassay tests found rBlo t 10 sensitisation rates of between 20% and 29% in atopic subjects. As in the case of other specific Blomia allergens, some allergic individuals had unique IgE epitopes for Blo t 10.
Sensitisation to Blo t 11 has been reported in 10% of 80 B. tropicalis-sensitive Taiwanese patients. A study using rBlo t 11 found sensitisation in 52% of 63 sera from asthmatic patients.
Of 80 B. tropicalis-sensitive Taiwanese patients, 16.3% were allergic to Blo t 12. In a study with Bt6 (Blo t 13), the frequency of IgE binding of allergic sera was generally low (11%) and weak, with the exception of 1 serum which did show strong specific IgE reactivity.
Blo t 21 shares 39% identity with Blo t 5. It is present in the midgut and hindgut contents as well as in faecal particles of B. tropicalis. IgE antibodies to Blo t 21 were detected in 93% (40/43) of B. tropicalis sensitised individuals by means of ELISA and 95% (41/43) by means of skin reactivity in an evaluation of 43 adult patients with ongoing persistent allergic rhinitis. However, sera of 494 consecutive individuals attending outpatient allergy clinics over 18 months showed that 57.9% (286/494) were sensitised to Blo t 21. Although the majority (>75%) of sensitised individuals were co sensitised to both Blo t 5 and Blo t 21, these 2 allergens had a low to moderate degree of cross-reactivity.
A study evaluated the presence of IgE, IgG1, and IgG4 to concanavalin A-binding antigens (Bt-Con-A) isolated from B. tropicalis (Bt)-total extract in sera of 121 patients with allergic rhinitis. Skin reactivity for B. tropicalis was found in 58% of the patients. Proteins of 14-152 kDa were isolated from Bt-total, and components >27 kDa from the Bt-Con-A extract. The authors concluded that Con-A-binding components isolated from B. tropicalis constitute major allergens and are involved in both allergen sensitisation (IgE response) and homeostasis maintenance (IgG1 and IgG4 responses) (40).

IgE-mediated reactions
Several investigations have demonstrated that allergens from B. tropicalis may play an important role in sensitisation and allergic symptoms. Sensitisation to B. tropicalis has been associated with acute asthma that requires emergency room treatment both among children and adults.

B. tropicalis occurs in a significant percentage of homes in tropical and subtropical regions of South America and Asia, as well as in the United States and Europe. In these areas, B. tropicalis has been shown to be a clinically important allergenic component of house dust, inducing IgE antibody response in patients with allergic diseases such as asthma and rhinitis. In a Brazilian study, patients with atopic dermatitis showed a high degree of sensitisation to B. tropicalis, and the authors suggested that exposure to it can thus be considered a risk factor for the development of AD exacerbations.

In a study in Tampa, Florida, subjects with allergic rhinitis were challenged with B. tropicalis extracts. Ten out of 12 (83%) subjects had positive nasal challenge responses to B. tropicalis, as measured by rhinometry. The authors concluded that B. tropicalis should be considered a risk factor for allergic rhinitis when a patient is evaluated who lives in an area where it is endemic.
In studies in Lima, Peru, Cartagena, Colombia, Singapore and Malaysia, B. tropicalis was the mite most frequently detected. A study in Tampa, Florida, identified B. tropicalis in 30% of the dust samples from homes in the area.

In the Canary Islands, in a study of patients who were sensitised to 2 mite species, D. pteronyssinus and B. tropicalis, it was confirmed that individuals may react only to 1 of these, supporting the evidence that, although there is some in vitro and in vivo allergenic cross-reactivity between B. tropicalis and D. pteronyssinus, clinical symptoms induced by the inhalation of B. tropicalis and D. pteronyssinus seem to be species-specific; however, some patients may react to common allergens.

Among Thai patients, skin reactivity to D. pteronyssinus was found in 62.5% of 40 adults and 51.1% of 45 children; and to B. tropicalis in 37.5% and 40%, respectively. In a study in Taiwan and Singapore, although Der p 1, Der p 2 and Blo t5 were found to be major sensitising allergens in both countries, Blo t 5 was found to be a more potent one in Singapore than in Taiwan, probably reflecting the high level of exposure to Blomia in that country. Similarly, in a Taiwanese study of 498 atopic children aged 2 to 16, a high prevalence of sensitisation – 90.2% to D. pteronyssinus, 88.2% to D. farinae, 79.5% to D. microceras, and 76.7% to Blomia tropicalis – was documented.

In a study of 124 individuals with allergic rhinitis in Malaysia and Singapore, it was found that sensitisation to Blo t extract was positive in 73% of 124 individuals, while sensitisation to Blo t 5 was positive in 50%. Among 105 patients without rhinitis, sensitisation to Blo t extract was found in 57%, and to Blo t 5 in 23%. Of Malaysian asthmatic adults, 37% were sensitised to Blo t 5, and of the asthmatic children, 90% were sensitised to Blo t 5. The study clearly demonstrated that dual sensitisation to B. tropicalis and D. pteronyssinus was common in the general populations of Singapore and Malaysia, and that sensitisation to Blo t 5 was more prevalent than to Der p 1 and Der p 2. In a subsequent study of 175 patients with newly diagnosed allergic rhinitis, with a mean age of 7.9 years (range 2-16), 39% reported a concomitant diagnosis and/or clinical complaints of bronchial asthma, and 48% of atopic dermatitis. Skin prick test results were positive for familiar House dust mites (D. pteronyssinus and D. farinae mix) in 85% of patients, and for B. tropicalis in 62%. The authors concluded that in this population, B. tropicalis sensitisation is more prominent in children with pure respiratory allergy.

In Taiwan, 73.3% of asthmatic patients were reported to be sensitised to Blomia. Concurrent sensitisation to both B. tropicalis and D. pteronyssinus occurred in 63.3% of these patients.

A number of studies from South America have demonstrated the importance of Blomia as a sensitising agent on that continent. B. tropicalis sensitisation was shown to occur, among allergic patients, in prevalences ranging from 47% in Mexico City to 93.7% in São Paulo. Even very young children may be sensitised to this allergen, the mean age in São Paulo being 2.9 years. In Caracas the prevalence of sensitisation was 77.8%. In a repeat study in Caracas ten years later, the prevalence had increased to 91.6% for B. tropicalis, and 97.2% for D. pteronyssinus.

A high prevalence of sensitisation to B. tropicalis has also been reported in patients with persistent allergic respiratory symptoms in Venezuela. Skin reactivity in 92.2% of 115 patients was shown to either B. tropicalis or D. pteronyssinus or both; 70.4% were positive to both, 10.4% only to D. pteryonyssinus, and 11.3% only to B. tropicalis. IgE antibodies to either or both were detected in 93%, in 69.6% to both, in 11.3% only to D. pteronyssinus, and in 12.2% only to B. tropicalis. In a second Venezuelan study, 204 allergic patients attending specialised clinics in Caracas were studied. Sensitisation to B. tropicalis was documented in 90.6%. Monosensitisation to B. tropicalis occurred in 2.4%, whereas none reacted exclusively to B. kulagini.

In a Brazilian study, the presence of skin specific IgE to B. tropicalis was found in 61.8% of patients with atopic dermatitis and 83.33% of asthmatic patients, and in 12.5% of the control group. IgE antibodies were present in 44.1% of those with atopic dermatitis and in 61.9% of asthmatic patients, but in none of the control group. Among 110 Brazilian patients with allergic rhinitis with or without asthma, 56% had skin reactivity to B. tropicalis, 51% to both B. tropicalis and D. pteronyssinus, and 6% to B. tropicalis only. IgE antibodies for B. tropicalis were found in 43% of these patients.

In Brazil, nasal challenges with B. tropicalis in a group of sensitised patients were positive in 60% of cases (and 90% had positive challenges to D. pteronyssinus). In Singapore, positive nasal challenges to B. tropicalis were demonstrated; it was also shown that B. tropicalis may provoke a concomitant asthmatic response during the late-phase reaction. A clinical study was recently made of patients with allergic respiratory disease who attended an allergy clinic in Brazil. Of 212 medical records evaluated, 61.7% were of patients sensitised to Der p, 59.9% to Der f and 54.7% to B. tropicalis. The high prevalence of sensitisation is not surprising, considering the high level of B. tropicalis infestation of dwellings. In an investigation of mites and the presence of Blo t 5 on beds used by individuals with different socioeconomic backgrounds in Salvador, a major Brazilian city, 89% of the beds analyzed were found to harbour at least 1 mite species. B. tropicalis was found in 71.8% and D. pteronyssinus in 39.9%. B. tropicalis was found with a similar frequency in beds of both socioeconomic groups, whereas D. pteronyssinus was found more frequently in the beds of the wealthy than of the poor group .

In Valdivia, Chile, among 100 consecutive asthmatic paediatric patients evaluated, 80 were confirmed to have skin specific IgE to at least 1 mite species. Sixty patients had asthma and allergic rhinitis, 12 asthma and eczema, and 8 asthma, allergic rhinitis and eczema. All patients with skin reactivity for mites were positive to D. pteronyssinus, 99% to D. farinae, 92% to Euroglyphus maynei, 80% to Lepidoglyphus destructor, 73% to Tyrophagus putrescientae, 72% to B. tropicalis, 70% to Acarus siro and 68% to Chortoglyphus arcuatus. All of the patients with severe persistent asthma, 85% of those in the moderate group, and 73% of those in the mild group had skin reactivity to mites. Ninety-five percent of patients with asthma and allergic rhinitis were shown to have skin reactivity to mites, along with 92% of patients with asthma and eczema and 100% of patients with asthma, allergic rhinitis and eczema.

D. pteronyssinus, D. siboney and B. tropicalis have also been reported to be the most important allergenic mites in Cuba. A total of 88.4% of patients were positive to D. siboney, 87.1% to D. pteronyssinus, and 68.1% to B. tropicalis. Sensitisation to Dermatophagoides species was predominant, as demonstrated by the fact that 31.9% of patients showed positive SPT to either D. siboney or D. pteronyssinus only, whereas only 5.6% was sensitised solely to B. tropicalis. Nevertheless, most patients (58.6%) were polysensitised to the 3 species.

Although a very high rate of sensitisation to B. tropicalis has been found in atopic individuals in tropical and subtropical environments, studies have reported high prevalences of sensitisation in countries with temperate climates; the species Blomia tjibodas, B. kulagini, and B. thori appear to partake of this phenomenon.

In Germany, a high rate of IgE antibodies to B. tjibodas and B. tropicalis in allergic city dwellers and farmers was reported. In a study of B. tropicalis-sensitive patients in Florida, 83% had a positive nasal challenge with B. tropicalis extract, suggesting that the presence of IgE antibodies to this mite is a good predictor of allergic symptoms due to inhalation of allergens from the mite.

Other reactions Occupational allergy to Blomia kulagini present on cheese rind has been reported.
Systemic anaphylaxis can occur after the ingestion of heated or unheated mite contaminated foods. This problem may be more prevalent in tropical and subtropical countries than previously recognised. The most common symptoms following the ingestion of mite-contaminated flour were breathlessness, angioedema, wheezing, and rhinorrhoea, and these started between 10 and 240 minutes after eating.

Cyclic Vomiting Syndrome (CVS)

What is cyclic vomiting syndrome (CVS)?

  Cyclic vomiting syndrome (CVS) is a chronic functional disorder of unknown etiology that is characterized by paroxysmal, recurrent episodes of vomiting and was first described in children by Samuel Gee in 1882. Although this was initially thought to occur mostly in children, it is being recognized with increasing frequency in adults. CVS is characterized by episodes or cycles of severe nausea and vomiting that last for hours, or even days, that alternate with intervals with no symptoms. 

  Although the pathophysiology is unknown, various mechanisms such as corticotropin-releasing factor (CRF) and a heightened sympathetic response may play a role. Data also suggest a strong genetic component, with evidence of mitochondrial heteroplasmies that predispose to cyclic vomiting syndrome and other related disorders, such as migraine and chronic fatigue syndrome.

  Each episode of CVS is similar to previous ones, meaning the episodes tend to start at the same time of day, last the same length of time, and occur with the same symptoms and level of intensity. Although CVS can begin at any age, in children it starts most often between the ages of 3 and 7. Episodes can be so severe that a person has to stay in bed for days, unable to go to school or work.

  The exact number of people with CVS is unknown, but medical researchers believe more people may have the disorder than commonly thought. Because other more common diseases and disorders also cause cycles of vomiting, many people with CVS are initially misdiagnosed until other disorders can be ruled out. CVS can be disruptive and frightening not just to people who have it but to family members as well.

The Four Phases of CVS

There are 4 phases in CVS:
Symptom-free interval phase. This phase is the period between episodes when no symptoms are present.
Prodrome phase. This phase signals that an episode of nausea and vomiting is about to begin. Often marked by nausea―with or without abdominal pain―this phase can last from just a few minutes to several hours. Sometimes, taking medicine early in the phase can stop an episode in progress. However, sometimes there is no warning; a person may simply wake up in the morning and begin vomiting.
Vomiting phase. This phase consists of nausea and vomiting; an inability to eat, drink, or take medicines without vomiting; paleness; drowsiness; and exhaustion.
Recovery phase. This phase begins when the nausea and vomiting stop. Healthy color, appetite, and energy return.

What triggers CVS?

  Many people can identify a specific condition or event that triggered an episode, such as an infection. Common triggers in children include emotional stress and excitement. Anxiety and panic attacks are more common triggers in adults. Colds, allergies, sinus problems, and the flu can also set off episodes in some people.
Other reported triggers include eating certain foods such as chocolate or cheese, eating too much, or eating just before going to bed. Hot weather, physical exhaustion, menstruation, and motion sickness can also trigger episodes.

What are the symptoms of CVS?

  A person who experiences the following symptoms for at least 3 months―with first onset at least 6 months prior―may have CVS:
 - vomiting episodes that start with severe vomiting―several times per hour―and last less than 1 week
 - three or more separate episodes of vomiting in the past year
 - absence of nausea or vomiting between episodes

  A person with CVS may experience abdominal pain, diarrhea, fever, dizziness, and sensitivity to light during vomiting episodes. Continued vomiting may cause severe dehydration that can be life threatening. Symptoms of dehydration include thirst, decreased urination, paleness, exhaustion, and listlessness. A person with any symptoms of dehydration should see a health care provider immediately.

How is CVS diagnosed?

CVS is hard to diagnose because no tests―such as a blood test or x ray―can establish a diagnosis of CVS. A doctor must look at symptoms and medical history to rule out other common diseases or disorders that can cause nausea and vomiting. Making a diagnosis takes time because the doctor also needs to identify a pattern or cycle to the vomiting.

Pathophysiology

  The etiology and pathophysiology in cyclic vomiting syndrome are not unknown. Over the last decade, studies have proposed several potential brain-gut mechanisms. Migraine-related mechanisms have been proposed, and patients with cyclic vomiting syndrome have a significantly higher prevalence of family members with migraine headaches (82% vs 14% of control subjects with a chronic vomiting pattern). Furthermore, 28% of patients with cyclic vomiting syndrome whose vomiting subsequently resolved developed migraine headaches. Finally, 80% of affected patients with family histories positive for migraine respond to antimigraine therapy.

  Mitochondrial DNA (mtDNA) mutations may be involved in the pathogenesis of cyclic vomiting syndrome. Boles et al have demonstrated that, among children with cyclic vomiting syndrome and neuromuscular disease, 86% have a history of migraines on the matrilineal side. Boles and colleagues also reported a large mitochondrial DNA deletion in a single child with cyclic vomiting syndrome and have identified additional mutations concentrated in the D-loop, a hypervariable locus of the control region, in other children with cyclic vomiting syndrome.

  In children with cyclic vomiting syndrome, two mtDNA polymorphisms (16519T and 3010A) are expressed with a high degree of frequency and may serve as a surrogate marker for predisposition to the disease. The mtDNA polymorphism, 16519T, was found to be 6 times more common in pediatric cyclic vomiting syndrome than in control populations.

  Another common mtDNA polymorphism, 3010A, was noted to increase the odds ratio for developing cyclic vomiting syndrome in subjects with 16519T as much as 17 times. These mtDNA polymorphisms may account for the clustering of functional conditions and symptoms in the same individuals and families. Unlike pediatric cyclic vomiting syndrome, adult-onset cyclic vomiting syndrome is not associated with these mtDNA polymorphisms, suggesting a degree of genetic distinction.

  Children with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) syndrome are known to have both severe migraines and episodic vomiting, as in cyclic vomiting syndrome. Several children with cyclic vomiting syndrome, including 4 members of an Italian family, have been reported to have various mitochondrial mutations. Sympathetic hyperresponsivity and autonomic dysfunction also appear to contribute to the pathogenesis of cyclic vomiting syndrome. Many associated symptoms, such as pallor, flushing, fever, lethargy, salivation, and diarrhea, are mediated by the autonomic nervous system.

  Several studies support altered autonomic function in cyclic vomiting syndrome. Rashed et al and To et al demonstrated a heightened sympathetic cardiovascular tone in patients with cyclic vomiting syndrome. Kasawinah et al reported the successful use of dexmedetomidine, an alpha-2 adrenergic agonist, to treat cyclic vomiting syndrome. In a small study involving 6 children with cyclic vomiting syndrome, all patients had sympathetic autonomic dysfunction, affecting mainly the vasomotor and sudomotor systems. Symptoms developed during tilt testing in half of these patients, suggesting that these findings may play a role in the pathophysiology of this disorder.

  To evaluate this association with autonomic dysfunction, a cross-sectional study using the Ohio dysautonomia (ODYSA) questionnaire was administered to 21 patients with cyclic vomiting syndrome (3 children) and 46 patients with migraines. Both the cyclic vomiting syndrome and the migraine groups had similar comorbid conditions, with fibromyalgia noted in 38% of subjects with cyclic vomiting syndrome, orthostatic intolerance noted in 47% of subjects with cyclic vomiting syndrome, functional dyspepsia in 9.5% of subjects with cyclic vomiting syndrome, and complex regional pain syndrome in 24% of subjects with cyclic vomiting syndrome. The limitation of this study was the findings were not corroborated with either a physical examination or standard autonomic function test findings. However, the findings of orthostatic intolerance are of clinical significance because the use of pharmacological therapy such as fludrocortisone and beta blockers may be considered in these patients.

  The stress response, mediated by the hypothalamic-pituitary-adrenal (HPA) axis, can also potentially induce episodes of cyclic vomiting syndrome. Infectious, psychological, and physical stressors are known triggers of episodes. Sato et al documented increased levels of adrenocorticotropic hormone (ACTH) and cortisol, associated with extreme lethargy and hypertension, before the onset of vomiting. Furthermore, Taché has definitively shown that central CRF induces gastric stasis, emesis, or both in animals. Therefore, CRF may be a potential brain-gut mediator of cyclic vomiting syndrome that directly connects stress and vomiting. If this theory holds true, CRF receptor antagonists currently in development could theoretically ablate the vomiting by blocking the CRF receptor's vagally mediated actions.

  How these pathways fit together is still unclear. Li and Misiewicz have proposed that heightened neuronal excitability due to enhanced membrane ion permeability (ion channelopathy), mitochondrial energy deficits (due to dysfunction), or hormonal state (eg, menstrual periods) may be present.

  Both physical (infection) and psychologic stressors (excitement) can initiate a known cascade that releases hypothalamic CRF, the suspected neuroendocrine trigger, resulting in vomiting. Altered brainstem regulation of these autonomic signals may be the necessary abnormality that allows the dysautonomia to feed forward and become self-sustained for days on end.

How is CVS treated?

  Treatment varies, but people with CVS generally improve after learning to control their symptoms. People with CVS are advised to get plenty of rest and sleep and to take medications that prevent a vomiting episode, stop one in progress, speed up recovery, or relieve associated symptoms.

  Once a vomiting episode begins, treatment usually requires the person to stay in bed and sleep in a dark, quiet room. Severe nausea and vomiting may require hospitalization and intravenous fluids to prevent dehydration. Sedatives may help if the nausea continues.

  Sometimes, during the prodrome phase, it is possible to stop an episode from happening. For example, people with nausea or abdominal pain before an episode can ask their doctor about taking ondansetron (Zofran) or lorazepam (Ativan) for nausea or ibuprofen (Advil, Motrin) for pain. Other medications that may be helpful are ranitidine (Zantac) or omeprazole (Prilosec), which help calm the stomach by lowering the amount of acid it makes.

  During the recovery phase, drinking water and replacing lost electrolytes are important. Electrolytes are salts the body needs to function and stay healthy. Symptoms during the recovery phase can vary. Some people find their appetite returns to normal immediately, while others need to begin by drinking clear liquids and then move slowly to solid food.
People whose episodes are frequent and long-lasting may be treated during the symptom-free intervals in an effort to prevent or ease future episodes. Medications that help people with migraine headaches, such as propranolol (Inderal), cyproheptadine (Periactin), and amitriptyline (Elavil), are sometimes used during this phase, but they do not work for everyone. Taking the medicine daily for 1 to 2 months may be necessary before one can tell if it helps.

  The symptom-free interval phase is a good time to eliminate anything known to trigger an episode. For example, if episodes are brought on by stress or excitement, a symptom-free interval phase is the time to find ways to reduce stress and stay calm. If sinus problems or allergies cause episodes, those conditions should be treated. During an episode, anti-migraine drugs such as sumatriptan (Imitrex) may be prescribed to stop symptoms of migraine headache. However, these agents have not been studied for use in children.

What are the complications of CVS?
The severe vomiting that defines CVS is a risk factor for several complications:

• Dehydration. Vomiting causes the body to lose water quickly. Dehydration can be severe and should be treated immediately.
• Electrolyte imbalance. Vomiting causes the body to lose important salts it needs to keep working properly.
• Peptic esophagitis. The esophagus—the tube that connects the mouth to the stomach—becomes injured from stomach acid moving through it while vomiting.
• Hematemesis. The esophagus becomes irritated and bleeds, so blood mixes with vomit.
• Mallory-Weiss tear. The lower end of the esophagus may tear open or the stomach may bruise from vomiting or retching.
• Tooth decay. The acid in vomit can hurt teeth by corroding tooth enamel.

How to Help Someone with Depression

-- by GARRETT WONG DPsych (Melb), M.Sc. (Melb)

A lot of people don't realize that depression is an illness. I don't wish it on anyone, but if they would know how it feels, I swear they would think twice before they just shrug it. - Jonathan Davis

Depression is a dangerous and torturous disease and in fact, many of you would have experienced it at some point of your life be it yourself or someone around you. At times, we are at lost to how to deal with depression and at lost with what to say and how to react. Below, there are ways of helping anyone tackle depression and by merely being there and saying the right things to care. You can make a huge difference in overcoming Depression.

What are the positive things you can say and do to help someone with depression? Here are some ideas written by someone who has experienced deep depression and been helped greatly by family and friends.

1. Be On Their Side

• Someone with depression will often get defensive, so an accusatory tone is not helpful. Try to convey a sense of understanding. It isn’t helpful to say “Why can’t you just get out of bed?” Instead try “You seem to have trouble getting out of bed in the mornings. What can I do to help you in this area?”

• The person may have lost perspective on how big a problem actually is. They will find it hard to hear that what is insurmountable for them is actually not such a big deal. It is unhelpful to say “What’s your problem? You’re upset about nothing.” Instead try “You seem to be finding this issue a big deal at the moment. Can we solve it together?”

• When I was very sick, I often thought that my wife was trying to ruin my life. To counter that kind of thinking she would often say “We are a team. I am on your side.”

• Depression is an awful illness, a whole world away from pure sympathy-seeking. So you should treat it as such. “I trust you. If you had a choice in the matter you wouldn’t choose to have depression. How about we search for ways to deal with depression together?”

2. Give Plenty of Reassurance

• Many people suffering with depression feel unworthy of being loved. You need to reassure them frequently. For example “I love you for who you are. I am not going to leave you.”

• In a similar vein, they may have lost the ability to recognize their positive attributes. You might reaffirm them with “You are a sensitive person who cares for others” or “People really love you a lot. They think you’re a great person.”

• If said repeatedly and with absolute sincerity then it is helpful to say “If you ever need a friend, I am here.”

3. Give Understanding and Sympathy

• Someone with depression can spend a lot of time ruminating on their situation and feeling sorry for themselves. Pointing it out to them is not helpful. Instead, try to sympathize.

• “I can’t imagine how hard it is for you, but you have all my sympathy.”

• “All I want to do is give you a hug and a shoulder to cry on.”

• “I can’t honestly say that I know how you feel, but I want to help in any way I can.”

4. Offer to Help

• “Let me do anything you need me to do to help.”

• If you ask “What is the best thing I can do to help you right now?” don’t be offended if the reply is “Leave me alone”. Helping someone with depression can sometimes mean doing nothing. On the other hand, depression can leave a person feeling incapable of even the simplest tasks. Offering some practical help, like picking up things from the shops, could provide them with great relief.

• Well meaning people often attempt to immediately fix the problem. “Have you tried aromatherapy? There was an article about it in the paper…” . This kind of comment can come across as trivializing the illness. If you want to introduce a treatment idea, make sure you are respectful about the seriousness of depression. “It’s important that you stay on your medication and keep seeing your doctor. I’ve found some information on aromatherapy. Would you like to look into it with me?”

• While it is important to accept the person in the state they are in, don’t let it totally consume your life. Otherwise, you’ll fall in a heap and won’t be much help to anyone. You need to take care of yourself. “I am committed to you and to helping you. But I also need to eat / shop / go out for coffee / ring a friend / see a movie to recharge my batteries. Then I can look after you better.”

The Science Behind a Bad Mood and What You Can Do About It

 - written by Dr. GARRETT WONG DPsych (Melb), M.Sc. (Melb)

The Science Behind a Bad Mood and What You Can Do About It

Bad moods knock us all out of alignment now and again. But why do they happen? And is there anything we can do about it? Let's look at the science behind a bad mood, what it does in your system, and what you can do to keep it at bay.

A bad mood can appear due to all kinds of different events. Maybe you eat lunch an hour late, you get some bad customer service, or your morning commute stuffs you into road rage mode. The triggers of a bad mood are often dependent on the person and the stresses in their lives. But what's going on inside your body and your brain when you're in a temporary bad mood? Let's take a look.

The Physical and Mental Reaction of a Bad Mood

Some psychologists believe a bad mood originates due to ego depletion. This idea,founded by researcher Roy Baumeister, suggests when people use up their willpower to avoid temptation they drain cognitive resources. In effect, if you're withholding something, say, food because you're on a diet, or yelling at someone because they gave you poor customer service, it drains your brain and makes you irritated. Essentially, the harder you push your mind to avoid something, the more likely you are to get irritated.

You can think of it as a sort of stress-threshold. When you pass the line you get in a bad mood and that might manifest itself as anger, irritability, or cynicism. All of these cause your blood pressure to fluctuate. They can also increase your level of the stress hormone cortisol. This causes you to get even more flustered. In some cases it's also a reflection of an acute stress reaction. We've talked about how this works before, but it's often a cause of a bad mood because it raises blood pressure, stops digestion, and elevates your heart rate. If nothing else, it makes you feel drained and a bit cranky after a long day.

We also have evidence that a bad mood changes the way you view the world. In a 2009 study published in the Journal of Neuroscience, researchers found that being in a bad mood gives you a sense of tunnel vision and narrows your field of vision. In contrast, if you're in a good mood, you see a wider view of your surroundings.

 What You Can Do About a Bad Mood

Thankfully, getting over a bad mood isn't hard if you're willing to do a few things. We're assuming this is a temporary issue, not a long lasting case of depression, but even still, a number of these tricks can perk up even the most down-and-out.

Eat: Theoretically, doing anything you like can increase your mood, but food works in a number of ways. First, it regenerates nutrients you've lost over the course of the day. If you're in a bad mood because you haven't eaten and your blood sugar level is low, you should already feel better after a few bites. As it turns out, there's also a chance fatty acids can have a positive effect on emotion. If fatty foods aren't your thing, eating spicy foods are known to release endorphins, the same boost you get from exercising. Basically, eating can often reverse a bad mood, but be careful not to overdo it.

Exercise: Exercise increases endorphins and can naturally switch a mood from bad to good in a matter of a few minutes. You can get an endorphin boost from exercise by exerting a moderate or high level of exercise. When your breathing starts to get a bit difficult, the body releases endorphins which can be associated with feelings of happiness. The euphoria isn't long lasting, but it should be enough to make you forget about the guy who cut you off in traffic.

Listen to Music: Music can trigger a release of dopamine into your brain. This is associated with a pleasurable feeling and subsequently can turn a frown upside down in the span of a three-minute pop song. Basically, as you're following a tune, you are anticipating what's going to happen next and the reward for doing so is a little shot of pleasure.

Embrace It: A bad mood can trigger more attentive, careful thinking and allows you to zero in on specific tasks. As we mentioned above, it gives you a sort of tunnel vision, which also means your focus is dedicated to one project. Since you can pay more attention to specific details it's a good time to get started on complex projects, rework old hair-brained ideas, or tackle a task that requires your total attention. It can even give you a slight competitive advantage because your focus is driven directly toward a task. It can also make you more persuasive because it promotes concrete ideas and communications styles. It might not be the most pleasurable way to deal with a case of the Monday's, but at least you'll get a bunch of work done because of it.

Everyone has different things that put them in bad moods. It can be as complex as a stress caused by work or as simple as getting cut off in traffic. Knowing what your brain and body are doing when this happens is helpful in figuring out what to do about.

The Clique Fruits Calorie Chart

How much calories do you get from 100g (3.53 ounces) of fruits?
Below is a reference for you:

Do you realise that Durians and Avocados are not only high in calories, but also high in fat?
Dried fruits after being dried out of water contents, are concentrated with sugar.
Something to think about when planning your diet.

Clique Hypertension Diet Guide

For people who are having risks of developing hypertension, or at the prehypertension category, or already developed hypertension, diet plays a very important part of the disease prevention, control and progression.

The following are important points to take back:

1. Minimal salt intake in your daily food

Salt is used in high contents in our normal daily diet. Salt is not only used to preserve food, but also as add-on to increase taste in food. Avoiding daily consumption of processed food, instant noodles, carbonated drinks or sports drinks can reduce the amount of sodium intake. Also, you can have better control on your sodium/salt intake by making your own meals versus eating out or go to a restaurant. Using salt substitute such as vinegar and curry powder can help increase tastes without using sodium.

2. Vegetables in every meal, and a fruit a day

Vegetables and fruits has many anti-oxidants properties, vitamins and minerals that helps reducing your blood pressure.

Baked white potato, banana, avocados, tomato, grapefruit, and soy beans provide ample potassium. When potassium is low, the body retains sodium (and too much sodium raises blood pressure). When potassium is high, the body gets rid of sodium. Eating potassium-rich foods is important for maintaining a healthy balance of both minerals and, by extension, for keeping blood pressure low.

Green beans, broccoli, tofu contains high calcium, where as spinach, legumes, sunflower seeds and beans are all loaded with magnesium, key ingredients for lowering and maintaining healthy blood pressure levels. These foods also provide lots of potassium, a primary nutrient in the fight against high blood pressure.

Celery, is known not only providing calming properties, but it also helps reducing blood pressure.

Onion, spring onion, scallion, and seaweed reduces blood pressure, blood clots, and cholesterol levels in your blood.

3. Skim milk
Skim milk provides calcium and vitamin D, two nutrients that work as a team to help reduce blood pressure by about 3 to 10 percent. It could add up to about 15 percent reduction in risk for cardiovascular disease.

4. Dark chocolate
Eating about 30 calories a day was associated with a lowering of blood pressure without weight gain or other adverse effects, according to a study in the July 4, 2007, issue of JAMA (Journal of the American Medical Association).